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2 Blackwell’s Five-Minute Veterinary Consult A Abortion, Spontaneous (Early Pregnancy Loss)—Cats

Physical Examination Findings peritonitis; trauma; impending parturition or Purulent, mucoid, watery, or sanguineous dystocia vaginal discharge; dehydration, fever, CBC/BIOCHEMISTRY/URINALYSIS BASICS r r abdominal straining, abdominal discomfort. May be normal. Inflammatory leukogram DEFINITION CAUSES or stress leukogram depending on systemic r r Spontaneous abortion—natural expulsion Infectious disease response. Hemoconcentration and of fetus(es) prior to the point at which they r r Bacterial—organisms implicated in causing azotemia with dehydration. can sustain life outside the uterus. Early abortion via ascending infection include OTHER LABORATORY TESTS pregnancy loss—generalized term for any loss Escherichia coli, Staphylococcus spp., Infectious Causes of conceptus including early embryonic death Streptococcus spp., Chlamydia spp., Pasteurella r and resorption. Cytology and bacterial culture of vaginal spp., Klebsiella spp., Pseudomonas spp., discharge, fetus, fetal membranes, or uterine PATHOPHYSIOLOGY Salmonella spp., Mycoplasma spp., and r r contents (aerobic, anaerobic, and myco- r Infectious causes result in pregnancy loss Ureaplasma spp. Protozoal—Toxoplasma plasma). FeLV—test for antigens in queens r r directly by affecting the embryo, fetus, or fetal gondii Viral—FHV-1, FIV, FIP,FeLV, FPLV. using ELISA or IFA. FHV-1—IFA or PCR membranes, or indirectly by creating Non-infectious from corneal or conjunctival swabs, viral debilitating systemic disease in the queen. r r Uterine—cystic endometrial hyperplasia, isolation from conjunctival, nasal, or pharyn- r Non-infectious causes of pregnancy loss pyometra, chronic endometritis, anatomical geal swabs. FIP—submit fetal tissue for result from any factor other than infection abnormalities of the uterus, mechanical histopathology and immunohistochemistry. r r that leads to the death or premature expulsion trauma to uterus or fetus. Ovarian—early FIV—ELISA: confirm positive results with r of the conceptus (e.g., uterine disease, termination of corpora lutea function causes a Western blot. FPLV—viral isolation from inadequate maternal nutrition, endocrine decline in serum progesterone concentrations fetuses submitted for necropsy; document dysfunction, toxicity, genetic defects). resulting in early parturition/abortion. seroconversion in the queen. SYSTEMS AFFECTED Primary hypoluteoidism is rare but secondary Non-infectious Causes r r r r Endocrine Reproductive Other hypoluteoidism may result from certain drugs, To rule out anovulatory cycle, confirm prolonged stress and uterine inflammation. systems—any debilitating illness can result in r progesterone rise > 1.5 ng/mL one week r pregnancy loss. Fetal—chromosomal abnormalities following mating. Hypoluteoidism—serum resulting in abnormal or arrested development GENETICS r progesterone level < 1.0 ng/mL prior to and embryonic or fetal death. Systemic— Genetic defects are more prevalent in highly abortion indicates luteal failure but does not malnutrition or nutritional disorders such as inbred individuals; heritability of suscep- determine whether the luteal failure was taurine deficiency; vitamin A deficiency or r tibility to FIPV thought to be very high. primary or secondary Disorder of sexual toxicity; severe non-reproductive illness; INCIDENCE/PREVALENCE development can be evaluated with exogenous drug administration: estrogens, description of external genitalia, karyotype, Unknown—pregnancy frequently not glucocorticoids, PGF2𝛼, and dopamine and histopathology of reproductive tract. confirmed, owners may not recognize late agonists (cabergoline, bromocriptine) will IMAGING pregnancy loss if the queen is fastidious; early disrupt normal corpora lutea function; r embryonic death is difficult to document. fetotoxic or teratogenic drugs: Abdominal ultrasound in early gestation SIGNALMENT chemotherapeutic agents, antifungal agents, (21–25 days post-breeding) to confirm pregnancy and screen for evidence of Species some antibiotics (trimethoprim-sulfonamides, tetracyclines, gentamicin); modified live resorption. Later pregnancy, evaluate health Cat vaccines. and viability of fetus(es) and associated fluid Breed Predilections RISK FACTORS and membranes; abnormal uterine fluid Purebred cats—higher incidence of r accumulation and non-reproductive disease. Previous history of pregnancy loss r non-infectious abortion; inbreeding increases r r Radiograph— evaluates relative size, Concurrent systemic disease Recent risk of genetic disease. Predisposition to r number, and position of fetal skeletons; can trauma Purebred cat with high degree of developing FIP increased in some breeds r also be used to screen for fetal monsters, fetal inbreeding Very young or old queen including Bengal, Birman, and Himalayan. r malpresentation, and non-reproductive Previous use of progestins to suppress estrus r r disease. Mean Age and Range Malnourishment Homemade and raw Infectious abortion seen in all ages; r DIAGNOSTIC PROCEDURES COPYRIGHTEDdiets Overcrowded or unsanitary MATERIALr non-infectious abortion seen more commonly environment Genetic defects—necropsy aborted in young and aged queens. fetus(es); submit samples from aborted and r SIGNS stillborn fetus for karyotyping. Nutrition— General Comments submit sample of diet for nutritional analysis: of particular importance when queen is fed a Early embryonic death and resorption DIAGNOSIS r homemade and/or raw diet. Pedigree frequently have no clinical symptoms; any DIFFERENTIAL DIAGNOSIS analysis to evaluate inbreeding coefficient combination of historical and physical r r Evaluate cattery for vaccination protocols, examination findings may occur, with some Early pregnancy loss—failure to conceive, feeding regime, general sanitation procedures, queens displaying no symptoms. disorder of sexual development, anovulatory r and quarantine procedures for pregnant cycle Vulvar discharge—pyometra, r Historical Findings mucometra, uterine stump pyometra; queens and new arrivals. Submit Failure to deliver litter at expected time, vaginitis, metritis, cystitis; impending reproductive tract (uterus, ovaries, uterine return to estrus sooner than expected, parturition or dystocia; neoplasia or trauma of tubes) and aborted, stillborn, mummified decrease in abdominal diameter and weight urinary bladder, urethra, vagina, or uterus; fetus(es) and fetal membranes (fresh, loss, discovery of fetal material, behavior estrus—very little discharge typically seen refrigerated, on wet ice) for evaluation of r change, anorexia, vomiting, diarrhea. Abdominal straining or discomfort: urethral anatomic and pathologic changes, gross obstruction; intestinal foreign body; JWST589-A12-01 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:10 279mm×216mm

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necropsy, histopathology, cultures, and viral serum progesterone concentration and isolation. tocodynamometry. CONTRAINDICATIONS r MISCELLANEOUS Terbutaline—cardiac or respiratory disease, AGE-RELATED FACTORS pyometra, infectious disease, hypertension. r r Queens > 6 years old have higher incidence TREATMENT Progesterone in oil—diabetes, pyometra, r infectious disease, CEH. of infertility. Pregnancy loss seen most APPROPRIATE HEALTH CARE frequently in very young and old queens. r PRECAUTIONS Outpatient management: typically no r ZOONOTIC POTENTIAL medical management required for Use of tocolytics to maintain pregnancy non-infectious stable queens; primary requires accurate documentation of breeding Toxoplasma gondii hypoluteoidism—can be managed on an dates to know when treatment should be SEE ALSO r r outpatient basis with tocolytic drugs in discontinued; tocolytics used most Breeding, Timing Sexual Development combination with tocodynamometry. successfully in combination with Disorders r Surgical management: OHE for queens tocodynamometry to establish desired dosing ABBREVIATIONS interval based on increasing preterm uterine r with severe illness due to pyometra or metritis. r CEH = cystic endometrial hyperplasia activity. Terbutaline can cause hypertension r ACTIVITY ELISA = enzyme-linked immunosorbent r leading to increased hemorrhage from the r r Isolation for queens with infectious disease. assay FeLV = feline leukemia virus FHV-1 r placental sites during parturition or at the r No activity restrictions for most non- = feline herpesvirus 1 FIPV = feline r time of c-section. r infectious pregnancy losses. Restrict activity infectious peritonitis virus FIV = feline r as indicated for pregnancy loss due to trauma. POSSIBLE INTERACTIONS immunodeficiency virus FPLV = feline r r Progesterone administration during panleukopenia virus IFA = indirect DIET r pregnancy is associated with masculinization fluorescent antibody OHE = ovario- Feed commercially available diet labeled for r of female fetuses; do not administer in the = use in pregnancy. Correct diets with hysterectomy PGF2𝛼 prostaglandin F2𝛼 first half of pregnancy and use with informed inappropriate taurine or vitamin A r INTERNET RESOURCES consent thereafter. Use of tocolytics to r concentrations. Avoid feeding raw meats or www.theriojournal.com maintain pregnancy is associated with r allowing queens to hunt during pregnancy to www.whelpwise.com increased risk of dystocia, failure of normal reduce risk for ingestion of pathogenic placental separation at parturition, lack of Suggested Reading bacteria and T. gondii. mammary gland development and milk Lamm CG. Clinical approach to abortion, CLIENT EDUCATION r production, and poor maternal behavior for stillbirth, and neonatal death in dogs and Infectious diseases—verify client is follow- the first few days postpartum. cats.VetClinNorthAm:SmallAnimPract ing good vaccination protocols and disease 2012, (42)3:501–513. surveillance measures and is utilizing Pretzer SD. Bacterial and protozoal causes of quarantine facilities for pregnant queens and r pregnancy loss in the bitch and queen. new arrivals. Breeding management— FOLLOW-UP Theriogenology 2008, 70(3):320–326. discuss normal reproductive behavior and Verstegen J, Dhaliwal G, Verstegen-Onclin K. good breeding management; advise clients to PATIENT MONITORING r Canine and feline pregnancy loss due to keep detailed records related to reproductive Serial ultrasound evaluation q 5–7 days to viral and non-infectious causes: a review. performance, pedigree analysis, and social evaluate fetal viability for queens receiving Theriogenology 2008, 70(3):304–319. behavior of queens within the cattery. tocolytics. r Author Milan Hess Nutrition—discuss routine diet PREVENTION/AVOIDANCE Consulting Editor Sara K. Lyle r recommendations for breeding queens; advise Institute infectious disease prevention, r homemade diets undergo nutritional analysis. control, and surveillance plan. Replace r Client Education Handout Genetic disease—increase in inbred infertile queens with more reproductively fit individuals; many reproductive traits are r available online r individuals. Avoid exposure to abortifacient, heritable. Discuss risk of zoonotic disease teratogenic, or fetotoxic drugs. from Toxoplasma gondii. POSSIBLE COMPLICATIONS r r Depends on etiology. Metritis, endometritis, uterine rupture, sepsis, shock. r MEDICATIONS Diabetes, CEH, masculinization of female fetuses with progesterone treatment. DRUG(S) OF CHOICE EXPECTED COURSE AND PROGNOSIS r Will depend on etiology. r r Infectious disease—normal pregnancy, Amoxicillin-clavulanic acid 13.75 mg/kg repeated abortion, or infertility possible with r PO q12h or enrofloxacin 5 mg/kg/day PO viral disease. Poor prognosis for normal based on bacterial culture results. r r pregnancy in queens with severe CEH. Fair Tocolytic therapy to prevent uterine prognosis for successful pregnancy with contractions and help maintain pregnancy: treatment for primary hypoluteoidism; Terbutaline 0.03–1.0 mg PO as needed based significant monitoring required for good r on tocodynamometry; 0.03 mg/kg PO q8h if outcome. Pregnancy loss due to genetic tocodynometry not available. r abnormalities likely to recur if queen is bred Hypoluteoidism: progesterone in to tom with similar pedigree. oil—2.0–3.0 mg/kg IM as needed based on JWST589-A13-02 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:16 279mm×216mm

4 Blackwell’s Five-Minute Veterinary Consult A Abortion, Spontaneous (Early Pregnancy Loss)—Dogs

r Mycoplasma and Ureaplasma. OTHER LABORATORY TESTS r r Miscellaneous bacteria—E. coli, Serologic testing—B. canis, canine Streptococcus, Campylobacter, Salmonella. herpesvirus, and Toxoplasma, Neospora; collect BASICS r Miscellaneous viruses—distemper virus, serum as soon as possible after abortion; DEFINITION parvovirus, adenovirus. repeat testing for raising titers for canine r Loss of a fetus because of resorption in early Uterine herpesvirus, Toxoplasma, Neospora. Slide test r stages or expulsion in later stages of pregnancy. Cystic endometrial hyperplasia and for B. canis—very sensitive; negative results r PATHOPHYSIOLOGY pyometra. Trauma—acute and chronic. reliable; prevalence of false positives as high as r r r 60% (D-Tec CB®, Synbiotics Corp., Direct causes—congenital abnormality, Neoplasia. Embryotoxic drugs. r r r r (800)733-5500); PCR for B. canis now Chemotherapeutic agents. Estrogens. r infectious disease, trauma. Indirect r available; Definitive diagnosis made via Glucocorticoids—high dosages. r causes—infectious placentitis, abnormal culture. Tube agglutination test for ovarian function, abnormal uterine Ovarian r B. canis—gives titers; titers > 1:200 environment. Prostaglandins—lysis of corpora lutea. considered positive; titers from 1:50–1:200 r r SYSTEMS AFFECTED Dopamine agonists—lysis of corpora lutea considered suspicious. Agar gel r r via suppression of prolactin; bromocryptine, Reproductive. Any dysfunction of a major r immunodiffusion test for B. canis—effectively body system can adversely affect pregnancy. cabergoline. Hypoluteoidism—abnormal differentiates between false positives and true luteal function in the absence of fetal, uterine, GENETICS positives in agglutination tests; detects r or placental disease: progesterone No genetic basis for most causes of abortion. < cytoplasmic and cell surface antigens (Cornell r concentrations 1–2 ng/mL, most often seen University Animal Health Diagnostic Lymphocytic hypothyroidism—single-gene at 40–45 days gestation. r recessive trait in borzois. Laboratory, (607)253-3900). Baseline T4 Hormonal Dysfunction serum concentration (when no infectious INCIDENCE/PREVALENCE r r r Hypothyroidism; new data shows this is less agents are identified)—hypothyroidism is a True incidence unknown. Resorption common than previously thought. r r common endocrine disease and has been estimated between 11–13%, some estimates Hyperadrenocorticism. Environmental suggested as a cause for fetal wastage; role in up to 30% of at least one resorption. r factors—endocrine disrupting contaminants pregnancy loss unclear; subnormal T4 Incidence of stillbirth reported as 2.2–4.4%; have been documented in human and wildlife concentrations indicate need for further r increases with dystocia up to 22.3%. instances of fetal loss. testing (see Hypothyroidism). Serum SIGNALMENT Fetal Defects progesterone concentration (when no r r Species Lethal chromosomal abnormality. Lethal infectious agents are identified)— Dog organ defects. hypoluteoidism may cause fetal wastage; dogs depend on ovarian progesterone production Breed Predilections RISK FACTORS r throughout gestation (minimum of 2 ng/mL r Exposure of the brood bitch to carrier Familial lymphocytic hypothyroidism r r required to maintain pregnancy); collect reported in borzoi—prolonged interestrus animals Old age Hereditary factors sample and determine as soon as possible after interval, poor conception rates, abortion r abortion; in subsequent pregnancies, start midgestation, stillbirths. Many breeds weekly monitoring at week 3, which may be considered at risk for familial hypothyroidism before pregnancy can be documented with (see Hypothyroidism). DIAGNOSIS ultrasound; start biweekly sampling around Mean Age and Range the gestational age of previous loss. Pregnancy r DIFFERENTIAL DIAGNOSIS Infectious causes, pharmacologic agents r loss typically occurs during the seventh week Differentiate infectious from non-infectious r causing abortion, fetal defects—seen in all of gestation (see Premature Labor). Vaginal r causes—B. canis of immediate and zoonotic ages. Cystic endometrial hyperplasia— r culture—B. canis with positive serologic test; concern. Differentiate resorption from usually > 6 years old. Mycoplasma, Ureaplasma, other bacterial infertility—helped by early diagnosis of r agents; all except B. canis can be normal flora, Predominant Sex pregnancy. Historyofdruguseduring therefore diagnosis difficult from vaginal Intact bitches pregnancy—particularly during the first cultures alone; Salmonella associated with SIGNS trimester, or use of drugs (e.g., systemic illness in the bitch. Historical Findings dexamethasone, prostaglandins, ketoconazole, r r IMAGING Failure to whelp on time. Expulsion of griseofulvin, doxycycline, tetracycline, r Radiography—identifies fetal structures recognizable fetuses or placental tissues. dantrolene, among others) known to cause r r after 45 days of gestation; earlier, can Decrease in abdominal size; weight loss. fetal death. Vulvar discharges during r r determine uterine enlargement but cannot Anorexia. Vomiting, diarrhea. diestrus—may mimic abortion; evaluate r assess uterine contents. Behavioral changes. discharge and origin to differentiate uterine r from distal reproductive tract disease. Ultrasonography—identifies uterine size Physical Examination Findings r r Necropsy of aborted fetus, stillborn and contents; assesses fluid and its Sanguineous or purulent vulvar discharge. r puppies, and placenta(s)—enhances chances consistency; assesses fetal remains or fetal Disappearance of vesicles or fetuses of a definitive diagnosis, refrigerate but do not viability by noting heartbeats (normal, r previously documented by palpation, freeze prior to submission. History of > 200 bpm; stress, < 150 or > 280 bpm). ultrasonography, or radiography. r systemic or endocrine disease—may indicate DIAGNOSTIC PROCEDURES Abdominal straining, discomfort. r r r problems with the maternal environment. r Depression. Dehydration. Fever in Vaginoscopy—identify source of vulvar CBC/BIOCHEMISTRY/URINALYSIS some patients. discharges and vaginal lesions; use a scope of r r sufficient length (16–20 cm) to examine the CAUSES Usually normal. Systemic disease, uterine r infection, viral infection, or endocrine entire length of the vagina. Cytologic Infectious examination and bacterial culture—vagina r r abnormalities—may produce changes in Brucella canis. Canine herpesvirus. may reveal an inflammatory process (e.g., r CBC, biochemistries, or urinalysis. Toxoplasma gondii, Neospora caninum. uterine infection); technique for culture: use a JWST589-A13-02 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:16 279mm×216mm

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guarded swab culture instrument to ensure an PREVENTION/AVOIDANCE r anterior sample (distal reproductive tract is Brucellosis and other infectious agents— normally heavily contaminated with bacteria), surveillance programs to prevent introduction MEDICATIONS r or collection of secretions via transcervical to kennel. OHE—for bitches with no r catheterization. DRUG(S) OF CHOICE breeding value. Use of modified-live r vaccines (e.g., some distemper, parvovirus, PATHOLOGIC FINDINGS PGF2𝛼 (Lutalyse, dinoprost Histopathologic examination and culture of tromethamine)—uterine evacuation after etc., vaccines). fetal and placental tissue—may reveal abortion; 0.05–0.1 mg/kg SC q8–24h; POSSIBLE COMPLICATIONS r infectious organisms; tissue culture, cloporostenol (Estrumate, cloprostenol)— Untreated pyometra—septicemia, toxemia, 𝜇 r particularly of stomach contents, to identify 1–5 g/kg SC q24h; not approved for use in death. Brucellosis—discospondylitis, infectious bacterial organisms. dogs, but adequate documentation legitimizes endophthalmitis, recurrent uveitis. its use; use only if all living fetuses have been EXPECTED COURSE AND PROGNOSIS expelled. r r Antibiotics—for bacterial disease; initially Pyometra—recurrence rate during subsequent cycle is high (up to 70%) unless TREATMENT institute broad-spectrum agent; specific agent r depends on culture and sensitivity testing of pregnancy is established. CEH—recovery of fertility unlikely; pyometra common APPROPRIATE HEALTH CARE vaginal tissue or necropsy of fetus. r r r complication. Hormonal dysfunction— Most bitches should be confined and Progesterone (Regu-Mate) at 0.088 mg/kg r often manageable; familial aspects should be isolated pending diagnosis. Hospitalization (1 mL/25 kg PO q24h); progesterone in oil at r r considered. Brucellosis—guarded; of infectious patients preferred. B. canis— 2 mg/kg IM q48–72h; progesterone ® extremely difficult to successfully eliminate highly infective to dogs; shed in high numbers (Prometrium ; 10 mg/kg PO q24h, adjust infection even if combined with neutering. during abortion; suspected cases should be daily dosage based on serum progesterone)— r isolated. Outpatient medical for documented hypoluteodism only to management—medically stable patients with maintain pregnancy, must have accurate due non-infectious causes of pregnancy loss, date to know when to discontinue therapy— endocrinopathies, or endometrial disease. inadvertently prolonging gestation will result MISCELLANEOUS r Partial abortion—may attempt to salvage in fetal death. AGE-RELATED FACTORS the live fetuses; administer antibiotics if a CONTRAINDICATIONS Older bitches more likely to have CEH bacterial component is identified. Progestogen supplementation— ZOONOTIC POTENTIAL NURSING CARE contraindicated in dogs with endometrial or B. canis—can be transmitted to humans, mammary gland disease. Dehydration—use replacement fluids, especially when handling the aborting bitch supplemented with electrolytes if imbalances PRECAUTIONS and expelled tissues; massive numbers of are identified by serum biochemistries. PGF2𝛼—metabolized in the lung; side effects organisms expelled during abortion. ACTIVITY are related to smooth muscle contraction, are Pathologists should be warned when B. canis Partial abortion—cage rest generally dose-related, and diminish with each is suspected. People that are recommended, although the positive effect on injection; panting, salivation, vomiting, and immunocompromised are at greatest risk for reducing further abortion is unknown. defecation common; dosing critical (LD50 for infection. DIET dinoprost—5 mg/kg). SEE ALSO r r r No special dietary considerations for ALTERNATIVE DRUG(S) Brucellosis Hypothyroidism Infertility, r uncomplicated cases Oxytocin—1 U/5 kg SC q6–24h for uterine Female—Dogs Premature Labor r CLIENT EDUCATION evacuation; should only be considered in cases Pyometra r where uterine evacuation is desired solely Critical for B. canis—if confirmed, ABBREVIATIONS through uterine contraction. r euthanasia recommended due to lack of CEH = cystic endometrial hyperplasia r r successful treatment and to prevent spread of OHE = ovariohysterectomy PGF2𝛼 = infection; may try OHE and long-term prostaglandin F2𝛼 antibiotics; discuss surveillance program for Suggested Reading kennel situations: monthly serology for all FOLLOW-UP Givens MD, Marley MSD. Infectious causes individuals, culling any positive animals, until PATIENT MONITORING of embryonic and fetal mortality. three consecutive negative tests are obtained; r r Partial abortion—monitor viability of Theriogenology 2008, 70(3):270–285. discuss zoonotic potential. Primary uterine remaining fetuses with ultrasonography; Verstegen J, Dhaliwal G, Verstegen-Onclin K. disease—OHE is indicated in patients with monitor systemic health of the dam for Canine and feline pregnancy loss due to no breeding value; cystic endometrial r remainder of pregnancy. Vulvar viral and non-infectious causes: A review. hyperplasia is an irreversible change. r discharges—daily; for decreasing amount, Theriogenology 2008, 70(3):304–319. Infertility or pregnancy loss—may recur in odor, and inflammatory component; for Author Julie T. Cecere subsequent estrous cycles despite successful r consistency (increasing mucoid content is Consulting Editor Sara K. Lyle immediate treatment. Prostaglandin r prognostically good). PGF 𝛼—continued Acknowledgment The author and editors treatment—discuss side effects (see Abortion, 2 r for 5 days or until most of the discharge ceases acknowledge the prior contribution of Beverly Termination of Pregnancy). Infectious r (range 3–15 days). B. canis—monitor after J. Purswell. diseases—establish surveillance and control neutering and antibiotic therapy; yearly measures. serologic testing to identify recrudescence. r SURGICAL CONSIDERATIONS Hypothyroidism—treat appropriately; Client Education Handout OHE—preferred for stable patients with no neutering recommended (hereditary nature); available online breeding value. see Hypothyroidism. JWST589-A14-03 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:36 279mm×216mm

6 Blackwell’s Five-Minute Veterinary Consult A Abortion, Termination of Pregnancy

efficacy compared to midgestation but canbe less distasteful to client (less discharge and r BASICS DIAGNOSIS recognizable fetuses are not passed). PGF2𝛼 r and bromocriptine given in combination— DEFINITION Confirm pregnancy first, less than 40% of improves efficacy of either drug given alone. Termination of an unwanted pregnancy. May mismated bitches become pregnant: NURSING CARE ◦ Abdominal palpation (bitch: 31–33 days be accomplished by drugs that alter embryo N/A transport in the oviduct impeding after LH surge; queen: 21–25 days after ◦ ACTIVITY establishment of a pregnancy, and/or cause breeding). Transabdominal ultrasound > luteal regression, terminating an established (bitch: 25 days after LH surge; queen: Normal > ◦ pregnancy. Due to their possible side effects 16 days after breeding). Abdominal DIET > (CEH, aplastic anemia and bone marrow radiographs (bitch: 45 days after LH surge; Avoid feeding prior to each treatment and for > ◦ suppression), drugs that impair embryonic queen: 38 days after breeding). Serum 1–2 hours after treatments (reduces nausea > transit through the oviduct (estrogens) are not relaxin concentration in the bitch ( 28 days and vomiting). ® commonly used or recommended. after LH surge) (Witness Relaxin, Synbiotics/ CLIENT EDUCATION Zoetis Corp., http://synbiotics.com/index.html; PATHOPHYSIOLOGY r r (800)733-5500). Ascertain that a breeding Discuss patient’s reproductive future with After fertilization the embryo travels the owner. If no litters are desired, then OHE is took place; a tie in the bitch and coital r oviduct in a timely manner before entering “after-reaction” in the queen. the best option. Discuss with the client the the uterus. Impaired embryo transport potential side effects of the treatment options; DIFFERENTIAL DIAGNOSIS through the oviduct leads to embryonic r r r reach a mutual agreement on the treatment Hydrometra Mucometra Hematometra degeneration and implantation abnormalities. r r plan. In the dog and cat, pregnancy maintenance is Pyometra Pseudopregnancy SURGICAL CONSIDERATIONS dependent on progesterone production from CBC/BIOCHEMISTRY/URINALYSIS r OHE is recommended for patients with no the corpora lutea. In dogs and cats, Within normal limits during first half of r reproductive value or when owners do not maintenance of the corpora lutea during the pregnancy in healthy patients. Decrease in desire future litters. second half of gestation is also supported by PCV during second half of pregnancy in prolactin. Drugs that cause luteal regression, bitches and queens is normal. r antagonize PRL, and/or compete with Recommended as screening test prior to progesterone receptors will terminate treatment in patients with suspected MEDICATIONS pregnancy. underlying disease. SYSTEMS AFFECTED OTHER LABORATORY TESTS DRUG(S) OF CHOICE r r r r r Cardiovascular Digestive Neurologic Vaginal cytology—determines stage of Confirmation of pregnancy before initiating (caused by drugs used for treatment) any of the treatment protocols suggested r r estrous cycle and presence of sperm (absence Reproductive Respiratory does not rule out a previous breeding). below is recommended. Lengths of treatment GENETICS Methods to increase detection of sperm: suggested may vary; treatments should be continued until abortion is complete. N/A infuse and recover 5–10 mL of saline from ◦ PGF 𝛼: causes luteal regression with INCIDENCE/PREVALENCE anterior vagina using standard AI pipette, 2 centrifuge, examine pellet; collect routine subsequent decline in progesterone N/A cytology and allow swab to sit in 1–2 mL of concentration, cervical relaxation, and GEOGRAPHIC DISTRIBUTION saline, express fluid, centrifuge, examine uterine contractions; bitches and cats low r 𝜇 N/A pellet. Serum progesterone concentration dose protocol: 10 g/kg SC q6h for determines if the female is in diestrus and 7–10 days or until pregnancy terminated SIGNALMENT 𝜇 monitors luteal regression during treatment. (in the bitch), then 25 g/kg q6h for Species 𝜇 IMAGING 1–2 days; then 50 g/kg q6h for 3–4 days Dog and cat r (the queen is more resistant to the luteolytic Transabdominal ultrasound (method of Breed Predilections effects of PGF2𝛼 than bitches—often higher choice): diagnose pregnancy and monitor N/A doses for longer periods are required); bitch uterine evacuation during treatment. standard dose protocol: 100 𝜇g/kg SC q8h Mean Age and Range r Abdominal radiographs. for 2 days, then 200 𝜇g/kg SC q8h until Postpubertal bitch and queen PATHOLOGIC FINDINGS pregnancy termination; queens: Predominant Sex N/A 0.5–1 mg/kg SC q12h every other day > Pregnant bitch or queen day 40, or 2 mg/cat IM q24h for 5 days > SIGNS day 33. r ◦ Depends on stage of gestation: ◦ None Cloprostenol (prostaglandin analogue): 𝜇 ◦ Vaginal discharge ◦ Fetal expulsion TREATMENT bitches: 2.5 g/kg SC q8 or q12h every CAUSES 48 hours until pregnancy termination APPROPRIATE HEALTH CARE (∼6 days after start of treatment). r r r Impaired oviductal transport Luteal Physical examination before initiation of ◦ Dexamethasone: mode of action is r r regression Progesterone receptor antagonism treatment. Monitor 30–60 minutes after unknown; bitches: 0.2 mg/kg PO q8–12h RISK FACTORS treatment for side effects (vomiting, for 5 days, then decreasing from 0.16 to N/A defecation, hypersalivation, hyperpnea, 0.02 mg/kg over the last five days; r micturition, tachycardia). Pregnancy status treatment failures not uncommon. in early diestrus is unknown; ultrasound ◦ Cabergoline (PRL antagonist): causes confirmation of pregnancy is not possible luteal regression; bitches: 1.65 𝜇g/kg SC r until ∼4 weeks after breeding. Treatment on q24h for 5 days or 5 𝜇g/kg PO q24h for day 6–10 of diestrus—may have reduced 5days> day 40; queens: 1.65 𝜇g/kg SC for JWST589-A14-03 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:36 279mm×216mm

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5days> day 30 or 5 𝜇g/kg PO q24h for ALTERNATIVE DRUG(S) EXPECTED COURSE AND PROGNOSIS r r 5days> day 35. The following drugs are recommended for The interestrous interval in bitches treated ◦ Bromocriptine (PRL antagonist): causes use in bitches but not available in the United with prostaglandins and PRL inhibitors may luteal regression; bitches: 50–100 𝜇g/kg States: ◦ Mifepristone (RU486; progestin and be shortened (∼1 month). Queens may q12h IM or PO for 4–7 days > day 35 glucocorticoid receptor antagonist): resume estrous behavior 7–10 days after r (50% effective); vomiting common side 2.5 mg/kg PO q12h for 4–5 days > day 32 of pregnancy termination. Subsequent estrus effect, reduce dose and give with meal. pregnancy (dog); no side effects have been fertility is not affected. ◦ Cloprostenol and cabergoline reported. ◦ Aglepristone (progestin and combination: bitches: cabergoline 5 𝜇g/kg glucocorticoid receptors antagonists): PO q24h for 10 days plus cloprostenol 10 mg/kg SC q24h for 2 days > 32 days 2.5 𝜇g/kg SC at start of treatment or post-LH surge (dog); pregnancy is terminated MISCELLANEOUS 1 𝜇g/kg SC at start of treatment and at day in 4–7 days; mild reaction at injection site 5 of treatment; treatment should be have been reported; mild vaginal discharge ASSOCIATED CONDITIONS initiated > 28 days post-LH surge; queen: may be observed. ◦ Aglepristone and N/A cabergoline 5 𝜇g/kg PO q24h plus cloprostenol combination: aglepristone AGE-RELATED FACTORS 𝜇 > cloprostenol 5 g/kg SC q48h ( 30 days (10 mg/kg SC) combined with cloprostenol N/A after breeding) until abortion is complete (1 𝜇g/kg SC) q24h for 2 days > 25 days ZOONOTIC POTENTIAL (∼ 9 days). pregnancy; pregnancy is terminated within ◦ Cloprostenol and bromocriptine 6 days. Side effects after treatment include N/A combination: bitches; bromocriptine vomiting and diarrhea. Vaginal discharge may PREGNANCY/FERTILITY/BREEDING 30 𝜇g/kg q8h PO for 10 days plus be observed. ◦ Aglepristone (10 mg/kg SC, N/A 𝜇 𝜇 cloprostenol 2.5 g/kg SC or 1 g/kg SC at q24h for 2 days) with intravaginal misoprostol SYNONYMS start of treatment and at day 5 of treatment; (200–400 𝜇g, depending on body size) daily Induced abortion treatment should be initiated > 28 days until abortion complete; abortion complete post-LH surge. within 7 days. Vomiting, diarrhea, polydipsia, SEE ALSO CONTRAINDICATIONS anorexia not observed with this regimen Breeding, Timing r ◦ GnRH antagonists (Acyline; blocks GnRH ABBREVIATIONS PGF2𝛼 and analogues: animals with r receptors at the pituitary gland, causing a CEH = cystic endometrial hyperplasia respiratory disease (bronchoconstriction); do r r decline in gonadotropins concentration): a GnRH = gonadotropin-releasing hormone not administer intravenously. Cabergoline 𝜇 r r single treatment with 110–330 g/kg SC is LH = luteinizing hormone OHE = and bromocriptine: avoid administration in r animals hypersensitive to ergot alkaloids; use recommended (dog); pregnancy is terminated ovariohysterectomy PCV = packed cell within 6–10 days after treatment; r with caution in patients with significantly volume PGF 𝛼 = prostaglandin F 𝛼 r r 2 2 impaired liver function. Estrogens may prepartum-like behavior has been observed; PRL = prolactin cause cystic endometrial hyperplasia, abortion may be followed by serosanguineous vaginal discharge for 2–3 days; not yet Suggested Reading pyometra, and bone marrow suppression Gobello C, Castex G, Corrada Y, Klima L, leading to pancytopenia. available in the US (currently in Phase I clinical trials for prostate cancer in men). De la Sota RL, Rodriquez R. Use of PRECAUTIONS prostaglandins and bromocriptine mesylate r PGF2𝛼 and analogues: side effects are for pregnancy termination in bitches. J Am dose-dependent and include vomiting, Vet Med Assoc 2002, 220(7):1017–1019. defecation, dyspnea, tachycardia, salivation, FOLLOW-UP Eilts BE. Pregnancy termination in the bitch restlessness, and anxiety; side effects subside and queen. Clin Tech Small Anim Pract within 60 minutes; the severity of effects can PATIENT MONITORING 2002, 17:116–123. be attenuated with premedication (> 15 In animals treated with luteolytic drugs FieniF,DumonC,TainturierD,BruyasJF. minutes) with a combination of atropine (prostaglandins and PRL antagonists), Clinical protocol for pregnancy termination (0.025 mg/kg); use extreme caution in dogs progesterone assays and transabdominal in bitches using prostaglandin F2𝛼.JReprod and cats with preexisting cardiopulmonary, Fertil Suppl 1997, 51:245–250. r ultrasound examinations should be performed liver, and renal diseases. Dexamethasone: to monitor decrease of serum progesterone Johnston SD, Root Kustritz MV, Olson PNS. polydipsia, polyuria, and polyphagia are concentration and complete evacuation of Prevention and termination of canine reported side effects. Long- term uterine contents. In patients treated with pregnancy. In: Canine and Feline administration has been associated with Theriogenology. Philadelphia: Saunders, r progesterone receptor antagonist drugs, hyperadrenocorticism. Cabergoline and transabdominal ultrasound examinations are 2001, pp. 168–192. bromocriptine: should be administered with recommended to monitor complete Johnston SD, Root Kustritz MV, Olson PNS. caution in patients with impaired liver evacuation of the uterus. Prevention and termination of feline function. Side effects may include vomiting PREVENTION/AVOIDANCE pregnancy. In: Canine and Feline and anorexia; prolonged use (> 2 weeks) may r Theriogenology. Philadelphia: Saunders, OHE for bitches and queens not intended cause coat color changes. r 2001, pp. 447–452. for breeding. Estrus suppression or Author Jose A. Len POSSIBLE INTERACTIONS confinement of bitches and queens intended r Consulting Editor Sara K. Lyle PGF2𝛼 and analogues: effect may be for breeding during a later cycle to avoid reduced by concomitant administration of mismating. progestins; use may enhance effects of r POSSIBLE COMPLICATIONS Client Education Handout oxytocin. Cabergoline and bromocriptine: Pregnancy termination may not be achieved available online cabergoline effects may be reduced with after one treatment protocol and continuation concomitant treatment with dopamine (D ) 2 or change in treatment protocol may be antagonists; avoid concomitant treatment necessary. with hypotensive drugs. JWST589-A15-04 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:24 279mm×216mm

8 Blackwell’s Five-Minute Veterinary Consult A Abscessation

r r History of traumatic insult or previous Neoplasia—variable growth; consistent; infection. painful. r A rapidly appearing painful swelling with or Draining Tracts BASICS r without discharge, if affected area is visible. Mycobacterial disease r DEFINITION Physical Examination Findings Mycetoma—botryomycosis, actinomycotic r An abscess is a localized collection of purulent Determined by the organ system or tissue mycetoma, eumycotic mycetoma r exudate contained within a cavity. affected. Neoplasia r r PATHOPHYSIOLOGY Classic signs of inflammation (heat, pain, Phaeohyphomycosis r r swelling, and loss of function) are associated Sporotrichosis Bacteria are often inoculated under the skin r with specific anatomic location of the abscess. Systemic fungal infection—blastomycosis, via a puncture wound; the wound surface r then seals. Inflammation and discharge from a fistulous coccidioidomycosis, cryptococcosis, r When bacteria and/or foreign objects persist tract may be visible if the abscess is superficial histoplasmosis, trichosporosis and has ruptured to an external surface. in the tissue, purulent exudate forms and r CBC/BIOCHEMISTRY/URINALYSIS collects. A variably sized, painful mass of fluctuant to r r CBC—normal or neutrophilia with or Accumulation of purulent exudates—if not firm consistency attached to surrounding without regenerative left shift. Neutropenia tissues may be palpable. quickly resorbed or discharged to an external r and degenerative left shift if sepsis present. Fever if abscess is not ruptured and draining. r surface, stimulates formation of a fibrous r Urinalysis and serum chemistry capsule; may eventually lead to abscess Sepsis occasionally, especially if abscess profile—depends on system affected. r rupture. ruptures internally. Prostatic—pyuria. r r Prolonged delay of evacuation—formation CAUSES Liver and/or pancreatic—high liver enzymes r of a fibrous abscess wall; to heal, the cavity Foreign objects. and/or total bilirubin. r r must be filled with granulation tissue from Pyogenic bacteria—Staphylococcus spp.; Pancreatic (dogs)—high amylase/lipase. r which the causative agent may not be totally Escherichia coli; 𝛽-hemolytic Streptococcus Diabetes mellitus—persistent eliminated; may lead to chronic or spp.; Pseudomonas; Mycoplasma and hyperglycemia and glucosuria. intermittent discharge of exudate from a Mycoplasma-like organisms (l-forms); OTHER LABORATORY TESTS draining sinus tract. r Pasteurella multocida; Corynebacterium; FeLV and FIV—for cats with recurrent or SYSTEMS AFFECTED Actinomyces spp.; Nocardia; Bartonella. r slow-healing abscesses. r r Skin/Exocrine—percutaneous (cats > dogs); Obligate anaerobes—Bacteroides spp.; CSF evaluation—increase in cellularity and anal sac (dogs > cats) Clostridium spp.; Peptostreptococcus; protein expected with brain abscess. r r Reproductive—prostate gland (dogs > cats); Fusobacterium. Adrenal function— evaluate for mammary gland RISK FACTORS hyperadrenocorticism. r r Ophthalmic—periorbital tissues Anal sac—impaction; anal sacculitis. r r IMAGING Hepatobiliary—liver parenchyma Brain—otitis interna sinusitis oral infection. r r r Radiography—soft-tissue density mass in Gastrointestinal—pancreas (dogs > cats) Liver—omphalophlebitis sepsis. r affected area; may reveal foreign body. r GENETICS Lung—foreign object aspiration bacterial Ultrasonography—determine if mass is pneumonia. N/A r fluid filled or solid; determine organ system Mammary gland—mastitis. INCIDENCE/PREVALENCE r affected; reveal flocculent-appearing fluid Periorbital—dental disease; chewing of characteristic of pus; may reveal foreign N/A wood or other plant material. r object. GEOGRAPHIC DISTRIBUTION Percutaneous—fighting, trauma, or surgery. r r Echocardiography—helpful for diagnosis of Prostate gland—bacterial prostatitis. N/A r pericardial abscess. r SIGNALMENT Immunosuppression—FeLV/FIV infection, CT or MRI—helpful for diagnosis of brain immunosuppressive chemotherapy, acquired abscess. Species or inherited immune system dysfunctions, Cat and dog underlying predisposing disease (e.g., diabetes DIAGNOSTIC PROCEDURES Breed Predilections mellitus, chronic renal failure, Aspiration r N/A hyperadrenocorticism). Reveals a red, white, yellow, or green liquid. r Protein content > 2.5–3.0 g/dL. Mean Age and Range r N/A Nucleated cell count—3,000–100,000 (or more) cells/𝜇L; primarily degenerative Predominant Sex DIAGNOSIS neutrophils with lesser numbers of Mammary glands (female); prostate gland macrophages and lymphocytes. r (male) DIFFERENTIAL DIAGNOSIS Pyogenic bacteria—may be seen in cells and SIGNS Mass Lesions free within the fluid. r r General Comments Cyst—less or only transiently painful; If the causative agent is not readily r slower growing. identified with a Romanowsky-type stain, Determined by organ system and/or tissue r affected. Fibrous scar tissue—firm; non-painful. specimens should be stained with an acid-fast r r Associated with a combination of Granuloma—less painful; slower growing; stain to detect mycobacteria or Nocardia and generally firmer without fluctuant center. PAS stain to detect fungus. inflammation (pain, swelling, redness, heat, r and loss of function), tissue destruction, Hematoma/seroma—variable pain (depends Biopsy r and/or organ system dysfunction caused by on cause); non-encapsulated; rapid initial Sample should contain both normal and accumulation of exudates. growth but slow increase once full size is abnormal tissue in the same specimen. r Historical Findings attained; unattached to surrounding tissues; Impression smears—stained and examined. r r Often presented for nonspecific signs such fluctuant and fluid filled initially but more Tissue—submit for histopathologic as lethargy and anorexia. firm with organization. examination and culture. JWST589-A15-04 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:24 279mm×216mm

Canine and Feline, Sixth Edition 9

(Continued) Abscessation A

r Contact the diagnostic laboratory for SURGICAL CONSIDERATIONS EXPECTED COURSE AND PROGNOSIS r specific instructions. Appropriate debridement and drainage— Depends on organ system involved and Culture may need to leave the wound open to an amount of tissue destruction. r Affected tissue and/or exudate—aerobic and external surface; may need to place surgical anaerobic bacteria and fungus. drains. r r Blood and/or urine—isolate bacterium Early drainage—to prevent further tissue responsible for possible sepsis. damage and formation of abscess wall. MISCELLANEOUS r r Bacterial sensitivity. Remove any foreign objects(s), necrotic tissue, or nidus of infection. ASSOCIATED CONDITIONS PATHOLOGIC FINDINGS r FeLV or FIV infection r r Pus-containing mass lesion accompanied by Immunosuppression inflammation. r AGE-RELATED FACTORS Palpable—variably firm or fluctuant mass. r Ruptured—may see pus draining directly MEDICATIONS N/A from the mass or an adjoining tract. DRUG(S) OF CHOICE ZOONOTIC POTENTIAL r r Exudate—large numbers of neutrophils in r Minimal for pyogenic bacteria. Antimicrobial drugs—effective against the r various stages of degeneration; other infectious agent; gain access to site of Mycobacteria and systemic fungal infections inflammatory cells; necrotic tissue. infection. carry some potential. r r Surrounding tissue—congested; fibrin; large Broad-spectrum agent—bactericidal and PREGNANCY/FERTILITY/BREEDING number of neutrophils; variable number of with both aerobic and anaerobic activity; until Teratogenic agents—avoid use in pregnant lymphocytes; plasma cells; macrophages. r results of culture and sensitivity are known. animals. Causative agent variably detectable. Dogs and cats: amoxicillin (11–22 mg/kg PO SEE ALSO q8–12h); amoxicillin/clavulanic acid r Actinomycosis (12.5–25 mg/kg PO q12h); clindamycin r Anaerobic Infections (5 mg/kg PO q12h); and trimethoprim/ r Colibacillosis TREATMENT sulfadiazine (15 mg/kg PO IM q12h). Cats r Mycoplasmosis with Mycoplasma and l-forms: doxycycline r APPROPRIATE HEALTH CARE Nocardiosis (5 mg/kg PO q12h). r r r Depends on location of abscess and Aggressive antimicrobial therapy—sepsis or Sepsis and Bacteremia treatment required. peritonitis. ABBREVIATIONS r r Outpatient—bite-induced abscesses. CSF = cerebrospinal fluid r CONTRAINDICATIONS r Inpatient—sepsis; extensive surgical CT = computed tomography N/A r procedures; treatment requiring extended FeLV = feline leukemia virus r hospitalization. PRECAUTIONS FIV = feline immunodeficiency virus r r Establish and maintain adequate drainage. N/A MRI = magnetic resonance imaging r r Surgical removal of nidus of infection or POSSIBLE INTERACTIONS PAS = periodic acid-Schiff foreign object(s) if necessary. r N/A Institution of appropriate antimicrobial Suggested Reading therapy. ALTERNATIVE DRUG(S) Birchard SJ, Sherding RG, eds., Saunders NURSING CARE N/A Manual of Small Animal Practice. r Philadelphia: Saunders, 1994. Depends on location of abscess. r DeBoer DJ. Nonhealing cutaneous wounds. Apply hot packs to inflamed area as needed. r In: August JR, ed., Consultations in Feline Use protective bandaging and/or Internal Medicine. Philadelphia: Saunders, Elizabethan collars as needed. FOLLOW-UP r 1991, pp. 101–106. Accumulated exudate—drain abscess; PATIENT MONITORING McCaw D. Lumps, bumps, masses, and maintain drainage by medical and/or surgical Monitor for progressive decrease in drainage, lymphadenopathy. In: Ettinger SJ, Feldman means. r resolution of inflammation, and improvement EC, eds., Textbook of Veterinary Internal Sepsis or peritonitis—aggressive fluid of clinical signs. Medicine, 4th ed. Philadelphia: Saunders, therapy and support. PREVENTION/AVOIDANCE 1995, pp. 219–222. ACTIVITY r Percutaneous abscesses—prevent fighting. Author Adam J. Birkenheuer r Restrict until the abscess has resolved and Anal sac abscesses—prevent impaction; Consulting Editor StephenC.Barr adequate healing of tissues has taken place. consider anal saculectomy for recurrent cases. Acknowledgment The author and editors r DIET Prostatic abscesses—castration possibly acknowledge the prior contributions of r Sufficient nutritional intake to promote a helpful. Johnny D. Hoskins. r positive nitrogen balance. Mastitis—prevent lactation (spaying). r r Depends on location of abscess and Periorbital abscesses—do not allow chewing Client Education Handout treatment required. on foreign object(s). available online CLIENT EDUCATION POSSIBLE COMPLICATIONS r r Discuss need to correct or prevent risk Sepsis. r factors. Peritonitis/pleuritis if intra-abdominal or r Discuss need for adequate drainage and intrathoracic abscess ruptures. r continuation of antimicrobial therapy for an Compromise of organ function. r adequate period of time. Delayed evacuation may lead to chronically draining fistulous tracts. JWST589-A16-05 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:44 279mm×216mm

10 Blackwell’s FiveMinute Veterinary Consult A Acetaminophen (apap) Toxicosis

INCIDENCE/PREVALENCE Other causes of methemoglobinemia r Common drug toxicity in cats; less frequent Onions/garlic r in dogs. Naphthalene BASICS r Chlorates GEOGRAPHIC DISTRIBUTION r DEFINITION Nitrites N/A r Sulfites Results from accidental animal ingestion or r SIGNALMENT Phenol owner administration of over-the-counter r Species Benzocaine acetaminophen-containing analgesic and r antipyretic medications. Cats more often than dogs Propylene glycol (cats) PATHOPHYSIOLOGY SIGNS CBC/BIOCHEMISTRY/URINALYSIS r When the normal biotransformation General Comments Methemoglobinemia and progressively mechanisms for detoxification Relatively common—owing to widespread rising serum concentrations of liver enzymes (ALT, AST)—characteristic. (glucuronidation and sulfation) are saturated, human use. r As hepatic function becomes impaired— cytochrome P450-mediated oxidation Historical Findings r decreased BUN, cholesterol, and albumin, produces a toxic metabolite (N-acetyl-p- Depression r and increased serum bilirubin. benzoquinone imine) that is electrophilic, Hyperventilation r r Heinz bodies (cats)—prominent in RBCs conjugates with glutathione, and binds to Darkened mucous membranes r within 72 hours. sulfhydryl groups leading to hepatic necrosis. Signs may develop 1–4 hours after dosing r Anemia, hemoglobinemia, and Dogs Physical Examination Findings r r hemoglobinuria or hematuria. Liver is most susceptible to toxicity. Progressive depression r r OTHER LABORATORY TESTS Signs commonly observed at exposures Salivation > r 100 mg/kg. Vomiting Acetaminophen plasma, serum, or urine r r Methemoglobinemia may develop at doses Abdominal pain concentrations > r 200 mg/kg. Tachypnea and cyanosis or muddy mucous IMAGING Cats membranes—reflect methemoglobinemia N/A r r Cannot effectively glucuronidate; more Edema—face, paws, and possibly forelimbs; DIAGNOSTIC PROCEDURES limited capacity for acetaminophen after several hours r N/A elimination than dogs. Chocolate-colored urine—hematuria and r Saturate glucuronidation and sulfation methemoglobinuria; especially in cats PATHOLOGIC FINDINGS r r biotransformation routes. Icterus Methemoglobinemia. r r r RBCs are most susceptible to oxidative Hypothermia Pulmonary edema. r r injury following glutathione depletion. Shock Centrilobular necrosis and congestion of the r r liver. Develop toxic cytochrome P450 metabolite Death r at much lower doses than dogs. CAUSES Renal tubular edema and degeneration with r proteinaceous tubular casts. Poisoned by as little as 50–60 mg/kg (often Acetaminophen toxicosis as little as one-half tablet); deacetylation of RISK FACTORS acetaminophen to p-aminophenol (PAP) r causes oxidative damage to RBCs, rapidly Nutritional deficiencies of glucose and/or sulfate producing methemoglobinemia by binding to r TREATMENT sulfhydryl groups on hemoglobin. Simultaneous administration of other r APPROPRIATE HEALTH CARE Slower-developing hepatotoxicosis may not glutathione-depressing drugs r be fully expressed before development of fatal With methemoglobinemia—must evaluate promptly. methemoglobinemia. r SYSTEMS AFFECTED With dark or bloody colored urine or r icterus—inpatient. Hemic/Lymph/Immune—RBCs are DIAGNOSIS NURSING CARE damaged by glutathione depletion, allowing DIFFERENTIAL DIAGNOSIS r oxidation of hemoglobin to methemoglobin. Gentle handling—imperative for clinically r Other causes of liver injury Hepatobiliary—liver necrosis (more r affected patients. Hepatotoxic mushrooms r commonindogs). r Induced emesis and gastric lavage—useful r Blue-green algae Cardiovascular (primarily cats)—edema of r within 4–6 hours of ingestion. Aflatoxins r the face, paws, and (to a lesser degree) r Anemia, hematuria, or hemoglobinuria— Iron, copper, zinc forelimbs through an undefined mechanism. r may require whole blood transfusion. Xylitol r GENETICS r Fluid therapy—maintain hydration and Cycad palms electrolyte balance. r r Cats—genetic deficiency in the glucuronide NSAIDs Oxygen therapy may be needed. r conjugation pathway makes them vulnerable. Drinking water—available at all times. r Food—offered 24 hours after initiation of treatment. JWST589-A16-05 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:44 279mm×216mm

Canine and Feline, Sixth Edition 11

(Continued) Acetaminophen (apap) Toxicosis A

ACTIVITY PREVENTION/AVOIDANCE SYNONYMS r r Restricted Never give acetaminophen to cats. Paracetamol r r DIET Give careful attention to the acetaminophen Tylenol N/A dose in dogs. SEE ALSO CLIENT EDUCATION POSSIBLE COMPLICATIONS Poisoning (Intoxication) Therapy r Warn client that treatment in clinically Liver necrosis and resulting fibrosis—may ABBREVIATIONS r affected patients may be prolonged and compromise long-term liver function in PAP = p-aminophenol r expensive. recovered patients. ALT = alanine aminotransferase r r Inform client that patients with liver injury EXPECTED COURSE AND PROGNOSIS AST = aspartate transaminase r r may require prolonged and costly Rapidly progressive methemoglobinemia— RBC = red blood cell r management. serious sign. D5W = 5% dextrose injection r SURGICAL CONSIDERATIONS Methemoglobin concentrations ≥ 50%— INTERNET RESOURCES grave prognosis. N/A r http://www.aspca.org/pet-care/poison- Progressively rising serum liver enzymes control/ 12–24 hours after ingestion—serious concern. r Expect clinical signs to persist 12–48 hours; Suggested Reading death owing to methemoglobinemia possible Plumb DC. Acetaminophen. In: Plumb DC, MEDICATIONS at any time. ed., Plumb’s Veterinary Drug Handbook, r DRUG(S) OF CHOICE Dogs and cats receiving prompt treatment 7th ed. Ames, IA: Wiley-Blackwell, 2011, r Activated charcoal 2 g/kg PO; immediately that reverses methemoglobinemia and pp. 6–8. after completion of emesis or gastric lavage. prevents excessive liver necrosis—may recover Plumlee KH. Hematic system. In: Plumlee r fully. KH, ed., Clinical Veterinary Toxicology. N-acetylcysteine (Mucomyst) 140 mg/kg r diluted in D5W as loading dose PO, IV; then Dogs—death as a result of liver necrosis St. Louis, MO: Mosby, 2004, p. 59. may occur within 72 hours. Schell MM, Gwaltney-Brant S. OTC drugs. 70 mg/kg diluted in D5W PO, IV, q6h for r 5–7 additional treatments. Cats—death as a result of methemo- In: Poppenga RH, Gwaltney-Brant SM, r S-adenosylmethionine (SAMe) as a globinemia occurs 18–36 hours after eds., Small Animal Toxicology Essentials. glutathione donor; 40 mg/kg PO × 1dose, ingestion. Chichester, UK: Wiley-Blackwell, 2011, then 20 mg/kg q24h PO × 7days. pp. 231–233. r Added benefit of using methylene blue, Sellon RK. Acetaminophen. In: Peterson ME, cimetidine, and/or ascorbic acid is Talcott PA, eds. Small Animal Toxicology, controversial. MISCELLANEOUS 3rd ed. St. Louis, MO: Elsevier, 2013, pp. 423–429. CONTRAINDICATIONS ASSOCIATED CONDITIONS Stockham SL, Scott MA. Fundamentals of Drugs that contribute to methemoglobinemia Keratoconjunctivitis sicca (KCS) may develop Veterinary Clinical Pathology, 2nd ed. or hepatotoxicity. in small-breed dogs as a sequela. Oxford: Blackwell, 2008, p. 186. PRECAUTIONS AGE-RELATED FACTORS Author Lisa A. Murphy Drugs requiring extensive liver metabolism or Young and small dogs and cats—greater risk Consulting Editor Lynn R. Hovda biotransformation—use with caution; expect from owner-given single-dose acetaminophen their half-lives to be extended. medications. Client Education Handout POSSIBLE INTERACTIONS ZOONOTIC POTENTIAL available online Drugs requiring activation or metabolism by None the liver have reduced effectiveness. PREGNANCY/FERTILITY/BREEDING Imposes additional stress and higher risk on exposed animals. FOLLOW-UP PATIENT MONITORING r Continual clinical monitoring of methemoglobinemia—vital for effective management; laboratory determination of methemoglobin percentage every 2–3 hours. r Serum liver enzyme activities (ALT, ALP) every 12 hours; monitor liver damage. JWST589-A17-06 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:54 279mm×216mm

12 Blackwell’s Five-Minute Veterinary Consult A Acidosis, Metabolic (Traditional Approach)

SYSTEMS AFFECTED Associated with Normochloremia (High r Cardiovascular—afallinpHresultsinan Anion Gap Metabolic Acidosis) r increase in sympathetic discharge but Renal: uremic acidosis, acute renal failure. BASICS r simultaneously causes a decrease in the Ketoacidosis: diabetic ketoacidosis, r DEFINITION responsiveness of the cardiac myocytes and starvation liver disease. Lactic acidosis: vascular smooth muscle to the effects of impaired perfusion, impaired carbohydrate A process in the body that leads to a decrease r in pH below the reference interval for that catecholamines. In mildly acidemic metabolism. Toxins: ethylene glycol, conditions (pH > 7.2), the effects of increased salicylate, paraldehyde, and methanol species. A decline in blood pH is specifically r termed acidemia. Associated with a decrease sympathetic stimulation predominate and intoxication. Hyperphosphatemia (see – result in a mild increase in heart rate and Hyperphosphatemia): raises the anion gap. At in plasma bicarbonate concentration (HCO3 ) (dogs, > 18 mEq/L; cats, > 16 mEq/L) and cardiac output. More severe acidemia a pH of 7.4, each 1 mg/dL increase in base excess (BE) (< – 4 mmol/L) with a (pH < 7.1), especially if acute, may decrease phosphate concentration is associated with a compensatory decrease in carbon dioxide cardiac contractility and predispose the heart 0.58 mEq/L increase in anion gap. to ventricular arrhythmias and ventricular tension (PCO2). r RISK FACTORS + r PATHOPHYSIOLOGY fibrillation. Respiratory—increased [H ] Chronic renal failure, diabetes mellitus, and r r stimulates peripheral and central hypoadrenocorticism Poor tissue perfusion Metabolic acidosis may develops either from r – chemoreceptors to increase alveolar or hypoxia—lactic acidosis Tumor lysis a loss of HCO3 (hyperchloremic acidosis) or a ventilation; hyperventilation decreases PCO2, syndrome or osteosarcoma— gain in acid (high anion gap acidosis). It is r which counters the effects of low plasma hyperphosphatemia Trauma, snake usually secondary to an accumulation of HCO – on pH. In dogs, a decrease of metabolically produced strong anions (strong 3 envenomation, or malignant hyperthermia— approximately 0.7 mmHg in PCO2 is rhabdomyolysis ion gap or high anion gap acidosis), expected for each 1 mEq/L decrease in plasma accumulation of weak acids – HCO3 . Little is known about compensation (hyperphosphatemia), corrected in cats, but it appears to be almost r hyperchloremia (hyperchloremic acidosis), or nonexistent. Renal/Urologic—the kidneys as a compensatory mechanism for respiratory r increase net acid excretion, primarily by DIAGNOSIS alkalosis. High anion gap acidosis: Increase + increasing excretion of NH4 and chloride. DIFFERENTIAL DIAGNOSIS in the concentration of other strong anions r This compensatory mechanism is not very Low plasma HCO – and hyperchloremia through addition (e.g., ethylene glycol effective in cats. 3 toxicity), excessive production (e.g., lactate may also be compensatory in animals with SIGNALMENT produced by prolonged anaerobic chronic respiratory alkalosis, in which PCO2 metabolism), or renal retention (e.g., renal Any breed, age, or sex of dog and cat is low and pH is high or near normal, despite – failure) of strong anions other than chloride SIGNALMENT decreased HCO3 and increase in chloride concentration. Blood gas determination is causes metabolic acidosis without increasing Historical Findings r required to differentiate. chloride concentration (so-called Chronic disease processes that lead to normochloremic or high AG metabolic LABORATORY FINDINGS r metabolic acidosis (e.g., renal failure, diabetes acidosis). Hyperphosphatemic acidosis: mellitus, and hypoadrenocorticism), acute Drugs That May Alter Laboratory Results Increase in plasma weak acids (e.g., inorganic circulatory shock (hemorrhagic), exposure to Potassium bromide is measured as chloride in phosphate) is associated with metabolic toxins (e.g., ethylene glycol, salicylate, and most analyzers, so potassium bromide acidosis and increased anion gap. At pH of paraldehyde), diarrhea, administration of administration artificially decreases the anion 7.4, a 1 mg/dL increase in phosphate carbonic anhydrase inhibitors (e.g., gap. concentration is associated with a 0.58 acetazolamide and dichlorphenamide). mEq/L decrease in HCO – and a 0.58 mEq/L Disorders That May Alter Laboratory 3 Physical Examination Findings Results increase in AG. Hyperphosphatemia r r Generally relate to the underlying disease. Too much heparin (> 10% of the sample) commonly develops with decrease renal r – r Depression, stupor, seizures, and or decreases HCO3 . Blood samples stored at phosphorous excretion (e.g., renal failure, > hypoparathyroidism, etc), cellular lysis (e.g., generalized muscle weakness in severely room temperature for 15 minutes have low r pH because of increased PCO . tumor lysis syndrome, trauma, acidotic patients. Tachypnea in some r 2 patients results from compensatory increase in Hypoalbuminemia lowers AG; negative rhabdomyolysis), bone neoplasms (increased r bone resorption), and hypervitaminosis D. ventilation. Kussmaul’s respiration, typically charges of albumin are the main component r Hyperchloremic acidosis: Hyperchloremic seen in human beings with metabolic acidosis, of the anion gap. is not commonly observed in dogs and cats. acidosis may be caused by chloride retention r Valid if Run in Human Laboratory? (e.g., renal failure, renal tubular acidosis) that Vomiting and/or diarrhea. Yes – typically occurs in response to HCO3 loss. CAUSES CBC/BIOCHEMISTRY/URINALYSIS – r Chloride and HCO3 are reciprocally related; Associated with Hyperchloremia – Low total CO2—total CO2 in serum alossofHCO3 generally results in retention (Hyperchloremic Metabolic Acidosis) samples handled aerobically closely r of chloride. Other mechanisms for Renal: Renal tubular acidosis; carbonic approximates the serum HCO – r 3 hyperchloremic acidosis include: excessive loss anhydrase inhibitors. GI: Diarrhea. concentration; unfortunately, patients with r of sodium relative to chloride (e.g., diarrhea, Other: Chloride-rich fluids (e.g., 0.9% chronic respiratory alkalosis also have low Addison’s) and administration of substances NaCl, KCl supplementation); total parenteral total CO , and the distinction cannot be 2 r containing more chloride than sodium as nutrition with cationic amino acids: lysine, made without blood gas analysis. Metabolic compared with normal extracellular fluid arginine, and histidine; rapid correction of acidoses are traditionally divided into composition (e.g., administration of KCl, hypocapnia (chronic respiratory alkalosis); hyperchloremic and high anion gap by means 0.9% NaCl). Acidemia is usually not severe in NH4Cl or HCl. of the anion gap. Anion gap, the difference patients with hyperchloremic acidosis. between the measured cations and the JWST589-A17-06 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:54 279mm×216mm

Canine and Feline, Sixth Edition 13

(Continued) Acidosis, Metabolic (Traditional Approach) A

measured anions, is calculated as AG = by reevaluation of blood gas status is safe in POSSIBLE COMPLICATIONS + – – + r [Na ]–(HCO3 + [Cl ]) or AG = ([Na ] + most patients. Hyperkalemia in acute hyperchloremic + – – ◦ r [K ]) – (HCO3 + [Cl ]), depending on the Potential complications of NaHCO3 acidosis Myocardial depression and preference of the clinician or laboratory. administration: volume overload resulting ventricular arrhythmias Normal values with potassium included in the from administered sodium, tetany from low calculation are usually 12–24 mEq/L in dogs ionized calcium concentration, increased and 13–27 mEq/L in cats. The negative affinity of hemoglobin for oxygen, charges of albumin are the major contributors paradoxical CNS acidosis, overshoot MISCELLANEOUS to the normal anion gap; this should be taken metabolic alkalosis, and hypokalemia. r ASSOCIATED CONDITIONS into account when evaluating anion gap in Hyperchloremic acidosis: NaHCO3 may be r r patients with hypoalbuminemia. At pH 7.4 in effective and considered whenever pH < 7.1. Hyperkalemia Hyperchloremia r dogs, a decrease of 1 g/dL in albumin is Uremic acidosis: efficacy of NaHCO3 in AGE-RELATED FACTORS associated with a decrease of 4.1 mEq/L in the acute therapy of uremic acidosis is related to r None anion gap. Normal anion gap (i.e., the shift of phosphate inside the cells and r PREGNANCY/FERTILITY/BREEDING hyperchloremic metabolic acidosis). High consequent amelioration of anion gap (i.e., normochloremic metabolic hyperphosphatemic acidosis. N/A r r acidosis). Hyperglycemia—see Lactic acidosis: NaHCO increases lactate SYNONYMS r 3 Hyperglycemia. Azotemia—see Azotemia. production and is of little to no value in lactic r r Dilutional acidosis—metabolic acidosis Hyperphosphatemia—see acidosis. Therapy should be directed at resulting from increased free water in plasma. r r Hyperphosphatemia. High lactate augmenting oxygen delivery to the tissues and Hyperchloremic acidosis—normal anion concentration—see Lactic Acidosis. reestablishing cardiac output. Small titrated r r gap acidosis. Hyperphosphatemic Hyperkalemia—see Hyperkalemia (formulas doses of NaHCO3 can be used as a acidosis—metabolic acidosis resulting from to adjust potassium concentration based on pH temporizing measure to maintain HCO – high phosphate concentration. 3 r changes should not be used). above 5 mEq/L, if needed. Non-respiratory acidosis. r r OTHER LABORATORY TESTS Diabetic ketoacidosis: NaHCO3 adversely Normochloremic acidosis—high anion gap r Blood gas analysis reveals low HCO –,low affects outcome in humans with diabetic acidosis. Organic acidosis—metabolic 3 ketoacidosis even when pH is < 7.0. PCO , and low pH. r acidosis resulting from accumulation of 2 Administration of NaHCO to ketoacidotic DIAGNOSTIC PROCEDURES 3 organic anions (e.g., ketoacidosis, uremic patients cannot be recommended at any pH. acidosis, and lactic acidosis). None Therapy should be direct at insulin and fluid SEE ALSO administration. Reestablishing plasma volume r r Azotemia Diabetes Mellitus with and renal perfusion will allow the kidneys to r Ketoacidosis Hyperchloremia excrete ketoanions, replacing them with r r Hyperkalemia Hyperphosphatemia chloride. r TREATMENT Lactic Acidosis r CONTRAINDICATIONS Acid-base disturbances are secondary r ABBREVIATIONS Avoid NaHCO in patients with respiratory r r phenomena; successful resolution depends on 3 r AG = anion gap BE = base excess diagnosis and treatment of the underlying acidosis because it generates CO . Patients r r 2 CNS = central nervous system with respiratory acidosis cannot adequately r r disease process. Restore blood volume and H+ = hydrogen ion HCO – = bicarbonate perfusion deficits before considering excrete CO , and increased PCO will further r 3 r 2 r 2 NaHCO = sodium bicarbonate decrease the pH. Avoid diuretics that act in r 3 r NaHCO3. Treat patients with blood pH O = oxygen PCO = carbon dioxide ≤ 7.1 aggressively while pursuing the the distal nephron (e.g., spironolactone). 2 2 r r tension definitive diagnosis. Discontinue drugs that Avoid carbonic anhydrase inhibitors (e.g., r r may cause metabolic acidosis. Nursing acetazolamide, dichlorphenamide). Avoid Suggested Reading < care—Isotonic, buffered electrolyte solution is NaHCO3 in acute ( 10 minutes) cardiac de Morais HA, Constable PD. Strong ion the fluid of choice for patients with mild arrest as it may impair tissue oxygen approach to acid-base disorders. In: metabolic acidosis and normal liver function. unloading. DiBartola SP, ed., Fluid, Electrolyte and PRECAUTIONS Acid-Base Disorders, 4th ed. St. Louis, MO: Saunders, 2012, pp. 316–330. Use NaHCO3 cautiously in patients with congestive heart failure because the sodium de Morais HA, Leisewitz AL. Mixed acid-base MEDICATIONS load may cause decompensation of the heart disorders. In: DiBartola SP, ed., Fluid, failure. Electrolyte and Acid-Base Disorders, 4th ed. DRUG(S) OF CHOICE St. Louis, MO: Saunders, 2012, pp. r POSSIBLE INTERACTIONS NaHCO3 may help patients with 302–315. hyperchloremic, hyperhosphatemic, or uremic None DiBartola SP. Metabolic acid-base disorders. acidosis, but not patients with lactic acidosis ALTERNATIVE DRUG(S) In: DiBartola SP, ed., Fluid, Electrolyte and or diabetic ketoacidosis. Acid-Base Disorders, 4th ed. St. Louis, MO: r None NaHCO3 may be considered for alkaline Saunders, 2012, pp. 271–280. diuresis in salicylate toxicity. Hopper K. Traditional Acid-Base Analysis. In: ◦ – Estimation of HCO3 dose: dogs, 0.3 × Silverstein DC, Hopper K, eds., Small × – Animal Critical Care Medicine, 2nd. ed. St. body weight (kg) (21 – patient HCO3 ); FOLLOW-UP cats, 0.3 × body weight (kg) × (19 – patient Louis, MO: Elsevier, 2015, pp. 289–299. – PATIENT MONITORING HCO3 ). Give half of this dose slowly IV Authors Helio S. Autran de Morais and and reevaluate blood gases before deciding Recheck acid-base status; frequency dictated Lee E. Palmer on the need for additional administration. by the underlying disease and patient Consulting Editor Carl A. Osborne An empirical dose of 1–2 mEq/kg followed response to treatment. JWST589-A18-07 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:31 279mm×216mm

14 Blackwell’s Five-Minute Veterinary Consult A Acne—Cats

PATHOLOGIC FINDINGS CONTRAINDICATIONS/POSSIBLE r Mild disease—follicular distention with INTERACTIONS r BASICS keratin (comedo), hyperkeratosis, and Benzoyl peroxide and salicylic acids—can be follicular plugging. irritating. r r OVERVIEW Severe disease—mild to severe folliculitis Some wipes contain alcohols that can be r Inflammatory dermatitis affecting the chin and perifolliculitis with follicular pustule irritating. r and lips formation leading to furunculosis and Systemic isotretinoin—use with caution, if r Symptoms may be recurrent or persistent pyogranulomatous dermatitis. animal will not allow application of topical r r Precise etiology unknown Bacteria and Malassezia in these lesions are medications; potential deleterious side effects SIGNALMENT considered secondary invaders and not in human beings (drug interactions and r causative agents. Cats r teratogenicity); container should be labeled r Demodex mites can be primary agents of this for animal use only and kept separate from Prevalence for sex, age, or breed not disease. reported human medications to avoid accidental use; currently difficult to obtain for animal SIGNS r patients. Cats may have a single episode, a life-long recurrent problem, or a continual disease. r TREATMENT Frequency and severity of each occurrence r varies with the individual. Initial treatment—gentle clipping and r soakings to soften crusts. FOLLOW-UP Comedones, mild erythematous papules, r r Continue one or a combination of the Monitor for relapses. serous crusts, and dark keratin debris develop r on the chin and less commonly on the lips. therapies listed below until all lesions have Maintenance cleansing programs can be r Swelling of the chin. resolved. used to reduce relapses. Affected cats are likely r r Severe cases—nodules, hemorrhagic crusts, Discontinue treatment by tapering to have variable numbers of comedones medication over a 2- to 3-week period. pustules, cysts, fistulae, severe erythema, r life-long, often are just cosmetic and alopecia, and pain. Recurrent episodes—once the recurrence treatment is not necessary. r Pain often associated with bacterial rate is determined, an appropriate furunculosis. maintenance protocol can be designed for each individual. CAUSES & RISK FACTORS r Continual episodes—life-long maintenance MISCELLANEOUS Precise etiology unknown; may be a disorder treatment necessary. of keratinization, poor grooming, abnormal PREGNANCY/FERTILITY/BREEDING sebum production, immunosuppression, viral Systemic isotretinoin should not be used on infection, or stress. breeding animals. MEDICATIONS Suggested Reading DRUG(S) Jazic E, Coyner KS, Loeffler DG, Lewis TP. An evaluation of the clinical, cytological, DIAGNOSIS Topical r infectious and histopathological features of Shampoo—once or twice weekly with DIFFERENTIAL DIAGNOSIS feline acne. Vet Dermatol 2006, 17(2): r antiseborrheic (sulfur-salicylic acid, benzoyl Bacterial folliculitis 134–140. r peroxide, or ethyl lactate). Demodicosis r Miller WH, Griffin CE, Campbell KL. Acne. r Cleansing agents—benzoyl peroxide, Malassezia infection In: Muller & Kirk’s Small Animal r salicylic acid, chlorhexidine- Dermatophytosis Dermatology, 7th ed. St. Louis, MO: r phytosphingosine. Neoplasia of sebaceous or apocrine glands r Elsevier, 2013, pp. 640–642. r Wet wipes—Douxo Chlorhexidine pads®, Eosinophilic granuloma Rosencrantz WS. The pathogenesis, diagnosis, r Malaseb® wipes, MalAcetic® wipes, Contact hypersensitivity and management of feline acne. Vet Med GlycoZoo® wipes. r 1993, 5:504–512. CBC/BIOCHEMISTRY/URINALYSIS Antibiotic ointment—mupirocin 2%. r Werner AH, Power HT. Retinoids in N/A Other topicals—clindamycin or veterinary dermatology. Clin Dermatol OTHER LABORATORY TESTS erythromycin solution or ointment. r 1994, 12(4):579–586. Combination topicals—benzoyl N/A White SD. Feline acne and results of peroxide-antibiotic gels (e.g., Benzamycin). IMAGING r treatment with mupirocin in an open Topical retinoids—Tretinoin (Retin-A clinical trial: 25 cases (1994–96). Vet N/A 0.01% gel). r Dermatol 1997, 8:157. DIAGNOSTIC PROCEDURES In severe inflammatory periods 10–14 days r Author David D. Duclos Skin scrapings—demodicosis. of oral prednisolone (1–2 mg/kg q24h) may r Consulting Editor Alexander H. Werner Fungal culture—dermatophytosis. help to reduce scar tissue formation. r Cytology—bacteria, Malassezia. Systemic r r Biopsy—rarely needed; necessary in selected Antibiotics—amoxicillin with clavulanate, cases to characterize changes such as cystic cephalosporin, or fluoroquinolone. r follicles, to differentiate acne from other Severe cases may warrant treatment with diseases such as demodicosis, infections isotretinoin (Accutane) or cyclosporine, (bacterial, yeast, or dermatophytes), or to modified (Atopica). r diagnose neoplasia. Demodicosis—oral ivermectin 400 𝜇g/kg daily until mites are cleared. JWST589-A19-08 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:46 279mm×216mm

Canine and Feline, Sixth Edition 15 Acne—Dogs A

DIAGNOSTIC PROCEDURES CONTRAINDICATIONS/POSSIBLE r Bacterial culture and sensitivity testing—in INTERACTIONS r BASICS patients with suppurative folliculitis and Benzoyl peroxide—may bleach carpets and furunculosis that are non-responsive to initial fabrics; may be irritating. r OVERVIEW antibiotic selection. Mupirocin ointments—greasy; may be r r Also called muzzle folliculitis and Biopsy—histologic confirmation for cases in prudent to reserve for use in which diagnosis is in question. furunculosis. r multidrug-resistant cases. r Skin scrape—demodicosis. r Chronic inflammatory disorder of the chin r Topical retinoids—may be drying and and lips of young animals. Dermatophyte culture—dermatophytosis. irritating. r r Characterized by folliculitis and PATHOLOGIC FINDINGS Topical steroids—may cause adrenal r furunculosis; rarely comedogenic as seen in Clinical signs and histopathologic findings suppression and thinning of skin with “true acneiform” lesions of human beings. are diagnostic. repeated use. r r r Recognized almost exclusively in Initial lesions—hairless follicular papules; Isotretinoin—may cause short-coated breeds. keratoconjunctivitis sicca, hyperactivity, ear r characterized histopathologically by marked Genetic predisposition and local trauma follicular keratosis, plugging, dilatation, and pruritus, erythema of mucocutaneous may play a more important role than perifolliculitis. junctions, lethargy with vomiting, abdominal r hormonal effects. Bacteria—not present and cannot be distension, anorexia with lethargy, collapse, SIGNALMENT isolated from lesions in early stages. and swollen tongue; CBC and chemistry r r Dogs. As disease progresses, papules enlarge and screen abnormalities include high platelet r Predisposed short-coated breeds—boxer, rupture, promoting a suppurative folliculitis count, hypertriglyceridemia, Doberman pinscher, English bulldog, Great and furunculosis. hypercholesterolemia, and high alanine Dane, Weimaraner, mastiff, rottweiler, transaminase. German shorthaired pointer, pit bull terrier. SIGNS r Ventral chin and lip margins may be TREATMENT r FOLLOW-UP minimally to markedly swollen with Depends on the severity and chronicity of numerous erythematous papules and pustules. the disease. PATIENT MONITORING r r r Initial lesions are sterile; bacteria may not be Reduce behavioral trauma to the chin (e.g., Continue antibiotics until lesions have isolated and lesions may not respond to rubbing on the carpet, chewing bones that healed. r antibiotics. increase salivation). Repeat bacterial culture/sensitivity if lesions r r Advanced stages—lesions may be exudative, Frequent cleaning with benzoyl peroxide worsen. r indicating secondary deep bacterial shampoo or gel. Discontinue topical corticosteroids when folliculitis-furunculosis. r r Mupirocin 2% ointment to reduce the possible. Lesions may be painful on palpation; most bacterial numbers on the surface of the skin. r EXPECTED COURSE AND PROGNOSIS are non-painful and non-pruritic. r r Instruct owners to avoid expressing the Long-term topical treatment may be Chronic resolved lesions may be scarred and lesions, which may cause internal rupture of required. lichenified. r the papule and massive inflammation. Chronic scarring may be prevented by early CAUSES & RISK FACTORS and aggressive therapy. Some short-coated breeds appear to be genetically predisposed to follicular hyperkeratosis and secondary bacterial MEDICATIONS infection. DRUG(S) MISCELLANEOUS Topical PREGNANCY/FERTILITY/BREEDING r Benzoyl peroxide shampoo or gel Synthetic retinoids—teratogens; do not use in (antibacterial). DIAGNOSIS r pregnant animals, animals intended for Mupirocin 2% ointment reproduction, or intact female animals; should DIFFERENTIAL DIAGNOSIS (antibacterial-staphylococcus). r r not be handled by women of childbearing age. Dermatophytosis Tretinoin (Retin-A)—may reduce follicular r Demodicosis keratosis. Suggested Reading r r Foreign body Corticosteroids—may be necessary to Miller WH, Griffin CE, Campbell KL. r Contact dermatitis reduce inflammation; limit frequency of use Muzzle folliculitis and furunculosis. In: Muller & Kirk’s Small Animal Dermatology, CBC/BIOCHEMISTRY/URINALYSIS to avoid local and systemic effects. 7th ed. St. Louis, MO: Elsevier, 2013, Systemic N/A r pp 201 and 640. OTHER LABORATORY TESTS Antibiotics appropriate for deep bacterial Author Karen Helton Rhodes infection—when indicated (e.g., cephalexin, Consulting Editor Alexander H. Werner N/A 22 mg/kg PO q8–12h for 6–8 weeks). r IMAGING May need to perform bacterial culture and N/A sensitivity test. r Isotretinoin (Accutane)—1–2 mg/kg/day. r Oral corticosteroids: tapering dosages of prednisolone (initial 0.5 mg/kg/day) to reduce significant inflammation; not for continued use. JWST589-A20-09 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:1 279mm×216mm

16 Blackwell’s Five-Minute Veterinary Consult A Acral Lick Dermatitis

r r Dermatophyte culture—fungal infection. Topical medications should be applied with r Epidermal cytology—bacterial infection. gloves. r r BASICS Bacterial culture and sensitivity—tissue Animals should be kept from licking the cultures may differ from surface culture. area for 10–15 minutes. r OVERVIEW Food-elimination diet—determine food CONTRAINDICATIONS/POSSIBLE r allergy. Chronic lesions directly caused by r INTERACTIONS self-trauma. Intradermal allergy testing—atopy. r r r Doxepin—caution using with monoamine A cycle of licking, pruritus, and secondary Biopsy—to rule out neoplasia, other infections. oxidase inhibitors, clonidine, anticonvulsants, infection develops. r Behavioral history. oral anticoagulants, steroid hormones, SYSTEMS AFFECTED r antihistamines, or aspirin. Neurologic and orthopedic evaluation. r Skin/Exocrine Antihistamines—may cause sedation. PATHOLOGIC FINDINGS r SIGNALMENT Psychotropic medications should be r Histopathology—epidermal hyperplasia, Dogs. combined and/or withdrawn carefully. r plasmacytic dermal inflammation, folliculitis, r Most common in large breeds—especially Cardiotoxicity and hepatoxicity—rare cases furunculosis, perihidradenitis, hidradenitis, in animals on TCAs. Routine monitoring Doberman pinschers, Labrador retrievers, and vertical streaking fibrosis. Great Danes, Irish and English setters, golden recommended. retrievers, Akitas, Dalmatians, boxers, Shar-Peis, and Weimaraners. r Age at onset—varies (especially with cause). r No sex predilection. TREATMENT FOLLOW-UP r r SIGNS Behavioral therapy: attempt to identify Monitor level of licking and chewing closely. r r Excessive licking of the affected area. psychological causes and remediate. Treat underlying disease to prevent r r Alopecic, eroded, thickened, and raised firm Physical restraints—Elizabethan collars and recurrence. bandaging permit healing. r plaques with scabs and exudation, usually r If no underlying disease is detected, suspect located on the dorsal aspect of the carpus, Therapeutic laser—one controlled study did psychogenic causes (compulsive or metacarpus, tarsus, or metatarsus. not demonstrate efficacy. self-mutilation disorder); prognosis is r r Lesions often occur singly or may be Diet—no modification unless food guarded. hypersensitivity is suspected. multiple. r CAUSES & RISK FACTORS Difficult to treat, especially if no underlying r cause is found; warn owner that patience and Focal trauma to the area initiating a time are necessary. lick-itch cycle. r MISCELLANEOUS r Surgery (laser or standard)—may cause Anything causing a local irritation or lesion increased licking and attention to a larger AGE-RELATED FACTORS may initiate response. r affected area; if underlying causes are not Dogs < 5 years old—strongly consider allergy Associated diseases—staphylococcal addressed, recurrence is likely. ZOONOTIC POTENTIAL furunculosis, hypersensitivity, r endocrinopathy, demodicosis, Transmitted to humans only if dermatophytosis, foreign body reaction, dermatophytosis is the underlying cause; exceedingly rare. neoplasia, underlying joint disease or arthritis, r trauma, neuropathy, psychogenic, or sensory MEDICATIONS Methicillin resistant Staphylococcus aureus nerve dysfunction. DRUG(S) may have zoonotic implications. Antibiotics ABBREVIATIONS r r Based on bacterial culture and sensitivity. ACTH = adrenocorticotropin hormone r r Administer until infection is completely LDDST = low-dose dexamethasone DIAGNOSIS suppression test resolved; often at least 6 weeks. r SSRI = selective serotonin reuptake DIFFERENTIAL DIAGNOSIS Systemic r r inhibitor Neoplasia Antihistamines—e.g., hydroxyzine r r TCA = tricyclic antidepressant Bacterial furunculosis (1–2 mg/kg PO q12h); chlorpheniramine r r TSH = thyroid stimulating hormone Focal demodicosis (4–8 mg/dog PO q12h; maximum of r 0.5 mg/kg q12h). Suggested Reading Focal dermatophytosis r CBC/BIOCHEMISTRY/URINALYSIS SSRIs: e.g., fluoxetine (1 mg/kg PO q24h); Shumaker AK, Angus JC, et al. paroxetine (0.5–1 mg/kg PO q24h). Microbiological and histopathological r Normal except in cases of endocrinopathy. Dopamine antagonists: e.g., naltrexone features of canine acral lick dermatitis. Vet OTHER LABORATORY TESTS (2.2 mg/kg PO q12–24h). Dermatol 2008, 19(5):288–298. r Endocrinopathy—free T4/TSH; ACTH TCAs: e.g., amitriptyline (1.1–2.2 mg/kg Author Alexander H. Werner stimulation test or LDDST. PO q12h; doxepin (3–5 mg/kg PO q12h; Consulting Editor Alexander H. Werner IMAGING maximum 150 mg q12h); clomipramine Acknowledgment The author and editors (1–3.5 mg/kg PO q12–24h). acknowledge the prior contribution of Radiology—neoplasia; local trauma; r radiopaque foreign bodies; bony proliferation Combine and/or withdraw administration Jean S. Greek. may be seen secondary to the chronic of these medications carefully. Topical irritation; evidence of underlying arthritis if r over a joint. Flunixin meglumine and fluocinolone in dimethyl sulfoxide (combined). DIAGNOSTIC PROCEDURES r r Topical capsaicin products. Skin scrapings—demodicosis. r Intralesional corticosteroids rarely helpful. JWST589-A21-10 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:3 279mm×216mm

Canine and Feline, Sixth Edition 17 Acromegaly—Cats A

CAUSES & RISK FACTORS septal and left ventricular free-wall r GH hypersecretion. thickening, systolic anterior motion of the r Progestins do not cause GH secretion and mitral valve, and diastolic dysfunction. BASICS r acromegaly in cats as they do in dogs. Radiographic changes include increased OVERVIEW oropharyngeal soft tissue, degenerative r Syndrome resulting from growth hormone arthropathy with periarticular osteophytosis, (somatotropin) hypersecretion by tumorous spinal spondylosis deformans, and variable or hyperplastic somatotrophs in the anterior DIAGNOSIS abdominal organomegaly. pituitary. r DIFFERENTIAL DIAGNOSIS Clinical signs are due to growth hormone’s r direct catabolic/diabetogenic effects and its Uncomplicated DM or DM secondary to hyperadrenocorticism indirect anabolic effects mediated through r TREATMENT insulin-like growth factor I, which is secreted Pituitary-dependent hyperadrenocorticism and acromegaly can both produce RADIOTHERAPY by the liver in response to growth hormone r stimulation. insulin-resistant DM with an associated The only currently available means of r Elevated IGF1 activity induces excessive soft pituitary mass lesion. Differentiation may reducing autonomous overproduction tissue growth, visceral organomegaly, bone require use of a low-dose dexamethasone of GH from the anterior pituitary. suppression test to rule out PDH. Unfortunately, radiotherapy is more suited to remodeling and thickening (especially in r bones formed from membranous ossification) Acromegaly and PDH can occur reducing the size of the tumor than achieving concurrently. clinically significant reductions in GH resulting in arthropathy, broad facial features, r and enlarged “clubbed” paws. Other disorders causing weight loss with secretion. r r Myocardial hypertrophy occurs in many polyphagia, polyuria, and polydipsia such as A total dose of between 3,500 and cats, but heart failure is uncommon. hyperthyroidism are not usually associated 5,500 cGY, administered in variably r The catabolic actions of GH result from with significant glucose intolerance. fractionated doses is often suggested. Recent r > insulin antagonism leading eventually to Insulin-resistant DM ( 2.0 U of reports suggest that the greatest success may pancreatic 𝛽 cell exhaustion and DM. insulin/kg/12h) is to be expected in all be achieved with a total dose of 3,700 cGy Between 25 and 33% of diabetic cats may acromegalic cats and the dose tends to administered as an incremental have acromegaly. increase over time, with doses of hypofractionated dosage protocol of r 12–50 U/cat/12h not uncommon. 10 doses. Using this method, 13 of 14 Like most diabetic cats the potential for r remission remains if the excessive GH Acromegaly should be suspected in any acromegalic cats had markedly improved production can be normalized; likelihood of diabetic cat demonstrating signs of otherwise diabetic control. remission is inversely related to the duration unexplained insulin resistance. SURGERY r of DM. CBC/BIOCHEMISTRY/URINALYSIS Hypophysectomy is considered the r SIGNALMENT Most abnormalities attributed to poorly treatment of choice in human r Cat controlled DM—hyperglycemia, glucosuria, hypersomatotropism. It has also proven to be r Median age—11 years (range of 6–17 years) and elevated fructosamine levels are consistent the only consistently effective and reliable r findings in most acromegalic cats. method to cure HS in cats. Approximately 80% are males r r Hyperproteinemia. An experienced neurosurgeon and SIGNS r r Traditionally associated with renal failure appropriate pre-, peri- and postoperative care Initial signs relate to unregulated DM with and hypertension, but more recent studies are essential for success. A transsphenoidal the vast majority of cases presenting with suggest this is not the case. approach is currently preferred (incising the polyuria, polydipsia, and often profound soft palate). OTHER LABORATORY TESTS r polyphagia accompanied with concurrent r IGF1—diabetic cats receiving insulin can In the long run, cats need to be weight gain (weight loss has also been supplemented with thyroid hormone and a reported). have higher IGF1 levels than normal; hence r glucocorticoid; synthetic ADH (DDAVP) Many patients gain weight and have there is significant potential for overlap between acromegalic and non-acromegalic supplementation can often be ceased increased body size due to increased bone and 6–8 weeks postoperatively. When performed soft tissue mass, not from increased adipose diabetic cats; however, dramatically elevated IGF1 levels (e.g., > 1,000 ng/ml) are strongly early in the disease process, diabetic remission tissue. Weight gain in an unregulated diabetic is a realistic outcome and often occurs within cat strongly suggests acromegaly. suggestive of the acromegaly. r r 2 months after the procedure. Broadening of facial features, prognathia IGF1 is well preserved across the species, so valid assays are commonly available. inferior, and increased paw size reflect r long-standing or severe disease. GH—elevated basal serum levels are r Organomegaly—most commonly bilateral diagnostic. However, as GH is not well renomegaly and hepatomegaly. preserved across the species, a validated fGH MEDICATIONS r Murmur and/or gallop rhythm occasionally assay has limited availability. Somatostatins and dopamine agonists have present; signs of heart failure uncommon. IMAGING r been used to try to inhibit GH secretion by Lameness may develop. r r Intracranial imaging to demonstrate a the pituitary, mostly without success. Neurologic signs referable to intracranial pituitary mass lesion; MRI is more Recently, a novel somatostatin analog, disease through an expanding pituitary mass sensitive than contrast-enhanced CT, pasireotide (Novartis, Basel, Switzerland) has lesion possible. r although the difference is modest and from a been shown to be effective at achieving this, Recent reports suggest the majority of cost-benefit perspective CT is generally although further research is required to acromegalic cats are indistinguishable preferred. evaluate the use of this drug, including dosing r phenotypically from non-acromegalic diabetic Echocardiographic abnormalities may regimes, in the long run. cats. include left atrial enlargement, asymmetric JWST589-A21-10 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:3 279mm×216mm

18 Blackwell’s Five-Minute Veterinary Consult

A Acromegaly—Cats (Continued)

PALLIATIVE TREATMENT r When definitive treatment is not possible, the focus should lie on gaining more control FOLLOW-UP MISCELLANEOUS of the diabetes mellitus and treating possible r comorbidities. Clinical signs that might be attributed to r Suggested Reading Eventually most cats tend to need high poor diabetic control (e.g., profound Berg RI, Nelson RW, Feldman EC, et al. dosages of insulin and/or combinations of polyphagia) will not improve with improved Serum insulin-like growth factor-I short-acting and long-acting insulin types to diabetic control; thus levels of glycated concentration in cats with diabetes mellitus ensure an adequate quality of life for both pet proteins or blood glucose levels are better and acromegaly. J Vet Intern Med 2007, and owner. indicators of diabetic control than clinical r 21(5):892–898. Nevertheless, a minority achieve an signs. r Niessen SJ, Petrie G, Gaudiano F, et al. Feline adequate quality of life. Serum IGF1 levels are not suitable for r acromegaly: an underdiagnosed Regular veterinary assessment is monitoring therapy as they do not change endocrinopathy? J Vet Intern Med 2007, recommended. during or after radiotherapy. r r 21(5):899–905. Iatrogenic hypoglycemia is a major Reported survival times vary Authors Deborah S. Greco and David concern given the pulsatile nature of GH enormously—from a few months to many Church secretion (and therefore associated insulin years, and dying from causes unlikely to be Consulting Editor Deborah S. Greco resistance). related to acromegaly. JWST589-A22-11 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:42 279mm×216mm

Canine and Feline, Sixth Edition 19 Actinomycosis A

r draining tracts and pleural or peritoneal Antibiotics—a retrospective study suggests effusions must be addressed. administration for a minimum of 3–4 months CBC/BIOCHEMISTRY/URINALYSIS after resolution of all signs; may need to be BASICS r r Nonspecific changes. Leukocytosis with a directed against other associated microbes. OVERVIEW r left shift and monocytosis—reported. Penicillins—considered the drug of choice; r r An infectious disease caused by Nonregenerative anemia—may develop. in most cases, oral therapy can be initiated r Gram-positive, branching, pleomorphic, Hypoglycemia and hyperglobulinemia— and parenteral is not needed; amoxicillin rod-shaped bacteria of the genus Actinomyces. reported. should be administered at 20–22 mg/kg q8h r PO. A. viscosus and A. hodeovulneris—most IMAGING commonly identified isolates (though most r CONTRAINDICATIONS/POSSIBLE Radiographs of infected bone—periosteal isolates are not identified to the species level); INTERACTIONS survives in microaerophilic or anaerobic new bone production, reactive osteosclerosis, r r r Metronidazole—avoid use; actinomycosis conditions. Rarely found as the single and osteolysis. Thoracic radiographs— r alveolar and interstitial lung patterns with unlikely to respond. Aminoglycosides—do bacterial agent in a lesion; more commonly, it not use; ineffective against anaerobic is a component of a polymicrobial infection. possible lung consolidation; pleural effusion; r r infections. A. hordeovulneris—cell-wall There may be synergism between pericardial effusion; subcutaneous masses on r r deficient variant (l-phase); does not usually Actinomyces and other organisms. Organ lateral thorax. Abdominal radiographs— ◦ peritoneal effusion; mass effect in abdomen. respond well to penicillin; consider systems affected may include: Skin r ◦ ◦ Vertebral column radiographs—periosteal clindamycin, erythromycin, and Respiratory Cardiovascular chloramphenicol. ◦ Musculoskeletal ◦ Nervous. new bone formation, especially T13–L3. SIGNALMENT DIAGNOSTIC PROCEDURES r r r Dogs and cats (uncommon). Most Pus or osteolytic bone fragments submitted in anaerobic specimen containers for culture common in young male dogs of sporting FOLLOW-UP breeds. (see Anaerobic Infections) can provide a definitive diagnosis; inform the lab to check SIGNS PATIENT MONITORING r for actinomycosis; advisable to submit aerobic Infections—usually localized; may be r Monitor patients closely for recurrence in the culture, as well. Fresh smears—Gram months after therapy discontinued. disseminated; cervicofacial area commonly staining, cytology, and acid-fast staining; r PREVENTION/AVOIDANCE involved. Cutaneous swellings or abscesses staining does not preclude the need for with draining tracts—yellow granules (“sulfur culture; Actinomyces does not stain acid-fast; Avoidance of contact with grass awns and granules”) may be seen in associated exudates. prevention of bite wounds. r r Nocardia is variable. Pain, fever, and weight loss. Exudative PATHOLOGIC FINDINGS POSSIBLE COMPLICATIONS pleural or peritoneal effusions; occasionally r Histopathologic examination—sulfur Concurrent immune-suppressive disease or pericardial effusion noted. Cough, dyspnea, therapy may complicate management. decreased ventral lung sounds (empyema). granules can be difficult to find so multiple r EXPECTED COURSE AND PROGNOSIS Retroperitonitis—lumbar pain; rear limb tissue sections should be submitted; special r paresis or paralysis. Osteomyelitis of stains may enhance visualization of Redevelopment of infection at the initial site vertebrae or long bones—probably secondary organisms; granules are a useful diagnostic may be expected in about half of all cases. to extension of cutaneous infection; lameness tool when present; pyogranulomatous or r or a swollen extremity may develop. Motor granulomatous cellulitis with colonies of and sensory deficits—reported with spinal filamentous bacteria is characteristic. r cord compression by granulomas. Pyothorax MISCELLANEOUS and subcutaneous bite wounds are the most AGE-RELATED FACTORS common presenting signs in cats. Young outdoor dogs. CAUSES & RISK FACTORS TREATMENT r r ZOONOTIC POTENTIAL Actinomyces spp. normal inhabitants of the Exudative fluid (thorax, abdomen, r subcutaneous tissue) should be drained and There are no reported cases of actinomycosis oral cavity of dogs and cats. Loss of normal r protective barriers (mucosa, skin), lavaged. A chest tube with continuous being transmitted from animals to man; immunosuppression, or change in the suction is needed for cats with pyothorax; transmission by bite wound may be possible bacterial microenvironment can predispose; dogs are best served with surgical exploration so appropriate attention should be given to thought to occur as an opportunistic of the chest prior to tube placement in order bite wounds. r to identify and remove any grass awns. infection. Specific risk factors—trauma (bite r Suggested Reading Diseased lung lobes may need to be wound), migrating foreign body (grass awn r Edwards DF. Actinomycosis and nocardiosis. or, in the western United States, a foxtail), removed. Dogs with solitary masses In: Greene CE, ed., Infectious Diseases of and periodontal disease. involving the thoracic or abdominal wall may the Dog and Cat, 3rd ed. St. Louis, MO: experience cure with radical surgical excision. Saunders Elsevier, 2006, pp. 451–461. Thomovsky E., Kerl ME. Actinomycosis and nocardiosis. Compend Contin Educ Pract DIAGNOSIS Vet 2008, 10:4–10. Author Sharon Fooshee Grace DIFFERENTIAL DIAGNOSIS MEDICATIONS Consulting Editor StephenC.Barr r DRUG(S) Nocardiosis—primary differential diagnosis; r Actinomyces not reliably distinguished from Important to distinguish between Nocardia spp. by Gram staining, cytology, or Actinomyces and Nocardia for appropriate r clinical signs. Other causes of chronic antimicrobial selection. JWST589-A23-12 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:34 279mm×216mm

20 Blackwell’s Five-Minute Veterinary Consult A Acute Abdomen

r r Male Dalmatians in particular have a higher Biliary obstruction, rupture, or necrosis may risk of urethral obstruction because of the lead to bile leakage and peritonitis. high incidence of urate urinary calculi. Gallbladder mucocele may be identified on BASICS r German shepherds with pancreatic atrophy ultrasound examination. r DEFINITION have a higher risk of mesenteric volvulus. Hepatic abscess. r An emergency condition characterized by Patients treated with corticosteroids and Spleen r historical and physical examination findings non-steroidal anti-inflammatory drugs are at Splenic torsion, splenic masses, splenic of a tense, painful abdomen. May represent a higher risk for gastrointestinal ulceration and thrombus, splenic abscess. perforation. life-threatening condition. Urinary Tract r PATHOPHYSIOLOGY SIGNS Distention is the main cause of pain in the r A patient with an acute abdomen has pain General Comments urinary tract. r associated with either distention of an organ, Clinical signs vary greatly depending on the Lower urinary tract obstruction can be due inflammation, traction on the mesentery or type and severity of the disease leading to an to tumors of the trigone area of the bladder or peritoneum, or ischemia. acute abdomen. urethra, urinary calculi, or granulomatous r The abdominal viscera are sparsely Historical Findings urethritis. r r innervated, and diffuse involvement is often Trembling, reluctance to move, Traumatic rupture of the ureters or bladder necessary to elicit pain; nerve endings also inappetence, vomiting, diarrhea, vocalizing, are associated with blunt trauma and exist in the submucosa-muscularis of the increased intra-abdominal pressure. and abnormal postures (tucked up or praying r bowel wall. Urethral tears can be associated with pelvic r position)—signs that the owner may notice. Any process that causes fluid or gaseous r fractures from acute trauma. Question owner carefully to ascertain what r distension (i.e., intestinal obstruction, gastric system is affected; for example, melena with a Free urine in the peritoneal cavity leads to a dilatation-volvulus, ileus) may produce pain. chemical peritonitis. r history of NSAID treatment may suggest GI r Inflammation produces abdominal pain by mucosal disruption (ulceration). Acute pyelonephritis, acute renal failure, releasing vasoactive substances that directly nephroliths, and ureteroliths are uncommon Physical Examination Findings stimulate nerve endings. r causes of acute abdomen. r Abnormalities include abdominal pain, Many nerves in the peritoneum are sensitive Genital Tract to a diffuse inflammatory response. splinting of the abdominal musculature, gas- r or fluid-filled abdominal organs, abdominal Prostatitis and prostatic abscess, pyometra; a SYSTEMS AFFECTED ruptured pyometra or prostatic abscess can r mass, ascites, pyrexia or hypothermia, Behavioral—trembling, inappetence, tachycardia, and tachypnea. cause endotoxemia, sepsis, and cardiovascular r collapse. vocalizing, lethargy, and abnormal postural Once abdominal pain is confirmed, attempt r changes such as the praying position to to localize the pain to cranial, middle, or Infrequent causes include ruptures of the achieve comfort. caudal abdomen. gravid uterus after blunt abdominal trauma, r r Cardiovascular—severe inflammation, Perform a rectal examination to evaluate the uterine torsion, ovarian tumor or torsion, and ischemia, and sepsis may lead to acute colon, pelvic bones, urethra, and prostate, as intra-abdominal testicular torsion circulatory collapse (shock). May be well as for the presence of melena. (cryptorchid). r associated with SIRS and septic shock. Rule out extra-abdominal causes of pain by Abdominal Wall/Diaphragm r r Gastrointestinal—vomiting, diarrhea, careful palpation of the kidneys and Umbilical, inguinal, scrotal, abdominal, or inappetence, generalized functional ileus; thoracolumbar vertebrae. peritoneal hernias with strangulated viscera. r r pancreatic inflammation, necrosis, and Pain associated with intervertebral disc Trauma or congenital defects leading to abscesses may lead to cranial abdominal pain, disease often causes referred abdominal organ displacement or entrapment in the vomiting, and ileus. r guarding and is often mistaken for true hernia will lead to abdominal pain if the Hepatobiliary—jaundice associated with abdominal pain. Renal pain can be associated vascular supply of the organs involved extrahepatic cholestasis from biliary with pyelonephritis. becomes impaired or ischemic. obstruction (including pancreatitis) and bile CAUSES RISK FACTORS peritonitis. Hyperbilirubinemia may occur r secondary to sepsis. Gastrointestinal Exposure to NSAIDs or corticosteroid r r Renal/Urologic—azotemia can be due to Stomach—gastritis, ulcers, perforation, treatment (increased risk when used prerenal causes (dehydration, hypovolemia, foreign bodies, gastric dilatation-volvulus. concurrently)—gastric, duodenal, or colonic r ulcers. and shock), renal causes (acute pyelonephritis Intestine—obstruction (foreign bodies, r and acute renal failure), and post-renal causes intussusception, hernias), enteritis, ulcers, Garbage or inappropriate food ingestion— perforations. pancreatitis. (ureteral obstruction, urethral obstruction r r and uroperitoneum from bladder rupture). Rupture after obstruction, ulceration, or Foreign body ingestion—intestinal r obstructions. Respiratory—increased respiratory rate due blunt or penetrating trauma, or due to tumor r Abdominal trauma—hollow viscus rupture. to pain or metabolic/acid-base disturbances. growth. r r Hernias—intestinal obstruction/ SIGNALMENT Vascular compromise from infarction, r mesenteric volvulus, or torsion. strangulation. Dogs and cats. r Dogs more commonly. Pancreas r r Younger animals tend to have a higher Pain associated with inflammation, abscess, ischemia. incidence of trauma-related problems, r DIAGNOSIS intussusceptions, and acquired diet- and Pancreatic masses or inflammation infection-related diseases; older animals have a obstructing the biliary duct/papilla may cause DIFFERENTIAL DIAGNOSIS greater frequency of malignancies. jaundice. r r Renal-associated pain, retroperitoneal pain, Male cats and dogs are at higher risk for Hepatic and Biliary System r spinal or paraspinal pain, and disorders urethral obstruction. Rapid distention of the liver and its capsule causing diffuse muscle pain may mimic can cause pain. abdominal pain; careful history and physical JWST589-A23-12 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:34 279mm×216mm

Canine and Feline, Sixth Edition 21

(Continued) Acute Abdomen A

examination are essential in pursuing the Abdominal Ultrasound r appropriate problem. A sensitive diagnostic tool for the detection r Parvoviral enteritis can present similarly to of abdominal masses, abdominal fluid, TREATMENT intestinal obstructive disease; fecal parvoviral abscesses, cysts, lymphadenopathy, and biliary antigen assay and CBC (leukopenia) are or urinary calculi. APPROPRIATE HEALTH CARE r r helpful differentiating diagnostic tests. FAST ultrasound is a published technique Inpatient management with supportive care CBC/BIOCHEMISTRY/URINALYSIS meaning Focused Assessment with until decision about whether the problem is r Inflammation or infection may be Sonography in Trauma. to be treated medically or surgically. Early associated with leukocytosis or leukopenia. Abdominal CT intervention with surgery is important when r r indicated. Anemia may be seen with blood loss Very sensitive diagnostic tool that may be r associated with GI ulceration. used especially when surgeon requires Aggressive therapy and prompt r Azotemia is associated with prerenal, renal, additional information. identification of the underlying cause is very and post-renal causes. important. r DIAGNOSTIC PROCEDURES r Electrolyte abnormalities can help to Many causes of acute abdominal pain Abdominocentesis/Abdominal Fluid evaluate GI disease (i.e., hypochloremic require emergency surgical intervention. Analysis r metabolic alkalosis with gastric outflow r Keep patient NPO if vomiting, until a Perform abdominocentesis on all patients obstruction) and renal disease (i.e., definitive cause is determined and addressed. presenting with acute abdomen. r hyperkalemia with acute renal failure or Intravenous fluid therapy is usually required Four-quadrant approach may improve yield. post-renal obstruction). because of the large fluid loss associated with r Fluid can often be obtained for diagnostic Hyperbilirubinemia and elevated hepatic an acute abdomen; the goal is to restore the evaluation even when only a small amount of enzymes help localize a problem to the liver or normal circulating blood volume. free abdominal fluid exists, well before r biliary system. If severe circulatory compromise (shock) r detectable radiographic sensitivity. Urine specific gravity (before fluid therapy) exists, supplement initially with isotonic Ultrasound is much more sensitive than is needed to help differentiate prerenal, renal, crystalloid fluids (90 mL/kg, dogs; 70 mL/kg, radiography for the detection of fluid and can and post-renal problems. cats) over 1–2 hours; hypertonic fluids or r be used to direct abdominocentesis. Blind Urine sediment may be helpful in acute colloids may also be beneficial if refractory to abdominocentesis can be performed safely renal failure, ethylene glycol intoxication, and isotonic crystalloids or hypoproteinemic. without ultrasound guidance. Abdominal r pyelonephritis. Evaluate hydration and electrolytes (with fluid analysis with elevated WBC count, OTHER LABORATORY TESTS appropriate treatment adjustments) r degenerate neutrophils, and intracellular frequently after commencement of treatment. Venous blood gas analysis including lactate bacteria is consistent with septic peritonitis DIET concentration may indicate acid-base and is an indication for immediate surgery. r abnormalities, and increased lactate may be Diagnostic peritoneal lavage can be Early nutritional support important, associated with hypoperfusion. especially in order to maintain GI mucosal r performed by introducing sterile saline Canine and feline pancreatic lipase (10–20 ml/kg) and performing barrier. Nutritional support can be enteral immunoreactivity can be useful in evaluating abdominocentesis with or without ultrasound (oral, nasoesophageal, esophageal tube, pancreatitis. guidance. gastrostomy tube, enterostomy tube) or r IMAGING Measurement of glucose concentration in parenteral. abdominal effusion in comparison with SURGICAL CONSIDERATIONS Abdominal Radiography r r peripheral blood may aid in the diagnosis of May see abdominal masses or changes in Many different causes of an acute abdomen septic abdomen. A blood-to-abdominal fluid shape or shifting of abdominal organs. (withbothmedicalandsurgicaltreatments) r glucose difference of > 20 mg/dL is consistent Loss of abdominal detail with abdominal exist; make a definitive diagnosis whenever with septic effusion. fluid accumulation is an indication for r possible prior to surgical intervention. Pancreatitis patients may have an abdominal r abdominocentesis. This can prevent both potentially r effusion characterized as a non-septic (sterile) Free abdominal gas is consistent with a unnecessary and expensive surgical procedures peritonitis. ruptured GI viscus or infection with r and associated morbidity and mortality. Creatinine concentration higher in r gas-producing bacteria and is an indication It will also allow the surgeon to prepare for abdominal fluid than in serum indicates for emergency surgery. the task and to educate the owner on the r urinary tract leakage. prognosis and financial investment. Use caution when interpreting radiographs r Similarly, higher bilirubin concentration in following abdominocentesis with an open abdominal fluid than in serum indicates bile needle. Free gas may be introduced with this peritonitis. technique. r Use caution when evaluating postoperative Sedation and Abdominal Palpation MEDICATIONS ∙ Because of abdominal splinting associated radiographs; free gas is a normal postoperative DRUG(S) finding. with pain, thorough abdominal palpation is r Ileus is a consistent finding with peritonitis. often not possible without sedation; this is Analgesics r r Characterize ileus as functional (due to particularly useful for detecting intestinal Pain medication may be indicated for control of abdominal discomfort. metabolic or inflammatory causes) or foreign bodies that do not appear on survey r mechanical (due to obstruction). radiographs. Opioids, such as hydromorphone or r Foreign bodies may be radiopaque. Exploratory Laparotomy fentanyl, are often good choices. r Upper GI barium contrast radiographs are Histamine H Antagonists ∙ Surgery may be useful diagnostically (as well r 2 useful in evaluating the GI tract, particularly Reduce gastric acid production. as therapeutically) when ultrasonography (or r for determination of GI obstruction. Famotidine 0.5–1.0 mg/kg IV, SC or IM r other advanced imaging) is not available or Loss of contrast or radiographic detail in the q12h. when no definitive cause of the acute r area of the pancreas can be observed with abdomen has been established with Ranitidine 2 mg/kg IV q12h pancreatic inflammation. appropriate diagnostics. JWST589-A23-12 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:34 279mm×216mm

22 Blackwell’s Five-Minute Veterinary Consult

A Acute Abdomen (Continued)

r Proton Pump Inhibitor PRECAUTIONS Pyelonephritis r Pantoprazole 1–1.5 mg/kg IV as a CRI over Gentamicin and most NSAIDs can be Prostatitis and Prostatic Abscess r 24 hours. nephrotoxic and should be used with caution Urinary Tract Obstruction Protectants in hypovolemic patients and those with renal ABBREVIATIONS r Sucralfate 0.25–1 g PO q8h. impairment. Opiates are preferred to NSAIDs GI = gastrointestinal for pain management as NSAIDs may cause r Antiemetics NSAID = nonsteroidal anti-inflammatory r GI complications. Metoclopramide 0.2–0.4 mg/kg IV q6–8h drug (or 24-hour continuous rate infusion Suggested Reading (1–2 mg/kg/24h). r Beal MW. Approach to the acute abdomen. Maropitant: dogs, 1–2 mg/kg SC; cats, Vet Clin North Am Small Anim Pract 2005, 1 mg/kg SC FOLLOW-UP r 35:375–396. Ondansetron 0.5–1 mg/kg IV slowly PATIENT MONITORING Heeren V, Edwards L, Mazzaferro EM. Acute q6–12h. r Patients usually require intensive medical care abdomen: Diagnosis. Compend Contin Dolasetron 1 mg/kg IV q24h. and frequent evaluation of vital signs and Educ Pract Vet 2004, 26:350–363. Antibiotics laboratory parameters. Heeren V, Edwards L, Mazzaferro EM. Acute r Antibiotics may be indicated if signs of abdomen: Treatment. Compend Contin infection (fever, elevated white blood cell Educ Pract Vet 2004, 26:3566–3673. count, positive culture) are seen or Mazzaferro EM. Triage and approach to the hemorrhagic diarrhea is present. acute abdomen. Clin Tech Small Anim r MISCELLANEOUS Broad spectrum for Gram-positive, Pract 2003, 18:1–6. Gram-negative, and anaerobic bacteria. SYNONYM Author Steven L. Marks r Gram stain and cultures prior to treatment Colic Consulting Editor Stanley L. Marks if possible, but do not delay intervention SEE ALSO r pending results. Gastric Dilation and Volvulus Syndrome r CONTRAINDICATIONS Gastroduodenal Ulceration/Erosion (GUE) r Gastrointestinal Obstruction Do not use metoclopramide if GI obstruction r Intussusception is suspected. Do not use barium if r gastrointestinal perforation is suspected. Use Pancreatitis iodinated contrast agent instead. JWST589-A24-13 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:51 279mm×216mm

Canine and Feline, Sixth Edition 23 Acute Respiratory Distress Syndrome A

GENETICS comparison of blood gases taken at different Certain humans are more prone to developing FiO2.PaCO2 is often low; hypercapnia tends ARDS than others due to specific gene to be a late (preterminal) development. BASICS r polymorphisms. This has not been Total protein of airway edema fluid DEFINITION investigated in the veterinary population. compared with serum total protein—ratio of r Acute respiratory distress syndrome (ARDS) INCIDENCE/PREVALENCE edema fluid to serum total protein < 0.5 is isasyndromeofacuteonsetofrespiratory Unknown supportive of low-protein hydrostatic pressure pulmonary edema (e.g., heart failure, fluid failure typified by diffuse bilateral pulmonary SIGNALMENT infiltrates on a dorsoventral thoracic overload); edema fluid/serum total protein radiograph with no clinical evidence of left Species ratio > 0.7 suggests a high-protein, increased Dog and cat permeability pulmonary edema such as ARDS atrial hypertension or volume overload. r ARDS results from an overwhelming Breed Predilections and pneumonia. Coagulation panel may inflammatory reaction in the alveolocapillary A familial form of ARDS has been reported in reveal hypocoagulable state supportive of DIC membrane in response to a systemic or a group of related Dalmatian dogs; it is or cause of pulmonary hemorrhage. pulmonary inflammatory insult. The end clinically indistinguishable from ARDS. IMAGING result is increased vascular permeability r Mean Age and Range Thoracic Radiographs r leading to edema. The 2012 Berlin Unknown Bilateral/diffuse pulmonary infiltrates. r Definition of ARDS defines three categories Severity of radiographic signs can lag SIGNS r of severity based on PaO2/FiO2 ratio and level behind clinical disease by 12–24 hours. Can of PEEP employed during ventilation, with Historical Findings r be difficult to distinguish from cardiogenic mild ARDS defined by a PF ratio of Acute onset of respiratory distress in a edema. Cardiac silhouette and pulmonary 200–300 mmHg with PEEP ≥ 5 mmHg, patient with a significant underlying disease r vascular size is usually normal in ARDS. moderate ARDS as a PF ratio of 100–200 or exposure to known risk factors. The ≥ Echocardiography mmHg with PEEP 5 mmHg, and severe patient is often hospitalized for its primary r < Attempt to rule out cardiogenic cause for ARDS as a PF ratio 100 mmHg with PEEP disease when it develops ARDS. r ≥ pulmonary edema. May be able to estimate 5 mmHg. Physical Examination Findings r r degree of pulmonary hypertension. PATHOPHYSIOLOGY Severe respiratory distress Crackles (if r present) heard bilaterally on auscultation DIAGNOSTIC PROCEDURES ARDS is due to a diffuse inflammatory r Fever—depends on underlying disease Pulmonary artery catheter to measure insult that causes widespread damage to r r alveolar endothelial and epithelial cells Cyanosis in more severe cases Signs pulmonary artery occlusion pressure can be resulting in thickening of the membrane and relevant to the primary disease process. used to rule out cardiogenic cause for edema; impaired gas exchange. This inflammatory by definition, ARDS is associated with PAOP CAUSES ≤ insult can be triggered by primary pulmonary 18 mmHg. Primary Pulmonary Causes disease or it can be of non-pulmonary origin, r r PATHOLOGIC FINDINGS Aspiration pneumonia Pneumonia and leads to exudative, proliferative, and r r r Pulmonary contusion Near drowning Gross Pathology fibrotic changes within the lung: First, r r Smoke inhalation An idiopathic form of Lungs are dark, heavy, and ooze fluid when excessive accumulation and activation of ARDS associated with acute interstitial cut. neutrophils, monocytes, and platelets in the pneumonia or idiopathic pulmonary fibrosis pulmonary microvasculature leads to Histopathology has been reported in humans and dogs. r increased alveolar endothelial permeability. Acute phase—pulmonary vascular Non-pulmonary Causes congestion with edema fluid and This causes protein-rich edema fluid and r r r r inflammatory cells to leak into the interstitial SIRS Sepsis Neoplasia Pancreatitis inflammatory cell accumulation in the r r r and alveolar spaces. Alveolar epithelial Severe trauma and shock Severe bee sting interstitium and alveoli; epithelial cell injury results from release of cytokines and envenomation damage, hyaline membrane formation, other inflammatory mediators from RISK FACTORS microthrombi, microatelectasis. r r leukocytes and platelets. Epithelial injury r r r r Proliferative phase—hyperplasia of type 2 SIRS Sepsis Severity of illness Multiple pneumocytes, interstitial mononuclear involves both type I and type II alveolar transfusions epithelial cells, and results in alveolar flooding infiltration, organization of hyaline and surfactant dysfunction. This causes membranes, and fibroproliferation. collapse and consolidation of alveoli with development of severe hypoxemia, and DIAGNOSIS hyaline membrane formation in the alveolar r spaces. Microthrombi in the pulmonary DIFFERENTIAL DIAGNOSIS TREATMENT r r vasculature, hypoxic pulmonary Left-sided congestive heart failure Fluid APPROPRIATE HEALTH CARE vasoconstriction, and release of endogenous r r r overload Diffuse pneumonia Pulmonary There is no specific therapy. General aims vasoconstrictors lead to pulmonary arterial hemorrhage are to maintain tissue oxygenation and to hypertension, which can lead to right-sided r CBC/BIOCHEMISTRY/URINALYSIS minimize iatrogenic lung injury while treating heart failure. Proliferation of type 2 alveolar r r r epithelial cells and pulmonary fibrosis occurs Leukocytosis or leukopenia Other changes the underlying disease. Oxygen in the late stages of ARDS. dependent on the underlying disease process therapy—no more than is required to maintain PaO > 60–80 mmHg to minimize OTHER LABORATORY TESTS 2 r SYSTEMS AFFECTED r r r Arterial blood gases—low PaO /FiO ratio oxygen toxicity. Positive-pressure ventilation Respiratory. Cardiovascular—right-sided 2 2 is essential in the management of ARDS heart failure secondary to pulmonary (where PaO2 is measured in mmHg and FiO2 = patients. It is indicated in patients that are hypertension; hemodynamic compromise is 0.21–1.0). Normal PaO2/FiO2 ratio 500; comparison of this ratio allows evaluation of hypoxemic despite oxygen therapy, patients may be associated with aggressive mechanical requiring high levels of inspired oxygen for ventilator settings. severity of lung disease and allows direct JWST589-A24-13 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:51 279mm×216mm

24 Blackwell’s Five-Minute Veterinary Consult

A Acute Respiratory Distress Syndrome (Continued)

r prolonged periods, or patients working so Antibiotics for the underlying disease where hard to breathe that they are at risk of indicated. r r exhaustion. ARDS is thought to be Vasoactive drugs to maintain blood pressure. r MISCELLANEOUS exacerbated by ventilator-induced lung injury Anesthetic drugs to allow positive-pressure associated with alveolar overdistension ventilation. ASSOCIATED CONDITIONS r compounded by cyclic opening and collapse Analgesia as appropriate. r Systemic inflammatory response syndrome, of atelectatic alveoli. Therefore, Low-dose corticosteroid—use remains multiple organ dysfunction syndrome, sepsis. lung-protective strategies of positive-pressure controversial with conflicting reports of SYNONYMS ventilation with moderate to high PEEP, low efficacy for low-dose steroids in early or late r r Acute hypoxemic respiratory failure Acute tidal volumes, and permissive hypercapnia are ARDS. r interstitial pneumonia Adult respiratory recommended to minimize ventilator-induced r ALTERNATIVE DRUG(S) distress syndrome High-protein pulmonary lung injury. Tidal volumes of 6 mL/kg have r Furosemide may produce pulmonary venous edema Shock lung been found to increase survival significantly in dilation and improve lung function, as an SEE ALSO human ARDS patients compared to tidal intermittent bolus of 1 mg/kg IV q6–12h or r r r Dyspnea and Respiratory Distress Panting volumes of 12 mL/kg. Recruitment as a CRI of 0.2 mg/kg/h IV. Beware r and Tachypnea Pulmonary Edema, maneuvers and high levels of PEEP can both dehydration and effects on organ function. r cause significant hemodynamic compromise Noncardiogenic Sepsis and Bacteremia and patients should have constant direct ABBREVIATIONS r arterial blood pressure monitoring. ARDS = acute respiratory distress r r Intensive supportive care of the syndrome CRI = constant rate infusion FOLLOW-UP r cardiovascular system and other organ systems DIC = disseminated intravascular r is vital, as these patients are at high risk for PATIENT MONITORING coagulation PAOP = pulmonary artery development of multiple organ dysfunction. Arterial blood gases, pulse oximetry, end-tidal occlusion pressure (formerly pulmonary r NURSING CARE carbon dioxide, thoracic radiographs, arterial capillary wedge pressure [PCWP]) PEEP = r r blood pressure, ECG, temperature, urine positive end-expiratory pressure PF ratio = Monitor temperature closely, especially if r output, CBC, coagulation profiles, serum PaO /FiO ratio PPV = positive-pressure using an oxygen cage, as animals with 2 2 r excessive work of breathing can easily become chemistry, blood cultures, monitoring for ventilation SIRS = systemic inflammatory r hyperthermic. Ventilator patients require other organ dysfunction. response syndrome frequent position changes and physical PREVENTION/AVOIDANCE INTERNET RESOURCES r therapy; regular oral care with a dilute Aggressive therapy of primary disease http://www.ardsnet.org chlorhexidine solution is important to reduce processes to reduce the inflammatory insult to r Suggested Reading oral colonization with bacteria as a source of the lung. Intensive cardiovascular ARDS Definition Task Force, Ranieri VM, sepsis, and frequent endotracheal tube monitoring and support of critically ill Rubenfeld GD, et al. Acute respiratory suctioning is needed to prevent occlusion. animals to ensure adequate tissue perfusion. r distress syndrome: the Berlin Definition. J Inflate cuff carefully and change endotracheal Careful management of recumbent animals Am Med Assoc 2012, 307(23):2526–2533. cuff position regularly to prevent tracheal to reduce the chance of aspiration, especially r Matthay MA, Ware LB, Zimmerman GA. damage. Blood pressure monitoring, as if patient has neurologic disease or upper The acute respiratory distress syndrome. J septic patients are prone to hypotension. airway disorders that reduce the ability to r r Clin Invest 2012, 122(8):2731–2740. Fluid therapy is important to support the protect the airway. Judicious use of blood Parent C, King LG, Van Winkle TJ, Walker cardiovascular system and to maintain products in patients with inflammatory or LM. Respiratory function and treatment in normovolemia while avoiding fluid overload, severe systemic disease. as this will negatively affect lung function. dogs with acute respiratory distress POSSIBLE COMPLICATIONS ACTIVITY r syndrome: 19 cases (1985–1993). J Am Vet Multiorgan dysfunction syndrome—acute Med Assoc 1996, 208:1428–1433. If not anesthetized for ventilation, strict cage kidney injury, DIC, and gastrointestinal Syrja P, Saari S, Rajamaki M, Saario E, confinement. disease are the more common forms of organ r Jarvinen A-K. Pulmonary histopathology in DIET dysfunction seen. Barotrauma—can result Dalmatians with familial acute respiratory Nutritional support is important but in pneumothorax. Incidence is thought to be distress syndrome (ARDS). J Comp Pathol less with lower tidal volume ventilation challenging. Enteral feeding is desired over r 2009, 141(4):254–259. parenteral nutrition, but must consider high strategies. Ventilator-associated Ware LB, Matthay MA. The acute respiratory risk of regurgitation and aspiration in a pneumonia—patients on PPV have increased distress syndrome. N Engl J Med 2000, recumbent patient. risk of pneumonia that may be difficult to 342:1334–1349. CLIENT EDUCATION differentiate from worsening of the initial Wilkins PA, Otto CM, Baumgardner JE, lung injury. Airway cultures should be Clients need to be aware of the guarded et al. Acute lung injury and acute considered in deteriorating patients. prognosis and high costs of therapy. r respiratory distress syndromes in veterinary Oxygen toxicity may be unavoidable due to medicine: consensus definitions: The SURGICAL CONSIDERATIONS severity of hypoxemia in spite of PPV. Oxygen Dorothy Russell Havemeyer Working The underlying disease may require surgery. toxicity is indistinguishable from ARDS on GrouponALIandARDSinVeterinary histopathology making the incidence of this Medicine. J Vet Emerg Crit Care (San problem impossible to determine. Antonio) 2007, 17(4):333–339. EXPECTED COURSE AND PROGNOSIS Authors Casey J. Kohen and Kate Hopper r MEDICATIONS Mortality in human patients remains at Consulting Editor Lynelle R. Johnson r DRUG(S) OF CHOICE 40–60%. Mortality in veterinary patients r No specific drug therapy. likely approaches 100%. JWST589-A25-14 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:5 279mm×216mm

Canine and Feline, Sixth Edition 25 Adenocarcinoma, Anal Sac A

r DIAGNOSTIC PROCEDURES then every 6 months thereafter. Incomplete r Fine-needle aspiration of anal sac mass to resection—monitor tumor size and blood BASICS rule out conditions other than calcium and renal values. adenocarcinoma; while differentiation of EXPECTED COURSE AND PROGNOSIS OVERVIEW benign versus malignant neoplasm of perianal r r Guarded prognosis with both local Malignant neoplasm derived from apocrine masses is difficult, apocrine gland r r progression and metastasis occurring. Cures glands of the anal sac. Locally invasive. adenocarcinoma of the anal sac will have a may occur if tumor is found early and treated r r High metastatic rate, often to sublumbar neuroendocrine appearance and can be aggressively. Growth of the tumor may be r differentiated from perianal gland tumors. lymph nodes. Frequently associated with r slow and debulking lymph node metastatic hypercalcemia, secondary to parathyroid Fine-needle aspiration of enlarged lymph disease may significantly prolong survival. nodes, liver, or splenic nodules to confirm r hormone–related peptide secretion. r Hypercalcemia is variably associated with a r r Prognosis guarded to fair. metastasis. Incisional biopsy for poor prognosis. Four papers (involving SIGNALMENT histopathology required for definitive 200 dogs) showed median survival times of 6 r diagnosis, although excisional biopsy may be Older dogs; extremely rare in cats. to 20 months, depending on stage and r appropriate if location of mass and cytology r Females overrepresented in some studies. treatment. A recent report on 16 dogs r are supportive of anal gland neoplasia. English cocker spaniels significantly without metastasis showed a median survival time not met with a follow-up of 33 months. overrepresented, springer and Cavalier King r Charles spaniels also overrepresented. Dogs with lymph node metastasis lived significantly longer if the nodes were SIGNS r TREATMENT extirpated. Ultimately, dogs that cannot r Historical Findings Surgical resection—treatment of choice. have their tumors excised completely r Signs may be due to physical obstructive Resection of primary tumor and enlarged succumb to hypercalcemia-related r nature of primary tumor (rectal mass, lymph nodes may prolong survival. If mass complications or mass effect from primary tenesmus) or enlarged local lymph node is large and regionally invasive at diagnosis, tumor or sublumbar nodal metastases. metastasis (tenesmus, constipation, surgery often palliative, not curative. r stranguria), or systemic manifestations due to Debulking all disease present may control hypercalcemia (anorexia, polyuria/polydipsia, hypercalcemia until tumor recurrence. r lethargy). Saline diuresis (200–300 mL/kg/day) MISCELLANEOUS Physical Examination Findings preoperatively if hypercalcemia is severe. r r ASSOCIATED CONDITIONS Mass associated with anal sac; may be quite Radiation may help delay local recurrence small despite massive metastatic disease. Hypercalcemia as a paraneoplastic syndrome r and control growth of sublumbar metastases. Sublumbar lymphadenopathy—on rectal or ABBREVIATION abdominal palpation. PTHrP = parathyroid hormone-related CAUSES & RISK FACTORS peptide None definitively identified MEDICATIONS Suggested Reading DRUG(S) Anderson CL, Mackay CS, Roberts GD, Fidel r Limited reports of partial responses to J. Comparison of abdominal ultrasound and platinum compounds in dogs—cisplatin magnetic resonance imaging for detection of DIAGNOSIS (70 mg/m2 IV with 6-hour saline diuresis— abdominal lymphadenopathy in dogs with metastatic apocrine gland adenocarcinoma DIFFERENTIAL DIAGNOSIS 18.3 mL/kg/h), carboplatin (300 mg/m2 IV r r of the anal sac. Vet Comp Oncol 2013, doi: Anal sac abscess Perianal adenoma/ as a slow bolus) every 3 weeks. r r 2 10.1111/vco.12022. adenocarcinoma Mast cell tumor Mitoxantrone (5 mg/m IV every 3 weeks r r Emms SG. Anal sac tumours of the dog and Lymphoma Squamous cell carcinoma for five treatments) in combination with r radiation therapy used in one small case series. their response to cytoreductive surgery and Perineal hernias r Possible role for melphalan after debulking chemotherapy. Australian Vet J 2005, CBC/BIOCHEMISTRY/URINALYSIS 2 83:340–343. r surgery (7 mg/m PO q24h for 5 days every Hypercalcemia—25–50% of cases. London C, Mathie T, Stingle N, et al. r 3 weeks). Secondary renal failure may develop. r Preliminary evidence for biologic activity of Toceranib phosphate reported to have some ® OTHER LABORATORY TESTS benefit (partial response or stable disease) in toceranib phosphate (Palladia )insolid 28 dogs with measurable tumor. tumours. Vet Comp Oncol 2012, If hypercalcemia is present, and tumor cannot 10(3):194–205. be identified, parathyroid hormone and CONTRAINDICATIONS/POSSIBLE Polton GA, Brearley MJ. Clinical stage, PTHrP levels can be assessed—high PTHrP INTERACTIONS therapy, and prognosis in canine anal sac support neoplasia as the cause of r Avoid platinum chemotherapeutic agents in gland carcinoma. J Vet Intern Med 2007, hypercalcemia. r dogs with renal insufficiency. Do not use 21:274–280. IMAGING Williams LE, Gliatto JM, Dodge RK, et al. r cisplatinincats. Abdominal radiography—to evaluate Carcinoma of the apocrine glands of the sublumbar lymph nodes and lumbar and anal sac in dogs: 113 cases (1985–1995). r pelvic bones. Thoracic radiography—to J Am Vet Med Assoc 2003, 223:825–831. evaluate for pulmonary metastasis. Author Laura D. Garrett r FOLLOW-UP Abdominal ultrasonography—may identify Consulting Editor Timothy M. Fan PATIENT MONITORING mildly enlarged sublumbar lymph nodes not r Complete resection—physical examination, visible radiographically, also nodules in Client Education Handout r thoracic radiography, abdominal liver/spleen. MRI—recently shown to available online identify lymphadenopathy with greater ultrasonography, and serum biochemistry at sensitivity than ultrasound. 1, 3, 6, 9, and 12 months postoperatively, JWST589-A26-15 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:58 279mm×216mm

26 Blackwell’s Five-Minute Veterinary Consult A Adenocarcinoma, Lung

well-circumscribed mass; must be performed CONTRAINDICATIONS/POSSIBLE in cats presenting with multiple digit tumors INTERACTIONS to screen for primary lung tumor (lung-digit r BASICS r Doxorubicin—monitor patients with syndrome). Ultrasonography—may help underlying cardiac disease carefully; consider OVERVIEW with obtaining an aspirate or biopsy specimen pretreatment with diphenhydramine and r Comprises 75% of primary pulmonary from lung, or to evaluate abdomen. serial echocardiograms and ECGs. r r r tumors in dogs and cats. Strongest CT—most accurate assessment of surgical Cisplatin—do not give to cats (fatal); do predictors of outcome are tumor grade, node feasibility, lymphadenopathy (93% accuracy), not use in dogs with pre-existing renal disease; r r involvement, and clinical signs. May metastatic disease. Dogs—most common in never use without appropriate and concurrent r metastasize. May be associated with right caudal lung lobe and accessory lobe; diuresis. hypertrophic osteopathy. cats—most common in left caudal lung lobe. SIGNALMENT DIAGNOSTIC PROCEDURES r Dogs Thoracocentesis with cytologic examination r r r 1% of all tumors Mean age of affected (for pleural effusion). Cytology— FOLLOW-UP r transthoracic fine-needle aspiration (83% animals 10 years No sex predilection, PATIENT MONITORING agreement with histopathology). though more females in some reports r r r Percutaneous tissue biopsy—use Tru-Cut Serial thoracic radiographs—consider every Medium to large breeds overrepresented r instrument. Open lung biopsy—specimen 3 months; administer a minimum of two Cats cycles of chemotherapy before evaluating r r via thoracotomy, or minimally invasive r Rarer than in dogs Mean age of affected r thoracoscopy. response to treatment. Perform CBC (with animals 11 years No breed predilection PATHOLOGIC FINDINGS any chemotherapy), biochemical analysis SIGNS r (cisplatin), and urinalysis (cisplatin) before Adenocarcinoma—classified according to each chemotherapy treatment. Historical Findings location (bronchial, bronchiolar, r POSSIBLE COMPLICATIONS Related to presence of a lung mass: bronchiolar-alveolar, or alveolar) and degree r r ◦ Nonproductive cough (> 50% of dogs) of differentiation. Thyroid transcription Following diagnostic procedures or ◦ Dyspnea (may be related to pneumothorax) factor-1 positivity may distinguish primary thoracotomy: pneumo- or hemothorax r r r ◦ Tachypnea ◦ Hemoptysis Paraneoplastic from metastatic carcinoma. Cats tend to Resulting from chemotherapy: signs: ◦ Lameness—bone metastasis or have less differentiated tumors, corresponding myelosuppression, fever, sepsis, nausea hypertrophic osteopathy (dogs or cats), to more aggressive behavior. EXPECTED COURSE AND PROGNOSIS r weight-bearing lytic digit metastasis (cats) Metastasis to the tracheobronchial lymph ◦ Polyuria or polydipsia—hypercalcemia or nodes—single best prognostic indicator; hyperadrenocorticism from ectopic median survival without metastasis ◦ production of ACTH Fever TREATMENT approaches 1 year and with metastasis, Physical Examination Findings r 60 days. More common (75%) in cats. r Surgery—mainstay of treatment: partial or r May be asymptomatic or lack respiratory Postoperative survival in dogs (∼1yr)is r r complete lobectomy with tracheobronchial signs Tachypnea and dyspnea Fever better than in cats (∼4 mo), but around r r lymph node biopsy or removal; thoracoscopic Limb swelling Ascites, pleural effusion 2 years in either species if positive prognostic r removal possible at limited centers and offers r Caval syndrome factors are present. Other patient, tumor, less postoperative morbidity. CAUSES & RISK FACTORS r and treatment factors influencing prognosis— Radiotherapy—reports are anecdotal, but complete surgical excision; size of the primary Some evidence correlates risk to urban r certain patients may benefit. Chemotherapy tumor (< 5 cm better); metastasis (better if environment; controversial should be considered following surgery for none); degree of cell differentiation (histologic tumors that are high grade, undifferentiated, score, better if well differentiated), lack of and/or have nodal involvement. Intracavitary clinical signs prior to surgery. chemotherapy can be used to treat malignant DIAGNOSIS pleural effusion. r r Fine-needle aspirate cytology Tissue biopsy or definitive resection MISCELLANEOUS DIFFERENTIAL DIAGNOSIS r MEDICATIONS PREGNANCY/FERTILITY/BREEDING Granulomatous lesion (fungal, foreign body, r r DRUG(S) Chemotherapy is not advised in pregnant parasitic) Pulmonary abscess Other r animals. primary lung tumor: ◦ Squamous cell Chemotherapy—vinorelbine concentrates ABBREVIATIONS carcinoma ◦ Sarcomas (osteo-, chondro-, in lungs and responses have been seen. r r lipo-) Metastatic lung tumor Pneumonia ◦ Doxorubicin, cisplatin, carboplatin, ACTH = adrenocorticotrophic hormone r r Asthma Pulmonary thromboembolism mitoxantrone, vinorelbine, and/or r r Suggested Reading Congenital cyst Lung torsion or vindesine—rational choices for palliation ◦ Rissetto KC, Lucas P, Fan TM. An update on hematoma Platinum based or gemcitabine diagnosing and treating primary lung CBC/BIOCHEMISTRY/URINALYSIS chemotherapy may be superior tumors. Vet Med 2008, 103(3):154. ◦ Toceranib Phosphate (Palladia) has shown No specific abnormalities Author Kim A. Selting some anecdotal success OTHER LABORATORY TESTS r Consulting Editor Timothy M. Fan Chemotherapy can be toxic; seek advice if Acknowledgments The author and editors Coagulation tests unfamiliar with cytotoxic drugs. acknowledge the prior contribution of Renee IMAGING r Al-Saraff. Thoracic radiography—usually demonstrates a focal, solitary, JWST589-A27-16 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:0 279mm×216mm

Canine and Feline, Sixth Edition 27 Adenocarcinoma, Nasal A

r CAUSES Regional lymph node metastasis < 10% at Dolichocephalic morphology, p53 mutations, time of diagnosis but up to 45% at necropsy. BASICS and COX-2 overexpression may all play a role. RISK FACTORS DEFINITION Urban environment and second-hand smoke Malignant neoplasm involving the nasal may be risk factors. TREATMENT cavity and paranasal sinuses. APPROPRIATE HEALTHCARE PATHOPHYSIOLOGY r Radiation therapy is the standard of care. r Progressive local and regional invasion of the Radiation therapy can be administered with nasal cavity, paranasal sinuses, and DIAGNOSIS curative intent (definitive) or for palliation of surrounding tissues by neoplastic epithelial clinical signs. DIFFERENTIAL DIAGNOSIS r and glandular epithelial cells. r Other sinonasal tumors (e.g., squamous cell Definitive radiation involves multiple SYSTEMS AFFECTED fractions for a high total dose. r carcinoma, lymphoma, sarcomas, olfactory r Respiratory—congestion, obstruction, neuroblastoma) Palliative radiation uses a low total dose to r dyspnea, epistaxis, mucopurulent nasal Intracranial neoplasia minimize toxicity while improving the quality discharge r of life through reduction of tumor size. r Viral infection—cats r Nervous—seizures, altered mentation r Novel radiation techniques including IMRT r Fungal infections including aspergillosis Ophthalmic—exophthalmos, epiphora (dogs) and cryptococcosis (cats) and stereotactic radiation therapy may r INCIDENCE/PREVALENCE Bacterial sinusitis decrease risk of late toxicity while improving r r tumor control. Parasites (e.g., nasal mites) r In dogs, less than 2% of all tumors are nasal r tumors. Foreign body Combining radiation therapy with novel r r In dogs, adenocarcinoma is more common Trauma drug therapy (toceranib phosphate (Palladia), r others) appears safe and well tolerated. than squamous cell carcinoma, Tooth root abscess and oronasal fistula r r Radiation therapy followed by surgery to chondrosarcoma, and other histologies, Coagulopathies r debulk residual mass may improve local comprising 31.5% of all nasal tumors. Ehrlichiosis, leishmaniasis r r control time but results in higher risk of late In cats, nasal tumors comprise < 1% of all Systemic hypertension toxicity. tumors. In cats, adenocarcinoma and r CBC/BIOCHEMISTRY/URINALYSIS Surgery alone considered ineffective with lymphoma are most common. r Usually normal most tumors relapsing within 6 months. GEOGRAPHIC DISTRIBUTION r Occasional blood loss anemia NURSING CARE Nasal adenocarcinomas are more commonly r OTHER LABORATORY TESTS During radiation therapy, supportive care reported in urban areas. r Cytologic examination: occasionally helpful for radiation related mucositis may involve SIGNALMENT (e.g., aspirates of the subcutaneous mass if r softening food, rinsing mouth with saline, Dog and cat. facial deformity) r r dilute black tea, and administration of Median age in dogs is 10 years and 13 years Coagulation profile medications to control discomfort. r in cats. IMAGING These side effects are temporary butmay r r In dogs, medium to large breeds affected Survey skull radiography—not sensitive; cause discomfort for 10–14 days. more commonly with a possible may show asymmetrical destruction of ACTIVITY overrepresentation of mesocephalic and r turbinates accompanied by a soft tissue mass Limit activity to minimize risk of epistaxis dolichocephalic breeds. effect; may see fluid density in the frontal and dyspnea. SIGNS sinuses secondary to outflow obstruction. r r Using a harness instead of a collar during Historical Findings Thoracic radiography—evaluate for lung walks may help minimize epistaxis. r metastasis (uncommon). Intermittent and progressive history of r DIET unilateral to bilateral epistaxis and/or CT or MRI best imaging method for local r staging and observing integrity of cribriform Soften food if needed during radiation mucopurulent discharge that initially therapy. plate or orbital invasion, and also used for r responds to antibiotic therapy (median Avoid extremes of temperatures and salty duration, 3 months). therapeutic planning. r foods with radiation therapy-related Sneezing and increased upper respiratory DIAGNOSTIC PROCEDURES mucositis. noises including reverse sneezing. r r Blood pressure. CLIENT EDUCATION Open-mouth breathing. r r Oral exam under anesthesia. Halitosis. r Nasal adenocarcinoma may be painful even r Rhinoscopy may permit visual observation Anorexia (more frequent in cats). of the mass and aid biopsy.. though the pet is not showing visible signs of r r pain. Seizures (secondary to invasion of cranial Tissue biopsy necessary for definitive r vault). diagnosis. Biopsies may be performed blind, Consider the use of medications for discomfort and congestion. Physical Examination Findings following advanced imaging, using pinch r r Radiation therapy is the most effective Nasal discharge (blood, mucopurulent) biopsy instrument including retroflex r rhinoscopic biopsy of nasopharynx, cannula option and is well-tolerated using modern Decreased or absent airflow in the nasal radiotherapy techniques. passages (unilateral or bilateral) (closed suction), or hydropulsion techniques. r r r Radiation side effects may impact the Facial deformity, exophthalmos, epiphora Cytologic evaluation of regional lymph r nodes to detect regional metastatic disease. patient’s quality of life during treatment, but Pain upon nasal or paranasal sinus palpation most pets enjoy a relatively normal quality of or upon opening the mouth PATHOLOGIC FINDINGS r life following treatment. Regional lymphadenomegaly (rare) r r Bilateral involvement and osteolysis Abnormal mentation or other neurologic common. findings (rare) JWST589-A27-16 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:0 279mm×216mm

28 Blackwell’s Five-Minute Veterinary Consult

A Adenocarcinoma, Nasal (Continued)

r Intermittent congestion and sneezing may SEE ALSO r occur post therapy due to increased sensitivity Squamous cell carcinoma, nasal r from the tumors’ destruction of the nasal Chondrosarcoma, nasal FOLLOW-UP r turbinates. Lymphoma, nasal SURGICAL/ANESTHETIC PATIENT MONITORING ABBREVIATIONS r r CONSIDERATIONS CT or MRI are needed to assess response to CT = computed tomography r Anesthetic recovery—ensure airway is therapy and are recommended 2–3 months MRI = magnetic resonance imaging post radiation treatment. maintained until animal is sternal to prevent r INTERNET RESOURCES Other staging tests including thoracic r apnea in patients with bilateral nasal http://veterinarymedicine.dvm360.com/ obstruction. radiography or CT and lymph node evaluation are generally recommended in vetmed/Medicine/Canine-and-feline-nasal- 3-month intervals during/following therapy. tumors/ArticleStandard/Article/detail/735167 r r Routine staging with CT/MRI and http://smallanimal.vethospital.ufl.edu/ monitoring of recurrent clinical signs can clinical-services/oncology/types-of-cancer- and-treatment/nasal-tumors-dogs/ MEDICATIONS detect early recurrence. r http://www.ncbi.nlm.nih.gov/pmc/articles/ DRUG(S) OF CHOICE POSSIBLE COMPLICATIONS r r PMC2643460/ Chemotherapy is considered ineffective for Dyspnea r durable tumor control, but may benefit some Epistaxis Suggested Reading r patients if radiation therapy is not a viable Secondary infections Adams WA, Bjorling DE, McAnulty JF, et al. r option. Various drugs have been described Weight loss Outcome of accelerated radiotherapy alone r including cisplatin (dogs only), carboplatin, Anorexia or accelerated radiotherapy followed by r doxorubicin, and piroxicam. Toceranib Chemotherapy or radiation toxicity exenteration of the nasal cavity in dogs with phosphate (Palladia) exerts therapeutic EXPECTED COURSE AND PROGNOSIS intranasal neoplasia: 53 cases (1990–2002). activity against nasal carcinoma. r J Am Vet Med Assoc 2005, 227:936–941. r Untreated—median survival around 2–6 Consult with an oncologist for more details. Henry CJ, Brewer WG, Tyler JW, et al. r months. r Survival in dogs with nasal Adequate analgesic therapy should be Radiation therapy—median survival times employed as needed in patients suffering from adenocarcinoma:64 cases (1981–1995). J around 12–18 months in dogs and 12–20 Vet Intern Med 1998, 12:436–439. invasive disease with bone destruction, signs months in cats; 1-year survival rate 20–57% of pain, and radiation therapy side effects. LaDueTA,DodgeR,PageRL,etal.Factors (dogs and cats); 2-year survival rate 20–48% influencing survival after radiotherapy of CONTRAINDICATIONS (dogs and cats). r nasal tumors in 130 dogs. Vet Radiol Cisplatin—never use in cats. Presence of cribriform lysis, brain Ultrasound 1999, 40:312–317. PRECAUTIONS involvement or metastatic disease (advanced Langova V, Mutsaers AJ, Phillips B, Straw R. r stage) are poor prognostic indicators. Most chemotherapeutics have r Treatment of eight dogs with nasal tumours gastrointestinal, hematologic, and other Ophthalmic complications of radiation with alternating doses of carboplatin and therapy—more likely in dogs than cats. potential side effects and should be r doxorubicin in conjunction with oral administered and monitored by an oncologist. Incidence and severity of ophthalmic piroxicam. Aust Vet J 2004, 82:676–680. r Piroxicam can cause gastric ulceration so toxicity are decreasing with advanced Lawrence JA, Forrest LJ, Turek MM, et al. careful monitoring of appetite, vomiting, and radiation therapy techniques now commonly Proof of principle of ocular sparing in dogs used. stool color (melena) is recommended. r with sinonasal tumors treated with Chronic rhinitis is possible following POSSIBLE INTERACTIONS intensity-modulated radiation therapy. Vet radiation therapy for sinonasal tumors and Radiol Ultrasound 2010, 51(5):561–570. Concurrent radiation therapy and may require periodic symptomatic therapy. chemotherapy will increase the risk of side Rassnick KM, Goldkamp CE, Erb HN, et al. effects but have not shown to significantly Evaluation of factors associated with improve tumor control. survival in dogs with untreated nasal carcinomas: 139 cases (1993–2003). J Am ALTERNATIVE DRUGS r MISCELLANEOUS Vet Med Assoc 2006, 229:401–406. Palladia, a tyrosine kinase inhibitor, may AGE-RELATED FACTORS Theon AP, Peaston AE, Madewell BR et al. have anticancer activity in some carcinomas Irradiation of nonlymphoproliferative including nasal adenocarcinomas. It is None neoplasms of the nasal cavity and paranasal currently being investigated at the labeled PREGNANCY/FERTILITY/BREEDING sinuses in 16 cats. J Am Vet Med Assoc dose alone and in combination with radiation Chemotherapeutic drugs and general 1994, 204(1):78–83. therapy. r anesthesia are a risk to the fetus and would Author Jayme Looper Objective responses have been documented not be recommended in pregnant animals. Consulting Editor Timothy M. Fan with use of Palladia alone. SYNONYMS Acknowledgment The author and editors r Nasal carcinoma acknowledge the prior contribution of r Nasal tumor Louis-Philippe de Lorimier. JWST589-A28-17 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:38 279mm×216mm

Canine and Feline, Sixth Edition 29 Adenocarcinoma, Pancreas A

IMAGING r Abdominal radiographs may reveal a mass BASICS or loss of serosal detail associated with FOLLOW-UP concurrent pancreatitis or peritoneal effusion. r OVERVIEW Ultrasonography may reveal one or more POSSIBLE COMPLICATIONS r r Malignant tumor of ductal or acinar origin masses or concurrent pancreatitis (mixed Intestinal obstruction r arising from the exocrine pancreas. echogenicity, large pancreas, hyperechoic Biliary obstruction r r Usually metastatic by the time of diagnosis, peripancreatic fat). Pancreatic thickening, Pancreatic abscess r affecting regional lymph nodes and visceral abdominal effusion, and single to multiple Peritonitis r abdominal organs (liver) and associated nodules of varying size may be identified. Metastasis peritoneal cavity. Sonographic findings may be impossible to EXPECTED COURSE AND PROGNOSIS distinguish from pancreatic nodular SIGNALMENT Progression to death is often rapid given that r hyperplasia. Rarely the ultrasound of the Rare in dogs—0.5–1.8% of all tumors there is no successful curative treatment r pancreas may appear normal except for Rare in cats—2.8% of all tumors available. Despite the grave prognosis, r dilation of the pancreatic duct. Older female dogs and Airedale terriers at individual patients treated with complete higher risk than others DIAGNOSTIC PROCEDURES resection of their tumor and chemotherapy, in r r Median age (dogs)—9.2 years Surgical biopsy—definitive. the absence of systemic metastasis, may have r r Mean age (cats)—11.6 years Fine-needle aspirate cytology—supportive. prolonged survival. SIGNS In many cases, where the tumor is not r resectable, the fine-needle aspirates may Nonspecific—fever; vomiting; weakness; provide strong enough evidence to start anorexia; icterus; malabsorption syndrome; medical treatment. weight loss. MISCELLANEOUS r Abdominal pain—variable. r ASSOCIATED CONDITIONS Abdominal effusion—malignant. r Gastrin-secreting pancreatic carcinoma Metastasis to bone and soft tissue common. r (gastrinoma) has been reported in dogs and Pathologic fractures secondary to metastasis TREATMENT cats. Clinical signs are associated with reported. r r None reported curative. hypergastrinemia, which results in Palpable abdominal mass (cats). r r Palliation of pain with aggressive analgesic inappropriate hydrochloric acid secretion by Paraneoplastic syndromes of epidermal combinations is necessary. r the stomach, leading to gastroduodenitis. necrosis, hyperinsulinemia, and Surgical intervention to alleviate intestinal hyperglucagonemia may be present. and biliary obstruction, if necessary. Suggested Reading r r Average duration of clinical signs (cats): Surgery is typically not a good option in Linderman MJ, Brodsky EM, de Lorimier LP, 41 days, range 2–180 days. many cases, due to the extent of the disease at Clifford CA, Post GS. Feline exocrine CAUSES & RISK FACTORS the time of diagnosis. pancreatic carcinoma: a retrospective study r Unknown If surgery is an option, partial or total of 34 cases. Vet Comp Oncol 2013, pancreatectomy may prolong survival. 11(3):208–218. r Treat concurrent pancreatitis. Cave T, Evans H, Hargreavest J, et al. r Antiemetics and supportive care (hydration Metabolic epidermal necrosis in a dog and caloric requirements). associated with pancreatic adenocarcinoma, DIAGNOSIS hyperglucagonaemia, hyperinsulinaemia, DIFFERENTIAL DIAGNOSIS and hypoaminoacidaemia. J Small Anim r Primary pancreatitis; may be concurrent Pract 2007, 48:522–526. and complicate or delay early diagnosis Hecht S, Penninck DG, Keating JH. Imaging r MEDICATIONS Pancreatic pseudocyst findings in pancreatic neoplasia and nodular r DRUG(S) Pancreatic nodular hyperplasia hyperplasia in 19 cats. Vet Radiol r r Hepatic neoplasia Gemcitabine is used in humans for the Ultrasound 2006, 48:45–50. r Other causes of vomiting and icterus treatment of pancreatic carcinoma, and while Quigley KA, Jackson ML, Haines DM. r Peritoneal carcinomatosis used in dogs with cancer, it has not been Hyperlipasemia in 6 dogs with pancreatic or r Other causes of abdominal effusion in cats established as the standard of care for dogs hepatic neoplasia: Evidence for tumor lipase with pancreatic adenocarcinoma. production. Vet Clin Pathol 2001, CBC/BIOCHEMISTRY/URINALYSIS r r Always consult a veterinary oncologist for 30:114–120. Usually nonspecific changes (e.g., mild updates in treating this rare neoplasm. Author Nick Dervisis anemia and neutrophilia). r CONTRAINDICATIONS/POSSIBLE Consulting Editor Timothy M. Fan Hyperamylasemia less reliable than Acknowledgment The author and editors hyperlipasemia. INTERACTIONS r acknowledge the prior contribution of Lipase concentrations are often markedly N/A Wallace B. Morrison. elevated and may serve as a non-invasive biochemical marker of neoplasia in dogs. OTHER LABORATORY TESTS Rarely there may be significant metabolic alterations that affect glucagon, insulin, and amino acid concentrations. JWST589-A29-18 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:48 279mm×216mm

30 Blackwell’s Five-Minute Veterinary Consult A Adenocarcinoma, Prostate

CBC/BIOCHEMISTRY/URINALYSIS r Inflammatory leukogram possible. r BASICS Alkaline phosphatase may be high if skeletal MEDICATIONS metastases exist. r OVERVIEW Post-renal azotemia may be present if DRUG(S) r urethral obstruction exists. r Prostatic adenocarcinoma is a malignant r Chemotherapy—carboplatin, tumor that occurs in both neutered and intact It is prudent to evaluate urine samples via mitoxantrone, or doxorubicin; may offer male dogs. cystocentesis and free-catch techniques, as short-term benefit. r r Although this neoplasm represents < 1% of hematuria, pyuria, and malignant epithelial Pain relief with NSAIDs, morphine-derived all canine malignancies, it is the most cells may be observed in free-catch samples drugs. r common prostatic disorder in neutered male but are unusual in samples obtained by Aminobisphosphonates for the relief of dogs. cystocentesis. painful skeletal metastases. r r Metastases to regional lymph nodes, lungs, OTHER LABORATORY TESTS Stool softeners to relieve tenesmus. and the lumbosacral skeleton are common. Serum and seminal plasma markers such as CONTRAINDICATIONS/POSSIBLE Skeletal metastases can adopt an osteoblastic acid phosphatase, prostate specific antigen, INTERACTIONS appearance. and canine prostate specific esterase are not N/A SIGNALMENT elevated in dogs with PAC. r Dog and rarely cat IMAGING r r Medium- to large-breed intact or neutered Thoracic radiography—metastases may male dogs r appear as pulmonary nodules or increased FOLLOW-UP Median age of 9–10 years interstitial markings. r SIGNS Abdominal radiography—sublumbar PATIENT MONITORING Historical Findings lymphadenomegaly, mineralization of the Ability to urinate and defecate, pain secondary r to skeletal metastases, quality of life. Tenesmus (with the production of prostate, lytic lesions to the lumbar vertebrae ribbon-like stool) or pelvis as a consequence of direct tumor PREVENTION/AVOIDANCE r Weight loss extension from regionally infiltrated lumbar Keeping dogs sexually intact may decrease r Stranguria and dysuria lymph nodes may be seen. risk. r r Rear limb lameness or neurologic weakness Abdominal ultrasonography—focal to r POSSIBLE COMPLICATIONS Lethargy multifocal hyperechogenicity with asymmetry r r Urethral obstruction Exercise intolerance and irregular prostatic outline, ± prostatic r mineralization. Metastasis to regional lymph nodes, Physical Examination Findings r skeleton, and lungs r Contrast cystography may help differentiate A firm, asymmetrical, and immobile prostatic from urinary bladder disease. EXPECTED COURSE AND PROGNOSIS prostate gland. r DIAGNOSTIC PROCEDURES Guarded to poor, survival of 2–6 months Prostatomegaly is common, but is not r depending upon presenting clinical always present. Prostatic aspirate (percutaneous or r transrectal). symptoms. Treatment early in the course of Pain may be elicited in response to r disease with curative-intent radiation and abdominal or rectal palpation. Prostatic wash. r r systemic chemotherapy can extend survival Caudal abdominal mass, cachexia, pyrexia, Prostatic biopsy performed percutaneously or surgically. times to 12 months. and dyspnea may also be identified in r advanced cases of disease. Percutaneous biopsy has been associated CAUSES & RISK FACTORS with tumor seeding along the biopsy tract. Neutered males are at increased risk for MISCELLANEOUS prostatic neoplasia ASSOCIATED CONDITIONS TREATMENT None r Prostatectomy if local disease (success of this AGE-RELATED FACTORS DIAGNOSIS procedure depends on the skill of the surgeon None and extent of disease). DIFFERENTIAL DIAGNOSIS r ABBREVIATIONS r Radiation therapy may palliate signs and r Other primary neoplasia (i.e., squamous cell prolong survival. NSAID = nonsteroidal anti-inflammatory carcinoma, transitional cell carcinoma). r drug r Prostatic urethral stenting can alleviate r Metastatic or locally invasive neoplasia (i.e., urethral obstruction. PAC = prostatic adenocarcinoma transitional cell carcinoma). r r Neutering—however, most tumors are not Suggested Reading Acute or chronic prostatitis, benign androgen responsive. Bryan JN, et al. A population study of prostatic hypertrophy, prostatic abscess, and neutering status as a risk factor for canine prostatic cysts are possible differentials in prostate cancer. Prostate 2007, intact male dogs but are highly unlikely in 67:1174–1181. neutered dogs. Author Ruthanne Chun Consulting Editor Timothy M. Fan JWST589-A30-19 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:35 279mm×216mm

Canine and Feline, Sixth Edition 31 Adenocarcinoma, Renal A

r Biochemistry may be normal, or may reveal PREVENTION/AVOIDANCE azotemia. N/A r Urinalysis may show hematuria, POSSIBLE COMPLICATIONS BASICS r proteinuria, bacteriuria, or casts. Renal failure OVERVIEW r OTHER LABORATORY TESTS Metastatic disease r < r Accounts for 1% of all reported Urine culture and sensitivity Invasion of local vital structures (vena cava, neoplasms in dogs. r IMAGING aorta) Renal tumors tend to be highly metastatic r Thoracic radiographs—metastatic disease EXPECTED COURSE AND PROGNOSIS via hematogenous dissemination, locally r invasive, and often bilateral. reported in up to 16% of patients. Adenocarcinoma—median reported r r Renal cystadenocarcinoma, a rare heritable Abdominal radiographs—mass visualized in survival of 49 dogs was 16 months (range 81% of patients. 0–59 months). syndrome with a less aggressive behavior and r r better long-term prognosis than renal Abdominal ultrasonography, CT, or contrast Cystadenocarcinoma—few large studies of adenocarcinoma, has been described in radiography—useful in identifying and this rare disease, reported median survival of German shepherd dogs. staging the disease. Advanced imaging can 12+ months with no definitive therapy. guide decisions regarding surgical resectability. SIGNALMENT r DIAGNOSTIC PROCEDURES Adenocarcinoma—older (8–9 years) dogs, r Renal biopsy (ultrasound-guided or 1.6:1 male-to-female ratio, no breed MISCELLANEOUS predilection. surgical) for definitive diagnosis. r r Cystadenocarcinoma—German shepherd Percutaneous fine-needle aspirate can be ASSOCIATED CONDITIONS used for supportive diagnosis. r dogs, often female. The paraneoplastic syndromes of SIGNS hypertrophic osteopathy, polycythemia, and a r Adenocarcinoma—insidious, non-specific neutrophilic leukocytosis have been reported in isolated cases. signssuchasweightloss,inappetance, r TREATMENT Renal failure. lethargy, hematuria, and pale mucous r r membranes. Possibility for paraneoplastic Aggressive surgical excision is the treatment Nodular dermatofibrosis and uterine polycythemia. of choice for unilateral disease. leiomyomas are commonly associated with r r Cystadenocarcinoma—may present for Successful chemotherapeutic management cystadenocarcinoma. nodular dermatofibrosis, a syndrome of of either disease has not been described. ABBREVIATION r r painless, firm, fibrous lesions of the skin and Supportive management for patients in CT = computed tomography subcutaneous tissues. renal failure may be necessary. Suggested Reading CAUSES & RISK FACTORS r Bryan JN, et al. Primary renal neoplasia of Adenocarcinoma—unknown. r dogs. J Vet Intern Med 2006, Cystadenocarcinoma—heritable in German 20:1155–1160. shepherd dogs. MEDICATIONS Knapp DW. Tumors of the urinary system. DRUG(S) In: Withrow SJ, Vail DM, eds., Small None Animal Clinical Oncology, 4th ed. Philadelphia: Saunders, 2007, pp. 649–658. DIAGNOSIS Author Ruthanne Chun DIFFERENTIAL DIAGNOSIS Consulting Editor Timothy M. Fan r Other primary neoplasia (i.e., lymphoma, FOLLOW-UP nephroblastoma) r PATIENT MONITORING Metastatic neoplasia (i.e., r Renal failure—measure serum urea nitrogen hemangiosarcoma) r and creatinine; urinalysis. Renal adenoma or cyst r r Quality of life if bilateral or otherwise Pyelonephritis non-surgical disease. CBC/BIOCHEMISTRY/URINALYSIS r CBC may show paraneoplastic polycythemia or leukocytosis, or anemia. JWST589-A31-20 JWST589-Tilley Printer: Yet to Come August 1, 2015 10:55 279mm×216mm

32 Blackwell’s Five-Minute Veterinary Consult A Adenocarcinoma, Salivary Gland

be indicated for treatment/palliation of metastatic disease. BASICS DIAGNOSIS CONTRAINDICATIONS/POSSIBLE INTERACTIONS OVERVIEW DIFFERENTIAL DIAGNOSIS r r N/A Tumor arising from major (e.g., parotid, Squamous cell carcinoma r mandibular, sublingual, or zygomatic) or Mucocele r minor salivary glands. Abscess r r Mandibular or parotid glands constitute Soft tissue sarcoma, e.g., fibrosarcoma r 80% of cases. Lymphoma FOLLOW-UP r r Mandibular gland most frequently affected Sialadenosis PATIENT MONITORING in dogs. r CBC/BIOCHEMISTRY/URINALYSIS Evaluations—physical examination and Parotid gland most frequently affected in Results often normal thoracic radiographs every 3 months cats. r reasonable if aggressive surgery and/or Locally invasive and regionally metastatic. IMAGING r r radiation therapy employed. Cats typically have more advanced disease Regional radiographs usually are normal; POSSIBLE COMPLICATIONS than dogs at time of diagnosis. may see periosteal reaction on adjacent bones r or displacement of surrounding structures. Temporary acute side effects (e.g., moist Metastasis—regional lymph node r involvement in 39% of cats and 17% of dogs MRI or CT imaging allows superior dermatitis and alopecia) expected with at diagnosis; distant metastasis reported in discrimination of tumor for surgery and/or definitive radiation therapy in dogs, but radiation treatment planning. uncommon in cats. Consultation with a 16% of cats and 8% of dogs at diagnosis but r may be slow to develop. Thoracic radiographs indicated to check for radiation oncologist is recommended r Other salivary gland neoplasms— lung metastases. regarding specific, anatomic site-related side carcinoma; squamous cell carcinoma; mixed DIAGNOSTIC PROCEDURES effects associated with planned dose and field neoplasia. r size. r Cytologic examination of aspirate may Epithelial malignancies—constitute roughly EXPECTED COURSE AND PROGNOSIS differentiate salivary adenocarcinoma from r 85% of salivary gland tumors. mucocele and abscess. Improved survival time in dogs without r r Fibrosarcomas, lipomas, mast cell tumors, Needle core or wedge biopsy for evidence of nodal or distant metastasis at and lymphomas have involved the salivary histopathology—definitive diagnosis. diagnosis; clinical stage not prognostic for glands by direct extension and invasion. A cats. r concurrent malignant fibrous histiocytoma Median survival 550 days for dogs and (giant cell type) and malignant mixed tumor 516 days for cats in retrospective study. r (likely of ductal origin) within the salivary TREATMENT Local control obtained through radiation gland has also been described. r r and/or surgery remains critical. Adenomas comprise only 5% of salivary Aggressive surgical resection—when tumors. possible; most are invasive and difficult to excise completely. SIGNALMENT r r Radiotherapy—good local control and Dog and cat. MISCELLANEOUS r prolonged survival in three reported cases. Mean age, 10–12 years. r r Aggressive local resection (usually ABBREVIATIONS Siamese cats—may be at relatively higher histologically incomplete) followed by r risk. CT = computed tomography r adjuvant radiation can achieve local control r Male cats affected twice as often as female MRI = magnetic resonance imaging and long-term survival, but further studies are cats. r needed to determine the most effective Suggested Reading No other breed or sex predilection has been treatment, including the possible role for Hammer A, Getzy D, Ogilvie G, et al. determined. chemotherapy. Salivary gland neoplasia in the dog and cat: SIGNS Survival times and prognostic factors. J Am r Unilateral, firm, painless swelling of the Anim Hosp Assoc 2001, 37:478–482. upper neck (mandibular and sublingual), ear Author Anthony J. Mutsaers base (parotid), upper lip or maxilla MEDICATIONS Consulting Editor Timothy M. Fan (zygomatic), or mucous membrane of lip (accessory or minor salivary tissue). DRUG(S) r Other signs may include halitosis, weight Chemotherapy (mitoxantrone or carboplatin) loss, anorexia, dysphagia, exophthalmus, efficacy is largely unreported; however, may Horner’s syndrome, sneezing, and dysphonia. CAUSES & RISK FACTORS Unknown JWST589-A32-21 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:11 279mm×216mm

Canine and Feline, Sixth Edition 33 Adenocarcinoma, Skin (Sweat Gland, Sebaceous) A

DIAGNOSTIC PROCEDURES r Biopsy for histopathology and definitive diagnosis BASICS r FOLLOW-UP Cytologic examination or biopsy of draining r OVERVIEW lymph nodes Sebaceous gland adenocarcinoma—little is Malignant growth originating from sebaceous PATHOLOGIC FINDINGS known about the metastatic potential of this r or apocrine sweat glands of the skin. Apocrine gland adenocarcinomas are malignancy, but may be rapidly metastatic to SIGNALMENT typically invasive into the underlying stroma regional lymph nodes in some patients; r and blood vessels, and often show poorly long-term prognosis is anecdotally good with Apocrine sweat gland—rare in dogs, multimodal therapy combining aggressive uncommon in cats. demarcated borders and a high mitotic index. r r surgery, chemotherapy, and radiation therapy. Sebaceous gland adenocarcinomas often r Sebaceous gland—rare in both dogs and Apocrine gland adenocarcinoma—fair to cats. reveal lymphatic vessel invasion. r good long-term prognosis; the histologic Middle-aged to older pets. r finding of vascular invasion is a negative Female dogs overrepresented for apocrine prognostic factor predicting systemic adenocarcinoma in one study. metastases; aggressive surgical resection (local SIGNS TREATMENT and regional tumor control) followed by r r May appear as solid, firm, raised, superficial Aggressive en bloc surgical excision, adjuvant chemotherapy is recommended to skin lesions. improve survival. A study reported a r including resection of draining lymph node, May be ulcerated and bleeding and recommended for both types. post-excisional median survival time of accompanied by inflammation of the Histopathologic analysis of lymph nodes 30 months in dogs. surrounding tissue. r assists with determining prognosis and Apocrine sweat gland—often poorly establishing adjuvant treatment plan. r circumscribed, ulcerated; very invasive into Margins of entire tissue specimen must be underlying tissue; may occur anywhere on the evaluated histologically to assess completeness MISCELLANEOUS body, frequently affecting the trunk in dogs. of resection. r r Sebaceous gland—often ulcerated and Radiation therapy may be recommended for Suggested Reading inflamed, moderate risk of lymph node treatment of draining lymph nodes after Carpenter JL, Andrews LK, Holzworth J. involvement. Tumors and tumor like lesions. In: r resection to prevent recurrence and Dermal and lymphatic tracking can be development of regional metastasis; radiation Holzworth J, ed., Diseases of the Cat: observed early in disease course. therapy of primary tumor site recommended Medicine and Surgery. Philadelphia: CAUSES & RISK FACTORS when wide and complete resection not Saunders, 1987, pp. 406–596. Pakhrin B, Kang MS, Bae IH, et al. Unknown possible. Retrospective study of canine cutaneous tumors in Korea. J Vet Sci 2007, 8:229–236. Simko E, Wilcock BP, Yager JA. A MEDICATIONS retrospective study of 44 canine apocrine DIAGNOSIS sweat gland adenocarcinomas. Can Vet J DIFFERENTIAL DIAGNOSIS DRUG(S) 2003, 44(1):38–42. r r Other more frequent skin tumors Chemotherapy has been used anecdotally Hauck ML. Tumors of the skin and r Cutaneous histiocytic diseases for the treatment of both tumor types, in subcutaneous tissues. In: Withrow SJ, Vail r Immune-mediated skin diseases both species. DM, Page RL, eds., Small Animal Clinical r r Bacterial/fungal infections Contact a veterinary oncologist for any Oncology, 5th ed. St. Louis, MO: Elsevier updated treatments that may be available. Saunders, 2013, pp. 305–320. CBC/BIOCHEMISTRY/URINALYSIS r Nonsteroidal anti-inflammatory drugs and Haziroglu R, Haligur M, Keles H. Normal other analgesics are recommended, as Histopathological and immunohisto- OTHER LABORATORY TESTS indicated, for pain control. chemical studies of apocrine sweat gland N/A CONTRAINDICATIONS/POSSIBLE adenocarcinomas in cats. Vet Comp Oncol 2014, 12(1):85–90. IMAGING INTERACTIONS Author Louis-Philippe de Lorimier Thoracic radiographs recommended at the None Consulting Editor Timothy M. Fan time of diagnosis to assess for distant metastases. JWST589-A33-22 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:13 279mm×216mm

34 Blackwell’s Five-Minute Veterinary Consult A Adenocarcinoma, Stomach, Small and Large Intestine, Rectal

OTHER LABORATORY TESTS Fecal occult blood may be positive; diet may BASICS affect results—can recheck to confirm after FOLLOW-UP feeding non-meat diet for 3 days. OVERVIEW IMAGING Physical examination, thoracic radiographs, r r and abdominal ultrasound—at 1, 3, 6, 9, and Uncommon tumor arising from the Ultrasound—may reveal a thickened epithelial lining of the gastrointestinal tract. 12 months post-surgery. r stomach or bowel wall; may see mass in the Prognosis guarded to poor. gastrointestinal tract, enlarged lymph nodes. EXPECTED COURSE AND PROGNOSIS r SIGNALMENT Positive contrast radiography—filling defect Dogs r r Dog more commonly affected than cat. (stomach); intraluminal space-occupying or Overall poor; pedunculated rectal tumors r Middle-aged to older (> 6 years) animals; annular constriction (small bowel); gastric do best; most cases recur locally, develop age range 3–13 years. neoplasm most often found in distal metastasis, or both rapidly. r r No breed predisposition. two-thirds of stomach. Median survival gastric—2 months. r r r More common in males than females. Double contrast radiography—large Median survival small intestinal— intestine and rectum; polypoid or annular 10 months. SIGNS r space-occupying masses. Mean survival large intestinal—annular Historical Findings r r Advanced imaging with contrast CT or 1.6 months versus pedunculated 32 months. Stomach—vomiting, anorexia, weight loss, MRI can provide highest quality images of Cats hematemesis, and melena. r r gastrointestinal tract. Guarded. Small intestine—vomiting, weight loss, DIAGNOSTIC PROCEDURES r borborygmus, flatulence, and melena. Few reported cases, but may have prolonged r r > Large intestine and rectum—mucus and Ultrasound-guided fine-needle aspirate of survival ( 1 year). blood-tinged feces and tenesmus. bowel mass or enlarged lymph node may reveal carcinoma cells on cytology, which can Physical Examination Findings r be useful to rule out lymphoma. Stomach—nonspecific. r r Endoscopic biopsy may be non-diagnostic MISCELLANEOUS Small intestine—may feel mid-abdominal because tumors are frequently deep to the mass; distended, painful loops of small bowel; ABBREVIATIONS mucosal surface; thus surgical biopsy r melena on rectal exam. CT = computed tomography r frequently required. r Large intestine and rectum—palpable mass MRI = magnetic resonance imaging per rectum, may form annular ring, or multiple nodular lesions protruding into the Suggested Reading Seim-Wikse T, Jorundsson E, Nodtvedt A, colon; bright red blood on feces. TREATMENT CAUSES & RISK FACTORS et al. Breed predisposition to canine gastric r r carcinoma–a study based on the Norwegian Unknown. Surgical resection—treatment of choice; r seldom curative. canine cancer register. Acta Vet Scand Nitrosamines—reported as causative agent r Gastric—usually non-resectable. 2013;55:25. in experimental literature. r r Small intestine—remove by resection and vonBaboV,EberleN,MischkeR,etal. Possible genetic cause—gastric Canine non-hematopoietic gastric adenocarcinomas in related Belgian shepherds anastomosis; metastasis to regional lymph nodes and the liver common. neoplasia. Epidemiologic and diagnostic and Dutch Tervuren shepherds. r Large intestine and rectal—may characteristics in 38 dogs with post-surgical occasionally be resected by a pull-through outcome of five cases. Tierarztl Prax Ausg K surgical procedure; metastasis common; Kleintiere Heimtiere 2012;40(4):243–249. transcolonic debulking may provide palliation Crawshaw J, Berg J, Sardinas JC, et al. DIAGNOSIS of obstruction. Prognosis for dogs with nonlymphomatous DIFFERENTIAL DIAGNOSIS small intestinal tumors treated by surgical r excision. J Am Anim Hosp Assoc 1998, Foreign body r 34:451–456. Inflammatory bowel disease r Swann HM, Holt DE. Canine gastric Lymphoma MEDICATIONS r adenocarcinoma and leiomyosarcoma: A Parasites r DRUG(S) retrospective study of 21 cases (1986–1999) Leiomyoma r r and literature review. J Am Anim Hosp Leiomyosarcoma Chemotherapy—only anecdotal reports, r usually unsuccessful. Assoc 2002, 38:157–164. Pancreatitis r Piroxicam 0.3 mg/kg PO q24 h can provide Author Laura D. Garrett CBC/BIOCHEMISTRY/URINALYSIS Consulting Editor Timothy M. Fan r palliation for large intestinal and rectal Stomach and small intestine—may see tumors. r microcytic, hypochromic anemia Aggressive combination analgesics should be (iron-deficiency anemia). Mild and persistent instituted. elevations in blood urea nitrogen in the face CONTRAINDICATIONS/POSSIBLE of normal creatinine can support intestinal blood loss. INTERACTIONS r Large intestine and rectum—no Seek advice before initiating treatment with characteristic changes. cytotoxic drugs. JWST589-A34-23 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:18 279mm×216mm

Canine and Feline, Sixth Edition 35 Adenocarcinoma, Thyroid—Dogs A

Historical Findings required and allows for controlled hemostasis r Palpable mass/swelling in cervical neck, in the event of bleeding. BASICS coughing, dyspnea, dysphagia, dysphonia, Cytology facial edema, neck pain. r r Examination of fine-needle aspirates from DEFINITION If functional thyroid tumor—may see tumor and palpable regional lymph nodes. r A malignant tumor arising from the follicular polyuria, polydypsia, polyphagia, weight loss, Specimen almost always heavily restless behavior, diarrhea. or parafollicular cells (medullary/C-cells) of r contaminated with blood owing to highly the thyroid gland. If hypothyroid—may see poor hair coat, vascular nature of tumor. r PATHOPHYSIOLOGY weight gain, lethargy. Homogeneous population of epithelial cells, r Physical Examination Findings sometimes with colloid and/or About 60% of patients are euthyroid, 30% r Freely movable or fixed cervical mass, tyrosine-containing granules. hypothyroid, and 10% hyperthyroid. r r unilateral or bilateral. Unable to differentiate malignant from Typically very invasive tumors with high r rate of metastasis (lungs, retropharyngeal Rarely may see Horner’s syndrome, or benign thyroid cells; but almost all thyroid cranial vena cava syndrome. neoplasms in dogs are malignant. lymph nodes, liver), with up to 35–40% of r dogs having metastasis at the time of If hyperthyroid—cardiac arrhythmias or PATHOLOGIC FINDINGS murmurs. diagnosis. Gross r r Animals with bilateral tumors have a sixteen CAUSES Characterized by high vascularity with areas times greater risk of developing metastatic Unknown of hemorrhage and necrosis. r disease than animal with unilateral tumors. RISK FACTORS Usually poorly encapsulated; often invade SYSTEMS AFFECTED r adjacent tissues (e.g., trachea and esophagus, r Untreated hypothyroidism has been shown Cardiovascular—hyperthyroid dogs are to be a risk factor in a colony of beagles. and surrounding vasculature); may adhere to r usually tachycardic and may have systemic Breed predilection. the jugular vein, carotid artery, and r hypertension; may see anemia and DIC in Iodine deficiency. vagosympathetic trunk. advanced disease. Histopathology r r Endocrine/Metabolic—affected dogs may Three main types—follicular, papillary, and be hypothyroid, euthyroid, or hyperthyroid; compact (solid); mixed follicular and solid hypercalcemia may be seen as a paraneoplastic tumors most common in dogs. DIAGNOSIS r syndrome or secondary to concurrent C-cell (e.g., parafollicular, medullary) parathyroid hyperplasia or parathyroid DIFFERENTIAL DIAGNOSIS r carcinomas less common. adenocarcinoma. r Other primary neoplasms—lymphoma; soft Respiratory—dogs may be dyspneic owing tissue sarcoma; salivary gland to a space-occupying mass adjacent to the adenocarcinoma; parathyroid carcinoma; trachea; metastasis to the lungs common. carotid body tumor. r TREATMENT Large compressive masses can result in caval Secondary tumors—metastatic oral syndrome manifested as facial edema. squamous cell carcinoma; oral melanoma. APPROPRIATE HEALTH CARE r Inflammatory—abscess or granuloma. r GENETICS r Definitive treatment is dependent on tumor Unknown Salivary mucocele. stage (tumor size, mobility, and evidence of CBC/BIOCHEMISTRY/URINALYSIS metastatic disease). INCIDENCE/PREVALENCE r r Usually normal. Complete surgical excision recommended Accounts for 1.2–3.8% of all canine tumors r for freely movable thyroid tumors. May see non-regenerative normocytic r and represents 10–15% of all primary head Full course external beam radiation therapy and neck tumors. normochromic anemia of chronic disease, leukocytosis. recommended preoperatively for large GEOGRAPHIC DISTRIBUTION r Rare—hypercalcemia; isosthenuria; DIC. tumors, as a sole therapy for non-resectable tumors, or postoperatively for incompletely May be more common in iodine-deficient OTHER LABORATORY TESTS areas. surgically removed tumors. Thyroid hormone (T and/or free T levels) r SIGNALMENT 4 4 Palliative radiation and/or chemotherapy and endogenous TSH levels. recommended for tumors that are metastatic Species IMAGING at presentation. r r Dog Thoracic radiography (3 view)—evaluation Also can use iodine-131 but doses are very Breed Predilections of lungs and other thoracic structures for large (60–100 mCi) and therefore there are Boxers, golden retrievers, Siberian huskies, metastasis. limited facilities that offer this therapy. r r and beagles at increased risk but seen in any Cervical ultrasonography, computed Toceranib phosphate (Palladia) can exert breed. tomography, and magnetic resonance cytoreductive activity. Mean Age and Range imaging—evaluation of tissue of origin, NURSING CARE Older dogs (median 9–15 years; range vascularity, invasion, and cervical lymph Varies with signs on examination. nodes. 4–18 years) r ACTIVITY Predominant Sex Technetium-99m scintigraphy to evaluate for ectopic thyroid tissue or metastatic lesions. Restrict activity if dyspneic. No gender predilection. r Radioiodine studies—may provide DIET SIGNS information about the tumor’s ability to N/A General Comments produce thyroid hormone. r CLIENT EDUCATION r Usually not diagnosed until a large mass is DIAGNOSTIC PROCEDURES Warn owners of the importance of palpable. r Biopsy controlling heart rate and rhythm in Approximately 65% are unilateral, 35% are Tru-Cut not recommended owing to high risk hyperthyroid patients and of the possibility of bilateral. of severe hemorrhage; open biopsy usually episodes of collapse. JWST589-A34-23 JWST589-Tilley Printer: Yet to Come August 1, 2015 11:18 279mm×216mm

36 Blackwell’s Five-Minute Veterinary Consult

A Adenocarcinoma, Thyroid—Dogs (Continued)

r r r Warn owners of possible postoperative Cisplatin is nephrotoxic; do not give to For animals treated with full course external laryngeal paralysis and intraoperative animals with renal disease. beam radiation therapy—progression-free hemorrhage. survival at 1 year—80%, and 72% at 3 years r PRECAUTIONS Warn owners of acute radiation therapy Chemotherapy can cause gastrointestinal, in one study and in another study MST toxicities—moist desquamation, laryngitis, 24.5 months. bone marrow, cardiac, and other toxicities— r tracheitis, esophagitis. seek advice from a medical oncologist if Palliative radiation therapy in 13 dogs— SURGICAL CONSIDERATIONS MST 24 months. unfamiliar with cytotoxic drugs. r 131 See “Appropriate Health Care” I therapy in combination with surgery— POSSIBLE INTERACTIONS MST 34 months, or 131I alone MST Risks Verapamil—may potentiate doxorubicin- 30 months. r r Marked hemorrhage—tumors highly induced cardiotoxicity. Animals treated with cisplatin alone vascular and invasive into surrounding ALTERNATIVE DRUG(S) (13 dogs)—overall response rate was 53%, structures including vasculature; may need N/A median progression-free interval for blood transfusion and intensive postoperative responders was 202 days and overall MST was care. r 98 days. Laryngeal paralysis—owing to trauma to recurrent laryngeal nerve. r Damaged parathyroid glands—may occur FOLLOW-UP during surgery. PATIENT MONITORING r MISCELLANEOUS Serum calcium concentration—if bilateral ASSOCIATED CONDITIONS thyroidectomy was performed; signs of r Non-thyroidal malignancies common hypocalcemia (agitation, panting, muscle r MEDICATIONS tremors, tetany, and seizures) may be Multiple endocrine neoplasia reported DRUG(S) OF CHOICE observed. AGE-RELATED FACTORS r ◦ Treat with 10% calcium gluconate Chemotherapeutic agents: None (1–1.5 mL/kg IV over 10–20 minutes). ◦ Chemotherapy is recommended as a sole PREGNANCY/FERTILITY/BREEDING ◦ Maintain serum calcium with therapy, or possibly in combination with dihydrotachysterol (vitamin D) orally. It is not recommended to breed animals with surgery and/or radiation therapy. r Thyroid hormone—supplementation with cancer. Chemotherapy is teratogenic—do not ◦ Cisplatin (60 mg/m2 every 3 weeks), thyroxine may be necessary after bilateral give to pregnant animals. carboplatin (300 mg/m2 every 3 weeks), or thyroidectomy. SYNONYMS doxorubicin (30 mg/m2 every 3 weeks)— r TSH concentration—a goal of thyroxin Thyroid carcinoma reported to effect partial remission in supplementation is to downregulate the approximately 50% of cases. ABBREVIATIONS body’s secretion of TSH. r ◦ Toceranib (2.5–3 mg/kg 3 times a r DIC = disseminated intravascular Site of primary tumor—physical week)—had biologic activity in 80% of coagulation examination and cervical ultrasound; thoracic r cases (26% partial remission, 53% stable MST = median survival time radiographs every 3 months to detect r disease). TSH = thyroid stimulating hormone pulmonary metastasis. ◦ Cisplatin—nephrotoxic; must use with PREVENTION/AVOIDANCE Suggested Reading saline diuresis (18.3 mL/kg/hour IV over Lunn KF, Page RL. Tumors of the endocrine 6 hours; give cisplatin after 4 hours). Unknown r system. In: Withrow SJ, Vail DM, Page RL, Antiemetics for cisplatin therapy: POSSIBLE COMPLICATIONS ◦ r eds., Small Animal Clinical Oncology, 5th Maropitant 1 mg/kg SC before cisplatin, Tumor—anemia; thrombocytopenia; ed. Philadelphia: Saunders, 2013, pp. or hypercalcemia; DIC; respiratory distress. ◦ r 513–515. Dolasetron 0.6–1 mg/kg IV or PO q24 h, Chemotherapy—dilated cardiomyopathy; Klein MK, Powers BE, Withrow SJ, et al. or ◦ renal failure; pancreatitis; sepsis; Treatment of thyroid carcinoma in dogs by Butorphanol 0.4 mg/kg IM before and gastrointestinal upset. surgical resection alone: 20 cases after cisplatin. r r Surgery—hemorrhage; hypothyroidism; (1981–1989). J Am Vet Med Assoc 1995, Thyroid management: ◦ hypoparathyroidism leading to hypocalcemia; 206:1007–1009. Thyroxine—maintenance doses to laryngeal paralysis. r Liptak JM. Canine thyroid carcinoma. Clin decrease TSH production have been Radiotherapy—acute side effects—moist Tech Small Anim Pract 2007, 22(2):75–81. recommended; some tumors contain TSH desquamation, pharyngeal mucositis; Pack L, Roberts RE, Davson SD, Dookwah receptors; value of hormone replacement esophagitis; tracheitis; late side effects— HD. Definitive radiation therapy for therapy in affected dogs not determined. ◦ alopecia, and skin or coat color change (at infiltrative thyroid carcinoma in dogs. Vet Methimazole 5 mg PO q8 h for medium radiation site). Radiol Ultrasound 2001, 42:471–474. to large dogs; may be beneficial for EXPECTED COURSE AND PROGNOSIS Nadeau ME, Kitchell BE. Evaluation of the hyperthyroid patients. r use of chemotherapy and other prognostic ◦ 𝛽-blockers—may be indicated for Prognosis—related to stage of disease (tumor size, mobility and evidence of variables for surgically excised canine tachycardia or hypertension in hyperthyroid thyroid carcinoma with and without patients. metastatic disease) with small, non-attached unilateral, non-metastatic tumors having best metastasis. Can Vet J 2011, 52(9):994–998. CONTRAINDICATIONS prognosis. Author Rebecca G. Newman r r Doxorubicin is cumulatively toxic to cardiac MST after surgical removal of unilateral Consulting Editor Timothy M. Fan myocytes causing decreased myocardial thyroid tumors is 1462 days vs. 365 days for Acknowledgment The author and editors function. Do not give to animals with poor patients undergoing bilateral thyroidectomy. acknowledge the prior contribution of Linda cardiac function or dilated cardiomyopathy. S. Fineman. JWST589-A01-32-24 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:52 279mm×216mm

Canine and Feline, Sixth Edition 37 Aggression to Unfamiliar People and Unfamiliar Dogs A

increased aggression, fear, agitation, and/or injuries and should be avoided. If safety BASICS DIAGNOSIS cannot be insured, dogs should be removed from the household. OVERVIEW DIFFERENTIAL DIAGNOSIS r r Behavior Therapy Fear aggression Territorial aggression r A variety of different motivations exist, r r Structured interactions (also known as learn Possessive aggression Conflict aggression including fear, territoriality, conflict and r to earn or say please by sitting) where the dog possessiveness. Aggression is directed toward a Generalized anxiety disorder is consistently taught to sit for anything it person or dog that does not live in the CBC/BIOCHEMISTRY/URINALYSIS values (before feeding, petting, play, going for household. Regular visitors may also be Usually unremarkable. Abnormalities suggest a walk) gives the dog control of its resources targets. May be within the range of normal an underlying medical condition. by sitting calmly, provides structure and behavior, but may be compounded by OTHER LABORATORY TESTS predictability in all interactions, teaches fearfulness. impulse control and trains the dog that good SYSTEMS AFFECTED Usually unremarkable things happen by sitting calmly. r r IMAGING r Behavioral. Sympathetic stimulation (e.g., Commands: teach the dog to focus on the tachypnea, tachycardia). MRI if CNS disease suspected. Other owner for guidance using eye contact and imaging as needed to rule out underlying hand target (e.g., dog touch nose to owner’s INCIDENCE/PREVALENCE r medical conditions. hand). Teach the dog to sit and relax on Stranger-directed aggression represents 32.5% verbal cue in neutral situations using food of canine behavioral referral caseload. rewards; teach to go to mat, bed or crate to SIGNALMENT settle; teach to walk on loose leash. Train with r Can occur at any age. Signs may begin to TREATMENT head halter or muzzle if needed to insure emerge as primary socialization wanes safety. Private session with a force-free trainer (approximately 12–16 weeks of age) or may CLIENT EDUCATION should be considered to achieve basics before arise or intensify at social maturity Treatment is aimed at controlling the any exposure. (approximately 18–36 months). Genetic problem, not at achieving a “cure.” Successful Behavior Modification: Systematic concerns and poor prognosis if signs arise treatment, resulting in a decrease in aggressive Desensitization and Counter-conditioning r incidents, depends on owner understanding (DS/CC) before 12 weeks. Territorial aggression more r common in intact males—initial signs usually of basic canine social behavior, risks involved, When owner can effectively control and r present by 1 year. Aggression toward how to follow safety and management calm in the absence of stimuli, begin exposure unfamiliar people and dogs overrepresented in recommendations, correct identification of by determining the limit (distance, location, r males. Breed predilection for inter-dog the aggression-eliciting stimuli, and effective person, dog) at which the dog will orient but aggression in “fighting breeds” (e.g., pit bull implantation of reward-based behavior not yet react. Have the dog focus on the terriers) and terriers. modification. owner or continue walking calmly (heel) and SIGNS Safety Recommendations give favored (highest value) rewards to make r r positive associations with each stimulus Aggression (barking, growling, lip-lifting, Owners’ main responsibility is safety by r exposure. Gradually (baby steps) increase snarling, snapping, lunging, biting) toward avoiding situations that may evoke a fearful or stimulus intensity, staying below the threshold unfamiliar people and dogs. May be aggressive reaction. Avoidance is also that would result in fear and/or aggression by accompanied by fearful or submissive body necessary to insure the pet’s welfare and decreasing distance, increasing distractions, or postures/facial expressions (head down, prevent further learning of aggressive r moving to more challenging environments. crouching, backing away, ears back, tail behaviors. Owners should be advised that r Progress is slow (typically months). tucked, looking away, lip licking) or confident dog owners may be liable for bites and could Carefully monitor body language to avoid body postures (standing straight up, approach face civil/criminal prosecutions should a r r r setbacks. If the dog is not calm, shows with tail up, ears forward). Territorial person be injured. Successful treatment is aggression or precursors to aggression (e.g., aggression arises in familiar locations or spaces more likely if a period of preventing exposure r fixating on the stimulus) reduce the level of (e.g., home, yard, car). May be confident, to aggression-provoking stimuli is instituted r r stimulation by moving farther away or taking fearful or conflict. Fear aggression more prior to behavior modification. Confine dog the dog out of the situation. Future sessions likely when dog is cornered or cannot escape. away from potential victims, avoid walks or r should be at greater distances, or in locations May be more frequent or severe on- than parks where stimulus exposure might occur, or with stimuli where success can be achieved. off-leash. or have dog under direct physical control of a For example, if the dog is calm when CAUSES & RISK FACTORS responsible adult whenever an aggression- r provoking situation could arise (e.g., public unfamiliar people pass on a walk, but when May be a normal canine behavior. location, when visitors are at the house). strangers pass the house the dog barks, revert r r Strongly influenced by previous experience Confine territorial dogs to where they to practicing DS/CC with the dog on walks (e.g., early socialization, painful conditions, and work up more slowly to practicing cannot see/hear visitors approaching territory r rough handling, inappropriate punishment, before they become aggressively aroused. around the house. Owners must always be previous fear-evoking experience with r r Introduce a head halter (e.g., Gentle Leader) vigilant for the approach of stimuli that might unfamiliar people or dogs). Underlying and basket muzzle for easier and safer control. incite fear or aggression. r medical conditions, especially pain. Owners should be advised that punishment/ SURGICAL CONSIDERATIONS r dominance-based training can lead to Castration reduced aggression by at least 50% toward unfamiliar dogs in < 20% of JWST589-A01-32-24 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:52 279mm×216mm

38 Blackwell’s Five-Minute Veterinary Consult

A Aggression to Unfamiliar People and Unfamiliar Dogs (Continued)

dogs studied and toward human territorial anticholinergic effects, cardiac conduction EXPECTED COURSE AND PROGNOSIS intruders in < 10% of dogs studied. disturbances if predisposed, and increased There is no cure. Prognosis is more favorable Castration reduced inter-male aggression in aggression. if aggression is motivated by fear, at a low r 62% of dogs. Military working German Alpha-2 agonists intensity, and occurs only in a few predictable r shepherds spayed at 5–10 months of age were Clonidine 0.01–0.05 mg/kg PO PRN situations. Prognosis is highly dependent on more reactive 4–5 months post-surgery to 1.5–2 hours before eliciting trigger, up to owner compliance. approach by an unfamiliar person walking q12h. r with an unfamiliar dog than intact dogs. Side effects: transient hyperglycemia, hypotension, collapse, and bradycardia (responsive to atropine), and increased MISCELLANEOUS aggression. ASSOCIATED CONDITIONS MEDICATIONS 𝛼 Serotonin 2 antagonist/reuptake Other fear- or anxiety-based conditions (e.g., SUPPLEMENTS inhibitors noise phobias, separation anxiety) Aggression r r Consider for mild fear or as an adjunct to Trazodone 2–5 mg/kg PRN prior to to other stimuli eliciting trigger up to q8h. Titrate to drug therapy. ZOONOTIC POTENTIAL r 8–10 mg/kg if no adverse effects. Supplements are not a substitute for and r Human injury from bite wounds should only be used to facilitate behavior Side effects: sedation, anorexia, ataxia, GIT modification. effects, cardiac conduction disturbances, and PREGNANCY/FERTILITY/BREEDING increased aggression. Do not breed dogs with extremely fearful L-theanine (Anxitane®) r PRECAUTIONS behavior or fear/aggression. 2.5–5 mg/kg q12h. r r Use caution as any psychotropic medication SEE ALSO Active ingredient in green tea purported to r may disinhibit, resulting in an increase rather Aggression toward Familiar People—Dogs increase serotonin, dopamine and GABA. r r r than decrease in aggression. Do not Aggression, Food and Resource Guarding— Side effects: none reported. r ® combine SSRIs, SARIs, TCAs, MAO Dogs Aggression—Between Dogs in the Alpha-casozepine (Zylkene ) r r inhibitors (e.g., amitraz, selegiline), opiods 15 mg/kg PO q24h (canine). Discontinue if Household Fear and Aggression in (e.g., tramadol) or other medications that no effect after 10 days. Veterinary Visits r increase serotonin—can result in potentially Purported to increase GABA. ABBREVIATIONS r fatal serotonin syndrome. r r Side effects: none reported. CNS = central nervous system DS/CC = r Alpha-casozepine also in Royal Canin Calm desensitization and counter-conditioning r r Canine. GABA = gamma-aminobutyric acid GIT r = gastrointestinal tract MAO = DRUG(S) r r FOLLOW-UP monoamine oxidase MRI = magnetic There are no medications licensed for r resonance imaging SSRI = selective treatment of canine aggression. Owners must PATIENT MONITORING r r be aware that the use of medications is Clients need ongoing assistance and should serotonin reuptake inhibitor SARI = Serotonin 2a antagonist/reuptake inhibitor off-label. Note in the patient’s record that receive at least one follow-up call within the r owners were informed of potential risks and first 1–4 weeks after consultation. Provisions TCA = tricyclic antidepressant side effects. A signed informed consent form for further follow-up should be made. Suggested Reading is advisable. NEVER use medications without Ongoing communication improves client Herron ME, Shofer SS, Reisner IR. Survey of concurrent behavior modification. Before compliance. the use and outcome of confrontational and prescribing medication, be sure that owners PREVENTION/AVOIDANCE non-confrontational training methods in r understand the risks and liability in owning Treatment recommendations are life-long— client-owned dogs showing undesired an aggressive dog, will follow safety aggression may recur with treatment lapses behaviors. Appl Anim Behav Sci 2009, procedures, and do not expect medications to and continued exposure to fear- and 177:47–54. insure safety. In fact, medication may not be aggression-producing stimuli. Owners must Author Meredith E. Stepita appropriate in all situations (e.g., households always be vigilant and in control of the dog’s Consulting Editor Gary M. Landsberg r with small children, or individuals that have behavior. Appropriate early socialization Acknowledgment The author and editors disabilities). r and habituation may help prevent fear-based acknowledge the prior contribution of Laurie There is a strong placebo effect when using behaviors later in life. Puppies that are not Bergman. drugs for behavior therapy in dogs. Studies socialized during the first three months of life have not shown a robust effect of drug are more likely to be fearful, defensive, and treatment on aggression. possibly aggressive later in life. Socialization Selective Serotonin Reuptake Inhibitors r may include attending well-structured, Fluoxetine 0.5–2 mg/kg PO q24h. r positive reinforcement puppy classes starting Paroxetine 0.5–1 mg/kg PO q24h. r during the sensitive period for socialization Sertraline 1–3 mg/kg PO q24h. r from 7–12 weeks (perhaps up to Side effects: sedation, irritability, GIT 14–16 weeks). One study found that effects, increased aggression; anorexia is vaccinated puppies that attended puppy common and usually transient. socialization classes were at no increased risk Tricyclic Antidepressants of parvovirus. r Clomipramine 1–3 mg/kg q12h POSSIBLE COMPLICATIONS (label-restricted for aggression). r Human injuries; euthanasia or Side effects: sedation, GIT effects, relinquishment of patient JWST589-A36-29-25 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:5 279mm×216mm

Canine and Feline, Sixth Edition 39 Aggression Toward Children—Dogs A

CBC/BIOCHEMISTRY/URINALYSIS CONTRAINDICATIONS/POSSIBLE Baseline profile to rule out medical INTERACTIONS r BASICS contributing factors. Psychotropic medication can increase OTHER LABORATORY TESTS agitation and anxiety or disinhibit aggression. OVERVIEW r Use with safety recommendations to prevent Anecdotal evidence (only) correlates canine r Children are the most frequent victims of hypothyroidism with increased aggression; bites. Avoid the following combinations: ◦ ◦ reported dog bites and tend to be injured however, no data-based evidence. SSRI + TCA SSRIorTCA+ tramadol r ◦ more severely than adults. Unnecessary supplementation with thyroid SSRIorTCA+ MAOI including amitraz ◦ SIGNALMENT hormone may predispose to agitation or SSRI + NSAID (caution, due to increased Any breed, age, gender, and neuter status. aggression. risk of GI or other hemorrhage). Breed DIAGNOSTIC PROCEDURES r Breed reports vary with demographics. Thorough physical examination. A detailed Breed identification may be unreliable. history of the bite event and the behavior of r Breeds most commonly presenting to a both dog and child to determine motivation. FOLLOW-UP behavior referral service that had bitten a PREVENTION/AVOIDANCE r child include English springer spaniel, Do not rely on training alone to eliminate r German shepherd, Labrador retriever, golden aggression. Preventive measures are most retriever, and American cocker spaniel. r TREATMENT important in management of canine Most fatal attacks (uncommon) are r SAFETY WITH FAMILIAR DOGS aggression to children. Even well-trained, attributed to rottweilers, pit bulls, and their r socialized dogs may bite. r Never leave infants or young children mixes. Larger breeds and mixed breeds may POSSIBLE COMPLICATIONS be more likely to inflict severe injury. unsupervised with dogs. Securely separate r r infants from dogs when alone, if both asleep. Family may not acknowledge risks. Smaller breeds can also be dangerous. r r r If one adult is present, separate dog from Disease may aggravate aggression. Family Sex r r r young children. If more than one adult is may not be compliant. Psychotropic drug More frequent in males than females. may be unrealistically relied upon or r present, assign responsibility for one adult to r Neutering will not significantly reduce the r ineffective. Young children may be risk. dog, and one to child. Do not allow child to approach or interact with dog when dog is impulsive and difficult to control. Age r r lying down. Do not allow child to remove EXPECTED COURSE AND PROGNOSIS Any age, but more frequent in socially r r r any object from dog. Do not allow child to Aggressive behavior can often be reduced mature dogs (2+ years old). Risk may hug, kiss, bend over, or lie down beside dog. and controlled. However, lifetime compliance r r increase in geriatric dogs because of pain, Separate dog when eating or chewing valued is needed. Prognosis is poor if social/ sensory impairment, or irritability. items. physical environment cannot be controlled. r CAUSES & RISK FACTORS SAFETY WITH UNFAMILIAR DOGS In some cases it may be necessary to rehome r r Clinical Categories/Motivation for Do not tether unsupervised. Do not allow or euthanize dog, while in others the dog’s Aggression young children to interact with unfamiliar behavior may improve as the child grows r r r r r Fear-related Pain-related Play-related older. r r r dogs. Securely lock gates in yards. Avoid Conflict-related Predatory Territorial r underground electric fences, which do not Resource (food/toy/bed) guarding prevent entry of children into yard. Dog-Associated Risk Factors BEHAVIOR MODIFICATION THROUGH r r Disease and associated irritability. Pain- LEARNING/TRAINING MISCELLANEOUS r related aggression and resource guarding are Redirect dog’s attention: teach “look” or ABBREVIATIONS the most common reasons for bites to familiar r r r “touch” cues. Establish secure, separate “safe GI = gastrointestinal MAOI = children < 6 years old. Generalized anxiety. r r r r haven” for dog. Restrict fearful or reactive monoamine oxidase inhibitor NSAID = Fearful behavior. Dog lying down, r dog on lead and offer food at safe distance nonsteroidal anti-inflammatory drug particularly under or on furniture. Parent/ r from children, to turn a negative situation SSRI = selective serotonin reuptake littermate aggression. r r into a positive one. Do not rely on training inhibitor TCA = tricyclic antidepressant Environmental/Social Risk Factors r alone; safe practices require prevention. Younger children most likely bitten by the Suggested Reading r family pet or other familiar dogs. Presence Herron ME, Shofer FS, Reisner IR. Survey of of infants (risk of predatory attacks). the use and outcome of confrontational and r r Presence of young children. Presence of non-confrontational training methods in r MEDICATIONS food, edible toys. Punishment-based client-owned dogs showing undesired r training. Inadequate supervision by parents/ DRUGS behaviors. Appl Anim Behav Sci 2009, r caregivers. History of growling, snapping, Anxiolytic drug may be indicated for dogs 117:47–54. r biting. Hugging, kissing, bending over with generalized or situational anxiety or Reisner IR, Shofer FS, Nance ML. Behavioral anxious, fearful, or conflict-aggressive dog. fearful behavior. assessment of child-directed canine aggression. Inj Prev 2007, 13:348–351. Selective Serotonin Reuptake Inhibitors r Author Ilana R. Reisner Fluoxetine 0.5–2.0 mg/kg q24 h r Consulting Editor Gary M. Landsberg Sertraline 0.5–3 mg/kg q24 h DIAGNOSIS Tricyclic Antidepressants DIFFERENTIAL DIAGNOSIS Clomipramine 1–3 mg/kg q12 h See “Clinical Categories/Motivations for Aggression” JWST589-A37-30-26 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:55 279mm×216mm

40 Blackwell’s Five-Minute Veterinary Consult A Aggression Toward Familiar People—Dogs

when another approaches). Aggression may be IMAGING seen in other contexts, e.g., denied access to MRI if CNS disease is suspected; other BASICS items or activities, when resting, when imaging may be needed to rule out other confronted or punished, or during medical conditions. DEFINITION uncomfortable or fear-evoking interactions Aggression, directed toward household (e.g., ear cleaning, grooming, bathing). members or people with an established History-taking should attempt to establish triggers and frequency/severity of aggressive relationship with the dog, often in situations r TREATMENT involving access to resources. May be episodes. Aggression may not be directed uniformly toward each household member. ACTIVITY status-related/dominance, conflict, impulsive, r competitive or possessive aggression. Confident/dominant body postures Insure behavioral needs are being met. PATHOPHYSIOLOGY (stiffening, staring, standing straight up, ears DIET forward, tail up, and/or approaching/direct These dogs may show anxiety or be impulsive Low-protein/tryptophan-supplemented diets contact with the person) may be associated may help reduce aggression. and unpredictable. When the aggression is with aggressive behavior, or the motivation CLIENT EDUCATION guarding of resources, or in response to fear may be fear (tensing, head down, crouching, eliciting stimuli (e.g., threats, punishment, General Comments backing away, ears back, tail tucked, looking r possibly handling) might be normal. Treatment is aimed at controlling the away, lip licking). Owners may report a r SYSTEMS AFFECTED combination of confident and submissive problem, not achieving a “cure.” Successful Behavioral postures representing uncertainty (conflict). treatment, resulting in a decrease in aggressive r GENETICS Owners may describe dog as “moody” and incidents, depends on owner understanding of basic canine social behavior and Pedigree analyses have shown increased may be able to predict when aggression is communication, risks involved in living with occurrence in related dogs. May be genetic likely to occur. Early on the dog may show an aggressive dog, and how to implement factors associated with impulse dyscontrol in fear (e.g., eye aversion, tail tucked, avoidance) safety and management recommendations. English springer spaniel and English cocker that may diminish and the dog may give less r Owners must be aware that the only certain spaniel. May be more common in show than warning as it becomes more confident that aggression will be effective (negative way to prevent future injuries is euthanasia. field lines. r r reinforcement). Anxiety may be noted in Owners must be educated about the risks of INCIDENCE/PREVALENCE pet-owner interactions and other situations. using physical punishment and training 20–44% of behavioral referral caseloads. Physical Examination Findings techniques that rely on “dominating” their r r GEOGRAPHIC DISTRIBUTION Usually unremarkable. Medical dogs. Improper and inappropriate use of Regional breed differences exist. conditions, especially pain, may contribute to physical punishment/dominance techniques SIGNALMENT the expression of aggression. such as alpha rolls, corrections with choke chains or prong collars, or even yelling “no” Species CAUSES r can lead to human injury, increased Dog May be part of normal canine social aggression and anxiety, and disruption of the Breed Predilections behavioral repertoire, but its expression is human-animal bond. influenced by environment, learning, and Spaniel (English springer and cocker), terrier, r Safety Recommendations genetics. Display of aggression may be r but may be exhibited by any breed. If owners elect not to euthanize, they must influenced by underlying medical conditions be aware that their main responsibility is Mean Age and Range (especially pain), early experiences (learning preventing human injury by diligently Usually manifested by social maturity that aggression is effective to control avoiding all situations that might evoke an (12–36 months of age). May be seen in situations), and inconsistent or lack of clear aggressive response including situations that younger dogs. rules and routines in the household and in r incite fear even if not aggression. Treatment Predominant Sex human-pet interactions. must begin with prevention of exposure to all Males (castrated and intact). RISK FACTORS aggression-provoking stimuli prior to any r SIGNS Inconsistent or inappropriate physical behavior modification. Use patient history General Comments punishment and inconsistent owner to identify each situation or trigger for owners Detailed history-taking is needed to make a interactions. to avoid. This may include not allowing on diagnosis, assess risks, and devise a safe and furniture or beds where aggression might realistic treatment plan. Mild signs of arise, not giving valuable treats or toys (e.g., aggression (e.g. staring, growling, baring rawhides) except when confined away from teeth) often precede bites. Details of early DIAGNOSIS family members, and limiting physical contact aggressive episodes are vital to establish the DIFFERENTIAL DIAGNOSIS with the dog including petting in any place or r r diagnosis and prognosis. Often anxiety or fear Fear-based aggression Conflict aggression situation where the dog might resist or bite. r r based but may be motivated by desire to Anxiety conditions Disease conditions Instead provide the dog with opportunities control, e.g., personal space, resources. associated with aggression (e.g., painful (control) to avoid undesirable interactions Historical Findings conditions, endocrinopathies) (e.g., safe haven, crate). Reward the dog for r entering the safe haven and for leaving Aggression (barking, growling, lip-lifting, r CBC/BIOCHEMISTRY/URINALYSIS (coming out). Do not physically punish or snarling, snapping, lunging, biting) directed Usually unremarkable. Abnormalities may r toward family members. Aggression may reprimand the dog. Introducing a head indicate an underlying or contributing halter (e.g., Gentle Leader) with a lightweight occur around resources such as resting areas, medical condition. food, or toys, handling (e.g., petting and 8- to 10-foot leash attached or a basket muzzle reaching toward), or favored possessions OTHER LABORATORY TESTS whenever in contact with people or in any (including resting with one family member As indicated to rule out underlying diseases. situation where problems might arise, makes Rule out hypothyroidism. controlling potentially dangerous situations JWST589-A37-30-26 JWST589-Tilley Printer: Yet to Come August 26, 2015 10:55 279mm×216mm

Canine and Feline, Sixth Edition 41

(Continued) Aggression Toward Familiar People—Dogs A

r easier and safer. Use the long leash to safely be aware that the use of medications is may recur if preventive strategies not remove the dog from situations that may elicit off-label. Note in the patient’s record that maintained. aggression; do not reach for the dog directly. owners were informed of potential risks and POSSIBLE COMPLICATIONS Behavioral Therapy side effects. A signed informed consent form r Human injuries; euthanasia or Behavior modification—use is advisable. NEVER use medications without relinquishment of patient. concurrent behavior modification. Before non-confrontational methods and EXPECTED COURSE AND PROGNOSIS reward-based training to achieve desirable prescribing medication, be sure that owners There is no cure. Prognosis is more favorable outcomes and teach the dog behaviors understand the risks and liability in owning if aggression is at a low intensity and occurs in without experiencing fear or becoming an aggressive dog, will follow safety r relatively few predictable situations. Prognosis aggressive. Structured interactions (also procedures, and do not expect medications to is highly dependent on owner compliance. known as learn to earn or say please by insure safety. In fact, medication may not be sitting) where the dog is consistently taught to appropriate in all situations (e.g., households sit for anything it values (before feeding, with small children or individuals with disabilities). petting, play, going for a walk) gives the dog r control of its resources by sitting calmly, There is a strong placebo effect when using MISCELLANEOUS drugs for behavior therapy in dogs. Studies provides structure and predictability in all ASSOCIATED CONDITIONS interactions, teaches impulse control and have not shown a robust effect of drug treatment on aggression. Other forms of aggression, including interdog trains the dog that good things happen by aggression, resource guarding, and aggression sitting calmly. Owners must ignore the dog Selective Serotonin Reuptake Inhibitors r to unfamiliar people or dogs. Aggressive dogs until it sits or train “sit”, whenever soliciting Fluoxetine 0.5–2 mg/kg PO q24 h. r r often have underlying anxiety. attention. Use positive reinforcement (e.g., Paroxetine 0.5–2 mg/kg PO q24 h. r food, toys, play, petting) for response Sertraline 1–3 mg/kg PO q24 h. ZOONOTIC POTENTIAL r substitution (or counter commanding) to Side effects: sedation, irritability, GIT Human injury. teach behaviors that are incompatible with effects, increased aggression; anorexia is PREGNANCY/FERTILITY/BREEDING those that have resulted in aggression. common and usually transient. Do not breed aggressive dogs. Desensitization and Counter-Conditioning r Tricyclic Antidepressants SYNONYMS Decreasing reactivity to situations that have r r r Clomipramine 1–3 mg/kg q12 h in dogs Competitive aggression Conflict resulted in aggression by making positive r (label restriction for aggression) aggression Dominance-related aggression associations with each interaction. Do not r r r Side effects: sedation, GIT effects, Rage syndrome Status-related aggression begin until owner can insure success with anticholinergic effects, cardiac conduction reward-based training and sit for all ABBREVIATIONS r disturbances if predisposed, and increased r r interactions. Teach the dog strategies to CNS = central nervous system GIT = aggression. r relax (sit, down, go to your bed) on verbal cue gastrointestinal tract MAO = monoamine CONTRAINDICATIONS r in neutral situations using food rewards. oxidase MRI = magnetic resonance imaging r r Expose the dog to a sufficiently reduced Use caution as any psychotropic medication SSRI = selective serotonin reuptake r stimulus where no fearful or aggressive may reduce fear-based inhibition resulting in inhibitor TCA = tricyclic antidepressant reaction is elicited (e.g., owner passing by an increase rather than decrease in aggression. r SEE ALSO PRECAUTIONS r resting dog at sufficient distance). Reward Aggression Toward Unfamiliar People and r calm, non-fearful/aggressive behavior (e.g., Any psychotropic medication may increase Unfamiliar Dogs—Dogs Aggression, Food verbal praise, tossing favored treats). r rather than decrease aggression. and Resource Guarding—Dogs r Gradually increase the level of stimulation, Corticosteroids are contraindicated in Aggression—Between Dogs in the staying below the threshold that would result r food-aggressive dogs; polyphagia can lead to Household in fear and/or aggression. Progress is slow increased frequency/intensity of aggression. (typically months) and careful monitoring is POSSIBLE INTERACTIONS Suggested Reading essential to understand and respect the dog’s Herron ME, Shofer SS, Reisner IR. Survey of r Do not combine SSRIs, TCAs, MAO limits. Train on cue those behaviors needed the use and outcome of confrontational and inhibitors (e.g., amitraz, selegiline), opioids to manage specific problems, e.g., go to your non-confrontational training methods in (e.g., tramadol), and other medications that bed (for dogs that are protective of resting client-owned dogs showing undesired increase serotonin—can result in potentially areas) or “drop it” (for resource guarding). behaviors. Appl Anim Behav Sci 2009, fatal serotonin syndrome. SURGICAL CONSIDERATIONS 177:47–54. r Sueda KL, Malamed R. Aggression toward Castration reduced aggression by at least people—a guide for practitioners. Vet Clin 50% toward family members in N Am 2014, 14:599–628. approximately 30% of dogs studied. r FOLLOW-UP Author Meredith E. Stepita Females that start to show dominance Consulting Editor Gary M. Landsberg aggression at less than 6 months of age may be PATIENT MONITORING Acknowledgment The author and editors less aggressive if spaying delayed until mature. Clients need ongoing assistance and should acknowledge the prior contribution of Laurie receive first follow-up call within the first Bergman. 1–4 weeks after consultation. Provisions for further follow-up (by phone or in person) MEDICATIONS should then be made. Client Education Handout PREVENTION/AVOIDANCE DRUG(S) available online r Treatment, including safety There are no medications licensed for recommendations, are life-long—aggression treatment of canine aggression. Owners must JWST589-A38-31-27 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:0 279mm×216mm

42 Blackwell’s Five-Minute Veterinary Consult A Aggression Toward Humans—Cats

mydriasis; may hiss and growl before turning ACTIVITY r to bite person. Play-motivated: cat should be provided with CAUSES & RISK FACTORS increased opportunity for appropriate BASICS r Play-motivated: lacking in opportunities for play—either in the form of toys, human DEFINITION interaction, or additional housemate. normal play—no other cats, insufficient r Human-directed aggression in cats and/or inappropriate toys; history of owner Redirected: cat should be denied access to PATHOPHYSIOLGY using hands/feet to play with kitten and/or windows where outside cats can be seen. playing roughly with the kitten. DIET The more common causes for human-directed r r aggression in cats include play, Fear: poor socialization with humans and/or Hill’s Science Diet c/d Multicare Feline feral living, an aversive event associated with a Urinary Stress fear/pain-related, redirected, maternal, and r person, or people in general. Royal Canin Feline Calm petting intolerance. Context is going to r r contribute greatly when making the correct Pain-related: obvious medical/physical Either may be beneficial in helping to condition. decrease anxiety. diagnosis. For example, play aggression is r likely to be seen in a young, solitary cat, while Redirected: occurs during interference in, or CLIENT EDUCATION r pain-related/fear aggression is a common interruption of, situations that have caused Play-motivated: normal play behavior and behavior seen in the clinic setting. the cat to become aggressively aroused—such the importance for opportunities for SYSTEMS AFFECTED as a cat fight (between familiar household appropriate play. r cats), the presence of a cat outside or noise. r Behavioral r Fear: avoidance of fear-inducing r Maternal: recent birth of litter. r situations—ongoing exposure may worsen Gastrointestinal—decreased appetite if fear Petting intolerance: exact etiology and/or pain-related signs, cause severe stress, and compromise r unknown. Cats tend to groom each other on animal welfare. Hemic/Lymphatic/Immune—chronic stress head/neck so human grooming of cat in other r effects on immune function Redirected: importance in addressing r locations may contribute to aggressive primary stimuli—such as outside cats. Ophthalmic—dilated pupils in response to reaction. r autonomic nervous system stimulation Maternal: normal maternal and r Skin/Exocrine—may show displacement kitten-protective behavior—same as for fear-motivated aggression. behaviors such as overgrooming r GENETICS Petting intolerance: normal feline grooming DIAGNOSIS patterns; observation of cat’s warnings so that There is no known genetic basis for behavior does not escalate. human-directed aggression in cats. DIFFERENTIAL DIAGNOSIS Behavior Modification Exercises INCIDENCE/PREVALENCE See causes above CBC/BIOCHEMISTRY/URINALYSIS Desensitization and Counter-Conditioning Aggression is second only to inappropriate (DS & CC) r elimination for feline cases seen by veterinary Rule out contributing medical conditions Desensitization: exposing cat to the behavior specialists. based on presentation. fear-inducing stimulus (scary person) at a low GEOGRAPHIC DISTRIBUTION OTHER LABORATORY TESTS level so the cat does NOT react fearfully or r Senior cats: a complete thyroid panel. aggressively. Over time, the intensity of the None r SIGNALMENT Urinalysis if inappropriate elimination stimulus is increased (i.e., the distance and/or urine marking is presented as part of between the cat and stimulus is decreased) Cats of any age, gender/ neuter status, breed the aggression. without causing fearful responses. can be affected. Play-motivated aggression r Counter-conditioning: rewarding the cat more likely in juvenile, solitary cat. IMAGING with a special treat, toy, grooming, petting, SIGNS Based on clinical examination and/or r suspected pain component for relaxation. Play-motivated: cat approaches its “victim,” Classical Conditioning (CC) crouches in wait, stalks and chases; tail is DIAGNOSTIC PROCEDURES Classical conditioning: pairing the stimulus twitching and ears are forward. Typically will Thorough behavioral history including a (person threatening to the cat) with a tasty attack moving target. description of the cat’s postures during r treat, toy, petting. Example: scary person = Fear/Pain-related: ears back, body and tail aggression and injuries inflicted, context, tuna fish. lowered, piloerection, pupils dilated; may hiss presence of outside cats, early historical and growl. Avoidance of person(s) who elicit information, litter box use, food the aggression. Attacks possible if approached consumption, and hiding behaviors. and/or cornered. Extreme cases: expression of PATHOLOGIC FINDINGS MEDICATIONS anal glands, urination, and/or defecation. N/A Hiding behavior. The short-term use of medication may be r Redirected: cat is highly aroused by stimulus necessary to decrease overall levels of anxiety and seeks out less appropriate target. and reactivity in more severe cases. Aggression can be very severe given the cat’s DRUG(S) OF CHOICE level of arousal. TREATMENT r Azapirones Maternal: usually predictable and APPROPRIATE HEALTH CARE Buspirone 0.5–1.0 mg/kg PO q12h. Most self-limiting. Queen will act to protect her Applicable only if health/medical issue useful for fearful and withdrawn cats. kittens. r diagnosed. Decreases anxiety and may increase Petting intolerance: cat signals its NURSING CARE “self-confidence.” Anecdotal reports of “displeasure” by twitching its tail and skin “increase in affection”; therefore might be when being petted in an undesired location Applicable only if health/medical issue useful in severe cases of petting intolerance. and/or for too long. Ears are usually back; diagnosed. Response noted in 1–2 weeks. JWST589-A38-31-27 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:0 279mm×216mm

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(Continued) Aggression Toward Humans—Cats A

r Selective Serotonin Reuptake Inhibitors Specific recommendations for the use of until the new behavior is stable (8–12 weeks) (SSRIs) diazepam: baseline physical exam, CBC, and and wean off slowly, usually over weeks. If r Fluoxetine, paroxetine, sertraline blood chemistries to confirm good health. aggressive behavior recurs, return to the last 0.5–1.5 mg/kg PO q24h. Repeat the blood chemistries at 3–5 days. dose that controlled the anxiety/reactivity and r SSRIs must be given daily. May take Elevated ALT or AST, discontinue the continue treatment. 4–8 weeks to reach peak effects. medication. Tricyclic Antidepressants (TCAs) ALTERNATIVE DRUGS r Amitriptyline 0.5–2.0 mg/kg PO q12–24h. Pheromones r r Clomipramine 0.25–1.3 mg/kg PO q24h. Used alone or concurrently with drugs MISCELLANEOUS r r TCAs must be given daily. May take Feliway—available in diffuser, spray and ASSOCIATED CONDITIONS 4–8 weeks to reach peak effects. wipes—facial pheromone r N/A Benzodiazepines NurtureCALM 24/7 collar—maternal r AGE-RELATED FACTORS Alprazolam 0.125–0.25 mg/cat PO q8–24h. pheromone r Play-motivated: typically seen in young, Diazepam 0.1–1.0 mg/kg PO q12–24h Supplements r solitary cat in household. (rarely used due to potential hepatopathies). Used alone or concurrently with drugs r r Can be given “as needed” for specific Anxitane—contains L-theanine, a calming ZOONOTIC POTENTIAL encounters with people inducing the fear compound found in green tea People injured during an aggressive attack r response and during desensitization, Zylkene—contains alpha-casozepine, a should seek prompt medical attention. counter-conditioning and classical GABA agonist Infection by Bartonella henselae can result conditioning sessions. r from a cat scratch or bite. Can be used in conjunction with PREGNANCY/FERTILITY/BREEDING azapirones, SSRIs, and TCAs. Avoid medications in breeding/nursing cats. CONTRAINDICATIONS/ FOLLOW-UP SYNONYMS PRECAUTIONS/POSSIBLE PATIENT MONITORING N/A INTERACTIONS r Weekly follow-up is recommended in the SEE ALSO None of the drugs listed are approved for r early stages of treatment, especially when on Aggression Overview—Cats use in cats. r r medication(s). Monthly follow-up once Fears, Phobias, and Anxieties—Cats All of the medications are to be stable. For cats on medication, follow-up ABBREVIATIONS administered orally, as they have not been blood testing recommended every r CC = classical conditioning shown to be effective through transdermal 6–12 months. r dosing. DS & CC = desensitization and r PREVENTION/AVOIDANCE counter-conditioning Azapirones: side effects are uncommon but r r occasional excitement is noted. Should not be Play-motivated: provide opportunities for MAOI = monoamine oxidase inhibitor appropriate play. r given in combination with an MAOI. Avoid r SSRI = selective serotonin reuptake Fear: avoidance of the fear-inciting stimuli if inhibitor use in the aggressor cat; may increase any r “bully” behavior. at all possible. Early socialization to people TCA = tricyclic antidepressant r and events may help prevent some Neither SSRIs nor TCAs should be given Suggested Reading with each other, nor in combination with occurrences of fear-related responses to people. Horwitz DF, Neilson JC. Blackwell’s MAOIs. r r Pain: treat underlying condition(s). Five-Minute Veterinary Consult Clinical SSRIs: side effects include mild sedation r Companion Canine & Feline Behavior. and decreased appetite, constipation, and Redirected: address possible arousing stimuli—indoors and outdoors. Ames, IA: Blackwell, 2007, pp. 109–178. urinary retention. Competitive inhibition of r Maternal: as for fear. Landsberg GM, Hunthausen W, Ackerman cytochrome P450 liver enzymes; when r Petting intolerance: limit amount of time L. Behavior Problems of the Dog and Cat, administered concurrently with medication 3rd ed. Saunders Elsevier, 2013, utilizing the P450 enzymes, elevated plasma petting the cat; desensitization and counter-conditioning to increase petting time. pp. 327–343. levels of the medications may increase, Overall K. Manual of Clinical Behavioral causing toxic levels. POSSIBLE COMPLICATIONS r Medicine for Dogs and Cats. St. Louis, TCAs: side effects include sedation, Potential human injury in all of the above MO: Mosby, 2013, pp. 390–426. constipation, diarrhea, urinary retention, cases, especially if the cat is approached or Seksel K. Behavior problems. In: The Cat: appetite changes, ataxia, decreased tear cornered and/or when highly aroused. Clinical Medicine and Management. production, mydriasis, cardiac arrhythmias, EXPECTED COURSE AND PROGNOSIS St. Louis, MO: Saunders, 2012, tachycardia, and changes in blood pressure. r pp. 219–224. Benzodiazepines: side effects include Progress occurs slowly. Relearning is a process and each case is individual. If medications are Author Terr y Marie Curtis sedation, ataxia, muscle relaxation, increased Consulting Editor Gary M. Landsberg appetite, paradoxical excitation, and increased indicated, begin at a low dose and work up as friendliness. Idiopathic hepatic necrosis has necessary. To discontinue medication, wait been reported in cats. JWST589-A39-25-28 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:3 279mm×216mm

44 Blackwell’s Five-Minute Veterinary Consult A Aggression, Food and Resource Guarding—Dogs

r Use positive reinforcement (e.g., food, toys, play) to teach behaviors that are incompatible BASICS TREATMENT to those that lead to aggression including a calm sit and watch before giving any food, OVERVIEW CLIENT EDUCATION chews or toys, and “drop it” to release toys for r r valued rewards. Aggressively guarding food (e.g., in food Treatment is aimed at control, not achieving r bowl, rawhides, bones, stolen/found items) or a “cure.” Successful treatment resulting in a Prevent access to items that might be stolen objects (e.g., toys, stolen objects). decrease in aggressive incidents, depends on or guarded by supervising with leash if r Usually within the range of normal owner understanding of basic canine social necessary, dog proofing or confinement training. behavior; genetics, learning or early behavior, risks involved in living with an r experience may contribute to excessive aggressive dog, and ability to follow safety and “Booby trap” items by applying an aversive expression of aggression. management recommendations. substance such as hot sauce. r r SYSTEMS AFFECTED If safety cannot be insured, pet should be Systematic desensitization and counter- conditioning to specific aggression-provoking Behavioral removed from the home. Safety Recommendations stimuli if safety and owner compliance can be SIGNALMENT r insured. The owner’s main focus must be on r No breed or sex predilections. Find the threshold (distance, location) at preventing injury by diligently avoiding which the dog shows no anxiety or aggression SIGNS situations that may evoke an aggressive when in possession of food or chews and Aggression (barking, growling, lip-lifting, reaction. r make positive associations by tossing small snarling, snapping, lunging, biting) toward Owners may be more compliant with food treats each time the owner walks by— people or other animals in the presence of avoidance recommendations if they the goal is for the dog to associate the owner’s valued food items or objects. understand both the risk and the potential presence with positive outcomes. If successful, CAUSES & RISK FACTORS liability if the dog causes injury. r training can very gradually proceed to closer r Successful treatment is more likely if a May be part of normal canine behavior. proximities—level of improvement will be period of preventing exposure to aggression- Strongly influenced by previous experiences of limited by safety and the dog’s motivation to provoking stimuli is instituted prior to successfully defending food, or objects retain the resource. behavior modification. throughaggressionandbyresource r availability/novelty. Always confine the dog away from potential r Underlying medical conditions and victims or the dog must be under the direct physical control of a responsible adult medications, especially those causing MEDICATIONS polyphagia, or calorie-restricted diets may whenever an aggression-provoking situation could arise. increase level of food aggression. r DRUG(S) Give food and any other objects that the Medications are generally not indicated in the dog might guard in a confinement/safe haven treatment of resource guarding. location away from people and other animals; prevent access to items that may evoke DIAGNOSIS aggression. r DIFFERENTIAL DIAGNOSIS Teach the dog to be comfortable wearing a r FOLLOW-UP Fear aggression head halter (e.g., Gentle Leader) and basket r Social status/dominance or conflict muzzle for safer control of potentially PATIENT MONITORING dangerous situations. aggression r Clients usually need ongoing assistance with CBC/BIOCHEMISTRY/URINALYSIS Punishment/dominance-based training at least one follow-up call within the first techniques are contraindicated as they cause 1–3 weeks after the consultation. Provisions Usually unremarkable. Abnormalities suggest further fear, agitation, defensive aggression, an underlying or contributing medical for further follow-up should be determined at and further learning (fear of approach and that time. condition. negative reinforcement if successful). OTHER LABORATORY TESTS PREVENTION/AVOIDANCE Behavior Modification r Management recommendations (avoiding Usually unremarkable. Command-response-reward program (say triggers) are life-long.. IMAGING please by sitting): to increase owners’ control POSSIBLE COMPLICATIONS MRI if CNS disease suspected. Other of resources, make the dog more responsive to imaging as needed to rule out underlying the owner, and create structure and Human injuries; euthanasia or medical conditions. predictability in the dog’s life. relinquishment of patient. DIAGNOSTIC PROCEDURES N/A JWST589-A39-25-28 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:3 279mm×216mm

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EXPECTED COURSE AND PROGNOSIS SEE ALSO Herron, M.E., Shofer, S.S., Reisner, I.R.. r There is no cure. Prognosis for improvement Aggression Toward Unfamiliar People and Survey of the use and outcome of is more favorable if aggression is at a low Unfamiliar Dogs—Dogs confrontational and non-confrontational r intensity, occurs in only a few predictable Aggression Toward Familiar People—Dogs training methods in client-owned dogs r situations, and can be effectively and Aggression Between Dogs in the showing undesired behaviors. Appl Anim practically prevented. Household—Dogs Behav Sci 2009, 177:47–54. ABBREVIATIONS Landsberg G, Hunthausen W, Ackerman L. r CNS = central nervous system Behavior Problems of the Dog and Cat. r MRI = magnetic resonance imaging Oxford: Butterworth-Heinemann, 2013. MISCELLANEOUS Author Meredith E. Stepita Suggested Reading Consulting Editor Gary M. Landsberg ASSOCIATED CONDITIONS deKeuster T, Jung H. Aggression toward Acknowledgment The author and editors Fear and dominance/conflict aggression familiar people and animals. In: Horwitz acknowledge the prior contribution of Laurie ZOONOTIC POTENTIAL DF, Mills D, eds., BSAVA Manual of Bergman. Human injury and bite wounds Canine and Feline Behavioural Medicine, 2nd ed. Gloucestershire, UK: BSAVA, 2009, PREGNANCY/FERTILITY/BREEDING pp. 182–210. Do not breed dogs with extreme aggression. JWST589-A40-26-29 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:27 279mm×216mm

46 Blackwell’s Five-Minute Veterinary Consult A Aggression, Intercat Aggression

Aggressor (usually offensive) RISK FACTORS r r Covert signs: staring, displacing other cats, Singleton and/or bottle-raised kittens. r stiff body language/movements while Lack of social exposure and experience with BASICS r approaching the other cat. Overt signs: conspecifics during the socialization period r DEFINITION Growling, yowling, spitting, hissing, swatting, (2–7 weeks) and beyond. Male intact cats in r Intercat aggression—offensive or defensive lunging, chasing/stalking, and/or biting other multi-cat households. Postpartum females cats, dilated pupils, may be accompanied by with kittens in multi-cat households. aggression between cats consisting of staring, r displacing, vocalizing (growling, yowling, body language of fear (e.g., the classic Separating and returning housemate (e.g., Halloween cat stance—piloerection, back following veterinary visit, groomer). shrieking), spitting, hissing, swatting, lunging, r chasing/stalking, and/or biting other cats. arched, tail up) or more offensive body Changes in social group such as the language (stiff muscles, tail head elevated but addition of a “new” cat to a home of resident PATHOPHYSIOLOGY r r rest of tail down, back straight or slightly cats. Scratching and biting during the first May be normal behavior or abnormal. r slanted toward the head, ears forward or to introduction risks future intercat aggression. r May be caused by underlying medical the side), excessive facial marking, and Access to the outdoors and/or intrusion of r disease (e.g., CNS) or the indirect result of perhaps urine marking. unfamiliar cats onto the territory. Crowding concurrent medical disease lowering the Victim (usually defensive) or lack of adequate social space and access to threshold for irritable responses (e.g., pain, r r Covert: avoidance of aggressor, hiding, resources (food, water, litter boxes, and resting hyperthyroid). May be multiple motivations change in grooming and eating habits, stations). r including predatory/play, disputes over hypervigilance, dilated pupils. Overt: territory, sexual, fear, anxiety, and redirected. hissing, swatting, running, vocalizing SYSTEMS AFFECTED (including growling), Halloween cat stance, r r Behavioral. Skin/Exocrine—secondary to may escalate to defensive attack if cornered. r DIAGNOSIS traumatic injury. Immune—chronic stress Elimination Outside of the Litter Box r r may alter the immune response. Secondary Aggressor may block access to the litter box DIFFERENTIAL DIAGNOSIS infection (cat bite abscesses) are not area, forcing victims to choose alternative Behavioral Differentials r r uncommon. Nervous. elimination locations; secondary substrate Fear-related aggression—cat may hiss, spit, and/or location preferences and aversions can GENETICS r arch the back, display piloerection and develop. Both victims and aggressors may No specific genetic basis, although some r attempt to flee unless escape is thwarted; urine mark. Extremely fearful cats may pupil dilation will accompany a fear response. evidence to suggest that friendliness is mostly r genetic and related to paternal effects. urinate or defecate in midst of aggressive Status-related aggression—may occur with events. INCIDENCE/PREVALENCE change or instability of social hierarchy and Physical Examination Findings the control of access to resources; it is Unknown r None except injury from fights or if undecided if cats have dominance hierarchies GEOGRAPHIC DISTRIBUTION r or if conflict is better explained by territorial underlying medical issues. Stress may affect r None eating and self-grooming (increased or defense. Territorial aggression—in response SIGNALMENT decreased). to threat to the territory; boundaries are often delineated by marking with urine, feces, or Breed Predilections CAUSES r r scent glands. Redirected aggression— Lack of appropriate socialization to other None r exposure to agitating stimuli (cats in the yard, Mean Age and Range cats prior to 7 weeks of age. May be a r r visitors, noises, scents, etc.) with aggression Can occur at any age when due to changes component of normal social behavior. Social directed toward a target other than the r in social environment (e.g., addition of a new and environmental instability such as the agitating stimuli. Failure of recognition— cat, return of a cat from the veterinarian) or addition of a new cat, loss of a resident cat, r aggression between feline housemates after redirected. Previously stable cat odor stimuli (return of a cat from the returning from separation (e.g., veterinary relationships can deteriorate as cats reach veterinarian or giving one cat a bath), aging or visit, grooming); most likely due to change in illness of one or both cats, cats reaching social r social maturity (2–4 years of age). r odor and visual cues of victim. Maternal maturity. Household change, e.g., moving, Predominant Sex aggression—aggression during the r changing furniture or resting areas. Intact males more likely to initiate intercat r periparturient period; females guard kittens Genetically unrelated cats and cats that have and nesting sites from unfamiliar individuals. aggression (related to territory, and/or r r recently moved in together are more likely to Intermale aggression—between males in proximity to females). Females will defend show aggressive behaviors toward each other. their young from unfamiliar individuals. r response to territorial disputes, hierarchical r Resident cats commonly need prolonged status, or mates; aggression may be more Male kittens are more likely to initiate exposure to new cats before accepting them r intercat aggression related to the predatory r pronounced at social maturity. Sexual into group. Resource limitation (not aggression—male typical behavior of chasing, components of play. enough vertical and/or horizontal space, lack SIGNS pouncing, biting on the nape of the neck, and of appropriate hiding areas, and limited food, mounting with or without intromission. Historical Findings water, and litter boxes, etc.) in multi-cat r r r Predatory/play-related aggression— May arise spontaneously and vary in households. Exposure to arousing stimuli r predatory components of play directed frequency and intensity. Owners most likely (cats in the yard, visitors, noises, scents, etc.) toward another cat; the recipient is often an can cause redirected aggression after which to seek behavioral intervention if there are r older cat that is not interested in playing. aggression might persist. Medical problems physical injuries, the welfare of the aggressor Medical Differentials and /or victim is compromised, or fighting including CNS disorders, hyperthyroidism, or r r Any illness causing malaise, pain, or any disorder that causes pain and/or increased r becomes sufficiently distressing. Human increased irritability Endocrine, e.g., irritability. r intervention in an attempt to interrupt hyperthyroidism Neurologic: fighting may result in human-directed space-occupying lesions, e.g., meningioma, aggression/injury. lymphoma, encephalitis, seizures, feline JWST589-A40-26-29 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:27 279mm×216mm

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ischemic encephalopathy, trauma, sensory or For Cases that have a Low Frequency of increasing vertical space (e.g.,. resting areas on r r cognitive decline Infectious: rabies, Intense, Injurious Aggressive Outbursts shelves, window sills). No new cats should r toxoplasmosis, aberrant parasitic migrations Separate the cats when they cannot be be added to the house. r r (e.g., cuterebriasis), FIV, FeLV Iatrogenic: supervised (create “safe zones”). Either keep For Cases where the Cats Cannot be in medications that increase irritability or them separate in the same areas each day in an the Same Room without Immediately disinhibit aggression (e.g., mirtazapine, effort to form separate core territories for each Becoming Agitated r r benzodiazepines, buspirone) Toxins: lead, cat, or “time share” the space between cats. Separate cats completely when r r illicit substances Confine the newly introduced cat or the unsupervised. Meet each cat’s needs for play, CBC/BIOCHEMISTRY/URINALYSIS aggressor to the smaller, less familiar area. litter boxes, food, water, perching, resting, and r r Baseline CBC, biochemistry, urine to rule out For multiple cats, separate by stability of attention. A large wire dog kennel or vertical relationship between cats. Any despotic/bully medical causes and as a baseline if drug r orientated wire cat cage (with shelving) may therapy indicated. cats should be confined alone. Consider be better tolerated than smaller cat kennels “artificial allomarking” to form a communal and can be used for controlled exposure. OTHER LABORATORY TESTS r r r scent between the cats that are fighting; a Cats may be taught to tolerate harnesses and FeLV/FIV Cats > 6 years should have towel (facecloth) may be rubbed leashes so that they can be used during total T measured 4 (cephalocaudally) to obtain the scent of one training and controlled reintroduction. This is IMAGING cat and then rubbed onto the other cat and r r especially valuable for the aggressor. Set up As indicated based on history and physical vice versa. Towels should be left in the desensitization and counter-conditioning signs environment to allow for habituation to each sessions daily; initially utilize physical and other’s scent especially if the cats are kept r DIAGNOSTIC PROCEDURES r visual barriers. Introduce the cats (in their r separated. Reward cats with food, play, Obtain a detailed behavioral and medical kennels or on leash and harness) at a distance r and/or attention for being in the same room from each other that prevents overt/covert history of the patients. Identify if there is a together without having aggressive events. clear aggressor and/or victim and if aggression aggression. Feed the cats or engage in play for r Cats should stay at a distance that allows for r is overt or covert. If multiple cats determine r classical counterconditioning. Over many calm participation. Engage cats in daily sessions gradually reduce the distance between which cats spend time together, mutually sessions of pleasurable activities (e.g., play, groom each other, and which cats physically the cats, being careful to stay far enough apart r training, eating delectable food treats) at avoid each other. Identify the preferred core during each session that no overt or covert distances that do not incite aggression. behavioral signs of aggression and/or fear are areas of each cat for feeding, play, and resting Gradually move the fun sessions closer to each and locations of any house soiling or marking. seen. Start and end all sessions on a successful r other, making sure to stay at a distance that r Identify: the number, location, types of note. Teach the cats a “come and/or go to r does not trigger overt/covert aggression. litter boxes and their management. Media in r place” cue using operant counterconditioning Teach the cats a “come and/or go to place” and positive reinforcement. Practice these the form of video, photographs, and/or drawn cue using positive reinforcement at times, in floor plans can provide spatial details and cues several times daily so each cat learns to situations, and with sufficient rewards that the respond reliably. Behavioral cues are best information regarding body language during r r r cats are most able to learn. Interrupt or taught when animals are not stressed. When social interactions. Note any other changes redirect the cats by cueing to come or go to its in demeanor, routine, eating, and grooming. ready to allow the cats more freedom with place, or by luring one or both cats to their each other, follow the instructions for less PATHOLOGIC FINDINGS safe zones with food and treats, wand toys, severe interact aggression (above). None unless concurrent medical diseases tossed toys, or laser pointers before aggression SURGICAL CONSIDERATIONS starts or as initial signs are seen (e.g., staring, r tail twitching, pupil dilation). Aversives Neutering intact males is approximately 90% and/or punishers can increase aggressive effective in reducing roaming, intercat TREATMENT behavior and increase negative associations aggression, and urine spraying. with other cats, so must be avoided or used Neutering/spaying is effective in reducing APPROPRIATE HEALTH CARE r mounting/sexual behavior. r cautiously. The goal of management and Treat as outpatients with behavior and safety is to prevent aggressive events. In an environmental modification± ( medication) r emergency, use of a laundry basket or blanket Current on routine vaccinations, including placed between or over the cats, can stop rabies aggression, and direct the cat to its safe area MEDICATIONS until calm, but should not be considered as a NURSING CARE r DRUG(S) OF CHOICE Supportive care if any injuries from fighting. treatment. Bell the aggressor (using a quick release or safety collar) so both the owners and As all medications are extra-label, insure that ACTIVITY victim can quickly identify his/her location. the client is informed, and review target r May need to be restricted if confinement Increase the number of resources and desirable outcomes and potential adverse required to prevent the perpetuation of locations (e.g., food, water, scratching, effects. aggression and negative emotional responses. perching, bedding, play and feeding toys) For the Aggressor and/or Victim Provide sufficient alternate outlets for each cat throughout the residence including each cat’s Selective Serotonin Reuptake Inhibitors during confinement area and during release. (SSRI) core area. The efficacy of multimodal r DIET environmental enrichment should not be Fluoxetine or paroxetine 0.5–1 mg/kg PO r q24 h. None (except possible therapeutic diet trial underestimated. Increase litter boxes to the r discussed below) number of cats plus one divided among Drugs of choice for aggression, anxiety, CLIENT EDUCATION multiple locations so that one cat cannot keep and/or urine marking, may decrease another from accessing the boxes; locations impulsivity. For chronic, severe cases or for aggression that r with more than one exit/entry are ideal. Side effects may include gastrointestinal does not respond to treatment, may require r Increase the number of hiding places and upset, decreased appetite, sedation, urinary permanent separation either by rehoming one resting areas; especially concentrate on of the cats or by splitting up the residence. JWST589-A40-26-29 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:27 279mm×216mm

48 Blackwell’s Five-Minute Veterinary Consult

A Aggression, Intercat Aggression (Continued)

retention (paroxetine), and increased cautiously or avoid with buspirone, tramadol, incomplete owner compliance. In one study agitation/irritability. and tryptophan due to possible serotonin 62% (30/48) were considered cured and 37% r Tricyclic Antidepressant (TCA) syndrome. Caution with concurrent (17/48) not cured (cat given away, euthanized r r Clomipramine 0.3–0.5 mg/kg PO q24 h: medications considered substrates of P450. or permanently separated). Recent and mild serotonin selective tricyclic: for anxiety and ALTERNATIVE DRUGS (low-intensity, low-frequency) cases may have aggression r better long-term outcomes. r Amitriptyline (TCA) 0.5–1 mg/kg PO Side effects include gastrointestinal upset, q12–24 h: for anxious cats especially if sedation, urinary retention, constipation, and comorbid recurrent FIC/FLUTD; not lowered seizure threshold. Do not use in selective for serotonin reuptake inhibition and r patients with arrhythmias or likely less effective for the aggressor. Dietary MISCELLANEOUS cardiomyopathies. supplementation with alpha-casozepine ASSOCIATED CONDITIONS Pheromones (Zylkene: Veotquinol), ROYAL CANIN r r Urine marking/spraying House soiling Feliway and Feliway Multicat (CEVA) and Veterinary Diet CALM (contains r r Excessive grooming Fearful/anxiety- Felifriend (CEVA, presently available in alpha-casezopine, l-tryptophan, and r related behavior Human-directed or Europe) are feline facial pheromones that may nicotinamide) or Hill’s Prescription Diet interspecies aggression be helpful in cases of intercat aggression when Multicare Feline Urinary Stress (contains used with a multimodal plan. l-tryptophan and milk protein hydrolysate). AGE-RELATED FACTORS For the Victim Predatory/Play-related aggression more Azapirone common in young active and playful cats Buspirone 0.5–1 mg/kg PO q8–24 h (feline housed indoors with more sedentary or aged dose): reserved for victims to increase social FOLLOW-UP individuals. confidence. r ZOONOTIC POTENTIAL Side effects rare; may include decreased PATIENT MONITORING r Humans intervening while cats are fighting sociability and increased agitation/irritability. Clinicians should monitor patients 2 weeks may be injured and contract infections May increase intercat aggression as victim after treatment initiation and monthly for the through cat bites and/or scratches. may be more confident and fight back.” first few months by phone or email; a Benzodiazepines follow-up visit should be scheduled 4–8 weeks PREGNANCY/FERTILITY/BREEDING r Lorazepam 0.125–0.25 mg/cat PO up to into treatment if drugs dispensed to assess Most behavioral medications are q12–24 h or oxazepam 0.2–0.5 mg/kg PO response and adjust dose if necessary. contraindicated in breeding animals. r q12–24 h for anxious or fearfully aggressive Benzodiazepines may rarely cause cases of SYNONYM cats and as an appetite stimulant helping to fatal hepatopathies; patients should be Feline intraspecies aggression facilitate classical counter conditioning. May rechecked immediately if any adverse events, r ABBREVIATIONS be used as needed with peak effects seen including anorexia. Medication should be r within 1 hour. used for at least 4–6 weeks after resolution of FeLV = feline leukemia virus r r Side effects may include increased appetite, signs, then gradually weaned by reducing the FIC/FLUTD = feline idiopathic cystitis/feline lower urinary tract disease ataxia, inhibited learning, and disinhibition of dosage no faster than 25% per day on a r r FIV = feline immunodeficiency virus aggression. weekly basis. Some patients require r r MAOI = monoamine oxidase inhibitor Note: controlled substance; dependence can long-term medication; recheck laboratory r SSRI = selective serotonin reuptake develop; Medication should be gradually work every 6 months to 1 year depending on r r = = weaned if used consistently for longer than health and age.. inhibitor T4 thyroxine TCA tricyclic antidepressant 2 weeks. PREVENTION/AVOIDANCE r SEE ALSO CONTRAINDICATIONS Proper socialization 2–7 weeks and ongoing. r r r Benzodiazepines should be used cautiously Gradual introduction more closely resembles Aggression, Overview—Cats Pediatric or avoided in cats with hepatopathies. the natural process through which new cats Behavior Problems—Cats r Paroxetine and TCAs may produce enter an existing group at the periphery and INTERNET RESOURCES anticholinergic side effects. Fluoxetine also may be accepted over time. Intercat http://indoorpet.osu.edu/cats/ occasionally reported to cause urine retention. aggression may be more common when r Suggested Reading SSRIs and TCAs should be used with unfamiliar cats are suddenly placed together. Heath S. Feline aggression. In: Horwitz DF, caution in patients with histories of cardiac A negative initial encounter is often associated Mills D, eds. BSAVA Manual of Canine and abnormalities, seizures, and liver disease. with future intercat aggression. Related and Feline Behavioural Medicine, 2 nd ed. familiar cats are less likely to have intense PRECAUTIONS Gloucestershire, UK: BSAVA, 2009, r intercat aggression. In stable multi-cat Any behavioral drug has the potential to pp. 223–235. households, avoid adding additional cats. produce paradoxical reactions, including fear, Landsberg G, Hunthausen W, Ackerman L. anxiety, hyperexcitability and/or aggression. POSSIBLE COMPLICATIONS r Feline aggression. In: Behavior Problems of Medications that alter serotonin levels have Abrupt withdrawal of behavioral medications the Dog and Cat, 3rd ed. Philadelphia: the potential to produce serotonin syndrome. may result in aggression and rebound anxiety. Elsevier Saunders, 2013, pp. 327–343. POSSIBLE INTERACTIONS EXPECTED COURSE AND PROGNOSIS Authors E’Lise Christensen Bell and Kenneth r r Avoid concurrent use of SSRIs and TCAs or The prognosis for most cases is fair; itis M. Martin MAO inhibitors such as selegiline and use complicated by prolonged duration, high Consulting Editor Gary M. Landsberg intensity, underlying medical conditions, and JWST589-A02-27-30 JWST589-Tilley Printer: Yet to Come August 27, 2015 14:13 279mm×216mm

Canine and Feline, Sixth Edition 49 Aggression, Overview—Cats A

Territorial Aggression (Toward People or need to be evaluated to accurately diagnose Other Animals) and treat aggression cases. r Some cats, particularly male cats, show SYSTEMS AFFECTED BASICS r territorial behaviors in domestic home settings Behavioral—vary with type of aggression, DEFINITION due to size and the presence of more resources r occur alone or in combination: tail swishing/ Aggression is a behavioral strategy used to (e.g., people, food, resting areas, feeding areas, r twitching, ears turned sideways or flattened, manage aversive situations. May be normal elimination sites, etc.) to defend in a smaller r r stiffening of shoulders/legs, crouching, and appropriate in certain contexts. May area. Territorial behaviors include marking dilation of pupils, hissing, spitting, growling, be abnormal with serious deleterious effects with urine, feces, or bunting (the rubbing of piloerection, staring, chasing, stalking, on the cat’s physical and emotional the cheeks on surfaces to deposit pheromones) r r pawing, lunging. Cardiovascular—signs well-being. Aggressivity: describes both and scratching (also deposits pheromones and associated with sympathetic activation and leaves visual marker) and may be associated r mood and temperament traits relating to the r HPA activation. Endocrine and propensity to show aggression when with aggression. In severe cases, the Metabolic—long-term aggression associated aggressor may seek out the other individuals environmental circumstances dictate it might r with fear/stress/anxiety, symptoms associated be used. and attack. Body posture with territorial with long-term activation of the HPA system. r OVERVIEW OF TYPES aggression is assertive and confident. Gastrointestinal—with chronic HPA Pain Aggression (Toward People and Play Aggression (Toward People) stimulation may see a cat more prone to r Animals) Typically refers to a cat who scratches and anorexia and GI ulcers. With acute fear r Cats who are in pain may show aggression bites the owners during play. Not true aggression: evacuation of the bowel and (hiss, growl, scratch, bite) when they are aggression but overzealous play without possible diarrhea. IBD possible in chronic physically handled or prior to or after r proper impulse control due to lack of training stress. Hemic/Lymphatic/Immune— r movements such as jumping onto or off a or proper intraspecific social feedback. The decreased immune response with chronic piece of furniture. cat’s intent is not to harm the person. HPA stimulation; stress leukogram. r r Behavior encouraged and rewarded by Maternal Aggression Musculoskeletal—an outcome of the owners through rough play with a kitten; A female cat may show aggressive behaviors aggression may result in damage to the muscles from damage by the nails and teeth. when larger and stronger, becomes perceived toward individuals approaching her kittens. r Both the victim and the aggressor may as aggression rather than overzealous Impulse Control Aggression suffer injuries. With chronic activation of the play. Cats who show intense aggressive responses to r HPA, may see muscle wasting. Nervous— mild stimuli without much or any warning Predatory Aggression (Toward People or increased reactivity for up to 72 hours may have an impulse control disorder arising Other Animals) following an aggressive outburst. May see an r from dysfunctional serotonin neural circuits. Cats have an innate drive to “hunt” or show increase in aggression with decreased predation behavior, which includes stalk, r Frustration-Induced Aggression (To provocation as the synapses in the amygdala hide, and pounce. Predation is not a direct r People and Other Animals) become sensitized. Some animals may have function of hunger. Typically stimulated by Some cats have very outgoing, social decreased serotonin, causing aggressive fast movements and can progress to the cat personalities and exhibit aggression if the outbursts. Depending on the type of hiding and waiting for an animal or person to captive life indoors does not meet their aggression, may see ritualized motor patterns, r r walk by. Play is a common way for young behavioral needs. shaking, or trembling. Ophthalmic— cats to perfect predation skills; play aggression Contact-Induced/Petting Aggression dilated pupils with sympathetic stimulation. r and predatory aggression may overlap. (Toward People) Renal/Urologic—may see associated r Redirected Aggression (Toward People Cats will show early signs of aversion when spraying or small amounts of urine on or Other Animals) horizontal surfaces. May exhibit signs r people stroke their cats, with their ears going Cats who see, hear, or smell a trigger and r consistent with FLUTD with aggression that back and tail swishing. If physical contact r direct aggressive behavior toward the closest r is due to stress/anxiety/fear. Respiratory— r continues, they typically bite. Owners often bystander. In some cases, one person or r tachypnea in acute cases or when stressed. miss the early warning signs. When cats r animal in the home becomes the designated groom one another, they typically limit the Skin/Exocrine—damage due to fights. r victim, and the cat may bypass a nearby grooming to the head region. Some cats Damage due to excessive grooming associated individual and look for the preferred victim. with fear-based aggression/anxiety/distress. r appear to be particularly sensitive to being Some cats may stay aroused for 24–72 hours r stroked along the dorsum, the common SIGNALMENT r after a triggered event. Common triggers method used by owners. There is preliminary evidence that inciting redirected aggression are seeing Intercat Aggression within a Home behavioral traits in cats vary by breed and r r another cat or wildlife outside or loud noises. Fifty percent of cat owners report fighting gender. Males were more likely to show r Fear/Defensive Aggression (Toward (scratching and biting) after introducing a aggression to cats than females. Abyssinian, r People or Other Animals) new cat to the home. The number of cats, Russian blue, Somali, Siamese, and chinchilla r r The cat will show body postures indicative gender, and age are not significant factors in breeds showed more aggression. Maine of fear/anxiety and may use aggression as a predicting which cats will show aggression. Coon, ragdoll, and Scottish folds showed the strategy to manage that aversive situation. r r Any of the above categories of aggression are least aggressiveness. Typical behaviors shown include a all possibilities for fights between or among SIGNS combination of any of the following: hissing, r r cats. Fear/anxiety is the most common cause May appear at social maturity (2–4 years of spitting, piloerection, arched back, turning of intraspecific aggression. age) except for play-related and should occur away, running away, cowering, rolling on its CONTRIBUTING FACTORS TO THE in specific social contexts/interactions. If onset back and pawing (defensive position, not PATHOPHYSIOLOGY occurs in an older cat, medical causes should submissive position) if cornered. r Behavior problems are typically multifactorial be ruled out first. General comments: most in cause, and Figure 1 is a diagram illustrating owners are able to detect overt signs of some of the more common components that aggression (biting, hissing, growling) but may JWST589-A02-27-30 JWST589-Tilley Printer: Yet to Come August 27, 2015 14:13 279mm×216mm

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counter-condition the cat to the triggers. medication. Recheck liver and kidney values Learning r Implement safety measures (nail caps, 2–3 weeks after starting medication. Recheck Communication wearing long pants/long sleeves, keep bloodwork annually in young healthy flattened cardboard boxes around home to patients, semiannually in older patients. r Social interactions place between yourself and your cat, redirect Repeat physical exams in older patients the behavior in early arousal phase). semiannually, as painful conditions may start r Environment Genetics Behavior modifications to redirect the cat to contribute to/exacerbate the pain. AGGRESSION and reduce arousal (specific plans are EXPECTED COURSE AND PROGNOSIS dependent upon the specifics of each case). r r Ultimately depends on the specific kind of Train your cat to commands such as “sit,” r aggression and the compliance of clients with Physiology “go to place,” etc. Implement r r the suggested treatment plan. Most cases of environmental enrichment. Teach owners to Learning aggression need a combination of behavioral identify early signs of arousal so the cat can be r modification, environmental modification, redirected or so they can avoid the cat. After training, and, when necessary, medication to r Figure 1. a very aggressive outburst, keep aggressor maximize chances of improvement. Some isolated in a room for at least 24 hours (as types of aggression can resolve or improve long as the cat remains aroused after an r r within a few weeks, whereas others may take r attack). Pheromones. Medications. several months or longer. Some forms of miss more subtle signs of aggression that aggression have a poor prognosis. typically occur between cats (staring) and the resulting anxious behaviors that can result in aggression (meatloaf position, averting gaze, MEDICATIONS etc.). Videotapes of intercat interactions allow the clinician to assess the behavior. DRUGS OF CHOICE MISCELLANEOUS r CAUSES SSRIs: fluoxetine or paroxetine 0.5 mg/kg AGE-RELATED FACTORS r PO q24h. r Underlying medical issues can cause r Older cats—cognitive decline, CNS disease, r aggression. Temperament/behavior is TCAs: clomipramine 0.5 mg/kg PO q24h. arthritis, meningioma, other medical r r influenced by genetics, rearing, socialization, Buspirone at 0.5–1.0 mg/kg q8–24h or conditions. Age 2–4—social maturity, when environment in which the cat lives, and types benzodiazepines such as oxazepam at cats may start to show certain kinds of of interactions the cat has with people. 0.2–0.5 mg/kg q12–24h might reduce fear aggression. and build confidence in the fearful cat that ABBREVIATIONS does not retaliate or fight back. r r CNS = central nervous system FCV = CONTRAINDICATIONS r r r feline calicivirus FeLV = feline leukemia Cats with renal or hepatic disease Caution r DIAGNOSIS r virus FIV = feline immunodeficiency virus r with TCAs and SSRIs in diabetics TCAs in FLUTD = feline lower urinary tract disease DIFFERENTIAL DIAGNOSIS patients with cardiac abnormalities r r r GI = gastrointestinal HPA = r CNS diseases (e.g., infections, toxins, POSSIBLE INTERACTIONS hypothalamic-pituitary-adrenal IBD = tumors, partial seizures, focal seizures) r r r r TCAs and SSRIs should not be used inflammatory bowel disease SAMe = Hyperthyroid Hepatic encephalopathy r r together. Mirtazapine should not be used in S-adenosyl-L-methionine-tosylate disulfate r r Any condition causing pain (e.g., arthritis, combination with a TCA or SSRI. Any SSRI = selective serotonin reuptake pancreatitis, dental disease, anal sacculitis) r r r r other medication the cat is on, the inhibitor TCA = tricyclic antidepressant Lead poisoning Rabies Diabetic practitioner should look up which liver SEE ALSO neuropathy (pain-induced aggression when r enzyme system is utilized in metabolism to Aggression—Intercat Aggression paws touched) r maximize safety in combining medications. Aggression Toward Humans—Cats CBC/CHEMISTRY/URINALYSIS ALTERNATIVE DRUGS r Suggested Reading Physical examination, baseline blood and Amitryptiline 0.5–1.0 mg/kg PO q12–24h r r Crowell-Davis SL, Murray T. Veterinary urine screening followed by additional SAMe: 100 mg PO q24h Zylkene 75 mg r Psychopharmacology. Ames, IA: Blackwell, diagnostics as indicated based on history, (15 mg/kg or greater) PO q24h Feliway 2006. examination and laboratory results. Multicat diffuser l-theanine 25 mg PO q24h r Levine ED. Feline fear and anxiety. Vet Clin OTHER LABORATORY TESTS Zylkene 75 mg PO SID r North Am Small Anim Pract 2008, Discuss Bartonella testing in any cat that r 38:1065–1079. bites or scratches people. Thyroid levels. r Levine ED, Perry P, Scarlett J, et al. Intercat Urinalysis ± culture if housesoiling is part r aggression in households following the of the aggression issue. Feline serology FOLLOW-UP introduction of a new cat. Appl Anim Behav (FCV, FeLV, FIV). PATIENT MONITORING Sci 2004, 90:325–336. r Call owners once every 1–2 weeks for the Author Emily D. Levine first 2 months after a treatment plan has been Consulting Editor Gary M. Landsberg Acknowledgment Karen L. Overall TREATMENT recommended. Determine implementation of r safety recommendations and the behavioral Never use physical correction/punishment; r r plan. If medications are involved, the Client Education Handout may escalate the aggression. Never try to medication dose should be reevaluated every physically handle or manipulate a cat in an r available online r 3–4 weeks. Frequency of follow-up will be aggressive state. Avoid known triggers. r dictated by the severity of the case and owner Identify triggers and desensitize and r compliance. CBC, chemistry, T4 prior to JWST589-A41-28-31 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:36 279mm×216mm

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r PATHOPHYSIOLOGY In the majority of cases, people are bitten by r Affective aggression involves arousal of the dogs that are known to them. BASICS sympathetic nervous system. Some pathologic GEOGRAPHIC DISTRIBUTION conditions are associated with an increase in Worldwide DEFINITION aggression because of CNS effects such as r pain or irritability. SIGNALMENT Action by one dog directed against another r organism with the result of, limiting, Abnormalities in the CNS serotonin Species depriving, or harming that organism. neurotransmitter system have been implicated Dog Aggression refers to any behavior along an in one type of impulsive human-directed Breed Predispositions r aggression continuum, from a stare, to aggression, colloquially called “rage,” directed Any breed or breed mix. r immobility (freeze), growl, snarl, lunge, air toward familiar persons over controlling Pit bull, German shepherd dog, and gestures. snap, single bit, multiple bite, multiple r rottweiler are the most common breed types attacks, and chase and attack. Aggression often has a learned component implicated in fatal dog bites in the US. r r Numerous functional types have been whereby dogs learn to use aggression to In the US, English springer spaniels appear posited. Here, aggression is classified on the manage distance from fearful stimuli or to be at risk for human-directed “dominance” basis of (1) affective aggression, (2) predatory control resources. aggression. aggression, and (3) play-related aggression. SYSTEMS AFFECTED r Mean Age and Range Affective (emotional) aggression is the focus Behavior. r Any age of this chapter. Affective states, such as fear Other, if there is an underlying medical Predominant Sex and arousal, and motivational factors, such as etiology. r Any sex. hunger and sexual drive, influence the GENETICS r probability of overt aggression, such as biting. r Males—intact or castrated are most Affective aggression may be human-directed In some breeding programs, aggressive commonly implicated in cases of or dog-directed. Within these contexts, there tendencies and bite styles have been selected human-directed “dominance” type aggression. for (or against). may be additional specificity, such as r Intact males are overrepresented in dog-bite One study in the United States linked fatalities. human-directed aggression toward unfamiliar r persons, or human-directed aggression English springer spaniels that display Females—spayed are most commonly directed toward familiar persons. Often dogs human-directed dominance aggression to one implicated in aggression to other female dogs display aggression in a single context. breeding sire, implicating a heritable in the home. In some studies, spayed females r component. Human-directed aggression toward familiar r are less likely than males to display human persons in response to controlling gestures is One study of human-directed dominance directed aggression. historically called dominance aggression, aggression among English cocker spaniels SIGNS reported that males were more aggressive than although newer terminology, such as conflict General Comments females, and dogs with solid coat color were r aggression, may be used to avoid Any dog can display aggression. Many often-erroneous semantic assumptions more aggressive than those with parti coat color. factors, including individual dog inherent in the term “dominance.” temperament and experience, influence the r INCIDENCE/PREVALENCE Human-directed aggression toward propensity to bite. r r unfamiliar persons specific to home location Canine aggression is the most common Dogs may display warning signs—including is called territorial aggression. diagnostic category seen by board-certified r immobility, growls, snarls, or air snaps that Predatory aggression refers to behaviors veterinary behaviorists in North America. r may provide time to avoid overt aggression. associated with chasing and hunting prey. It is According to the Centers for Disease These signs should not be punished, as this often considered nonaffective and may be Control and Prevention (2009), about might decrease the probability of warning socially facilitated by other dogs. Predatory 4.7 million people are bitten by dogs each signs without affecting the underlying risk, or behaviors may be triggered by movement or year in the US, although this number is may further intensify the aggressive high-pitched sounds and may be misdirected considered an underestimation as the majority (defensive) response. Instead, the animal to humans or objects. of dog bites are not reported. r r should be safely removed from the situation Play-related aggression involves aggressive In the US, it is estimated that one in five of and the underlying triggers for the affective gestures, such as growling and biting, in the those who are bitten require medical attention state should be addressed. context of play and is commonly displayed for dog bite–related injuries. r toward other dogs or humans. It is often Among children and adults, males are more initiated by signs of play, such as the play bow. likely than females to be bitten. r r In all cases, medical factors that might Based on emergency room data in the US, contribute to aggression (including pain) the rate of dog bite–related injuries is highest must be evaluated. for children aged 5–9 years. JWST589-A41-28-31 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:36 279mm×216mm

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r Historical Findings Unpredictability of aggressive behaviors, PATHOLOGIC FINDINGS r Variable. lack of warning signals. None r r Basis for risk analysis and details of Presence of children, elderly people, or treatment program. Important questions: other humans or animals at high risk living in Whoisthetarget?Whowaspresentto or visiting household. manage the dog? How severe were the TREATMENT resulting injuries? What are the circumstances APPROPRIATE HEALTH CARE (including location, time) in which aggression r Manage any underlying medical conditions. occurred? Are there any reliable triggers for DIAGNOSIS r the aggressive behavior? Abnormalities in Management success—combination of DIFFERENTIAL DIAGNOSIS multiple modalities: safe environmental mentation or awareness might indicate a r medical cause A thorough medical evaluation should be control, behavior modification to teach Physical Examination Findings conducted on all cases of aggression. animals appropriate behavior, and r r Usually unremarkable. Identify pathologic conditions associated pharmacotherapy. r r Use extreme care when handling aggressive with aggression before making a purely Consult a veterinarian with experience and dogs. behavioral diagnosis. training in aggression management. r r r A comfortable, well-fitting basket muzzle is Rule out developmental abnormalities Euthanasia should be discussed or recommended prior to examination of any (hydrocephaly, lissencephaly, hepatic shunts), recommended when the risk of injury is high. metabolic disorders (hypoglycemia, hepatic Note recommendation in medical record. dog with a history of human-directed r aggression. Basket-style muzzles allow dogs to encephalopathy, diabetes), Rehoming aggressive dogs may put those pant. neuroendocrinopathies (hypothyroidism, involved at liability risk. r Abnormalities on the neurologic hyperadrenocorticism), dermatopathy, NURSING CARE examination may suggest an organic disease neurologic conditions (intracranial neoplasm, A boarding facility able to safely manage the process (e.g., rabies, pain, blindness). Dogs seizures), toxins, inflammatory diseases dog might be used until a safe management can display aggression preictal, postictal or (encephalitis, rabies), cognitive dysfunction, plan can be implemented, or until an ictal period. acute or chronic pain, and iatrogenic causes, outcome decision can be made. such as glucocorticoid administration. CAUSES ACTIVITY r CBC/BIOCHEMISTRY/URINALYSIS Part of the normal range of behavior; r Since frustration and arousal may increase the strongly influenced by individual May be indicated to evaluate dog as incidence of aggression, an appropriate and candidate for behavioral medications. temperament, experience, early socialization r safe exercise regime should be incorporated (before 12 weeks), and other variables. Abnormalities may suggest underlying into the treatment program. r Harsh handling and confrontational metabolic, endocrine causes, or other medical conditions. DIET responses can escalate aggression and should r There is modest evidence that a low-protein be avoided. Usually no significant findings outside r diet may reduce territorial aggression in dogs, May be a manifestation of an organic laboratory range unless an underlying medical etiology is detected. an effect that might be enhanced with condition, such as hepatic encephalopathy or tryptophan supplementation. pain. OTHER LABORATORY TESTS r r In all cases, evaluate medical causes of Thyroid testing. CLIENT EDUCATION r r aggression. Others as indicated by history and physical Safe practices should dictate all decisions. RISK FACTORS exam. These practices include safe confinement, r physical barriers, head halters, leash control, Inadequate socialization during the canine IMAGING r muzzle use, and supervision by a competent critical period (3–12 weeks). May be indicated to identify sources of pain r adult. Traumatic/fearful/negative experience(s). or disease. r r r Situations that have led to aggression in the Predisposing environmental conditions— MRI or CT—particularly if cerebral past should be listed and a specific plan lack of training, inadequate restraint, harsh disease/neoplasia suspected. developed to avoid these situations and handling. r DIAGNOSTIC PROCEDURES associated locations in the future, and a r Inability of owner to safely confine or Collection of thorough behavioral history long-term management plan developed. r manage the dog in order to prevent future and evaluation of medical concerns. The dog should calmly be removed from r incidents. Helpful devices include a barrier Postmortem fluorescent antibody test is aggression-provoking situations. fence, a muzzle, a collar or head halter, a leash. r r indicated for any aggressive dog for which Safe, non-confrontational techniques that Previous aggression/bite history (number of rabies is a differential diagnosis, including any manage resources and use positive incidents, number of bites per incident, dog not quarantined for 10 days after a bite reinforcement to teach the dog appropriate target, severity of injury); legal citation for injury to a human or other animal. responses should be employed. biting. JWST589-A41-28-31 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:36 279mm×216mm

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r r Confrontational management techniques, Treatment duration: minimum 4 months, PREVENTION/AVOIDANCE r such as roll-overs, increase the probability of a maximum: lifetime. To prevent aggressive incidents, avoid all r defensive aggressive response, may lead to See Table 1 for drugs used to facilitate situations that have led to aggression in the human injury, and should be strictly avoided. management of aggression in combination past, using safe confinement, gates, halters, r Management (“dominance”) techniques with a safe management plan. collars, leashes, muzzles. r including punishment are associated with CONTRAINDICATIONS Reduce the risk of aggression in young dogs r defensive fear responses by the dog and an Fluoxetine is generally contraindicated in (3–12 weeks) with a positive socialization increased risk of human-directed aggression. cases of seizures. program; avoid intimidation techniques and r These should be avoided and replaced with Clomipramine is contraindicated in cases of negative, fear-inducing situations. positive management techniques. r cardiac conduction disturbances or seizures; POSSIBLE COMPLICATIONS r The client should be advised to consider in one open trial, clomipramine was no more Injury to humans or animals. r personal and legal liability risks of keeping the effective than control in cases of Liability to client, veterinarian. r dog. Human injury, bite-related lawsuits, and human-directed aggression. In cases of dog-directed aggression, homeowner’s insurance claims can result from although not the intended target, humans canine aggression. Such risk assessment may PRECAUTIONS Avoid the use of benzodiazepines (e.g., who interfere are often seriously injured either help the client objectively evaluate the by accident or by redirected aggression; situation. diazepam) in aggressive dogs because of the r risk of behavioral disinhibition. Aggression owners should not reach for fighting dogs; Euthanasia should be considered if safe pull apart with leashes. management cannot be employed, or when may increase when dogs lose their fear of the r repercussions of biting. Aggressive dogs are at risk for the risk of injury is high. relinquishment or euthanasia. POSSIBLE INTERACTIONS SURGICAL CONSIDERATIONS EXPECTED COURSE AND PROGNOSIS Castration of males may reduce the incidence Do not use SSRIs or TCAs with monoamine r oxidase inhibitors, including amitraz and Aggressive dogs weighing over 18.5 kg are at of inter-male aggression. increased risk for behavioral euthanasia. selegiline, or with each other because of the r risk of serotonin syndrome. Aggressive dogs may be successfully managed, but should not be considered ALTERNATIVE DRUG(S) r “cured.” L-Tryptophan (10 mg/kg PO q12 h). r MEDICATIONS r Prognosis is case-dependent due to risk Trazodone (4–8 mg/kg PO q12 h or PRN) DRUG(S) OF CHOICE factors and management features of each r may be used with the agents listed in Table situation. None approved by the FDA for the 1 to reduce anxiety and arousal. treatment of aggression. r r Clonidine (0.01–0.05 mg/kg PO q12 h or No drug will eliminate the probability of PRN), may be used with the agents listed in aggression. r Table 1 to reduce anxiety and arousal. Use drugs only when a safe management MISCELLANEOUS plan has been implemented. r ASSOCIATED CONDITIONS Inform the client of the extra-label nature of N/A medication and risk involved; document in the medical record, obtain signed informed FOLLOW-UP AGE-RELATED FACTORS consent. PATIENT MONITORING Onset of aggression in mature dogs suggests a r Drugs that increase serotonin may be Weekly to biweekly contact recommended in medical cause; carefully evaluate sensory helpful to reduce anxiety, arousal, and the initial phases to guide clients with acuity, sources of pain, endocrinopathy, impulsivity. behavior modification plans and medication cognitive function. management.

Table 1 Drugs and dosages used to manage canine aggression.

Drug Drug Class Oral Dosage in Dogs Frequency Side Effects-usually transient Fluoxetine SSRI 1.0–2.0 mg/kg q24 h Decreased appetite, sleepiness Paroxetine SSRI 1.0–2.0 mg/kg q24 h Constipation Sertraline SSRI 2.0–4.0 mg/kg q24 h Sleepiness Clomipramine TCA 1.0–3.0 mg/kg q12 h Sleepiness, vomiting JWST589-A41-28-31 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:36 279mm×216mm

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ZOONOTIC POTENTIAL INTERNET RESOURCES Herron ME, Shofer FS, Reisner IR. Survey of r r Dog bites are significant public health risk. American Veterinary Medical Association the use and outcome of confrontational and r Rabies is a potential cause of aggression. Dog Bite Prevention:. https://www.avma non-confrontational training methods in .org/public/Pages/Dog-Bite-Prevention.aspx client-owned dogs showing undesired PREGNANCY/FERTILITY/BREEDING r Tricyclic antidepressants are contraindicated Centers for Disease Control and Prevention behaviors. Appl Anim Behav Sci 2009, in breeding males and pregnant females. Dog Bites: http://www.cdc.gov/ 117(1–2):47–54. HomeandRecreationalSafety/Dog-Bites/ Landsberg G. Canine Aggression. In: r SYNONYM ASPCA Aggression in Dogs: Landsberg G. Hunthausen W, Ackerman L. Biting http://www.aspca.org/pet-care/virtual-pet- Behavior Problems of the Dog and Cat, 3rd SEE ALSO behaviorist/dog-behavior/aggression-dogs ed. New York: Saunders/Elsevier, 2013, pp. r Aggression—Between Dogs in the Suggested Reading 197–326. Luescher AU, Reisner IR. Canine aggression Household Casey RA, Loftus B, Bolster C, Richards GJ, r toward familiar people: A new look at an Aggression, Food and Resource Guarding— Blckwell EJ. Human directed aggression in old problem. Vet Clin North Am Small Dogs domestic dogs (Canis familiaris): r Anim Pract 2008, 38:1107–1130. Aggression to Unfamiliar People and Occurrence in different contexts and risk Authors Barbara L. Sherman and Margaret E. Unfamiliar Dogs factors. Appl Anim Behav Sci 2014, r Gruen Aggression Toward Children—Dogs 152:52–63. r Consulting Editor Gary M. Landsberg Aggression Toward Familiar People—Dogs deKeuster T, Jung H. Aggression toward ABBREVIATIONS familiar people and animals. In: Horwitz r CNS = central nervous system DF, Mills D, eds. BSAVA Manual of r Client Education Handout CT = computed tomography Canine and Feline Behavioural Medicine, r available online FDA = US Food and Drug Administration 2nd ed. Gloucestershire, UK: BSAVA, 2009, r MRI = magnetic resonance imaging pp. 182–210. r SSRI = selective serotonin reuptake inhibitor r TCA = tricyclic antidepressant JWST589-A35-24-32 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:39 279mm×216mm

Canine and Feline, Sixth Edition 55 Aggression—Between Dogs in the Household A

with other dogs, inappropriate punishment). understanding of basic canine social behavior r Breed predilections due to selective breeding and communication, risks involved in living r BASICS for interdog aggression. Aggression is likely with an aggressive dog(s), and willingness and to be more severe toward dogs of the same ability to follow safety and management r r OVERVIEW sex, especially two females. Instigators are recommendations. Owners must be aware usually newer to the household and younger that the only way to absolutely prevent future Aggression toward other dog(s) within a r household or those dogs that are otherwise than recipients. In cases of aggression within injuries is to continually separate the dogs or familiar and spend time together regularly. a household, there may be history of owners remove one from the home. Dogs can form stable social relationships interfering in normal canine communication, Safety Recommendations r quickly, sometimes within minutes of being especially when one dog appears to be The owner’s primary responsibility is to introduced. Aggression usually revolves denying another dog access to something that insure safety by identifying and avoiding all around resources (e.g., food, toys, owner the owners think they should “share.” This situations that may evoke an aggressive attention, resting places), but may be shift may actually support one dog in what response. Dogs within a household may fear-related or can occur at times of would be considered inappropriate “canine” initially need to be kept in separate housing r excitement/ behavior and result in escalation of the areas to prevent fighting. Owners should be arousal (e.g., visitors or other dogs on the interdog aggression. For example, an owner advised that they may be liable if their dog property). Usually within the range of normal calling dog “A” into a room when the other bites and could face civil/criminal r behavior, but may be abnormal or excessive dog “B” has blocked its access even though prosecutions should a person be injured. If due to learning, early environment, or “A” was willing to remain outside of the room needed, owners must be instructed in genetics (dogs bred for fighting). or the owner punishing dog “B” for blocking methods of safely breaking up dog fights. r SYSTEMS AFFECTED dog “A’s” access. Both of these situations Treatment is more likely to be successful if undermine dog “B” in its hierarchal position Behavioral aggression-provoking stimuli can be while it was subtly asserting control to which effectively prevented prior to behavior SIGNALMENT r r dog “A” was willing to defer. Underlying modification. The dogs must be confined medical conditions, especially pain, may Species r away from each other or under the direct Dog increase the level of aggression. If the physical control of a responsible adult Breed Predilections aggressor initiates or continues its attack whenever an aggression-evoking situation r despite deference from the other dogs, or if More common in purebreds with 50% could arise (e.g., around food/valued r the deferent dog is overly fearful or defensive, r being the same breed. Breed predilection in resources). Teaching the dogs to be then these may indicate abnormal responses “fighting breeds” (e.g., pit bull terrier) and comfortable wearing a head halter (e.g., that might have a poor prognosis (unable to terrier. Gentle Leader) with a lightweight 8- to socially communicate) or require drug Mean Age and Range 10-foot leash attached or a basket muzzle therapy to manage the abnormal behavior. makes controlling potentially dangerous Signs usually develop at social maturity situations easier and safer. If needed, use the (approximately 18–36 months of age). long leash both for prevention and to safely Predominant Sex remove the dog from situations that may elicit May be more common/intense between DIAGNOSIS aggression; do not reach for the dog directly. females. r DIFFERENTIAL DIAGNOSIS The more dominant dog typically asserts SIGNS r control of resources (e.g., staring, growling) r Play behavior/excited non-aggressive arousal r r with confident body postures directed toward Aggression (barking, growling, lip-lifting, Possessive aggression Fear aggression snarling, snapping, lunging, biting) toward r the more subordinate dog who relinquishes Others depending on circumstances the resource by moving or looking away. other dogs in the home. This may be r accompanied by fearful or submissive body CBC/BIOCHEMISTRY/URINALYSIS When there is competition over resources, postures/facial expressions (crouching, Usually unremarkable. Rule out underlying allow priority access to the more controlling/ backing away, ears back, tail tucked, looking medical contributing conditions with blood, dominant individual and encourage and urine and thyroid screening. reinforce deference in the other dog(s). away, lip licking) or confident/dominant body r postures (standing straight up, approaching/ OTHER LABORATORY TESTS Priority access may vary between resources direct contact with the other dog, tail up, ears (individual motivation), and contexts r As needed to rule out underlying medical forward). History prior to the onset of fights conditions. (location, who accesses first)—separate (time out) any dog displaying an inappropriate may include subtle signs of social/resource IMAGING r control/dominance (e.g., staring, lying across response. For some dogs problems may be doorways to block the other dog’s access to a MRI if CNS disease suspected; as needed to resolved if additional resources and sufficient rule out underlying medical conditions. distribution are provided to reduce room) and submission (e.g., turning away r from the staring dog or not entering the same DIAGNOSTIC PROCEDURES competition. Alternately, dogs may need to r room as the other dog). Dogs fighting in a N/A be separated when given resources that are a household may get along well except in source of repeated conflict. specific situations, especially over resources, Behavior Therapy r access to passageways/doorways, times of Depending on the situation, supporting and arousal. Dogs that fight over owner attention r TREATMENT reinforcing the hierarchal positions of the often described as “jealous.” Aggression dogs will result in rapid (e.g., 1–2 weeks) typically occurs when the owner is present. CLIENT EDUCATION resolution of the problem and a drastic CAUSES & RISK FACTORS General Comments decrease in aggressive incidents between dogs. r r May be a normal canine behavior; strongly Treatment is aimed at controlling the Fighting is likely to recur if support of the hierarchy by humans is not continued. influenced by previous experience (e.g., early problem, not achieving a “cure.” Successful r socialization, previous aggressive encounters treatment, as measured by a decrease in Separately, teach each dog those behaviors aggressive incidents, depends upon owner that will serve as a foundation for JWST589-A35-24-32 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:39 279mm×216mm

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management and control when together Tricyclic Antidepressants EXPECTED COURSE AND PROGNOSIS r including sit and relax, down-settle and Clomipramine 1–3 mg/kg PO q12h There is no cure. Prognosis for improvement teaching to go to mat, bed or crate to settle. (caution: label restriction for aggression). is more favorable if aggression is at a fairly low r r NEVER allow dogs to “fight it out” as Side effects: sedation, GIT effects, intensity and occurs in only a few predictable r serious injuries may occur. During times anticholinergic effects, cardiac conduction situations. Prognosis is highly dependent on together, use verbal cues or leave leash disturbances if predisposed, and increased owner compliance. Relationship issues may attached to train desirable and prevent or aggression. recur with changes in housing, health or age. r interrupt undesirable behavior. Structured Alpha-2 agonists r interactions (also known as learn to earn or Clonidine 0.01–0.05 mg/kg PO PRN say please by sitting) where each dog is 1.5–2 hours before eliciting trigger, up to r consistently taught to sit for anything it values q12h. Side effects: transient hyperglycemia, MISCELLANEOUS (before feeding, petting, play, going for a anticholinergic, hypotension, collapse, and ASSOCIATED CONDITIONS walk) provides structure and predictability in bradycardia (responsive to atropine), and all interactions, teaches impulse control and increased aggression. Other fear- or anxiety-based conditions; gives the dog control of its resources by sitting territorial aggression. r Serotonin 2a antagonist/reuptake calmly. Systematic desensitization and ZOONOTIC POTENTIAL inhibitors counter-conditioning to fear-provoking r Human injury and bite wounds when stimuli. Trazodone 2–5 mg/kg PO PRN prior to eliciting trigger, up to q6h—may titrate up to separating fighting dogs. r 8–10 mg/kg if no adverse effects. Side PREGNANCY/FERTILITY/BREEDING effects: sedation, anorexia, ataxia, GIT effects, Do not breed dogs with extreme interdog cardiac conduction disturbances, increased MEDICATIONS aggression. aggression. SEE ALSO r DRUG(S) CONTRAINDICATIONS Aggression to Unfamiliar People and r r There are no medications licensed for the Use caution as any psychotropic medication Unfamiliar Dogs Aggression, Food and treatment of canine aggression. Owners must may reduce fear-based inhibition resulting in Resource Guarding—Dogs be aware that the use of medication is r an increase rather than decrease in aggression. ABBREVIATIONS off-label. A signed informed consent form is PRECAUTIONS r r advisable listing potential risks and side CNS = central nervous system GIT = r Any psychotropic medication may increase r effects. NEVER use medications without gastrointestinal tract MAO = monoamine r irritability and aggression. Corticosteroids are r concurrent behavior modification. Before oxidase MRI = magnetic resonance imaging contraindicated in food-aggressive dogs; r prescribing medication, be sure that owners SSRI = selective serotonin reuptake polyphagia can lead to increased frequency/ r understand the risks in owning an aggressive inhibitor SARI = Serotonin 2a antagonist/ intensity of aggression. r dog, will follow safety procedures, and that reuptake inhibitor TCA = tricyclic they understand that medication will not POSSIBLE INTERACTIONS antidepressant r insure safety. Medication may not be Do not combine SSRIs, TCAs, MAO Suggested Reading appropriate in all situations (e.g., households inhibitors (e.g., amitraz, selegiline), opioids Herron ME, Shofer SS, Reisner IR. Survey of with small children, individuals that are (e.g., tramadol), and other medications that the use and outcome of confrontational and immunocompromised or have disabilities). increase serotonin—can result in potentially r non-confrontational training methods in Studies have not shown a robust effect of fatal serotonin syndrome. client-owned dogs showing undesired drug treatment on aggression. Placebo effect r behaviors. Appl Anim Behav Sci 2009, may be strong. Medications are most likely 177:47–54. to be helpful in situations where there is a Landsberg G, Hunthausen W, Ackerman L. strong fear/anxiety component, or where one FOLLOW-UP Behavior Problems of the Dog and Cat, 3rd or both dogs are behaviorally abnormal (e.g., ed. 2013, pp. 320–324. PATIENT MONITORING reactivity, impulsivity, intensity) as opposed to Wrubel KM, Moon-Fanelli AA, Maranda LS, situations where closely ranked dogs use Clients usually need ongoing assistance and et al. Interdog household aggression: aggression to establish resource control. should receive at least one follow-up call 38 cases (2006–2007). J Am Vet Med Assoc within the first 1–3 weeks after the Selective Serotonin Reuptake Inhibitors 2011, 238:731–740. r consultation. Provisions for further follow-up Fluoxetine 0.5–2 mg/kg PO q24h. Author Meredith E. Stepita r should be made at that time. Paroxetine 0.5–1 mg/kg PO q24h. Consulting Editor Gary M. Landsberg r r Sertraline 1–3 mg/kg PO q24h. Side PREVENTION/AVOIDANCE Acknowledgment The author and editors effects: sedation, irritability, GIT effects, Treatment recommendations are life-long. acknowledge the prior contribution of Laurie increased aggression; anorexia is common and POSSIBLE COMPLICATIONS Bergman. usually transient. Injuries to dogs and humans; euthanasia or relinquishment of patient. JWST589-A42-33 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:47 279mm×216mm

Canine and Feline, Sixth Edition 57 Alkalosis, Metabolic (Traditional Approach) A

nephron; and reducing glomerular filtration other organic anions with sodium (e.g., rate (GFR) which decreases the filtered load lactate, acetate, gluconate); administration of − BASICS of HCO3 and in the presence of volume cation-exchange resin with non-absorbable depletion, impairs renal excretion of the alkali (e.g., phosphorus binders). − r r DEFINITION excess HCO3 . Hypoalbuminemic alkalosis is Hypoalbuminemia—liver disease, protein due to a decrease in the level of plasma losing nephropathy or enteropathy, nephrotic A process in the body that leads to an r albumin. Plasma albumin is a weak acid. syndrome. Free water deficit—diabetes elevation in pH above the reference interval r for that species. An elevation in blood pH is Compensatory metabolic alkalosis occurs in insipidus; water deprivation; post-obstructive response to respiratory acidosis. This is diuresis; polyuric renal failure. specifically termed Alkalemia. Associated with r an increase in plasma bicarbonate associated with a low pH and elevated PCO2. Hypokalemia—see Hypokalemia. − > concentration (HCO3 )(dogs, 24 mEq/L; SYSTEMS AFFECTED RISK FACTORS > r r cats, 22 mEq/L) and base excess (BE) Nervous—muscle twitching and seizures Administration of loop or thiazide diuretics. > r r r ( 4 mmol/L) with a compensatory increase occur rarely in dogs. Metabolic alkalosis and Vomiting. Stomach drainage. Diseases in carbon dioxide tension (PCO2). associated hypokalemia may precipitate associated with hypoalbuminemia (e.g., PATHOPHYSIOLOGY hepatic encephalopathy in patients with liver nephrotic syndrome, liver failure). r r Metabolic alkalosis may develop from either failure. Urinary—the kidneys rapidly and a gain in bicarbonate or a loss in acid. effectively excrete excessive alkali. In patients ◦ Bicarbonate gain subsequent to: with chloride deficiency (and less importantly, Contraction alkalosis due to free water deficit; volume depletion), the kidneys cannot excrete DIAGNOSIS iatrogenic administration of alkalinizing the excess alkali. Therefore, metabolic DIFFERENTIAL DIAGNOSIS therapy (e.g., Na HCO−); metabolism of alkalosis is maintained. In these patients, 3 − organic ions (lactate, citrate, acetate, and chloride administration is required for renal High plasma HCO3 and hypochloremia may ketones); hypokalemia; and renal compensation to occur. Volume expansion also occur in animals compensating for ammoniagenesis. ◦ Acid loss subsequent to: will hasten compensation. Patients with chronic respiratory acidosis, in which PCO2 − gastric or renal acid loss (loop or thiazide mineralocorticoid excess have excessive is high and pH is low despite high HCO3 diuretic); mineralocorticoid excess; presence chloride loss. Therefore, chloride and low chloride concentration; blood gas of non-reabsorbable anions; decreased weak administration does not lead to determination required to differentiate. acids (hypoalbuminemia and hyperchloremia and correction of metabolic LABORATORY FINDINGS ◦ − alkalosis (so-called chloride-resistant hypophosphatemia). Renal HCO3 r Drugs That May Alter Laboratory Results metabolic alkalosis). Respiratory—low [H+] excretion is often very efficient in eliminating None an excess HCO− load, but is hindered by (elevated pH) reduces alveolar ventilation. 3 Disorders That May Alter Laboratory decreased effective circulating volume; Hypoventilation increases PCO2 and helps − Results hypokalemia, hypochloremia, and offset the effects of high plasma HCO3 on r pH.Indogs,foreach1mEq/Lincreasein Too much heparin (> 10% of the sample) hyperaldosteronism. Metabolic alkalosis − r − − decreases pH, PCO and HCO . Blood persists only if renal excretion of HCO is plasma HCO3 there is an expected increase of 2 3 3 samples stored at room temperature for more impaired. This primarily occurs from approximately 0.7 mmHg in PCO2. Limited than 15 minutes have low pH because of continued high rate of alkali administration, data is available for cats, but the degree of r increased PCO . Exposure to room air or some stimulus for the kidneys to retain respiratory compensation appears to be 2 r sodium in the presence of a relative chloride similar. decreases PCO2. Venous samples may have r deficit. Hypochloremic (corrected) metabolic SIGNALMENT pH 0.5–1 unit lower and PCO2 5–10 mmHg higher than an arterial sample. alkalosis results from loss of fluid rich in Any breed, age, or sex of dog and cat + Valid if Run in Human Laboratory? chloride and H primarily from the SIGNS alimentary tract or kidneys. Loss of chloride Yes + Historical Findings and H is associated with an increase in r CBC/BIOCHEMISTRY/URINALYSIS − Administration of loop diuretics (e.g., r plasma HCO3 concentration. With chloride r High total CO (total CO in samples furosemide) or thiazides Vomiting 2 2 loss and volume depletion, the kidneys handled aerobically closely approximates − r reabsorb sodium with HCO3 instead of Physical Examination Findings HCO−). Low blood ionized calcium r 3 r chloride, perpetuating the metabolic alkalosis. Signs related to the underlying disease or concentration. Serum electrolyte Hypochloremic alkalosis is divided into accompanying potassium depletion (e.g., abnormalities vary with underlying cause. chloride-responsive and chloride-resistant. weakness, cardiac arrhythmias, ileus, etc.). r r Hypochloremia—consider hypochloremic ◦ Chloride-responsive results primarily from Muscle twitching caused by low ionized r metabolic alkalosis, the most common reason the loss of chloride rich fluid and is calcium concentration. Dehydration in r for metabolic alkalosis in dogs and cats, which characterized by decreased extracellular fluid volume-depleted patients. Muscle twitching usually results from diuretic administration or r volume, hypochloremia, and low urinary and seizures in patients with neurologic vomiting of stomach contents. High sodium chloride levels. This type of alkalosis responds involvement (rare). but normal chloride concentration—consider to administration of chloride salt. CAUSES chloride-resistant metabolic alkalosis (e.g., ◦ Chloride-resistant is characterized by r Chloride-responsive—gastrointestinal losses hyperadrenocorticism or primary excessive mineralocorticoid leading to (e.g., gastric vomiting, nasogastric tube hyperaldosteronism) or administration of increased effective circulating volume and is r r suctioning); renal losses (diuretic therapy); alkali. Hypoalbuminemia—consider not responsive to chloride salt. Hypokalemia and rapid correction of chronic hypercapnia hypoalbuminemic metabolic alkalosis (e.g., may contribute to metabolic alkalosis by r (respiratory acidosis). Chloride-resistant— liver failure, protein-losing enteropathy, and shifting H+ intracellularly; stimulating apical hyperadrenocorticism and primary protein-losing nephropathy). In vitro, a H+/K+ ATPase in the collecting duct; r hyperaldosteronism. Oral administration of 1 g/dL decrease in albumin concentration is stimulating renal ammoniagenesis; impairing associated with an increase in pH of 0.093 in alkalinizing agents—sodium bicarbonate or r chloride ion reabsorption in the distal cats and 0.047 in dogs. Hypokalemia— JWST589-A42-33 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:47 279mm×216mm

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hypokalemia likely results from intracellular AGE-RELATED FACTORS potassium shifting due to metabolic alkalosis None or the underlying problem (e.g., vomiting of MEDICATIONS PREGNANCY/FERTILITY/BREEDING stomach contents or loop diuretic r N/A administration). Urinary chloride levels— DRUG(S) OF CHOICE SYNONYMS chloride-responsive metabolic alkalosis has Hypochloremic Alkalosis r < r Non-respiratory alkalosis. urine chloride levels 10 mEq/L while If chloride-responsive alkalosis occurs r chloride-resistant metabolic alkalosis involves Chloride-responsive metabolic alkalosis— > during an edematous state (e.g., congestive metabolic alkalosis that responds to chloride urine chloride levels of 20 mEq/L. r heart failure), oral compounds containing administration. Chloride-resistant OTHER LABORATORY TESTS chloride without sodium are recommended to − alkalosis—metabolic alkalosis secondary to Blood gas analysis reveals high HCO3 , correct the alkalosis. If diuresis is needed due increased mineralocorticoid activity that does PCO2, pH and base excess (BE). Unlike to volume overload, a carbonic anhydrase not respond to chloride administration. − r HCO3 , BE is independent of changes in and inhibitor (e.g., acetazolamide) or a potassium- Hypochloremic alkalosis—metabolic is considered a more reliable measure of sparing diuretic (e.g., spironolactone, alkalosis caused by low chloride metabolic acid-base changes. amiloride) can be used to correct the alkalosis. r r concentration. Hypoalbuminemic IMAGING H2-blocking agents such as famotidine alkalosis—metabolic alkalosis caused by low r None reduce gastric acid secretion and may be albumin concentration. Concentration considered as adjunctive therapy if gastric alkalosis—metabolic alkalosis resulting from DIAGNOSTIC PROCEDURES losses are ongoing. r r r decreased free water in plasma. Contraction Blood pressure—the combination of Antiemetics may help prevent further hypertension, hypernatremia, and alkalosis—metabolic alkalosis formerly gastric acid loss. attributed to volume contraction, but now hypokalemia with metabolic alkalosis may Hypoalbuminemic Alkalosis indicate the presence of hyperaldosteronism. r known to be caused by chloride depletion. r Treatment for hypoalbuminemic alkalosis Diagnostic testing for hyperadrenocorticism Volume depletion is a common but not should be directed at the underlying cause or primary hyperaldosteronism (e.g., plasma essential feature. and the decreased colloid oncotic pressure. renin and aldosterone levels). r SEE ALSO Foster enteral nutrition to increase r r Hypochloremia Hypokalemia endogenous albumin production. r ABBREVIATIONS Consider species-specific plasma or albumin r r (canine albumin) therapy. BE = base excess H+ = hydrogen ion TREATMENT r − r CONTRAINDICATIONS HCO3 = bicarbonate PCO2 = carbon r r dioxide tension Acid-base disturbances are secondary Avoid chloride-free fluids—they may phenomena. Diagnosis and treatment of the correct volume depletion but will not correct r Suggested Reading underlying disease process is integral to the hypochloremic alkalosis. Avoid using salts of de Morais HA. Chloride ion in small animal successful resolution of acid-base disorders. r potassium without chloride (e.g., potassium practice: The forgotten ion. J Vet Emerg Severe alkalemia is uncommon, but may be phosphate)—potassium will be excreted in Crit Care 1992, 2:11–24. life-threatening. Patients with chronic the urine and will correct neither the alkalosis de Morais HA, Constable PD. Strong ion respiratory disease and respiratory alkalosis are nor the potassium deficit. approach to acid-base disorders. In: at risk of developing severe alkalemia if they PRECAUTIONS DiBartola SP, ed., Fluid, Electrolyte and start vomiting or receive diuretics. r Acid-Base Disorders, 4th ed. St. Louis, MO: Discontinue drugs that may cause metabolic Do not use distal blocking agents (e.g., r spironolactone) in volume-depleted patients. Saunders, 2012, pp, pp. 316–330. alkalosis. Chloride-responsive—the fluids of de Morais HA, Leisewitz AL. Mixed acid-base POSSIBLE INTERACTIONS choice contain chloride; give patients with disorders. In: DiBartola SP, ed., Fluid, volume depletion an intravenous infusion of None Electrolyte and Acid-Base Disorders, 4th ed. balanced, buffered isotonic electrolyte ALTERNATIVE DRUG(S) St. Louis, MO: Saunders, 2012, replacement fluid supplemented with KCl; None pp. 302–315. patients with hypokalemia may require large DiBartola SP. Metabolic acid-base disorders. doses of KCl (see Hypokalemia). r In: DiBartola SP, ed., Fluid, Electrolyte and Chloride-resistant metabolic alkalosis can Acid-Base Disorders, 4th ed. St. Louis, MO: only be corrected by resolution of the Saunders, 2012, pp. 271–280. underlying disease; metabolic alkalosis is FOLLOW-UP r Robinson EP, Hardy RM. Clinical signs, usually mild in these patients. If the PATIENT MONITORING diagnosis, and treatment of alkalemia in metabolic alkalosis is associated with Acid-base status—frequency dictated by the dogs: 20 cases (1982–1984). J Am Vet Med hypokalemia and total body potassium underlying disease and patient response to Assoc 1988, 192:943–949. deficits, correcting the deficit with KCl isa treatment. Hopper K. Traditional Acid-Base Analysis. particularly effective way to reverse the POSSIBLE COMPLICATIONS In: Silverstein DC, Hopper K, eds. Small alkalosis. r r Animal Critical Care Medicine, 2nd. ed. Hypokalemia Neurologic signs NURSING CARE St. Louis, MO: Elsevier, 2015, Supportive care to maintain euhydration, pp. 289–299. euvolemia, adequate nutrition, etc. Authors Helio S. Autran de Morais, Stephen P. DiBartola, and Lee E. Palmer MISCELLANEOUS Consulting Editor Carl A. Osborne ASSOCIATED CONDITIONS r r Hypokalemia Hypochloremia JWST589-A43-34 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:56 279mm×216mm

Canine and Feline, Sixth Edition 59 Alopecia—Cats A

r r dermatitis. Often misdiagnosed as immunologic mechanisms. Possible r endocrine alopecia. The pattern of alopecia dramatic pigment accumulation along the r BASICS is frequently symmetrical without associated eyelid margins. Questionable association inflammation. with systemic disease or stressful event (e.g., DEFINITION inflammatory bowel disease, lupus-like r r Allergic Dermatitis Common problem Pattern of hair loss— r syndromes, upper respiratory tract infections). r Varies from mild partial alopecia with little varied or symmetrical Causes— inflammation to severe excoriation and Squamous Cell Carcinoma In Situ r r multifactorial ulceration. Barbering of the hair coat often Multicentric premalignant dermatosis in old r PATHOPHYSIOLOGY occurs clandestinely leading to a misdiagnosis cats. Associated with papilloma virus; r r Specific and unique for each cause of endocrine alopecia. Distribution—varied; Bowenoid in situ carcinoma. Slightly often the head and neck or ventral abdominal elevated, often pigmented, plaque-like or SYSTEMS AFFECTED r r r regions are most affected. Food allergy, papillated lesions with scaling and partially Endocrine/Metabolic Hemic/Lymphatic/ r r atopic dermatitis, contact allergy, and alopecic surfaces. Often misdiagnosed as Immune Skin/Exocrine ectoparasite hypersensitivity. seborrhea before distinct lesions develop. r SIGNALMENT Hyperthyroidism About 25% may convert to squamous cell r r No specific age, breed, or sex predilection. Partial to complete alopecia from carcinoma in situ lesions along the borders r r r Neoplastic and paraneoplastic associated self-barbering. Varied pattern. Middle- (histologically). r alopecias—generally recognized in older cats. aged to old cats. Often misdiagnosed in Epitheliotropic Lymphoma r SIGNS cases of allergic dermatoses, compulsive Early stages—varying degrees of alopecia r disorder, or other endocrine alopecia. associated with scaling and erythema. Later Depends on specific diagnosis r Diabetes Mellitus stages—plaques and nodules. Old cats. CAUSES r r Partial alopecia with an unkempt or greasy Alopecia Areata/Pseudopelade/ Neurologic/behavioral—compulsive r r hair coat and excessive scaling. Poor wound Lymphocytic Mural Folliculitis disorder. Endocrine—sex hormone alopecia, r healing. Increased susceptibility to (Lymphocytic Invasion of the Hair hyperthyroidism, hyperadrenocorticism, r r infections. Rarely, cutaneous xanthomatosis Follicle) diabetes mellitus. Immunologic—allergic r dermatitis, alopecia areata, alopecia mucinosa, secondary to hyperlipidemia (nodular to Often associated with an immunologic lymphocytic mural folliculitis, pseudopelade. linear, yellow-pink alopecic plaques that tend inciting cause; may occasionally be r r Parasitic—demodicosis, cheyletiellosis. to ulcerate). pre-neoplastic. Alopecia areata—rare; r Infections—dermatophytosis. Hyperadrenocorticism complete alopecia in a patchy distribution r r Physiologic/metabolic—sebaceous adenitis. Rare; characterized by alopecia and extreme with no inflammation; head, neck, ears; r r histologic lymphocytic accumulation around Neoplastic—paraneoplastic dermatitis, fragility of the skin. Truncal alopecia, with r squamous cell carcinoma in situ, or without a rattail and curling of the pinnal the hair bulb. Lymphocytic mucinotic r epitheliotropic lymphoma, thymoma with tips. Extreme skin fragility noted in mural folliculitis—diffuse alopecia of the face, r r exfoliative dermatitis. Idiopathic/ approximately 70% of cases. Occurs eyelids, muzzle; skin has a thick waxy feel; inherited—alopecia universalis, hypotrichosis, secondary to pituitary or adrenal tumors. histologic lymphocytic invasion of the spontaneous pinnal alopecia, anagen and r follicular outer root sheath and epidermis. r Iatrogenic form less common in cats than in r telogen defluxion. Injection site reaction. Pseudopelade—well-circumscribed r dogs; associated with frequent repositol Medication effect—corticosteroids. corticosteroid injections. non-pruritic alopecia that often starts on the r face; nails may slough; lymphocytic invasion Viral—FeLV- and FIV-associated disease Paraneoplastic Alopecia (giant cell dermatosis). r of the isthmus region of the hair follicle. Most cases associated with pancreatic RISK FACTORS exocrine adenocarcinomas, bile duct Feline Cutaneous Lymphocytosis FeLV/FIV—reported risk for demodicosis carcinomas, or exfoliative dermatitis with (Pseudolymphoma) r r (not all cases associated with viral infection). thymoma. Middle-aged to old cats Characterized by dermal lymphocytic r infiltrate rather than follicular or epidermal. (9–16 years). Pancreatic carcinoma/bile r duct carcinoma: acute onset, progress rapidly, Older cats; often solitary lesions of partial bilaterally symmetrical, ventrally distributed alopecia with scaling ± erythema and DIAGNOSIS (also located along the bridge of the nose and pruritus. periocular), hair epilates easily, rare pruritus, Alopecia Universalis (Sphynx Cat) r r DIFFERENTIAL DIAGNOSIS erythema with dry fissuring footpads, Hereditary. Complete absence of primary r Endocrine Alopecia/Sex Hormone glistening appearance to alopecic skin, skin is hairs; decreased secondary hairs. Thickened r r often thin and hypotonic, rapid weight loss. epidermis; normal dermis. Sebaceous and Non-inflammatory alopecias are rarely r Thymoma with exfoliative dermatitis: apocrine ducts open directly onto the skin hormonal in etiology; search for other causes r before exploring endocrine etiology. non-pruritic scaling dermatitis that starts on surface; oily feel to skin. Wrinkled r Hormonal causes—primarily castrated the head and neck. Brown waxy deposits foreheads; gold eyes; no whiskers; downy fur accumulate around the eyes and nasal region. on paws, tip of tail, and scrotum. males; alopecia along the caudal aspect of the r hind limbs, which may extend along the Surgical removal of the thymoma will cause Comedones with or without secondary r perineum. Excessive corticosteroid resolution of the dermatitis within a few folliculitis. administration; may also cause curling of months (typically 4–5 months). Feline Hypotrichosis r r pinnal tips. Megestrol acetate—may Sebaceous Adenitis Siamese and Devon Rex cats (autosomal r r produce lesions similar to/associated with Slowly progressive partial alopecia recessive alopecia). Poorly developed r diabetes mellitus or hyperadrenocorticism. associated with scaling along the dorsum of primary telogen hair follicles. Born with a r Compulsive Disorder the body and the extremities. Sebaceous normal coat; becomes thin and sparse as r Uncommon as sole source of symptoms. glands are, theoretically, selectively destroyed young adult. r Often misdiagnosed in cases of allergic by toxic intermediate metabolites or JWST589-A43-34 JWST589-Tilley Printer: Yet to Come August 1, 2015 12:56 279mm×216mm

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A Alopecia—Cats (Continued)

Spontaneous Pinnal Alopecia shampoo and topical therapy may relieve POSSIBLE COMPLICATIONS r r Siamese cats predisposed. May represent a secondary problems, such as hyperkeratosis in Determined by specific diagnosis form of alopecia areata or pattern baldness. sebaceous adenitis, crusting in demodicosis, EXPECTED COURSE AND PROGNOSIS Anagen and Telogen Defluxion secondary bacterial infection, and malodor for r Determined by specific diagnosis Acute loss of hair due to interference with greasy dermatoses. r the growth cycle. Causes—stress, infection, endocrine disorder, metabolic disorder, fever, surgery, anesthesia, pregnancy, drug therapy. MISCELLANEOUS Demodicosis MEDICATIONS r r ZOONOTIC POTENTIAL Rare. Partial to complete multifocal DRUG(S) r r Dermatophytosis—can cause skin lesions in alopecia of the eyelids, periocular region, r r Compulsive disorder—amitriptyline humans. Cheyletiellosis—can cause head, and neck; can generalize. Variable (10 mg/cat/day) as well as other behavior- pruritus with erythema, scale, and crust, and irritation in humans. r modifying medications, such as gabapentin ceruminous otitis externa. Demodex cati (5–10 mg/kg PO q12h). PREGNANCY/FERTILITY/BREEDING r (elongated shape) often associated with Endocrine alopecia (males)—testosterone Retinoids and griseofulvin should not be metabolic disease (e.g., FIV, systemic lupus supplementation. administered to pregnant animals. erythematosus, diabetes mellitus). r r Allergic dermatitis—antihistamines, SEE ALSO Short/blunted D. gatoi mite is rarely a r r restricted-ingredient diet, corticosteroids, Cheyletiellosis Demodicosis marker for metabolic disease; this form may r r cyclosporine (7.3 mg/kg/day initially), Dermatophytosis Diabetes Mellitus be transferable from cat to cat and has been r allergen-specific immunotherapy, ectoparasite without Complication, Cats Feline associated with pruritus most often affecting r control. Paraneoplastic Alopecia Hyperthyroidism the lateral thorax and abdomen. r r Hyperthyroidism—methimazole (tapazole) Sebaceous Adenitis, Granulomatous Cheyletiellosis or radioactive iodine therapy. r r r ABBREVIATIONS Variable pruritus with scaling. Not all Diabetes mellitus—regulation of glucose r ACTH = adrenocorticotropic hormone animals in the household may be affected. levels (insulin). r r r ANA = antinuclear antibody CT = Hyperadrenocorticism—surgery; no known r Dermatophytosis computed tomography FeLV = feline effective medical therapy. r Numerous clinical manifestations; always r leukemia virus FIV = feline associated with alopecia. Paraneoplastic alopecia—no therapy or r surgical excision of neoplasia; often fatal. immunodeficiency virus HDDST = CBC/BIOCHEMISTRY/URINALYSIS r high-dose dexamethasone-suppression test Epitheliotropic lymphoma—retinoids r Abnormalities may be noted with diabetes (isotretinoin), corticosteroids, interferon, LDDST = low-dose mellitus, hyperadrenocorticism, and cyclosporine, lomustine. dexamethasone-suppression test r hyperthyroidism. Sebaceous adenitis—retinoids, Suggested Reading OTHER LABORATORY TESTS corticosteroids, cyclosporine. Baer KE, Helton KA. Multicentric squamous r r FeLV and FIV—risk factors for Squamous cell carcinoma in situ—surgical cell carcinoma in situ resembling Bowens’ r demodicosis. Thyroid hormones— excision, retinoids (topical and oral), topical disease in cats. Vet Pathol 1993, r imiquimod cream. document hyperthyroidism. ANA titer— r 30:535–543. look for systemic lupus erythematosus. Alopecia areata—no therapy; possibly Helton Rhodes KA, Wallace M, Baer KE. r counterirritants. ACTH-response test, LDDST, and r Cutaneous manifestations of feline HDDST—diagnose hyperadrenocorticism. Demodicosis—lime sulfur dips at weekly hyperadrenocorticism. In: Ihrke PJ, Mason intervals for four to six dips. IMAGING r IS, White SD. Advances in Veterinary r Cheyletiellosis—topical parasiticides and Abdominal ultrasound—assess adrenals in Dermatology. New York: Pergamon, 1993. environmental control. hyperadrenocorticism and look for neoplasia r Helton Rhodes KA, Werner A. Blackwell’s Dermatophytosis—griseofulvin (caution: in animals with paraneoplastic syndrome. Five-Minute Veterinary Consult Clinical r idiosyncratic toxicity), itraconazole (hepatic Chest radiographs/ultrasound to rule out Companion; Small Animal Dermatology, r toxicity, vasculitis), terbinafine. thymoma. CT scan—look for pituitary or 2nd ed. Chichester: Wiley-Blackwell, 2011. other neoplasia tumors in animals with PRECAUTIONS Miller WH, Griffin CE, Campbell KL. hyperadrenocorticism. Toxicity with griseofulvin and itraconazole Miscellaneous alopecias. In: Kirk’s Small Animal Dermatology, 7th ed. St. Louis, DIAGNOSTIC PROCEDURES (see Dermatophytosis). r r r MO: Elsevier, 2013, pp 554–572. Skin biopsy Skin scrapes Dermatophyte POSSIBLE INTERACTIONS r Miller WH, Griffin CE, Campbell KL. culture Shirts/collar to prove self-trauma N/A r r Congenital and hereditary defects. In: Kirk’s Food elimination trials Intradermal allergy ALTERNATIVE DRUG(S) Small Animal Dermatology, 7th ed. St. test N/A Louis, MO: Elsevier, 2013, pp 573–617. Miller WH, Griffin CE, Campbell KL. Endocrine and metabolic diseases. In: Kirk’s Small Animal Dermatology, 7th ed. St. TREATMENT FOLLOW-UP Louis: Elsevier, 2013, pp 501–553. r Author Karen Helton Rhodes Therapy is specific for many of these r PATIENT MONITORING Consulting Editor Alexander H. Werner disorders. Behavioral modification or Determined by specific diagnosis protecting hair coat with a shirt may prevent r PREVENTION/AVOIDANCE self-barbering. Removal of an offending Client Education Handout dietary item may alleviate the symptoms of Determined by specific diagnosis r available online food allergy. If the pet is compliant, JWST589-A44-35 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:0 279mm×216mm

Canine and Feline, Sixth Edition 61 Alopecia—Dogs A

r r Sebaceous adenitis of short-coated breeds Pemphigus foliaceus—hair loss associated (now termed “idiopathic periadnexal with scale and crust formation. r BASICS pyogranulomatous dermatitis”)—annular to Keratinization disorders—alopecia polycyclic areas of alopecia and scaling. associated with excessive scale and greasy DEFINITION Symmetrical surface texture. r r Common disorder. Hyperadrenocorticism—truncal alopecia Specific Locations r r Characterized by a complete or partial loss associated with atrophic skin, comedones, and Pinnal alopecia/pattern of hair in areas where it is normally present. pyoderma. baldness—miniaturization of hairs and r r May be associated with multiple causes, be Hypothyroidism—thinning of truncal progressive alopecia; dachshund, greyhound, the primary problem, or be secondary to an haircoat; generalized alopecia is an American water spaniel, Portuguese water underlying cause. uncommon presentation; alopecic “rat” tail. spaniel, Boston terrier, Manchester terrier, r PATHOPHYSIOLOGY Non-inflammatory alopecia (alopecia X)— whippet, Italian greyhound, Chihuahua. r r Multiple causes. symmetrical truncal alopecia associated with Traction alopecia—hair loss on the top and r Represents removal of hair or disruption in hyperpigmentation; alopecia often starts lateral aspect of the cranium secondary to the growth of the hair from hypersensitivity, along the collar area of the neck; Pomeranian, having barrettes or rubber bands applied to chow chow, Akita, Samoyed, Keeshonden, the hair. infection, trauma, immunologic attack, r Alaskan malamute, and Siberian husky. Post-clipping alopecia—failure to regrow mechanical “plugging,” endocrine r abnormalities, neoplasia, drug reaction and/or Hyperestrogenism (females)—symmetrical after clipping; may be associated with hair alopecia of the flanks and perineal and growth cycle disruption. blockage of the receptor sites for stimulation r of the hair growth cycle. inguinal regions with enlarged vulva and Melanoderma (alopecia of Yorkshire SYSTEMS AFFECTED mammary glands; may also be associated with terriers)—symmetrical alopecia of the pinnae, r exogenous hormone exposure. bridge of the nose, tail, and feet. Endocrine/Metabolic r r r Hypogonadism in intact females—perineal, Seasonal/cyclic/canine flank alopecia— Hemic/Lymphatic/Immune flank, and truncal alopecia. serpiginous flank alopecia with r r Skin/Exocrine Testosterone-responsive dermatosis in hyperpigmentation; boxer, English bulldog, SIGNALMENT castrated males—slowly progressive truncal Airedale terrier. r alopecia. Black hair follicular dysplasia—alopecia of Breed predilection listed below r Male feminization from Sertoli cell tumor— the black-haired areas only. SIGNS r r alopecia of the perineum and genital region Dermatomyositis—alopecia of the face, tip May be acute in onset or slowly progressive. r with gynecomastia. of ears, tail, and digits; associated with scale Multifocal patches of circular alopecia— r Castration-responsive dermatosis—hair loss crusting and scarring. most frequently associated with folliculitis in the collar area, rump, perineum, and flanks. from bacterial infection and multifocal areas r Breed-Related Alopecia Estrogen-responsive dermatosis in spayed r of demodicosis. Alopecic breeds: Chinese crested, Mexican r female dogs—alopecia of the perineum and Large, more diffuse areas of alopecia—may hairless, Inca hairless, Peruvian Inca Orchid, genital regions. indicate a follicular dysplasia or metabolic r American hairless terrier (often associated Seasonal/cyclic/canine flank alopecia— component. with comedones, folliculitis, and r serpiginous flank alopecia with The pattern and degree of hair loss are furunculosis). hyperpigmentation; boxer, English bulldog, r important for establishing a differential Congenital hypotrichosis: cocker spaniel, Airedale terrier. diagnosis. Belgian shepherd, poodle, whippet, beagle, Patchy to Diffuse French bulldog, Yorkshire terrier, Labrador CAUSES r Demodicosis—often associated with retriever, bichon frise, Lhasa apso, basset Multifocal erythema, folliculitis, and hyperpigmentation. hound. r r r Localized demodicosis—partial to complete Bacterial folliculitis—multifocal areas of Color dilution alopecia: blue or fawn alopecia with erythema comedones, and mild circular alopecia to coalescing large patches of Doberman pinscher, silver Labrador, cream scaling; lesions may become inflamed and hair loss; epidermal collarettes. chow chow, blond Irish setter, blue pit bull r crusted. Dermatophytosis—often accompanied by terrier, other breeds with dilute coat colors. r r Dermatophytosis—partial to complete scale, erythema, and hyperpigmentation. Melanoderma with alopecia in Yorkshire r alopecia with scaling; with or without Sebaceous adenitis—alopecia with a thick terrier. erythema; not always ring-like. r r adherent scale; predominantly on the dorsum Seasonal/cyclic/canine flank alopecia— Staphylococcal folliculitis—circular patterns of the body, including the head and serpiginous flank alopecia with of alopecia with epidermal collarettes, extremities. hyperpigmentation; boxer, English bulldog, r erythema, crusting, and hyperpigmented Color mutant/dilution alopecia—brittle or Airedale terrier. macules. r r coarse hair, thinning of the blue or fawn Pinnal alopecia/pattern baldness— Injection reactions—inflammation with colored hair coat, and secondary folliculitis. miniaturization of hairs and progressive r alopecia and/or cutaneous atrophy from Follicular dysplasia—slowly progressive alopecia; dachshund, greyhound, American scarring. alopecia. water spaniel, Portuguese water spaniel, r r Rabies vaccine vasculitis—well-demarcated Anagen defluxion and telogen defluxion— Boston terrier, Manchester terrier, whippet, patch of alopecia observed 2–3 months acute onset of alopecia. Italian greyhound, Chihuahua. post-vaccination. r r r Hypothyroidism—diffuse thinning of the Non-inflammatory alopecia (alopecia X)— Localized scleroderma—well-demarcated, hair coat. symmetrical truncal alopecia associated with r shiny, smooth, alopecic, thickened plaque; Hyperadrenocorticism—truncal alopecia hyperpigmentation; alopecia often starts extremely rare; still considered a controversial with thin skin and formation of comedones. along the collar area of the neck; Pomeranian, diagnosis. r r Epitheliotropic lymphoma—diffuse, chow chow, Akita, Samoyed, Keeshonden, Alopecia areata—non-inflammatory areas of generalized truncal alopecia with scaling and Alaskan malamute, and Siberian husky. complete alopecia. intense erythema, later nodule and plaque formation. JWST589-A44-35 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:0 279mm×216mm

62 Blackwell’s Five-Minute Veterinary Consult

A Alopecia—Dogs (Continued)

r RISK FACTORS Sebaceous Adenitis, Granulomatous r N/A SertoliCellTumor ABBREVIATIONS MEDICATIONS r ACTH = adrenocorticotropic hormone DRUG(S) OF CHOICE r HDDST = high-dose DIAGNOSIS Varies with specific cause; see “Treatment.” dexamethasone-suppression test r DIFFERENTIAL DIAGNOSIS CONTRAINDICATIONS LDDST = low-dose r dexamethasone-suppression test Pattern and degree—important features for N/A formulating a differential diagnosis. PRECAUTIONS Suggested Reading r Inflammation, scale, crust, and epidermal Toxicity with griseofulvin, retinoids, Helton-Rhodes KA. Cutaneous collarettes—important for determining ivermectin, trilostane, lysodren, cyclosporine. manifestations of canine and feline diagnosis. POSSIBLE INTERACTIONS endocrinopathies. Probl Vet Med 1990, 12:617–627. CBC/BIOCHEMISTRY/URINALYSIS None Helton-Rhodes KA, Werner A. Blackwell’s Rule out metabolic causes such as ALTERNATIVE DRUG(S) hyperadrenocorticism Five-minute Veterinary Consult: Clinical None Companion: Small Animal Dermatology. OTHER LABORATORY TESTS r 2nd ed. Chichester: Wiley-Blackwell, 2011. Thyroid testing—diagnose hypothyroidism. r Miller WH, Griffin CE, Campbell KL. ACTH-response test, LDDST, and Congenital and hereditary defects. In: Kirk’s HDDST—evaluate for hyperadrenocorticism. r FOLLOW-UP Small Animal Dermatology, 7th ed. St. Sex hormone profiles (questionable Louis, MO: Elsevier, 2013, pp. 573–617. validity). PATIENT MONITORING Miller WH, Griffin CE, Campbell KL. IMAGING Determined by cause Endocrine and metabolic diseases. In: Kirk’s Ultrasonography—evaluate adrenal glands for POSSIBLE COMPLICATIONS Small Animal Dermatology, 7th ed. St. evidence of hyperadrenocorticism. N/A Louis, MO: Elsevier, 2013, pp. 501–553. DIAGNOSTIC PROCEDURES Miller WH, Griffin CE, Campbell KL. r Keratinization defects. In: Kirk’s Small Response to therapy as a trial r Animal Dermatology, 7th ed. St. Louis, Fungal culture r MO: Elsevier, 2013, pp. 630–646. Skin scraping MISCELLANEOUS r Miller WH, Griffin CE, Campbell KL. Cytology r ASSOCIATED CONDITIONS Miscellaneous alopecias. In: Kirk’s Small Skin biopsy—very useful to evaluate status N/A Animal Dermatology, 7th ed. St. Louis, of follicle/hair growth as well as epidermal AGE-RELATED FACTORS MO: Elsevier, 2013, pp. 554–572. changes associated with specific conditions. Schmeitzel LP. Growth hormone responsive N/A alopecia and sex hormone associated ZOONOTIC POTENTIAL dermatoses. In: Birchard SJ, Sherding RG, Dermatophytosis can cause skin lesions in eds., Saunders Manual of Small Animal TREATMENT people. Practice. Philadelphia: Saunders, 1994, r Demodicosis—amitraz, ivermectin, PREGNANCY/FERTILITY/BREEDING pp. 326–330. milbemycin. Avoid retinoids and griseofulvin in pregnant Author Karen Helton Rhodes r Dermatophytosis—griseofulvin, animals. Consulting Editor Alexander H. Werner ketoconazole, itraconazole, lime sulfur dips, SEE ALSO r terbinafine. Alopecia, Non-inflammatory—Dogs Client Education Handout r r Staphylococcal folliculitis—shampoo and Demodicosis available online r antibiotic therapy. Dermatomyositis r r Sebaceous adenitis—keratolytic shampoo, Dermatophytosis r essential fatty acid supplementation, Hyperadrenocorticism (Cushing’s retinoids, cyclosporine. Syndrome)—Dogs r r Keratinization disorders—shampoos, Hypothyroidism retinoids, vitamin D, cyclosporine. r r Pemphigus Endocrine—ovariohysterectomy, castration, Lysodren, trilostane, adrenalectomy. JWST589-A45-36 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:3 279mm×216mm

Canine and Feline, Sixth Edition 63 Alopecia, Non-inflammatory—Dogs A

SIGNS Historical Findings r BASICS Overall change in the hair coat—dry or DIAGNOSIS bleached because the hairs are not being DEFINITION replaced; lack of normal shed. DIFFERENTIAL DIAGNOSIS r r r Uncommon alopecic disorders that are Males with hyperestrogenism may attract Inflammatory causes of alopecia (pyoderma, associated with abnormal hair follicle cycling. other male dogs. demodicosis, and dermatophytosis)—should r Both endocrine and non-endocrine diseases Physical Examination Findings be ruled out; these diseases usually cause a can be associated with alopecia. r patchy rather than diffuse pattern of alopecia. r Alopecia—usually diffuse and bilaterally r Definitive diagnosis often requires ruling symmetrical truncal alopecia sparing the head Sebaceous adenitis – inflammatory cause of out the more common endocrine alopecias. alopecia that may affect specific breeds r and distal extremities. Uncommon with Alopecia X has also been called growth hyperandrogenism. (Samoyed, Akita). r r hormone-responsive alopecia, Hair coat—may be dry or bleached. Hypothyroidism and r castration-responsive alopecia, adrenal Secondary seborrhea, pruritus, pyoderma, hyperadrenocorticism—critical to rule out as hyperplasia-like syndrome, among others. comedones, ceruminous otitis externa, and these diseases may cause a very similar pattern PATHOPHYSIOLOGY hyperpigmentation—variable. of diffuse alopecia associated with lack of hair r r follicle cycling. There are many factors that affect the hair Enlargement of nipples, mammary glands, r cycle, both hormonal and non-hormonal. vulva, prepuce—may be associated with Follicular dysplasias including color- r Increased sex hormones can affect the hair hyperestrogenism. dilution alopecia and black hair follicular r dysplasia—alopecia should be color-restricted. cycle. Estrogen is a known inhibitor of Macular melanosis and linear preputial r anagen, the growth phase of the hair follicle. dermatitis—may be associated with Patterned alopecia of various breeds r hyperestrogenism. (dachshund, Boston terrier, greyhound, water The mechanism by which alopecia X r influences the hair cycle is not known. Abnormal-sized or different-sized testicles— spaniel, and others)—breed-specific alopecias r of unknown cause. Exposure to human exogenous hormone may be associated with hyperestrogenism or r hyperandrogenism. Seasonal/cyclic/canine flank alopecia— replacement therapy. r Testicles may also appear normal in size. alopecia of the flank and dorsum, often SYSTEMS AFFECTED r r Tail gland hyperplasia and perianal gland serpiginous patterns with hyperpigmentation, Behavioral r hyperplasia—usually associated with more often in short-coated breeds (boxer, Endocrine/Metabolic r hyperandrogenism. English bulldog, Airedale) and may recur Hemic/Lymphatic/Immune r r Systemic signs (PU/PD/polyphagia) are seasonally. Skin/Exocrine r usually NOT present. Post-clipping alopecia—hair fails to regrow GENETICS following clipping; however, hair regrowth CAUSES Breed predispositions exist for alopecia X; occurs within a year. Hyperestrogenism—Females r however, the mode of inheritance is unknown. r Telogen defluxion—alopecia occurs INCIDENCE/PREVALENCE Estrogen excess associated with cystic 1–2 months following an illness or severe r ovaries, ovarian tumors (rare), or exogenous stressful episode and is usually more sudden Hyperestrogenism and hyperandrogenism estrogen supplementation. in onset with relative ease of epilation. are uncommon to rare causes of alopecia. r r Animals with normal serum estrogen CBC/BIOCHEMISTRY/URINALYSIS Alopecia X is relatively common in concentrations may have increased numbers r Usually unremarkable. predisposed breeds. of estrogen receptors in the skin r Anemia and/or bone marrow hypoplasia or GEOGRAPHIC DISTRIBUTION (undocumented). aplasia can be associated with None Hyperestrogenism—Males r hyperestrogenism. SIGNALMENT Estrogen excess due to Sertoli cell tumor OTHER LABORATORY TESTS Species (most common), seminoma, or interstitial cell r tumor (rare). Serum sex hormone concentrations—often Dogs r Associated with male normal, treat according to suspected diagnosis Breed Predilections pseudohermaphrodism in miniature based on clinical signs and ruling out other r disorders. Hyperestrogenism and schnauzers. r hyperandrogenism—no breed predilections. Serum estradiol concentrations—sometimes r Alopecia X—miniature poodle and Hyperandrogenism—Males elevated in male dogs with testicular tumors plush-coated breeds such as Pomeranian, Androgen-producing testicular tumors or female dogs with cystic ovaries; however, chow chow, Akita, Samoyed, Keeshonden, (especially interstitial cell tumors). normal fluctuation of estradiol occurs Alaskan malamute, and Siberian husky. Alopecia X throughout the day, making interpretation of Mean Age and Range Hairs fail to cycle but an underlying estradiol concentrations difficult. r Hyperestrogenism and endocrine cause has not been identified. IMAGING hyperandrogenism—middle-aged to old RISK FACTORS Radiography, ultrasonography, and r intact dogs. Intact male and female dogs are at increased laparoscopy—identify cystic ovaries, ovarian r Alopecia X—1–5 years of age; however, risk for developing testicular tumors and tumors, testicular tumors (scrotal or older dogs may develop the condition. ovarian cysts/tumors, respectively. abdominal), adrenal tumors, sublumbar r Predominant Sex Cryptorchid males are at increased risk for lymphadenopathy, and possible thoracic r Hyperandrogenism, primarily intact males. developing testicular tumors. metastases of malignant tumors. r r Hyperestrogenism, primarily intact females Exogenous estrogen supplementation. DIAGNOSTIC PROCEDURES r r or males. Exposure to human exogenous hormone Preputial cytology—may demonstrate r replacement therapy. Alopecia X, neutered or intact dogs of either r cornification of cells in males with sex. There are no known risk factors for alopecia hyperestrogenism (similar to a bitch in estrus). r X other than breed predisposition. Skin biopsy. JWST589-A45-36 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:3 279mm×216mm

64 Blackwell’s Five-Minute Veterinary Consult

A Alopecia, Non-inflammatory—Dogs (Continued)

PATHOLOGIC FINDINGS This treatment works in approximately 40% POSSIBLE COMPLICATIONS Histologic changes associated with endocrine of cases. Because this treatment is the most None dermatoses (telogen hairs, follicular keratoses, benign, it is considered the treatment of EXPECTED COURSE AND PROGNOSIS r hyperkeratosis, excess trichilemmal choice following neutering. Once hair Female hyperestrogenism—improvement keratinization [flame follicles], thin epidermis regrowth has occurred, discontinue treatment. r should occur within 3–6 months after and thin dermis) may also be seen with Medroxyprogesterone acetate – 5–10 mg/kg ovariohysterectomy. r non-inflammatory alopecias including SC q4 weeks for 4 treatments. Hair regrowth Estrogen- and androgen-secreting hyperestrogenism and alopecia X. can take up to 6 months. This treatment tumors—resolution of signs should occur Histopathology will help rule out works in approximately 40–50% of cases. within 3–6 months after castration. r inflammatory causes of alopecia (pyoderma, CONTRAINDICATIONS Alopecia X—hair regrowth will only occur demodicosis, dermatophytosis, sebaceous None in a portion of dogs regardless of treatment adenitis) and some of the other differentials PRECAUTIONS chosen and hair loss may recur in spite of listed above. r Melatonin at high doses can cause insulin continued treatment. Therefore, if hair resistance; therefore, use caution in treating regrowth occurs, discontinue treatment to dogs with diabetes mellitus. preserve treatment for future recurrence of the r alopecia. Risk of treatment should be weighed TREATMENT Medroxyprogesterone acetate can cause mammary nodules and cystic endometrial with the fact that this is a cosmetic disease. APPROPRIATE HEALTH CARE hyperplasia with long term use. Diabetes N/A mellitus has been reported in a few dogs. POSSIBLE INTERACTIONS NURSING CARE MISCELLANEOUS N/A None ACTIVITY ALTERNATIVE DRUG(S) ASSOCIATED CONDITIONS r r None Mitotane—15–25 mg/kg—once daily as Pyoderma, seborrhea, comedones may be associated with the alopecia. DIET induction for 5–7 days, followed by twice r weekly maintenance; hair regrowth occurs in Behavioral changes associated with None a portion of dogs treated and can take up to hyperestrogenism or hyperandrogenism. CLIENT EDUCATION 3 months to become evident. Use of this drug AGE-RELATED FACTORS Alopecia X is a cosmetic condition resulting can result in an Addisonian crisis and other None in coat loss only and there is no definitive cure side effects as for treatment of Cushing’s ZOONOTIC POTENTIAL for the hair loss. The risk of treatment should syndrome. Electrolytes and cortisol with None be emphasized. Hair regrowth will only occur ACTH stimulation testing should be in a portion of dogs regardless of treatment monitored regularly. PREGNANCY/FERTILITY/BREEDING r chosen and hair loss may recur months to Trilostane—dosages as described for N/A—neutering is usually recommended for years later in spite of continued treatment. treatment of Cushing’s syndrome; hair managing these conditions. SURGICAL CONSIDERATIONS regrowth occurs in a portion of dogs treated SYNONYMS and can take up to 3 months to become Hyperestrogenism/Hyperandrogenism Alopecia X—growth hormone-responsive r evident. Use of this drug can result in an Castration—scrotal testicular tumors. alopecia, castration-responsive alopecia, r Addisonian crisis and other side effects as for Exploratory laparotomy—diagnosis and adrenal hyperplasia-like syndrome, among treatment of Cushing’s syndrome. Electrolytes surgical removal (ovariohysterectomy and others. and cortisol with ACTH stimulation testing castration) for ovarian cysts and tumors and ABBREVIATIONS should be monitored regularly. r abdominal testicular tumors. r ACTH = adrenocorticotropic hormone Growth hormone administration and r Alopecia X methyltestosterone may result in hair PU/PD = polyuria/polydipsia Neuter intact animals—a certain number will regrowth. Growth hormone can cause INTERNET RESOURCES regrow hair following neutering. Hair diabetes mellitus. Methyltestosterone can http://www.vet.utk.edu/hairloss/ regrowth can take up to 3 months to become result in increased aggression, evident. cholangiohepatitis, and seborrhea oleosa. Suggested Reading Therefore, these drugs are not recommended. Frank LA. Sex hormone and endocrine look-alike dermatoses. In: Birchard SJ, Sherding RG, eds., Saunders Manual of MEDICATIONS Small Animal Practice, 3rd ed. Philadelphia: Saunders, 2006, p. 517. DRUG(S) OF CHOICE FOLLOW-UP Frank LA, Watson JB. Treatment of alopecia General Treatments PATIENT MONITORING X with medroxyprogesterone acetate. Vet r r Topical antiseborrheic shampoos—for Medroxyprogesterone acetate—complete Dermatol 2013, 24:624–627. comedones and seborrhea associated with physical examination and chemistry panel Author Linda A. Frank alopecia. regularly. Consulting Editor Alexander H. Werner r r Antibiotics and topical antimicrobial Mitotane—electrolytes and cortisol with shampoos—for secondary skin infections ACTH stimulation testing regularly. r Client Education Handout associated with alopecia. Trilostane—electrolytes and cortisol with available online Alopecia X ACTH stimulation testing regularly. r Melatonin—3 mg q12h for small breeds and PREVENTION/AVOIDANCE 6–12 mg q12h for large breeds; hair regrowth None can take up to 3 months to become evident. JWST589-A46-37 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:6 279mm×216mm

Canine and Feline, Sixth Edition 65 Amebiasis A

direct spread from the nasal cavity through DIAGNOSTIC PROCEDURES the cribiform plate to the central nervous Brain biopsy—required to definitively BASICS system may occur, resulting in a diagnose neurologic forms antemortem. granulomatous amoebic meningoencephalitis. OVERVIEW r Facultative parasitic amoeba that infects people and non-human primates, including r TREATMENT dogs and cats. Found primarily in tropical DIAGNOSIS r areas throughout the world, including North Colitis (caused by E. histolytica)—responds DIFFERENTIAL DIAGNOSIS to metronidazole, although dogs continue to America. r Dogs shed organisms. Systemic forms SIGNALMENT r r r Causes of bloody diarrhea or tenesmus, (particularly neurologic disease)—invariably Dog and cat. Mainly young and/or including constipation; food intolerance/ fatal despite treatment. immunosuppressed animals are infected. allergy; parasitism (whip worms, SIGNS leishmaniasis, balantidiasis); HGE; foreign Dogs body; irritable bowel syndrome; inflammatory r Entamoeba histolytica infections are usually bowel disease; diverticula; infectious MEDICATIONS r asymptomatic. Severe infections—result in (parvovirus, clostridial enteritis, bacterial DRUG(S) ulcerative colitis to cause dysentery (may be overgrowth and other bacterial causes, fungal r r Tinidazole (44 mg/kg PO q24h for 6 days) fatal). Hematogenous spread—results in such as histoplasmosis or blastomycosis); in dogs—found to be more effective than failure states of the organs (invariably fatal). neoplasia; ulcerative colitis; endocrinopathy r metronidazole in treating amebiasis in Granulomatous amoebic (Addison’s disease); toxic (lead, fungal, or humans. meningoencephalitis (caused by plant); occasionally major organ disease r Metronidazole (20 mg/kg PO q12h for Acanthamoeba spp.)—causes signs similar to causing colonic ulceration such as renal r 7 days). distemper (anorexia, fever, lethargy, failure. Other causes of diffuse neurologic oculonasal discharge, respiratory distress, and disease in young animals, including infectious CONTRAINDICATIONS/POSSIBLE diffuse neurologic abnormalities). (distemper, fungal such as Cryptococcus, INTERACTIONS r Syndrome of inappropriate secretion of Blastomyces, Histoplasma, bacteria, protozoa High doses of metronidazole (usually antidiuretic hormone has been reported in a such as Toxoplasma and Neospora); toxic (lead, > 30 mg/kg) for extended periods may cause young dog with acanthamoebisis causing organophosphate); trauma; GME; neurologic signs in dogs. granulomatous meningoencephalitis with extracranial (hypoglycemia; hepatic invasion of the hypothalamus. encephalopathy); inherited epilepsy; Cats neoplasia. r Colitis—causing chronic intractable Cats r r FOLLOW-UP diarrhea (as per dogs). Systemic amebiasis or Other causes of diarrhea, including food Pets usually acquire infections from the same Acanthamoeba—not reported in cats. intolerance/allergy; inflammatory bowel source as their owners; veterinarians must CAUSES & RISK FACTORS disease; parasitism (giardiasis, parasites such as r warn owners of possible risk. Entamoeba histolytica—infection occurs by hookworms, roundworms, tritrichomonas); ingesting cysts from human feces. infectious (panleukopenia, FIV, FeLV r Encystment of trophozoites seldom occurs producing panleukopenia-like syndrome, in dogs or cats so they are not a source of bacterial including Salmonella, rarely r Campylobacter); drug (acetaminophen); MISCELLANEOUS infection. One of the few organisms neoplasia; pancreatitis; and major organ transmitted from man to pets but rarely from ABBREVIATIONS r dysfunction. r r pets to man. Trophozoites (the pathogenic CSF = cerebrospinal fluid FeLV = feline r stage)—inhabit the colonic lumen as CBC/BIOCHEMISTRY/URINALYSIS leukemia virus FIV = feline r commensals or invade the colonic wall but Normal; can reflect severe diarrhea. immunodeficiency virus GME = can disseminate to other organs (rare) granulomatous meningoencephalopathy OTHER LABORATORY TESTS r r including lungs, liver, brain, and skin. r H&E = hematoxylin and eosin HGE = r Microscopic examination—colonic biopsies r Trophozoites damage intestinal epithelial hemorrhagic gastroenteritis MRI = (H&E) obtained via endoscopy is the most r cells by secreting enzymes that lyse cells and r magnetic resonance imaging WBC = white r reliable method. Trophozoites in feces— disrupt intercellular connections. Certain very difficult to detect; methylene blue blood cell bacteria and a diet deficient in protein increase r r staining improves chances. Trichrome and Suggested Reading the virulence of the amoeba. The host’s iron-hematoxyline—the ideal fecal stains but Brofman PJ, Knostman KAB, Dibartola SP. immune response to invasion exacerbates r require a reference laboratory to perform. Granulomatous amebic pathology. Colonic ulceration results when r Fecal concentration techniques—no help. meningoenchephalitis causing the syndrome trophozoites in the submucosa undermine the r r CSF—elevated WBC count (70% of inappropriate secretion of antidiuretic mucosa. Acanthamoeba castellani and mononuclear cells), protein and hormone in a dog. J Vet Intern Med 2003, A. culbertsoni—free-living species found in xanthochromia in dogs with granulomatous 17:230–234. freshwater, saltwater, soil, and sewage; can r amebic meningoencephalitis due to Fung HB, Doan TL. Tinidazole: A infect dogs. Acanthamoeba spp.—infection Acanthamoeba. nitroimidazole antiprotozoal agent. Clin thought to be by inhalation of organisms IMAGING Ther 2005, 27:1859–1884. from contaminated water or colonization of Author StephenC.Barr the skin or cornea; hematogenous spread or MRI—shows brain granulomas. Consulting Editor StephenC.Barr JWST589-A47-38 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:7 279mm×216mm

66 Blackwell’s Five-Minute Veterinary Consult A Ameloblastoma

CBC/BIOCHEMISTRY/URINALYSIS Unaffected BASICS OTHER LABORATORY TESTS MEDICATIONS N/A OVERVIEW DRUG(S) r IMAGING Common oral tumor of odontogenic (tooth r N/A Skull or dental radiographs may show bone structure) ectoderm origin. CONTRAINDICATIONS/POSSIBLE r lysis deep to the superficial mass. Not Biologically these tumors are benign INTERACTIONS histologically but possess locally invasive particularly useful for diagnostic or treatment properties. planning. N/A r r Tumors may arise anywhere within the Regional and distant metastasis has not dental arcade. been described. r r Several histologic subtypes exist with similar Computed tomography is helpful for invasive behavior. planning surgery or radiation therapy, FOLLOW-UP especially in large or caudal tumors. SIGNALMENT Careful oral examination at 1, 3, 6, 9, and r DIAGNOSTIC PROCEDURES Middle-aged and old dogs 12 months after definitive treatment is r r Rare in cats Deep tissue biopsies are necessary and recommended to monitor for local recurrence. recommended for definitive diagnosis. SIGNS r r Squamous cell carcinoma may be Dogs may present with a smooth, firm, misdiagnosed as ameloblastoma. gingival mass that is usually non-ulcerated. r It may be incidental finding during dental MISCELLANEOUS prophylaxis/procedures. If involving rostral Suggested Reading dental arcade, incisor teeth can be displaced TREATMENT Amory JT, Reetz JA, Sanchez´ MD et al. and enveloped by proliferative tissue. r Computed tomographic characteristics of Surgical excision such as hemi- or total CAUSES & RISK FACTORS odontogenic neoplasms in dogs. Vet Radiol mandibulectomy or maxillectomy with N/A Ultrasound 2014, 55(2):147–158. > 1–2 cm margins is recommended as a Fiani N, Verstraete FJ, Kass PH, Cox DP. curative treatment option. Always submit Clinicopathologic characterization of resected tissue for histopathology, in order to odontogenic tumors and focal fibrous confirm the original diagnosis, and evaluate hyperplasia in dogs: 152 cases (1995–2005). DIAGNOSIS soft tissue and bone margins. r J Am Vet Med Assoc 2011, DIFFERENTIAL DIAGNOSIS Radiation therapy may provide long-term r 238(4):495–500. Epulis control in large tumors, or when the owners r Author Nick Dervisis Gingival hyperplasia decline surgery. r r Consulting Editor Timothy M. Fan Squamous cell carcinoma Intralesional chemotherapy with bleomycin r Acknowledgment The author and editors Amelanotic melanoma has been reported, but results are generally r acknowledge the prior contribution of Plasma cell tumor inferior to those of surgery or radiation. r Wallace B. Morrison. Other tumors related to the odontogenic apparatus JWST589-A48-39 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:10 279mm×216mm

Canine and Feline, Sixth Edition 67 Amitraz Toxicosis A

r Mydriasis r Death (prognosis is typically good with BASICS treatment) TREATMENT CAUSES & RISK FACTORS r OVERVIEW r Inpatient—severely affected patients. r Ingestion of impregnated collar or pieces of r Amitraz—formamidine acaricide; applied collar. Mild sedation after correctly applied r topically to control ticks, mites, and lice. Inappropriate direct dermal application. sponge-on solutions—often transient; may r r require no treatment. Amitraz-containing products (for Ingestion of undiluted product. r r dogs)—formulated as a 19.9% emulsifiable After application of properly diluted and Mild signs after topical application— concentrate in 10.6-mL bottles for dilution applied solutions—less common. wearing gloves, scrub with a hand r and sponge-on; as a 9% impregnated 25-inch Elderly, sick, toy-breed, or debilitated dishwashing detergent; rinse with copious 27.5-g collar and an 18-inch 18.5-g collar; as animals—may be predisposed. amounts of warm water; institute non-specific a 14.34% component of a 0.023 fl. oz., supportive therapy (e.g., intravenous fluids, 0.045 fl. oz., 0.113 fl. oz., 0.180 fl. oz.,or maintenance of blood pressure and normal 0.225 fl. oz. spot-on (discontinued); and asa body temperature, nutritional support); monitor 1–2 days until improvement is noted. 7.6% component of a 0.036 fl. oz., 0.072 fl. DIAGNOSIS r oz.,0.145 fl. oz., 0.217 fl. oz. spot-on Ingestion of collar possible—endoscopic r Systems affected—nervous; cardiovascular; DIFFERENTIAL DIAGNOSIS retrieval of the collar—removal of large r endocrine/metabolic (𝛽 cells of the pancreas); Recreational and prescription drugs— segments from the stomach may be beneficial; gastrointestinal. usually numerous small pieces are located r marijuana; opioids; barbiturates; Clinical signs—most associated with benzodiazepines; phenothiazines; throughout the gastrointestinal tract, making 𝛼 -adrenoreceptor agonist. removal unrealistic. r2 antihypertensive medications; skeletal muscle After high-dose oral administration relaxants; antidepressants (tricyclic, SSRIs), (dogs)—peak plasma concentration reached and other depressant drugs or chemicals. r at approximately 6 hours; elimination half-life Ivermectins, avermectins, milbemycins— as long as 24 hours; metabolites excreted in generally very high dose or exceptionally MEDICATIONS the urine. sensitive breed. r r DRUG(S) Ingestion of sustained-release- impregnated Macadamia nuts, tea tree oil, and albuterol collars—constant release and continued inhaler toxicosis. Collar Ingestion, Asymptomatic Patient r r systemic exposure until collar segments have Alcohols—ethanol; ethylene glycol Emetic—3% USP hydrogen peroxide passed in the stool. (2.2 mL/kg PO; maximum 45 mL after r (antifreeze); methanol (windshield washer Toxicosis—generally occurs when pieces of fluid); isopropyl alcohol (rubbing alcohol). feeding a moist meal); apomorphine and r especially xylazine not recommended. impregnated collar are ingested, when Tick bite paralysis, botulism, cranial r concentrated or improperly diluted solutions trauma, diabetes, hyperadrenocorticism, Activated charcoal has not been shown to be effective. are applied topically, or when solutions are hypothyroidism, severe anemia, cardiac r ingested or applied to the wrong size animal. Bulk diet (whole wheat bread, lactulose, r failure, and anaphylactic shock—marked Idiosyncratic reactions may occur. depression or weakness. pumpkin, psyllium husk [Metamucil]). r r SIGNALMENT Depends on clinical signs, history of Warm tap water enema (5–10 mL/kg); will r stimulate GI motility and help pass pieces of Thorough history—usually identifies topical exposure, or evidence of exposure and collar through the GI tract. or collar use; topically missing collar or pieces elimination of other causes. seen in dog’s environment or in the stool. CBC/BIOCHEMISTRY/URINALYSIS Marked Depression r r Dogs—common, owing to more common r May require pharmacologic reversal of the Hyperglycemia—common, related to 𝛼 use. insulin inhibition 2-adrenergic effects. r r r th Cats—more sensitive than dogs although Elevated liver enzymes—uncommon Atipamezole (Antisedan) 0.05 mg/kg 1/4 cats are less likely involved. IV 3/4th IM; reverse clinical signs within r IMAGING Predilection for old and toy-breed animals. minutes; repeat as needed; preferred over Abdominal radiography—may reveal a collar SIGNS yohimbine because of its higher buckle in the gastrointestinal tract; collar itself alpha-2 activities. r Historical Findings is not radioopaque.. Yohimbine (Yobine) 0.11–0.2 mg/kg IV, Develop acutely after exposure (topical or DIAGNOSTIC PROCEDURES administered slowly; reverses depression and oral) Identify amitraz on hair or in gastrointestinal bradycardia within minutes; improves GI Physical Examination Findings motility; objective is to keep the patient in a r contents—analytical methods described; Minor to severe depression/lethargy state of low-level depression with normal r useful only to prove exposure; no data Weakness heart rate, blood pressure, body temperature, r available correlating concentration with Ataxia and blood glucose concentrations. r clinical signs. r Bradycardia Collar ingestion—monitor for recurrence of r PATHOLOGIC FINDINGS Vomiting (pieces of collar) symptoms; may need additional yohimbine r High-dose, prolonged exposure—increased Hyperthermia/hypothermia until collar segments appear in the stool. r liver weight; slight enlargement of r Hyperglycemia; diabetic patients can show Yohimbine and atipamezole—may require hepatocytes; thinning of the zonae fasciculata significant hyperglycemia following exposure repeated administration (as needed) possibly r and reticularis; slight hyperplasia of the zona Hypotension every 2–8 hours, because their half-life in dogs r glomerulosa of the adrenal glands. Polyuria is short and amitraz elimination half-life is r Gastrointestinal stasis longer. JWST589-A48-39 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:10 279mm×216mm

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r r Atropine contraindicated because of Close observation for recurrence of clinical ABBREVIATIONS r potentiation of GI stasis. signs—required for 24–72 hours. CNS = central nervous system r r Yohimbine and atipamezole—requires GI = gastrointestinal CONTRAINDICATIONS/POSSIBLE r INTERACTIONS readministration in severe cases, because SSRI = selective serotonin reuptake reversal effects subside before collar segments inhibitor Yohimbine and atipamezole—excessive have passed or before amitraz has been Suggested Reading administration may result in apprehension, eliminated from the body. r Grossman MR. Amitraz toxicosis associated CNS stimulation, and rarely seizures. No long-term adverse effects expected. with ingestion of an acaricide collar in a dog. J Am Vet Med Assoc 1993, 203:55–57. Hugnet C, Buronfosse F, Pineau X, et al. Toxicity and kinetics of amitraz in dogs. Am FOLLOW-UP MISCELLANEOUS r J Vet Res 1996, 57:1506–1510. Body temperature, blood pressure, serum AGE-RELATED FACTORS Authors Steven R. Hansen and Safdar A. glucose, and heart rate—important r Khan parameters. Elderly, sick, or debilitated animals may take longer to fully recover. Consulting Editor Lynn R. Hovda JWST589-A49-40 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:17 279mm×216mm

Canine and Feline, Sixth Edition 69 Amphetamine and ADD/ADHD Medication Toxicosis A

r r Gastrointestinal—anorexia, vomiting, Pseudoephredrine, phenylephrine r diarrhea. 5 fluorouracil r BASICS INCIDENCE/PREVALENCE Ma huang, guarana, or ephedra N/A CBC/BIOCHEMISTRY/URINALYSIS DEFINITION r SIGNALMENT CBC—disseminated intravascular Acute gastrointestinal, neurologic, coagulopathy secondary to severe neuromuscular, and cardiac toxicosis as the Species hyperthermia (rare). r result of excessive consumption of Dogs and cats, although more prevalent in Chemistry— r amphetamine or a derivative. May be due to dogs. Azotemia: prerenal—secondary to ingestion of prescription medications or Breed Predilections dehydration; renal—secondary to illegal drugs. N/A rhabdomylosis and myoglobinuria (rare). r PATHOPHYSIOLOGY Mean Age and Range Elevated liver enzymes—secondary to r seizures and/or hyperthermia (rare). Amphetamine and its derivatives belong to N/A r Hypoglycemia. the CNS stimulant class phenylethylamines. Predominant Sex r Urinalysis—evidence of myoglobinuria, Various substitutions of the basic N/A phenylethylamine structure account for many urine specific gravity (high—prerenal SIGNS pharmaceutical and illicit compounds found azotemia; isosthenuria—renal failure). today. Historical Findings OTHER LABORATORY TESTS r r r Amphetamine is a sympathomimetic that is Abnormal behavior—usually hyperactivity, Electrolytes—imbalances secondary to GI structurally related to norepinephrine. anxiety or pacing, anorexia, fast heart rate, effects. r r Central action—stimulates cortical centers panting; observed or evidence of exposure by Acid-base status—acidosis may occur. owner/caretaker. r including cerebral cortex, medullary r Over-the-counter urine drug screens— respiratory center, and reticular activating Onset of signs typically begins within watch for false positive or negative. Consult systems. 30 minutes to 6 hours post-ingestion; user handbook for further information. r r Peripheral action—directly stimulates alpha depends on product formulation. Amphetamines are present in blood, urine, and beta receptors and stimulates the release Physical Examination Findings and saliva; consult with local veterinary r of norepinephrine from stores in adrenergic Nervous—hyperactivity, agitation, diagnostic lab or human hospital for nerve terminals. r restlessness, head bobbing, pacing, circling, availability and proper sample submission. Amphetamine may slow catecholamine vocalization, disorientation, hyperesthesia, IMAGING metabolism by inhibition of monoamine ataxia, lethargy or depression (less common). oxidase. r N/A r Cardiovascular—tachycardia or bradycardia Several different product formulations DIAGNOSTIC PROCEDURES (less common, may be reflexive), r including immediate and extended release hypertension. EEG for presence of any tachyarrhythmia or and topical patch. r less commonly bradyarrhythmia. r Neuromuscular—muscle fasciculation or r Amphetamines are well absorbed orally; tremors, seizures. Blood pressure—identification of r peak plasma levels are generally reached in Gastrointestinal—vomiting, diarrhea, hypertension. 1–3 hours; this may be delayed with extended anorexia, excessive salivation. PATHOLOGIC FINDINGS release formulations. r r Respiratory—tachypnea. On necropsy presence of amphetamines may Metabolism is minimal. r r Ophthalmic—mydriasis with possibly poor be found in the gastric contents, urine, The half-life, which varies from 7–34 hours, to unresponsive pupillary light response. r plasma, liver, kidney, or muscle. and rate of excretion of unchanged Other—hyperthermia. amphetamine in the urine are both dependent CAUSES upon urine pH, with shorter half-lives associated with more acidic urine. Accidental ingestion or administration, r Clinical signs may be seen at doses below malicious poisoning. TREATMENT 1mg/kg. RISK FACTORS r APPROPRIATE HEALTH CARE Oral lethal dose in dogs for most Households with children or adults currently Majority of cases require emergency inpatient amphetamines ranges from 10 mg/kg to taking prescription or illicit amphetamine or intensive care management. 23 mg/kg and for methamphetamine sulfate derivative. NURSING CARE it is 9–11 mg/kg. Oral lethal dose for r amphetamine sulfate is 20–27 mg/kg. Intravenous fluid therapy to correct r Amphetamine and its derivatives are used in dehydration and electrolyte imbalances as well humans to treat ADD/ADHD, narcolepsy, DIAGNOSIS as support renal function and promote and obesity. excretion of amphetamines. Use blood r DIFFERENTIAL DIAGNOSIS pressure to help guide fluid rate. Illicit use of amphetamines in humans is r r Strychnine Cool intravenous fluids, fans, cool water also prevalent. r Organochlorine insecticides baths for hyperthermia. SYSTEMS AFFECTED r r Methylxanthine ACTIVITY Cardiovascular—stimulation most r 4-aminopyridine common: tachycardia and hypertension. r Minimize activity and stimuli. r Metaldehyde Nervous—stimulation most common, r DIET Phenylpropanolamine depression uncommon. r r Albuterol Withhold food if moderately to severely Neuromuscular—stimulation: muscle r Nicotine affected. Bland diet for a few days tremors and seizures. r r Tremorgenic mycotoxins post-exposure if significant gastrointestinal Respiratory—stimulation, tachypnea. r r signs were noted. Ophthalmic—mydriasis. Hypernatremia JWST589-A49-40 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:17 279mm×216mm

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CLIENT EDUCATION PRECAUTIONS SYNONYMS r In case of an exposure, owner should contact N/A Common brand names of prescription local veterinarian or veterinary poison center POSSIBLE INTERACTIONS amphetamine drugs and their active r immediately. Amphetamines inhibit the metabolism of ingredient: Adderall (amphetamine and SURGICAL CONSIDERATIONS adrenergic blockers (doxazosin, dextroamphetamine); Ritalin, Metadate, and N/A phenoxybenzamine, prazosin, terazosin), Concerta (methylphenidate); Daytrana phenobarbital, and phenytoin. (methylphenidate transdermal patch); Focalin r Amphetamines potentiate the metabolism (dexmethylphenidate); Vyvanse of coumarin anticoagulants, monoamine (lisdexamfetamine), Cylert (pemoline), oxidase inhibitors, opioid analgesics, and Adipex-P (phentermine), Dexedrine MEDICATIONS (Dextroamphetamine). tricyclic antidepressants. r DRUG(S) OF CHOICE Illicit drug street names: ice, glass, crank, ALTERNATIVE DRUG(S) speed, uppers, ecstasy, meth, and many others. Decontamination r Phenobarbital, pentobarbital, and propofol SEE ALSO Induce emesis—if a recent exposure and pet for CNS stimulatory signs. r is not already symptomatic. Antidepressant Toxicosis—SSRIs and r SNRIs Apomorphine—0.04 mg/kg IV, r Antidepressant Toxicosis—Tricyclics subconjuctival. r r Pseudoephredrine/Phenylephrine Toxicosis Hydrogen peroxide 3%—2.2 mL/kg, FOLLOW-UP maximum dose 45 mL. ABBREVIATIONS r r Gastric lavage if extremely large ingestion or PATIENT MONITORING ADD = attention deficit disorder patient is already symptomatic. r r r Monitor in hospital until resolution of ADHD = attention deficit hyperactivity Activated charcoal with a cathartic. clinical signs. disorder r r CNS Signs of Stimulation If severely affected, monitor liver and CNS = central nervous system r r Acepromazine 0.05–1.0 mg/kg IV or IM kidney values every 24 hours for 72 hours or DIC = disseminated intravascular r Chlorpromazine 0.5 mg/kg IV, titrate up as until resolution. coagulation r needed. ECG = electrocardiogram r PREVENTION/AVOIDANCE r Cyproheptadine (serotonin antagonist): All medications and illicit drugs should be GI = gastrointestinal dogs, 1.1 mg/kg orally or rectally, may be kept out of pets’ reach at all times. INTERNET RESOURCES repeated q8h as needed for signs consistent r POSSIBLE COMPLICATIONS http://www.aspcapro.org/animal-poison- with serotonin syndrome; cats, 2–4 mg/cat, control-center-articles.php may repeat q12h as needed for signs Acute renal failure secondary to r myoglobinuria or DIC (rare). http://www.aspca.org/pet-care/animal- consistent with serotonin syndrome poison-control Methocarbamol (for muscle tremors): EXPECTED COURSE AND PROGNOSIS r r http://www.petpoisonhelpline.com/ 50–220 mg/kg IV, titrate to effect. Do not Expected course of clinical signs is exceed 330 mg/kg/day. 12–72 hours, depending on dose, product Suggested Reading Cardiovascular Signs formulation, effectiveness of decontamination Stern LA, Schell M. Management of r and treatment, and rate of elimination. attention-deficit disorder and attention- Tachyarrhythmia—beta blockers such as r propranolol 0.02–0.04 mg/kg IV or esmolol Prognosis—most patients do well with deficit/hyperactivity disorder drug or metoprolol. prompt and appropriate veterinary care. intoxication in dogs and cats. Vet Clin r Ventricular premature contractions— Seizures or severe hyperthermia may be a poor North Am Small Anim Pract 2012, lidocaine: dogs at 2–4 mg/kg IV (to prognostic indicator. 42(2):279–287. maximum of 8 mg/kg over a 10-minute Teitler, J.B. Evaluation of a human on-site period). Cats—start with 0.1–0.4 mg/kg and urine multi drug test for emergency use increase cautiously to 0.25–0.75 mg/kg IV with dogs. J Am Anim Hosp Assoc 2009, slowly if no response. Cats are reportedly very MISCELLANEOUS 45(2):59–66. sensitive to lidocaine, so monitor carefully if Volmer PA. “Recreational” drugs. In: Peterson ASSOCIATED CONDITIONS used. ME, Talcott PA, eds., Small Animal N/A Toxicology, 3rd ed. St. Louis, MO: Elsevier, Promote Elimination AGE-RELATED FACTORS 2013, pp. 309–334. Ascorbic acid or ammonium chloride—for Volmer, P.A. Human drugs of abuse. In: N/A urinary acidification to promote elimination; Bonagua JD, Twedt DC, eds., Current however, only use if can measure acid-base ZOONOTIC POTENTIAL Veterinary Therapy XIV. St. Louis, MO: status. Pets exposed to human waste products from Elsevier, 2009, pp. 144–145. CONTRAINDICATIONS those taking amphetamines or derivatives Wismer T. Amphetamines. In: Osweiler GD, r While diazepam has been successfully used could become symptomatic. Hovda LR, Brutlag AG, Lee JL, eds. to treat amphetamine exposures, there is PREGNANCY/FERTILITY/BREEDING Blackwell’s Five-Minute Veterinary Consult evidence that benzodiazepines may intensify Amphetamines are a known teratogen in Clinical Companion Small Animal neurologic signs. Toxicology. Ames, IA: Wiley-Blackwell, r humans. They have been found to cross the Urinary acidification if unable to monitor placenta in animals and may also be found in 2011, pp. 125–130. acid-base status or if myoglobinuria is present. Author Kirsten E. Waratuke r milk. Inducing emesis in a symptomatic patient. Consulting Editor Lynn R. Hovda JWST589-A50-41 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:21 279mm×216mm

Canine and Feline, Sixth Edition 71 Amyloidosis A

SIGNALMENT thromboembolism (e.g., dyspnea) or iliac or femoral artery thromboembolism (e.g., caudal Species r BASICS Dog and cat paresis). Chinese shar-pei dogs and Oriental shorthair and Siamese cats may have signs of Breed Predilections DEFINITION r hepatic disease (e.g., jaundice, cachexia, and Dog—Chinese shar-pei, beagle, collie, spontaneous hepatic rupture with A group of conditions of diverse cause in pointer, English foxhound, and walker intraperitoneal bleeding). which extracellular deposition of insoluble hound; German shepherd dog and mixed fibrillar proteins (amyloid) in various organs r CAUSES breeds are at lower risk. Cat—Abyssinian, r and tissues compromises their normal Oriental shorthair, and Siamese. Neoplasia and chronic infectious and function. Mean Age and Range non-infectious inflammatory conditions can PATHOPHYSIOLOGY r be found in 30–50% of dogs with reactive Cats—mean age at diagnosis 7 years; range r r r Patients usually affected by systemic reactive 1–17 years. Dogs—mean age at diagnosis is amyloidosis. Chronic inflammation— amyloidosis; tissue deposits contain AA, 9 years; range 1–15 years. Chinese shar-Pei systemic mycoses (e.g., blastomycosis, which is a fragment of an acute-phase reactant dogs—median age at diagnosis is 5 years; coccidioidomycosis), chronic bacterial r r protein called SAA. Phases of amyloid range 3.6–17 years. Prevalence increases infections (e.g., osteomyelitis, broncho- ◦ r deposition: Predeposition phase: SAA with age. Abyssinian cats—range pneumonia, pleuritis, steatitis, pyometra, r concentration is high but without amyloid < 1–17 years. Chinese shar-pei dogs— pyelonephritis, chronic suppurative deposits; colchicine administration during usually < 6 years of age when signs of renal dermatitis, chronic suppurative arthritis, r this phase may prevent development of the failure develop. Siamese cats with familial chronic peritonitis, nocardiosis, chronic ◦ disease. Deposition phase (rapid portion): amyloidosis of the liver and thyroid gland stomatitis), parasitic infections (e.g., amyloid deposits increase rapidly; colchicine usually develop signs of liver disease when dirofilariasis, leishmaniasis, hepatozoonosis), administration delays but does not prevent 1–4 years old. and immune-mediated diseases (e.g., systemic tissue deposition of amyloid; DMSO may lupus erythematosus). Amyloid deposits can Predominant Sex promote resolution of amyloid deposits and a be found in up to 35% of FIV-positive cats. Dogs and Abyssinian cats—females at a r persistent decrease in SAA concentration. Neoplasia (e.g., lymphoma, plasmacytoma, slightly higher risk (< 2:1). Female-to-male ◦ Deposition phase (plateau portion): net multiple myeloma, mammary tumors, ratio is higher in Chinese shar-pei dogs r deposition of amyloid changes little; neither testicular tumors). Familial (e.g., Chinese (∼ 2.5:1). DMSO nor colchicine is beneficial. shar-pei, English foxhound, and beagle dogs; r SIGNS Abyssinian, Siamese, and Oriental shorthair Clinical signs in dogs and cats usually are r associated with amyloid deposition in the General Comments cats). Others—cyclic hematopoiesis in gray r r kidneys. Dogs—amyloid deposits usually Depend on the organs affected, the amount collies; juvenile polyarteritis in beagles. found in the glomeruli leading to proteinuria of amyloid, and the reaction of the affected r r and nephrotic syndrome. Cats—amyloid organs to amyloid deposits. Usually caused deposits usually found in the medullary by kidney involvement; occasionally, hepatic interstitium but may occur in glomeruli. r involvement may cause signs in Chinese DIAGNOSIS Some Chinese shar-pei dogs with familial shar-pei dogs and Oriental shorthair and DIFFERENTIAL DIAGNOSIS amyloidosis have medullary amyloidosis Siamese cats. r r Dogs—GN; proteinuria tends to be more without glomerular involvement. Siamese Historical Findings and Oriental shorthair cats with familial r severe in dogs with glomerular amyloidosis r No clear history of a predisposing disorder than those with GN but there is great overlap. amyloidosis have hepatic amyloidosis. A r r in most (∼75%) cases. Anorexia, lethargy, Cats and Chinese shar-pei dogs with different type amyloid, pancreatic islet polyuria and polydipsia, weight loss, r medullary amyloidosis—consider other causes amyloid polypeptide, or amylin, deposits in vomiting. Ascites and peripheral edema in the pancreas of old cats. Amylin is a hormone r of medullary renal disease (e.g., animals with nephrotic syndrome. Chinese pyelonephritis, chronic interstitial disease). secreted along with insulin by the pancreatic shar-pei dogs may have a history of previous beta cells. Chronic increased stimulus for CBC/BIOCHEMISTRY/URINALYSIS episodic joint swelling and high fever that r secretion of amylin by beta cells (e.g., states of resolves spontaneously within a few days. Nonregenerative anemia is found in some insulin resistance) lead to pancreatic islet cell r dogs and cats with amyloid-induced renal Beagle dogs with juvenile polyarteritis may r amyloidosis. have a history of fever and neck pain that failure. Dogs—may see r > SYSTEMS AFFECTED persist for 3–7 days. Oriental shorthair and hypercholesterolemia ( 85%), azotemia > Renal/Urologic—predilection for renal AA Siamese cats may present with spontaneous ( 70%), hypoalbuminemia (70%), > deposition. Liver, spleen, adrenal glands, hepatic hemorrhage leading to acute collapse hyperphosphatemia ( 60%), hypocalcemia (50%), and metabolic acidosis. pancreas, tracheobronchial tree, and and hemoabdomen. r gastrointestinal tract also may be affected. Hypercholesterolemia—common finding in Physical Examination Findings > GENETIC r cats with renal disorders ( 70% of cats with Related to renal failure—oral ulceration, renal disease in one study) but does not (See “Breed Predilections.”) No genetic emaciation, vomiting, and dehydration; reliably predict glomerular disease. r involvement is clearly established; familial kidneys usually small, firm, and irregular in Hypoproteinemia—more common than affected cats; they may be small, normal-sized, amyloidosis occurs in Chinese shar-pei, r hyperproteinemia (24 vs. 8.5%) in dogs with English foxhound, and beagle dogs, and in or slightly enlarged in affected dogs. Signs amyloidosis; hyperglobulinemia common in of nephrotic syndrome (e.g., ascites, r Abyssinian, Oriental shorthair, and Siamese r cats. Proteinuria—with an inactive cats. subcutaneous edema). Related to the sediment common in dogs; mild or absent in primary inflammatory or neoplastic disease INCIDENCE/PREVALENCE r animals with medullary amyloidosis without process. Thromboembolic phenomena— Uncommon, occurs mostly in dogs; rare in glomerular involvement (most mixed-breed may occur in up to 40% of affected dogs; cats, except Abyssinians. cats, at least 25% of Abyssinian cats, and at signs vary with the location of the thrombus; least 33% of Chinese shar-pei dogs). In a patients may develop pulmonary retrospective study with 91 cases of renal JWST589-A50-41 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:21 279mm×216mm

72 Blackwell’s Five-Minute Veterinary Consult

A Amyloidosis (Continued)

amyloidosis in dogs, hypoalbuminemia was more common in non-Chinese shar-pei dogs (100%) versus shar-pei dogs (65%). r MEDICATIONS FOLLOW-UP Isosthenuria, and hyaline, granular, and waxy casts in some patients. DRUG(S) OF CHOICE PATIENT MONITORING r r Appetite and activity level daily by the OTHER LABORATORY TESTS Identify underlying inflammatory and r Proteinuria—urinary protein:creatinine ratio neoplastic processes and treat if possible. owner; body weight weekly. Serum r albumin, creatinine, and BUN concentrations to estimate severity. Manage renal failure according to the r every 2–6 months in stable patients. Can IMAGING principles of conservative medical treatment (see Renal Failure, Acute, and Renal Failure, assess degree of proteinuria serially by urine Abdominal Radiographic Findings r Chronic). protein:creatinine ratios. Kidneys usually small in affected cats. r r Normalize blood pressure in patients with PREVENTION/AVOIDANCE Kidneys small, normal-sized, or large in hypertension (see Hypertension, Systemic). r Do not breed affected animals. affected dogs. Patients with thromboembolic syndrome POSSIBLE COMPLICATIONS Abdominal Ultrasonographic Findings and nephrotic syndrome caused by r r Renal failure Nephrotic syndrome Kidneys usually hyperechoic and small in glomerular amyloidosis usually have a low r r affected cats; may be small, normal-sized, or plasma concentration of antithrombin; thus Systemic hypertension Hepatic rupture causing intraperitoneal hemorrhage large in affected dogs. heparin is relatively ineffective. Aspirin r Thromboembolic disease DIAGNOSTIC PROCEDURES (0.5 mg/kg PO q12h) has been suggested for dogs with glomerular disease; this low dosage EXPECTED COURSE AND PROGNOSIS Renal biopsy needed to differentiate is as effective in preventing platelet amyloidosis from GN. In dogs other than Disease is progressive and usually advanced at aggregation as is 10 mg/kg PO q24h. Chinese shar-pei, amyloidosis is primarily a r the time of diagnosis. Prognosis improves if DMSO—may help patients by solubilizing glomerular disease; diagnose by renal cortical an underlying immune, inflammatory, or amyloid fibrils, reducing serum concentration biopsy. In most domestic cats, some neoplastic disease is detected and successfully of SAA, and reducing interstitial Abyssinian cats, and some Chinese shar-pei treated. Survival for dogs with glomerular inflammation and fibrosis in the affected dogs, medullary amyloidosis can occur amyloidosis varied from 3 to 20 months in kidneys; may cause lens opacification in dogs. without glomerular involvement; diagnose by 1 study; some dogs may occasionally live Perivascular inflammation and local renal medullary biopsy. longer. Cats with renal failure because of thrombosis may occur if undiluted DMSO is amyloidosis usually survive < 1 year. Mildly PATHOLOGIC FINDINGS r administered intravenously. Subcutaneous affected cats may not develop renal failure and Small kidneys in cats; small, normal, or r administration of undiluted DMSO may be have an almost normal life expectancy. large kidneys in dogs. Amyloid deposits painful. The authors have used 90% DMSO appear homogeneous and eosinophilic when diluted 1:4 with sterile water subcutaneously stained by hematoxylin and eosin and viewed at a dosage of 90 mg/kg 3 times per week in by conventional light microscopy. They dogs. Whether or not DMSO treatment MISCELLANEOUS demonstrate green birefringence after Congo benefits renal amyloidosis in dogs remains red staining when viewed under polarized controversial. ASSOCIATED CONDITIONS r r r light. Evaluation of Congo red—stained Methylsulfonylmethane is an active Urinary tract infection Polyarthritis in r sections before and after permanganate metabolite of DMSO that can be given orally Chinese shar-pei Polyarteritis in beagle oxidation permits presumptive diagnosis of and lacks the smell of DMSO. It has been SEE ALSO AA amyloidosis (vs. other types) because AA used empirically in dogs with amyloidosis, r r Glomerulonephritis Nephrotic Syndrome amyloidosis loses its Congo red affinity after but there is no evidence that it benefits dogs r r r Proteinuria Renal Failure, Acute Renal permanganate oxidation. The liver is very with renal amyloidosis. r Failure, Chronic friable and usually contains extensive amyloid Colchicine—impairs release of SAA from ABBREVIATIONS deposits in cats presented with acute hepatic hepatocytes; prevents development of r r AA = amyloid A protein DMSO = hemorrhage. amyloidosis in humans with familial r dimethylsulfoxide GN = glomerula Mediterranean fever (a familial amyloidosis) r and stabilizes renal function in patients with nephritis SAA = serum amyloid A protein nephrotic syndrome but without overt renal Suggested Reading TREATMENT failure; no evidence of benefit once the patient BartgesJ,WallJ.Amyloidosis.InBartgesJ, develops renal failure; may cause vomiting, APPROPRIATE HEALTH CARE Polzin DJ. Nephrology and Urology of r diarrhea, and idiosyncratic neutropenia in Small Animals, Oxford: Wiley-Blackwell, Hospitalize patients with chronic renal dogs. Colchicine (0.01–0.04 mg/kg PO 2011, pp. 547–554. failure and dehydration for initial medical r q24h) is used particularly in shar-pei dogs Segev G, Cowgill, LD, Jessen, S et al. Renal management. Can manage stable patients with episodic fever or polyarthritis before amyloidosis in dogs: a retrospective study of and those with asymptomatic proteinuria as development of renal failure. 91 cases with comparison of the between outpatients. PRECAUTIONS Shar-pei and non-Shar-pei dogs. J Vet DIET r r Dosage of drugs excreted by the kidneys Intern Med 2012, 26:259–268. Patients with chronic renal failure—restrict may need adjustment in patients with renal Authors Helio S. Autran de Morais and phosphorus and moderately restrict protein. r r failure. Use nonsteroidal anti-inflammatory Stephen P. DiBartola Patients with hypertension—restrict drugs cautiously in patients with medullary Consulting Editor Carl A. Osborne sodium. amyloidosis; they can decrease renal blood CLIENT EDUCATION flow in dehydrated patients. r r Client Education Handout Discuss progression of the disease. Discuss available online familial predisposition in susceptible breeds. JWST589-A51-42 JWST589-Tilley Printer: Yet to Come August 1, 2015 13:25 279mm×216mm

Canine and Feline, Sixth Edition 73 Anaerobic Infections A

with non-healing wounds—test for FeLV and anaerobes and any aerobic components offers r FIV. Middle-aged and old animals—tumor the greatest chance of success. r BASICS invasion (e.g., in the gastrointestinal tract). Amoxicillin with clavulanate—in many CBC/BIOCHEMISTRY/URINALYSIS cases, considered the antibiotic of choice; OVERVIEW r Neutrophilic leukocytosis and monocytosis convenient and accessible; clavulanate r r improves activity against Bacteroides. Anaerobic bacteria (i.e., bacteria requiring common. Biochemical abnormalities r low oxygen tension) comprise a large portion depend on specific organ involvement. Imipenem—beta lactam with significant of the normal flora, especially on mucosal r activity against serious, resistant infections. r Systemic spread of infection suggested by r surfaces. May be Gram-positive or leukocytosis, hypoglycemia, increased ALP, Cefoxitin—a cephalosporin with reliable r activity against anaerobes. Gram-negative cocci or rods. Most common and hypoalbuminemia. r Clindamycin—may be especially useful for genera—Bacteroides, Fusobacterium, OTHER LABORATORY TESTS Actinomyces, Propionibacterium, r respiratory tract infections; concentrated Peptostreptococcus (enteric Streptococcus), Culture of anaerobic bacteria is often within leukocytes. r r Porphyromonas, and Clostridium. Most unrewarding because of their fastidious nature Chloramphenicol—good tissue penetration and errors in sample handling and anaerobic infections are polymicrobial and r but bacteriostatic and associated with adverse contain at least two different anaerobe species submission. Appropriate media and effects, especially in cats; concern for human admixed with facultative anaerobes or aerobic containers should be on-hand prior to sample exposure also limits use. r collection; diagnostic laboratories can provide r bacteria (especially E. coli). Individual r Metronidazole—useful against all clinically guidance. Samples should not be significant anaerobes (except Actinomyces). organisms vary in potential to withstand r r r refrigerated prior to submission. Suitable Aminoglycosides—uniformly ineffective. oxygen exposure. Injurious toxins and r enzymes may be elaborated by the organisms, samples for culture may include fluid (e.g., Trimethoprim-sulfa combinations— leading to extension of the infection into pleural, peritoneal, etc.) or tissue. ineffective; poor penetration into exudates. r r adjacent, healthy tissue. All body systems IMAGING Quinolones—routinely ineffective, are at potential risk for anaerobic infection. As required for the circumstances of the although newer expanded-spectrum SIGNALMENT individual patient (e.g., suspected bone quinolones do have activity against anaerobes (e.g., pradofloxacin). Dog and cat infection, peritonitis, etc.). DIAGNOSTIC PROCEDURES SIGNS r Cytologic inspection reveals abundant General Comments r degenerate neutrophils with morphologically Determined by the body system involved. r diverse forms of intracellular and extracellular FOLLOW-UP Certain areas more commonly associated bacteria; presence of large filamentous PATIENT MONITORING with anaerobic infection (mucous membrane r r bacteria is suggestive. If not performed proximity). It is possible to overlook Monitoring parameters will vary with the in-house, Gram staining should be requested circumstances of each patient. anaerobes in an infectious process, leading to when the sample is submitted. confusion in interpreting culture results and POSSIBLE COMPLICATIONS selection of antimicrobials. Localized infection may progress to systemic Physical Examination Findings infection if not appropriately identified and r A foul odor associated with a wound or treated. r MEDICATIONS exudative discharge. Gas in the tissue or EXPECTED COURSE AND PROGNOSIS r r associated exudates. Discolored tissue, Thoracic drainage—important with r r Dependent upon identification and resolution especially when black. Peritonitis, pyothorax (see specific chapter). Hyperbaric r of the underlying cause; long-term antibiotic pyothorax, or pyometra. Severe dental oxygen—some potential use; limited in r therapy may be required. disease. Wounds or deep abscesses that do availability. not heal as anticipated. SURGERY r CAUSES & RISK FACTORS Should not be delayed when anaerobes are r r Usually caused by normal flora of the body; suspected. Combined with systemic MISCELLANEOUS a break in protective barriers allows bacterial antimicrobial therapy—the best chance of a r r ASSOCIATED CONDITIONS invasion. Infection in the proximity of a positive outcome. Usually indicated when anaerobic organisms complicate pyometra, See “Causes & Risk Factors” mucous membrane should raise one’s index of r suspicion for anaerobe involvement. osteomyelitis, and peritonitis. Cleanse the ABBREVIATIONS r wound of toxins and devitalized tissue. r r Predisposing factors—immunosuppression, r r ALP = alkaline phosphtase FeLV = feline Enhance drainage of pus. Improve local r bite wounds, dental disease, open fractures, r leukemia virus FIV = feline abdominal surgery, and foreign bodies. blood flow. Increase oxygen tension. immunodeficiency virus DRUG(S) r Suggested Reading Antimicrobial therapy alone—unlikely to Hirsh DC, Jang SS. Anaerobic infections. be successful; poor drug penetration into In: Greene CE, ed., Infectious Diseases of DIAGNOSIS exudates. r the Dog and Cat, 3rd ed. St. Louis, MO: DIFFERENTIAL DIAGNOSIS Antibiotic selection—largely empiric, owing Saunders Elsevier, 2006, pp. 381–388. r to the difficulty of isolating anaerobes and the Author Sharon Fooshee Grace Wounds that fail to respond to appropriate delay in return of culture results. medical therapy—if aerobic cultures are r Consulting Editor StephenC.Barr r Because most anaerobic infections are negative, suspect anaerobic organisms. Cats polymicrobial, therapy targeted against both JWST589-A52-43 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:2 279mm×216mm

74 Blackwell’s Five-Minute Veterinary Consult A Anal Sac Disorders

r r Atopic dermatitis Identification of underlying causes of r Tapeworm infestation predisposing disease. r r Tail fold bacterial folliculitis Feeding high-fiber diets may help natural BASICS r Malassezia dermatitis expression of anal sacs. r OVERVIEW Compulsive disorder (anal licking) r r Colitis or other intestinal disorder Anal sacs are reservoirs for secretions r Keratinization disorder normally evacuated by compression during r defecation. Anal sac neoplasia (including MEDICATIONS r adenocarcinoma, squamous cell carcinoma) Normal gland secretions vary in consistency r Perianal adenoma DRUG(S) and color. r r r Perianal adenocarcinoma Infection—use of appropriate antibiotics: Disorders include impaction, infection r (sacculitis), abscess, and neoplasia. Perianal fistulae cephalexin (22 mg/kg q12h), amoxicillin r Treatment options include manual CBC/BIOCHEMISTRY/URINALYSIS trihydrate-clavulanate potassium (10–15 r mg/kg q12h), clindamycin (11 mg/kg q24h), expression, flushing, antibiotics, and surgical Usually normal r trimethoprim-sulfamethoxasole (15 mg/kg excision. Hypercalcemia—anal sac adenocarcinoma q12h); metronidazole (10–15 mg/kg q12h); SIGNALMENT OTHER LABORATORY TESTS r enrofloxacin (dogs, 10–20 mg/kg q24h; cats, Dogs and cats (rarely): no age or sex None unless indicated by an underlying cause 5 mg/kg/day), and orbifloxacin (5 mg/kg predisposition. r IMAGING q24h). Breeds predisposed: r ◦ None unless indicated by an underlying cause Chronic disease associated with perianal Impaction—miniature and toy poodle, fistulae; cyclosporine, modified (name brand American cocker and English springer DIAGNOSTIC PROCEDURES r preferred: Atopica 5 mg/kg q24h) and/or spaniel, Chihuahua. Digital palpation of the anal sacs—normal topical tacrolimus. ◦ Neoplasia (adenocarcinoma)—German anal sacs should not be palpable externally. r CONTRAINDICATIONS/POSSIBLE shepherd dog, golden retriever, American Normal anal sac contents vary widely in cocker and English springer spaniel. gross appearance and microscopic INTERACTIONS SIGNS characteristics; usually thin or watery, with N/A minimal cellularity and primarily extracellular Impaction/Infection r organisms, but may vary widely in numbers Anal pruritus—often manifested by of inflammatory cells and bacteria. “scooting” r r Impaction—generally more thick, pasty Perianal pruritus FOLLOW-UP r brown secretion; higher numbers of Hesitancy to defecate r r Malassezia and intracellular bacteria. Reassess patients weekly initially; then as Tenesmus r r Anal sacculitis and abscessation—purulent, necessary to monitor healing. Tail chasing r r often blood-tinged, foul-smelling discharge. Manually express anal sac contents and/or Foul-smelling, non-feces anal discharge r r Cytology of anal sac secretions—increased flush contents until sacs empty without Refusal to sit and/or lift tail intervention. r number of neutrophils, erythrocytes, r Cats—excessive licking of the ventral Malassezia, and intracellular bacteria indicate CBC, serum chemistry profile, and abdomen and tail head r infection; reports vary but Gram-positive urinalysis with culture—recommended every Abscess—often unilateral; localized pain cocci more common in normal secretions. 3–12 months for patients on chronic r and discharge Bacterial culture and sensitivity—normal corticosteroid or cyclosporine therapy. CAUSES & RISK FACTORS secretions may contain Proteus mirabilis, r Predisposing factors—soft feces or diarrhea Streptococcus spp., Escherichia coli, Bacillus spp., leading to retention of secretions within anal Clostridium perfringens,andPseudomonas sacs due to lack of expression; excessive aeruginosa. MISCELLANEOUS glandular secretions; dermatologic disorders SEE ALSO that alter the characteristics (cellularity and r Adenocarcinoma, Anal Sac organism colonization) of anal sac secretions. r r Perianal Fistula Retained secretions may lead to infection TREATMENT and abscess formation. r r Suggested Reading Other predisposing factors: Gentle manual expression of contents for Muse R. Diseases of the anal sac. In: ◦ impaction and sacculitis. Obesity r Bonagura JD, Twedt DC, eds., Kirk’s ◦ Infection – hypersensitivity and/or Sedation may be necessary to flush severely Current Veterinary Therapy, 14th ed. St. impacted or painful anal sacs. endocrinopathy. r Louis, MO: Saunders, 2009, pp. 465–468. Infusion of antibiotic and/or corticosteroid Zoran DL. Rectoanal disease. In: Ettinger SJ, medications directly into the anal sacs. r ed., Textbook of Veterinary Internal Drainage of abscesses. r Medicine, 6th ed. Philadelphia: Saunders, DIAGNOSIS Use of appropriate oral antibiotics and/or 2005, pp. 1408–1420. antiyeast medication. r Author Alexander H. Werner DIFFERENTIAL DIAGNOSIS Anal sac excision with chronic disease. r r Consulting Editor Alexander H. Werner Adverse food reaction or food Surgical excision and staging of anal sac hypersensitivity neoplasia; combine with chemotherapy. r Flea bite hypersensitivity JWST589-A53-44 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:4 279mm×216mm

Canine and Feline, Sixth Edition 75 Anaphylaxis A

Breed Predilections OTHER LABORATORY TESTS r r Dogs—numerous breeds documented as Intradermal skin testing to identify having a predilection for developing atopy. allergens. BASICS r r Cats—no breeds documented as having Radioallergosorbent test to quantify the DEFINITION predilection for atopy. concentration of serum IgE specific for a r Acute manifestation of a Type I Mean Age and Range particular antigen. r hypersensitivity reaction mediated through Dogs—age of clinical onset ranges from IMAGING the rapid introduction of an antigen into a 3 months to several years of age; most affected N/A host having antigen-specific antibodies of the animals 1–3 years old. r DIAGNOSTIC PROCEDURES IgE subclass. Cats—age of clinical onset ranges from r Limited because a severely allergic animal can The binding of antigen to mast cells 6 months to 2 years. develop an anaphylactic reaction when sensitized with IgE results in the release of Predominant Sex r exposed to even small quantities of antigen. preformed and newly synthesized chemical Dogs—atopy more common in females. mediators. r PATHOLOGIC FINDINGS r Cats—no reported sex predilection. r Anaphylactic reactions may be localized Lesions vary, depending on severity of (atopy) or systemic (anaphylactic shock). SIGNS reaction, from localized cutaneous edema to r Anaphylaxis not mediated by IgE is General Comments severe pulmonary edema (in cats) and visceral r designated an anaphylactoid reaction and will Initial clinical signs vary depending on the pooling of blood (in dogs). r not be discussed. route of exposure to the inciting antigen Other non-specific findings vary and are PATHOPHYSIOLOGY (allergen). characteristic of shock. r r r First exposure of the patient to a particular Shock—end result of a severe anaphylactic Non-specific characteristics of localized reaction. reactions include edema, vasculitis, and antigen (allergen) causes a humoral response r and results in production of IgE, which binds Shock organ—dogs, liver; cats, respiratory thromboembolism. and gastrointestinal systems. to the surface of mast cells; the patient is then r considered to be sensitized to that antigen. May be localized to the site of exposure but r Second exposure to the antigen results in may progress to a systemic reaction. Historical Findings TREATMENT cross-linking of two or more IgE molecules on r the cell surface, resulting in mast cell Onset of signs immediate (usually within APPROPRIATE HEALTH CARE degranulation and activation; release of mast minutes). r In an acutely affected animal, the reaction is cell granules initiates an anaphylactic reaction. Dogs—pruritus, urticaria, vomiting, r defecation, and urination. considered a medical emergency requiring Major mast cell-derived mediators include r histamine, eosinophilic chemotactic factor, Cats—intense pruritus about the head, hospitalization. arachidonic acid, metabolites (e.g., dyspnea, salivation, and vomiting. NURSING CARE prostaglandins, leukotrienes, and Physical Examination Findings Elimination of inciting antigen, if possible. r thromboxanes), platelet-activating factor, and Localized cutaneous edema at the site of Systemic Anaphylaxis r proteases, which cause an inflammatory exposure. Goal—emergency life support through the r response of increased vascular permeability, Hepatomegaly in some dogs. maintenance of an open airway, preventing r smooth muscle contraction, inflammatory cell Hyperexcitability possible in early stages. circulatory collapse, and reestablishing r influx, and tissue damage. Depression and collapse terminally. physiologic parameters. r r Clinical manifestations depend on the route CAUSES Administer fluids intravenously at shock of antigen exposure, the dose of antigen, and dosages to counteract hypotension. the level of the IgE response. Virtually any agent; those commonly reported include venoms, blood-based products, Localized Anaphylaxis SYSTEMS AFFECTED r vaccines, foods, and drugs. Goal—limit the reaction and prevent Gastrointestinal—salivation, vomiting, and RISK FACTORS progression to a systemic reaction. diarrhea r ACTIVITY Hepatobiliary (dogs)—because of portal Previous exposure (sensitization) increases the hypertension and vasoconstriction chance of the animal developing a reaction. N/A r Respiratory (cats)—dyspnea and cyanosis DIET r Skin/Exocrine—pruritus, urticaria, and If a food-based allergen is suspected edema (uncommon), avoid foods associated with GENETICS DIAGNOSIS hypersensitivity reaction. Familial basis reported for Type I DIFFERENTIAL DIAGNOSIS CLIENT EDUCATION r r hypersensitivity reaction in dogs. Other types of shock. Discuss the unpredictable nature of the r disease. INCIDENCE/PREVALENCE Trauma. r r r Localized Type I hypersensitivity reactions Depends on the major organ system Discuss the need to recognize that the not uncommon. involved or if reaction is localized; diagnosis animal has an allergic condition that may r Systemic Type I hypersensitivity reactions canbemadelargelyonthebasisofhistory require immediate medical care. rare. and clinical signs. SURGICAL CONSIDERATIONS GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS None None Because of the acute onset of disease, no tests SIGNALMENT available that reliably predict individual susceptibility. Species Dog and cat JWST589-A53-44 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:4 279mm×216mm

76 Blackwell’s Five-Minute Veterinary Consult

A Anaphylaxis (Continued)

POSSIBLE INTERACTIONS AGE-RELATED FACTORS N/A None MEDICATIONS ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL N/A None DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING Systemic Anaphylaxis r N/A Epinephrine hydrochloride parenterally (1:1,000; 0.01 mL/kg) for shock. SEE ALSO r FOLLOW-UP Corticosteroids for shock—prednisolone Shock, Cardiogenic sodium succinate (2 mg/kg IV q8h) or PATIENT MONITORING INTERNET RESOURCES dexamethasone sodium phosphate Closely monitor hospitalized patients for Merck Veterinary Manual: (0.25 mg/kg IV q12h). 24–48 hours. r www.merckvetmanual.com. Atropine sulfate (0.04 mg/kg IM) to PREVENTION/AVOIDANCE counteract bradycardia and hypotension. Suggested Reading r If inciting antigen (allergen) can be identified, Shmuel DL, Cortes Y. Anaphylaxis in dogs Aminophylline (10 mg/kg IM or slowly IV) eliminate or reduce exposure. in severely dyspneic patients. and cats. J Vet Emerg Crit Care (San POSSIBLE COMPLICATIONS Antonio) 2013, 23(4):377–394. Localized Anaphylaxis r None Author Paul W. Snyder Diphenhydramine hydrochloride Consulting Editor Alan H. Rebar (1–2 mg/kg IV or IM). EXPECTED COURSE AND PROGNOSIS r r Prednisolone (2 mg/kg PO). If localized reaction is treated early, r prognosis is good. Epinephrine hydrochloride (0.15 mL SC at r Client Education Handout site of initiation). If the animal is in shock on examination, r available online If shock develops, initiate treatment for a prognosis is guarded to poor. systemic anaphylaxis. CONTRAINDICATIONS None PRECAUTIONS MISCELLANEOUS Localized reaction can develop into systemic ASSOCIATED CONDITIONS reaction. None JWST589-A54-45 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:7 279mm×216mm

Canine and Feline, Sixth Edition 77 Anemia of Chronic Kidney Disease A

r CBC/BIOCHEMISTRY/URINALYSIS Target PCV is 25–30%. r r Normocytic, normochromic, May be given intermittently for prolonged BASICS hypoproliferative anemia (progressive; anemia management, although compatibility issues maybemaskedbydehydration). are likely to occur long term. r r DEFINITION Reticulocytes—low corrected indices and EPO support for progressive or absolute counts (≤ 10,000/𝜇L). symptomatic anemia (dogs, PCV ≤ 25%; Progressive decreases in PCV, RBC count, r and hemoglobin and hypoplasia of erythroid Moderate to advanced CKD—elevated cats, PCV ≤ 23%). elements of the bone marrow are predictable BUN, creatinine, and phosphorus; variably Erythropoietin Replacement r features of progressive CKD. Anemia is high calcium; variably low bicarbonate and Epoetin alfa (r-HuEPO)—original synthetic potassium. normocytic, normochromic, nonregenerative, r erythropoiesis stimulating protein, replica of and proportional to the stage of CKD. The High BUN:creatinine ratio may predict human erythropoietin (Epogen and Procrit); concurrent” gastrointestinal blood loss. underlying cause of the anemia of CKD is r provides consistent, rapid, and long-term multifactorial. Although factors such as Impaired urine-concentrating ability, correction of anemia in dogs and cats with gastrointestinal blood loss, reduced red blood possible proteinuria, and variably active CKD; potential for anti-r-HuEPO antibody cell survival, deficiencies in iron and/or folate, sediment. production and pure red cell aplasia. r cytokines and inflammatory mediators may OTHER LABORATORY TESTS Darbepoetin alfa (Aranesp), a new r be involved, the primary contributing factor Serum iron—normal or variably low. hyperglycolylated analogue of r-HuEPO with r to anemia of CKD is an inadequate Transferrin saturation—normal or variably prolonged half-life and sustained effects; very production of erythropoietin (EPO) by the low (< 20%). effective with significantly less tendency for r kidneys. Erythropoietin is a glycoprotein FeLV and FIV and/or haemobartonella antibody induction; should be used hormone that regulates red blood cell preferentially to epoetin alfa. testing (cats) or rickettsial titers or PCR (dogs) r generation at the level of the bone marrow. to exclude agent-induced myelodyscrasia. Target PCV—dogs, 30–35%; cats, 30%. r r Erythropoietin is produced in the peritubular Serum erythropoietin—normal Initial dosage: darbepoetin alfa—0.5– interstitial cells of the kidney in response to (inappropriately) or low. 2.0 𝜇g/kg SC/IV once weekly until PCV decrease in tissue oxygen. IMAGING reaches low end of target, then decrease to SIGNALMENT r q2–4 weeks as needed to maintain target. Small, irregular kidneys with loss or Recommend PCV prior to EVERY injection Middle-aged to old dogs and cats mostly disruption of renal architecture detected by to avoid overtreatment. affected; seen in young animals with heritable, radiography or ultrasonography. r r Epoetin alfa—50–100 U/kg SC thrice congenital, or acquired CKD. Enlarged, polycystic, hydronephrotic, weekly until low end of target, then decrease SIGNS infiltrative. to once to twice weekly. r r Anemia contributes to development of DIAGNOSTIC PROCEDURES If converting from epoetin alfa to anorexia, weight loss, fatigue, lethargy, Cytologic examination of bone marrow— darbepoetin—divide weekly units by 400 to depression, weakness, apathy, cold erythroid hypoplasia; myeloid:erythroid ratio establish 𝜇g to give once weekly. r intolerance, and behavior and personality normal or high; stainable iron normal or Individualize to each patient; life-long changes characterizing CKD. r variably low. treatment required. Pallor of the mucous membranes. r r If PCV exceeds target, discontinue until Tachypnea. r upper target range is achieved, then increase Tachycardia. r dosage interval. Systolic murmur. r r TREATMENT Serum iron and transferrin saturation Syncope and seizures (rare). r should be normalized before initiating and CAUSES & RISK FACTORS Stabilize azotemia in patients in with uremic during treatment. Injectable iron (10 mg/kg r crisis. All inherited, congenital, and acquired r IM) should be administered when indicated Ensure adequate and appropriate nutrition. forms of CKD (e.g., pyelonephritis, r on iron panel. Injectable iron is preferable and Stabilize any metabolic derangement (e.g., better tolerated than oral preparations. glomerulonephritis, amyloidosis, polycystic r kidney disease, and lymphoma). acidosis) that could contribute to shortened Species-specific erythropoietins for dogs and r RBC lifespan and or anorexia. cats are not currently commercially available. Exacerbated by iron deficiency, r r inflammatory or neoplastic disease, Minimize micronutrient deficiencies that Alternative erythropoietin-stimulating could negatively impact rbc production. gastrointestinal blood loss, hemolysis, and r treatments are under development. myeloproliferative disorders. Identify and manage GI blood loss (gastric acid suppression with H2 blockers or proton Anabolic Steroids pump inhibitors) (GI protectants such as Little or no efficacy or indication for use. sucralfate). r Ensure that patient is iron replete (serum DIAGNOSIS iron panel). r DIFFERENTIAL DIAGNOSIS Correct systemic hypertension. FOLLOW-UP r Anemia of chronic infectious, inflammatory, PATIENT MONITORING r or neoplastic disease; myeloproliferative PCV—weekly to semi-monthly for disease; chronic blood loss; aplastic anemia; 3 months, then monthly to bimonthly. r endocrine disease; drug reaction; and chronic MEDICATIONS Blood pressure—semi-monthly to monthly. r immune-mediated, toxic, viral, rickettsial, or DRUG(S) AND FLUIDS Iron and transferrin saturation—at 1, 3, and parasitic anemia; hemodilution. 6 months, then semiannually. r Blood Transfusion r Regenerative anemia excludes diagnosis of r Discontinue erythropoietin if patient Short-term, rapid correction if hypoxic anemia of CKD. develops evidence of erythrocythemia, local or r distress (typically PCV ≤ 15%)—give Generally masked until advanced CKD. systemic sensitivity, anti-r-HuEPO antibody compatible whole blood or packed RBCs. JWST589-A54-45 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:7 279mm×216mm

78 Blackwell’s Five-Minute Veterinary Consult

A Anemia of Chronic Kidney Disease (Continued)

r formation, pure red cell aplasia, or refractory Transfusion-Related FIV = feline immunodeficiency virus r r hypertension. Incompatibility reaction PCR = polymerase chain reaction r r Circulatory or iron overload PCV = packed cell volume POSSIBLE COMPLICATIONS r r Systemic hypertension RBC = red blood cell Erythropoietin-Related r r r Transmissible infection r-HuEPO = recombinant human Development of erythrocythemia, seizures, EXPECTED COURSE AND PROGNOSIS erythropoietin hypertension, iron depletion, injection pain, r and mucocutaneous reactions. Correction of anemia increases appetite, Suggested Reading r Development of a pure red cell aplasia activity, grooming, affection and playfulness, Chalhoub S, Langston C, Eatroff A. Anemia during the course of epoetin alfa treatment weight gain, and cold tolerance, and decreases of Renal Disease: What it is, what to do, sleeping. suggests formation of anti-r-HuEPO r and what’s new. J Feline Med Surg 2011, antibodies, which neutralize r-HuEPO and Use of erythropoietin replacement agents in 13:629–640. native erythropoietin, causing severe anemia dogs and cats requires careful assessment of Cowgill LD, James KM, Lew JK, et al. Use of the risks and benefits for individual patients. in 20–30% of animals; often reversible with r recombinant human erythropoietin for cessation of treatment. Short-term prognosis depends on the management of anemia in dogs and cats r severity of the renal failure. Development of anti-r-HuEPO antibodies r with renal failure. J Am Vet Med Assoc occurs in less than 5% of patients with Long-term prognosis is guarded to poor 1998, 212:521–528. darbepoetin alfa therapy. because of the underlying chronic renal Authors Sheri Ross and Ilaria Lippi r Signs associated with production of failure. Consulting Editor Carl A. Osborne anti-r-HuEPO antibodies while the patient is Acknowledgment The author and editors receiving epoetin alfa include decreasing PCV, acknowledge the prior contribution of Larry erythroid hypoplasia, absolute reticulocyte D. Cowgill. counts approaching zero, and MISCELLANEOUS myeloid:erythroid ratio ≥ 8. r ABBREVIATIONS Erythropoietin replacements should be used r CKD = chronic kidney disease cautiously or withheld if hypertension or iron r deficiency develop; treatment can be FeLV = feline leukemia virus reinstituted once hypertension and iron deficiency are corrected. JWST589-A55-46 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:17 279mm×216mm

Canine and Feline, Sixth Edition 79 Anemia, Aplastic A

r Thiacetarsamide OTHER DRUGS r r Ionizing radiation Antibiotics to treat secondary infections if r Mycotoxins (cats) fever and neutropenia present. BASICS r Whole or component blood transfusion if OVERVIEW indicated. r A disorder of hematopoietic precursor cells characterized by replacement of normal bone DIAGNOSIS marrow with adipose tissue. There is decreased DIFFERENTIAL DIAGNOSIS production of granulocytes, erythrocytes, and FOLLOW-UP platelets, resulting in pancytopenia in the Causes of pancytopenia with normal to increased bone marrow cellularity (e.g., PATIENT MONITORING peripheral blood. The disease is sometimes r myelodysplastic disorders, leukemia, Daily physical examination. also referred to as aplastic pancytopenia. r r myelofibrosis). CBC every 3–5 days to weekly. In the acute form, neutropenia and r thrombocytopenia predominate because of CBC/BIOCHEMISTRY/URINALYSIS Repeat bone marrow evaluation if necessary. r the shorter life spans of these cells; in the Leukopenia characterized by neutropenia PREVENTION/AVOIDANCE r chronic form, nonregenerative anemia also with or without lymphopenia. Castration of cryptorchid males. r r occurs. In both forms, the bone marrow Normocytic, normochromic, Vaccination for infectious diseases. r exhibits variable degrees of panhypoplasia. nonregenerative anemia. Frequent monitoring of CBC in cancer r r There are many precipitating causes of Thrombocytopenia. patients receiving chemotherapy or radiation. deficient hematopoiesis, including infectious OTHER LABORATORY TESTS POSSIBLE COMPLICATIONS diseases, drug administration, starvation and r r Immunologic tests for infectious diseases Sepsis toxin exposure; immune-mediated r (e.g., serologic titers, ELISA, IFA). Hemorrhage mechanisms are often suspected. r r PCR for infectious agents. r EXPECTED COURSE AND PROGNOSIS Hemic/lymphatic/immune systems affected. r Serologic test for antierythrocyte antibodies Guarded to poor. SIGNALMENT (Coombs’ test). r Dogs and cats, no apparent breed or sex Recovery of hematopoiesis may take weeks IMAGING to months, if it occurs at all. predilection. In one study, the mean age of r Spontaneous recovery occasionally occurs, nine affected dogs was 3 years. N/A DIAGNOSTIC PROCEDURES especially in younger animals. SIGNS r r Acute form: fever, petechial hemorrhages, Bone marrow aspiration—frequently an epistaxis, hematuria, melena; i.e., signs due to inadequate or fatty sample is obtained because neutropenia and thrombocytopenia. of decreased hematopoietic tissue and r replacement by adipocytes. MISCELLANEOUS Chronic form: pale mucous membranes, r weakness, lethargy; i.e., signs due to anemia, Bone marrow core biopsy—permits an SEE ALSO evaluation of architecture and reveals in addition to signs observed in acute forms. Pancytopenia hypoplasia of cell lines and replacement by CAUSES & RISK FACTORS ABBREVIATIONS adipose tissue. r Often not identified ELISA = enzyme-linked immunosorbent assay Infectious Agents r r FeLV = feline leukemia virus FeLV, FIV r r FIV = feline immunodeficiency virus Canine and feline parvovirus TREATMENT r r IFA = immunofluorescent antibody (test) Rickettsial organisms (e.g., Ehrlichia spp.) r Supportive treatment, antibiotics, blood NSAID = nonsteroidal anti-inflammatory Drugs and Chemicals r component therapy, as dictated by clinical drug Estrogen (exogenous administration, Sertoli r condition. PCR = polymerase chain reaction and interstitial cell tumors) r r rhG-CSF = recombinant human Methimazole (cats) r granulocyte colony-stimulating factor Chemotherapeutic drugs, including azathioprine, cyclophosphamide, cytosine Suggested Reading arabinoside, doxorubicin, vinblastine, and MEDICATIONS Brazzell JL, Weiss DJ. A retrospective study of hydroxyurea DRUG(S) OF CHOICE aplastic pancytopenia in the dog: 9 cases r r Antibiotics, including Cyclosporine A—10–25 mg/kg PO q12h (1996–2003). Vet Clin Path 2006, trimethoprim-sulfadiazine, cephalosporins, (dogs), 4–5 mg/kg PO q12h (cats). 35:413–417. and chloramphenicol r Weiss DJ. Aplastic anemia. In: Weiss DJ, r Recombinant hematopoietic growth factors Griseofulvin (e.g., rhG-CSF: 5 𝜇g/kg/day SC). Wardrop KJ, eds., Schalm’s Veterinary r r NSAIDs, including phenylbutazone and Androgen and corticosteroid administration Hematology, 6th ed. Ames, IA: Blackwell meclofenamic acid Publishing Ltd., 2010, pp. 256–260. r have been largely unsuccessful. Fenbendazole, albendazole Author R. Darren Wood r CONTRAINDICATIONS/POSSIBLE Captopril Consulting Editor Alan H. Rebar r Quinidine INTERACTIONS N/A JWST589-A56-47 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:10 279mm×216mm

80 Blackwell’s Five-Minute Veterinary Consult A Anemia, Heinz Body

or surgery to remove metallic items in gastrointestinal tract. BASICS DIAGNOSIS OVERVIEW DIFFERENTIAL DIAGNOSIS r r Heinz bodies cause hemolytic anemia and Other causes of regenerative, hemolytic r MEDICATIONS indicate oxidative damage to RBCs. Heinz anemia (e.g., immune mediated, r DRUG(S) OF CHOICE bodies form when oxidants overwhelm hemoparasites). Heinz bodies may be found protective reductive pathways in RBCs; in healthy or ill cats without anemia. Acetaminophen toxicity in cats—N- irreversible denaturation of the globin chains Diagnosis of a Heinz body anemia requires acetylcysteine (140 mg/kg PO or IV, followed in hemoglobin causes precipitation and documentation of a regenerative anemia, by seven additional treatments of 70 mg/kg attachment of altered hemoglobin to the cell supporting evidence of a hemolytic process q8h). r membrane. RBCs with Heinz bodies are (e.g. hyperbilirubinemia), identification of CONTRAINDICATIONS/POSSIBLE targeted for removal by macrophages in the Heinz bodies on a blood smear, and INTERACTIONS spleen, and occasionally undergo intravascular elimination of other causes of hemolysis or r Administration of methylene blue to treat lysis. The pitting function of the spleen may blood loss. methemoglobinemia may exacerbate Heinz remove Heinz bodies, resulting in r CBC/BIOCHEMISTRY/URINALYSIS body formation. spherocytes. Heinz bodies are usually caused r Regenerative anemia (decreased HCT, ALTERNATIVE DRUG(S) by exposure to chemical or dietary oxidants. r polychromasia, nucleated RBCs) is expected if Cats are particularly susceptible to Heinz The use of dietary antioxidants (e.g., there has been sufficient time for a bone bioflavonoids) is controversial but may help body formation because their hemoglobin marrow response; the severity of anemia contains more sulfhydryl groups than that of prevent further formation of Heinz bodies. r depends on dose of oxidant and duration of r dogs. Healthy cats may have Heinz bodies exposure. Hemoglobin concentration and with no anemia, possibly because cats have a MCHC may be falsely increased due to Heinz nonsinusoidal spleen with limited pitting r body interference with hemoglobin r function. Heinz bodies are reported in measurement. Heinz bodies are visible on a FOLLOW-UP hyperthyroidism (cats), lymphoma (cats, routinely stained blood smear as small, pale PATIENT MONITORING dogs), and diabetes mellitus (cats, dogs), red, round inclusions that may protrude from Serial CBCs and review of blood smears are possibly due to increased endogenous oxidants RBC surface. They may be difficult to identify (e.g., 𝛽-hydroxybutyrate in ketoacidosis). r recommended to assess RBC regeneration and r if there is marked poikilocytosis. Single, disappearance of Heinz bodies. Anemia may or may not be present. Heinz small (< 0.5 𝜇m) Heinz bodies may be found r PREVENTION/AVOIDANCE bodies may be accompanied by in RBCs of cats without anemia. Large methemoglobinemia (hemoglobin containing Counsel clients about preventing exposure to 3+ and/or multiple Heinz bodies in an anemic Fe ) and/or eccentrocytes (oxidative damage cat suggest a Heinz body hemolytic anemia. oxidants. r to RBC membranes causing adhesion of Dogs may have concurrent eccentrocytosis POSSIBLE COMPLICATIONS opposing membranes and displacement of r on a blood smear. Hyperbilirubinemia and N/A hemoglobin to one side of the cell). r bilirubinuria are possible. Hemoglobinemia EXPECTED COURSE AND PROGNOSIS SIGNALMENT and hemoglobinuria are uncommon but r r Prognosis is good with removal of oxidant and Dogs and cats No sex, breed, or age occur with severe intravascular hemolysis. r supportive care once the hemolytic crisis is disposition Neutrophilia and monocytosis may occur. over. SIGNS OTHER LABORATORY TESTS r Historical Findings New methylene blue stains Heinz bodies r r Exposure to oxidant. Sudden onset of blue, making them easy to identify and quantify on a blood smear, even with marked weakness, lethargy, or anorexia. r MISCELLANEOUS r poikilocytosis. Measure methemoglobin if Reddish-brown urine (hemoglobinuria) if r r blood is dark or chocolate colored. Serum SEE ALSO severe intravascular hemolysis. Signs related r zinc concentration if indicated. Acetaminophen (APAP) Toxicosis to underlying disease in animals with systemic r Anemia, Regenerative disease and Heinz bodies. IMAGING r r Physical Examination Findings Abdominal radiographs may reveal Methemoglobinemia Zinc Toxicosis r Pale and occasionally icteric mucous gastrointestinal metal objects in zinc toxicity. ABBREVIATIONS r r r membranes Dark or chocolate-colored HCT = hematocrit MCHC = mean r corpuscular hemoglobin concentration blood with methemoglobinemia Tachypnea, r tachycardia RBC = red blood cell CAUSES & RISK FACTORS TREATMENT Suggested Reading r r Dietary: onions (raw, cooked, dehydrated, Immediate identification and removal of Andrews D. Disorders of red blood cells. In: and powdered), garlic (dogs), propylene glycol Handbook of Small Animal Practice, 5th r oxidant may be sufficient, though it often (cats), Chinese chives (dog). Drugs: take several days after exposure for the severity ed. St. Louis: Saunders, 2008, pp. 632–635. r acetaminophen, phenacetin (cats), of anemia to reach nadir. Consider Desnoyers M. Anemias associated with phenazopyridine (cats), methylene blue, administration of emetics with recent oxidative injury. In: Schalm’s Veterinary r vitamin K1 or K3 (dogs), DL-methionine ingestion of an oxidant. Supportive care Hematology, 6th ed. Ames, IA: Blackwell, (cats), benzocaine (topical), phenylhydrazine 2010, pp. 239–245. r depends on the severity of the hemolytic crisis (dog), propofol (cats). Miscellaneous: zinc and includes IV fluids, RBC transfusions, Author Jennifer S. Thomas r (nuts, bolts, pennies, dermatologic creams), oxygen, and restricted activity. Endoscopy Consulting Editor Alan H. Rebar naphthalene (moth ball ingestion in dogs), skunk musk exposure (dogs). JWST589-A57-48 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:13 279mm×216mm

Canine and Feline, Sixth Edition 81 Anemia, Immune-Mediated A

r r Mean Age and Range Congenital feline porphyria Increased r Dogs,meanage5–6years(range osmotic fragility (Abyssinian, Somali) r 1–13 years) Cats, mean age 2 years (range CBC/BIOCHEMISTRY/URINALYSIS BASICS r 0.5–9 years) CBC—anemia, high MCV (3–5 days DEFINITION Predominant Sex r r post-hemolytic episode), spherocytes, Accelerated destruction or removal of RBCs Female dogs at higher risk Male cats polychromasia, increased RBC distribution due to a Type II hypersensitivity reaction. overrepresented width, leukocytosis with neutrophilia and left PATHOPHYSIOLOGY SIGNS shift, monocytosis, lymphocytosis (cats). r Anemia is nonregenerative in 30% of dogs Antibodies form against endogenous Historical Findings r r r and 50% of cats. Serum biochemistry— unaltered RBC surface antigens (primary Lethargy/weakness/collapse Anorexia r hyperbilirubinemia, hemoglobinemia, high IMHA) or altered RBC membrane antigens Exercise intolerance/dyspnea, tachypnea r r r r ALT. Urinalysis—hemoglobinuria, (secondary IMHA). Infectious organisms, Vomiting and/or diarrhea Dark red urine r bilirubinuria. drugs, exposure of previously unexposed Pica (cats) antigens, or adsorption of preformed OTHER LABORATORY TESTS Physical Examination Findings r antigen-antibody complexes to the RBC r Spontaneous saline agglutination test— Pale mucous membranes, tachycardia, r membrane can alter RBC membrane r r tachypnea. Splenomegaly/hepatomegaly. before and after washing RBCs. Positive antigens. Immunoglobulin deposits on RBC r Icterus and pigmenturia (hemoglobin or direct antiglobulin test (Coombs’ test)— membrane, causing either direct intravascular r positive in up to 75% of animals with IMHA. bilirubin). Fever/lymphadenomegaly. r hemolysis or accelerated removal by the r r r Systolic murmur. Petechiae, ecchymoses, Flow cytometric detection of membrane- monocyte/macrophage system. Intravascular bound immunoglobulin and complement. or melena (if concurrent thrombocytopenia or r hemolysis occurs when adsorbed antibodies r r DIC). Other findings possible (e.g., joint Reticulocytosis—absolute count (usually IgG) activate complement. In vivo > 60,000/𝜇L(dogs)or> 50,000/𝜇L(cats)in pain) when IMHA is component of SLE. r agglutination of RBCs occurs when IgM or r regenerative IMHA. Thrombocytopenia high titers of IgG molecules cause bridging of Necrosis of extremities and ear tips in r r cold-type IMHA (rare). 60% of dogs. Prolonged APTT and PT, RBCs. Extravascular removal of RBCs increased fibrin degradation products and occurs primarily in spleen, liver, bone marrow. CAUSES AND RISK FACTORS d-dimer, decreased antithrombin in animals r r Nonregenerative IMHA is believed to be Primary IMHA with DIC. Positive ANA titer and LE cell caused by immune-mediated destruction of r r Poorly characterized immune dysregulation test (animals with SLE). Positive serologic RBC precursors in the bone marrow. Rarely Secondary IMHA titers or PCR in secondary IMHA due to cold-acting antibodies cause in vivo hemolysis r r Infectious causes: hemotrophic Mycoplasma infectious causes. Evidence of hematologic and erythrocyte agglutination in peripheral spp., Ehrlichia spp., Anaplasma parasites in blood smears (secondary IMHA vasculature. phagocytophilum, Anaplasma platys, Babesia due to infectious causes). SYSTEMS AFFECTED IMAGING r spp., Leishmaniasis, Dirofilaria immitis, FeLV, Cardiovascular—tachycardia; low-grade r r r FIP, chronic bacterial infection. Neoplasia: Radiographic findings—hepatomegaly/ heart murmur. Hemic/Lymphatic/ lymphoma, lymphoid leukemia, splenomegaly; thorax usually normal; may see Immune—immune-mediated destruction of hemangiosarcoma, hemophagic histiocytic evidence of PTE (patchy alveolar pattern, RBCs, elaboration of proinflammatory r r sarcoma. Drugs: beta lactam antibiotics, interstitial pattern, pleural fluid), but dogs mediators, DIC. Hepatobiliary— propylthiouracil, methimazole, sulfonamides. with pulmonary embolism may have normal r r r r hyperbilirubinemia and icterus plus SLE Neonatal isoerythrolysis Hemolysis thoracic radiographs. Ultrasonographic bilirubinuria when hepatic function is due to DEA incompatible blood transfusion findings—hepatomegaly/splenomegaly; overwhelmed; centrilobular necrosis. r r Exposure to infectious agents, vaccination, liver/spleen can be mottled and hyperechoic Respiratory—tachypnea. PTE may result r chemicals/drugs, surgery, hormonal change, or hypoechoic. from hypercoagulable state. Skin—rarely or other stressful event is hypothesized as DIAGNOSTIC PROCEDURES cold-type IMHA may cause necrosis of r potential trigger for IMHA. Bone marrow aspirate usually reveals extremities and ear tips. r erythroid hyperplasia. With nonregenerative GENETICS IMHA, maturation arrest or erythroid r Cocker spaniels are at increased risk (absence hypoplasia may be evident. In chronic of dog erythrocyte antigen 7). DIAGNOSIS IMHA, myelofibrosis may be present. GEOGRAPHIC DISTRIBUTION DIFFERENTIAL DIAGNOSIS PATHOLOGIC FINDINGS r Secondary IMHA may have higher prevalence Hepatosplenomegaly, centrilobular hepatic Dogs r where associated infectious diseases are r necrosis Splenic and hepatic extramedullary Pyruvate kinase deficiency r endemic. r r hematopoiesis Reactive lymphadenomegaly Phosphofructokinase deficiency Toxicity r SIGNALMENT (zinc, onions, garlic, broccoli, copper, PTE and DIC r Species naphthalene, skunk musk) Snake/spider evenomation (coral snakes, recluse spiders) Dog and cat r r Breed Predilections Severe hypophosphatemia Anemia due to r TREATMENT Cocker spaniel at highest risk. Also, English hemorrhage (immune-mediated thrombocytopenia, rodenticide toxicosis) springer spaniel, Old English sheepdog, r APPROPRIATE HEALTH CARE Doberman pinscher, collie, bichon frise, Microangiopathic anemia due to splenic r neoplasia, DIC, splenic torsion Inpatient during acute hemolytic crisis; miniature pinscher, and Finnish spitz. outpatient when PCV stabilized, ongoing r Cats Domestic shorthair cats. r hemolysis controlled, and clinical signs of Toxicity (acetaminophen zinc, onions, r r anemia resolved. Inpatient if complications garlic) Severe hypophosphatemia such as DIC, PTE, thrombocytopenia, gastrointestinal bleeding, or a need for JWST589-A57-48 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:13 279mm×216mm

82 Blackwell’s Five-Minute Veterinary Consult

A Anemia, Immune-Mediated (Continued)

r r multiple transfusions. Chronic low-grade CONTRAINDICATIONS Centrilobular hepatic necrosis and renal r extravascular hemolysis can be treated on No heparin, enoxaparin, or aspirin in dogs tubular necrosis secondary to hypoxia. r outpatient basis if the patient not exhibiting with severe thrombocytopenia (< 80,000/𝜇L). Infection secondary to immunosuppressive r r clinical signs secondary to anemia. Do not use multiple cytotoxic drugs therapy. GI ulceration due to high-dose r NURSING CARE concurrently. glucocorticoids. Iatrogenic r Fluid therapy to maintain vascular volume PRECAUTIONS hyperadrenocorticism. r r and correct dehydration. Packed RBCs No azathioprine in cats because of risk of EXPECTED COURSE AND PROGNOSIS r r typed or cross-matched for naive recipient. bone marrow toxicity. Prednisone/ Mortality: 30–80% (dog), 25% (cat). r Blood should be cross-matched for recipients prednisolone can cause signs of Cushing’s Causes of death include thromboembolism, that have received prior transfusions. Whole syndrome and may increase risk of PTE, infection due to immunosuppression, DIC, r blood acceptable if packed RBCs not pancreatitis, diabetes mellitus, secondary persistent anemia. Hyperbilirubinemia r available. Transfusion volume = recipient infection, gastric ulcers (consider gastric > 5 mg/dL, autoagglutination, intravascular r weight (kg) × 85 (dog) or 50 (cat) × desired protectants). Cytotoxic drugs can cause hemolysis, severe thrombocytopenia, r PCV-current PCV/donor PCV. Transfusion bone marrow suppression, secondary hypoalbuminemia are associated with poorer r rate 0.25 mL/kg/hr for first 30 minutes then infection, pancreatitis (azathioprine), GI prognosis. Response to treatment may take r 5–10 mL/kg/h. Monitoring for upset (cyclosporine, azathioprine, weeks to months; nonregenerative IMHA complications such as PTE, bleeding mycophenolate mofetil), gingival hyperplasia, may have more gradual onset than typical r (especially GI), DIC, infection. Cage rest. papillomatosis (cyclosporine), infertility. IMHA and may be slower to respond to r CLIENT EDUCATION POSSIBLE INTERACTIONS treatment. IMHA may recur despite r IMHA and complications (e.g., DIC, PTE) Azathioprine and prednisone have been previous/current therapy. r can be fatal. Life-long treatment may be associated with development of pancreatitis. r needed; disease may recur. Side effects of ALTERNATIVE DRUG(S) treatment may be severe. r Dexamethasone (0.25–0.5 mg/kg/day MISCELLANEOUS SURGICAL CONSIDERATIONS IV)—can be used instead of prednisone/ r Splenectomy can be considered if medical prednisolone in animals that do not tolerate SYNONYMS management fails to control disease. oral drugs, until oral intake is possible. r r r Autoimmune hemolytic anemia Consider blood product administration Chlorambucil—for cats, 0.1–0.2 mg/kg PO r r Immune-mediated anemia preoperatively. q24h initially, then q48h. Cyclosporine— SEE ALSO microemulsion, e.g., Atopica—dogs, r r Anemia, Regenerative Chapters on causes 5–10 mg/kg/day PO divided twice daily; cats, r r of secondary IMHA Cold Agglutinin 0.5–3 mg/kg q12h. Mycophenolate mofetil r Disease Disseminated Intravascular 10–17 mg/kg q24h. MEDICATIONS Coagulation DRUG(S) OF CHOICE ABBREVIATIONS r r r Corticosteroids—prednisone ALT = alanine aminotransferase ANA = r 1–2 mg/kg/day q12h for 2–4 weeks. Use antinuclear antibody APTT = activated FOLLOW-UP r prednisolone in cats due to higher partial thromboplastin time DEA = dog r r bioavailability. Once PCV above 30%, PATIENT MONITORING erythrocyte antigen DIC = disseminated r r decrease dose to 1 mg/kg q12h. Then taper by Monitor heart rate, respiratory rate, intravascular coagulation FeLV = feline r r a maximum rate of 25–50% per month over a temperature frequently. Monitor for adverse leukemia virus FIV = feline 3- to 6-month period, depending upon PCV reactions to treatment (e.g., transfusion immunodeficiency virus IMHA = immune- r r and severity of side effects. If after reactions/overhydration). If PTE suspected, mediated hemolytic anemia LE = lupus r 3–6 months disease is in remission on a low monitor thoracic radiographs and arterial erythematosus MCV = mean cell volume r r r r q48h dose, try discontinuing the drug. Add blood gases frequently. During first days of PCR = polymerase chain reaction PCV = r additional immunosuppressive drug such as treatment, check PCV daily until stable, then packed cell volume PTE = pulmonary r azathioprine (dogs) cyclosporine (cats) if poor every 1-2 weeks for 2 months; if still stable, thromboembolism PT = prothrombin time r r response to prednisone after 5–7 days or if recheck PCV monthly for 6 months, then RBC = red blood cell SLE = systemic poor prognostic indicators (e.g., intravascular 2–4 times per year; rechecks need to be more lupus erythematosus hemolysis, serum bilirubin > 8–10 mg/dL, frequent if patient is on long-term medication r Suggested Reading persistent autoagglutination, Evans especially cytotoxic drugs. CBC and r Kohn B, Weingart C, Eckmann V, et al. syndrome). Azathioprine dose 2 mg/kg/day, reticulocyte count should be rechecked at Primary immune-mediated hemolytic can decrease to 0.5–1.0 mg/kg q48h if bone least monthly during treatment,; if the anemia in 19 cats: Diagnosis, therapy, and marrow suppression. Monitor for immuno- neutrophil count falls < 3,000 cells/𝜇L, outcome (1998–2004). J Vet Intern Med suppression, hepatotoxicosis, pancreatitis. discontinue cytotoxic drugs until count r 2006, 20:159–166. For prevention of thromboembolism (dogs) recovers; reinstitute at lower dosage. r Piek CJ. Canine idiopathic immune-mediated consider unfractionated heparin 300 U/kg SC Coombs’ tests and reticulocyte counts to haemolytic anaemia: A review with q6–8h (dose adjusted based on APTT assist in drug tapering. recommendations for further research. Vet prolongation or measurement of anti-Xa PREVENTION/AVOIDANCE Quart 2011, 31:129–141. activity) or ultra-low-dose aspirin Consider need for vaccination on case-by-case Author J. Catharine R. Scott-Moncrieff 0.5–1.0 mg/kg/day or enoxaparin (low- basis in dogs that developed IMHA after Consulting Editor Alan H. Rebar molecular-weight heparin) 0.8 mg/kg SC q6h vaccination. or 1.5 mg/kg q12h, or clopidogrel 2–3 mg/kg POSSIBLE COMPLICATIONS PO q24h (loading dose 10 mg/kg/day). r Client Education Handout r Pulmonary/multiorgan thromboembolism Address underlying cause (e.g., infection r available online and drugs) if secondary IMHA. (up to 80% of all cases at necropsy). DIC. JWST589-A58-49 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:15 279mm×216mm

Canine and Feline, Sixth Edition 83 Anemia, Iron-Deficiency A

from functional iron deficiency. Clinical Oral Iron Supplements r findings of inflammatory disease versus blood Ferrous sulfate powder—place in food or loss are required to differentiate cause of iron drinking water (100–300 mg PO q24h). BASICS r limited erythropoiesis. It is also possible that Ferrous gluconate—one (325 mg) tablet PO OVERVIEW inflammatory disease and true iron deficiency q24h. r may occur concurrently. Adults—caused by chronic external r CONTRAINDICATIONS/POSSIBLE hemorrhage. RBC morphologic changes—hypochromia r INTERACTIONS RBC produced by iron-limited (increased central pallor), oxidative lesions (e.g., keratocytes), fragmentation. Oral iron is associated with unexplained death erythropoiesis. r r Decreased MCHC not sensitive or specific. in kittens and should be avoided. Importance—prompts clinician to look for r Thrombocytosis may occur. chronic external blood loss. r SIGNALMENT Hypoproteinemia—consistent with blood r loss. Fairly common in adult dogs. r FOLLOW-UP Rare in adult cats. OTHER LABORATORY TESTS r r r Transient neonatal iron-deficiency anemia Hypoferremia (serum iron < 70 𝜇g/dL) and Monitor CBC every 1–4 weeks; if the < anemia is severe, more frequently as needed. may occur at 5–10 weeks of age in kittens. transferrin saturation 15% support the r SIGNS diagnosis. Effective treatment associated with an r increase in MCV and reticulocyte volume. r Serum iron values may be normal during r Signs of anemia (e.g., lethargy, weakness, iron repletion, if blood loss is intermittent. Erythrocyte histogram—effective treatment and tachypnea) and underlying disease. r r Fecal exam for hookworms. associated with microcytic subpopulation r Intermittent melena with gastrointestinal Fecal examination for occult blood or reduction over time; it may take a few months blood loss. r melena. to normalize the histogram. Possible heavy bloodsucking parasite load. IMAGING CAUSES & RISK FACTORS r Imaging studies—GI disease that may Chronic external blood loss. r account for blood loss. Common causes—GI lymphoma, MISCELLANEOUS hookworms, GI neoplasia. DIAGNOSTIC PROCEDURES r As indicated by underlying disease. ABBREVIATIONS Less common—skin (e.g., severe flea r CHr = reticulocyte hemoglobin content infestation) and urinary tract. r r GI = gastrointestinal Blood donor overuse. r MCHC = mean cell hemoglobin concentration TREATMENT r MCV = mean cell volume r r Identify / correct cause of blood loss. MCVr = mean reticulocyte volume DIAGNOSIS r r Administer iron until hematologic features PCV = packed cell volume r DIFFERENTIAL DIAGNOSIS of iron deficiency resolve. RBC = red blood cell r r < r Any cause of anemia, especially hemorrhage. If severe (i.e., PCV 15%), transfusion RDW = red cell distribution width r Microcytic anemia in portosystemic shunt may be required; whole blood (10–20 mL/kg IV) or packed RBC. Suggested Reading disease may or may not be due to iron Fry MM, Kirk CA. Reticulocyte indices in a deficiency. r canine model of nutritional iron deficiency. Anemia of inflammatory disease Vet Clin Pathol 2006, 35:172–181. iron-limited erythropoiesis. Radakovich LB, Santangelo KS, Olver CS. CBC/BIOCHEMISTRY/URINALYSIS MEDICATIONS r Reticulocyte hemoglobin content (CHr) PCV usually but not always decreased, DRUG(S) does not differentiate true from functional generally 10–40% in dogs. r Iron Supplementation iron deficiency in dogs. Vet Clin Pathol Anemia either regenerative or Parenteral Iron Supplementation 2015, 44 (in press). r non-regenerative. Initiate iron therapy with injectable iron. Steinberg JD, Olver CS. Hematologic and r r Microcytosis—indicated by low normal or Iron dextran—a slowly released form of biochemical abnormalities indicating iron low MCV, accompanied by increased injectable iron; one injection (10–20 mg/kg deficiency are associated with decreased heterogeneity, detected by erythrocyte IM) followed by oral supplementation. reticulocyte hemoglobin content (CHr) and histogram widening or increased RDW. Oral Iron Supplementation reticulocyte volume (MCVr) in dogs. Vet r r RBC changes include microcytosis, Animals with severe iron deficiency may Clin Pathol 2005, 34:23–27. hypochromia due to thin cell geometry, and have impaired intestinal iron absorption, Thrall MA. Regenerative anemias. In: Thrall keratocyte and schistocyte formation. r making oral therapy of little value until partial MA, et al., Veterinary Hematology and Newer erythrocyte indices MCVr and CHr, iron repletion has occurred. Clinical Chemistry. 2nd ed. Ames, IA: r are sensitive for detecting iron-limited Follow injected iron with oral iron Wiley-Blackwell, 2012, pp. 88–90. erythropoiesis; available on one hematology supplement for 1–2 months, or until resolved. Author Glade Weiser system. r r Kittens undergo spontaneous iron repletion Consulting Editor Alan H. Rebar Lab tests indicate iron-limited beginning at 5–6 weeks of age. erythropoiesis, but may not differentiate true JWST589-A59-50 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:19 279mm×216mm

84 Blackwell’s Five-Minute Veterinary Consult A Anemia, Metabolic (Anemias with Spiculated Red Cells)

r Normal mean corpuscular volume and mean corpuscular hemoglobin concentration in most animals. BASICS r FOLLOW-UP Normocytic, normochromic, and OVERVIEW nonregenerative. Monitor CBC periodically while treating the r r Sometimes occurs concomitantly with Polychromasia on blood films only with underlying condition. diffuse diseases of the liver, kidney, and, rarely, accompanying blood loss (as with hepatic spleen. hemangiosarcoma). r r In most animals with liver disease, WBC changes variable, based on underlying cause of hepatic or renal pathology. spiculated cells have 2–10 elongated, blunt, r MISCELLANEOUS finger-like projections from their surfaces and Inflammatory conditions likely to be SEE ALSO are classified as acanthocytes. accompanied by inflammatory leukogram. r r r Anemia of Chronic Kidney Disease Acanthocytic anemias can be associated Variable findings in liver and kidney r with renal disease; anemias of renal disease function tests (serum biochemistry and Hemangiosarcoma, Spleen and Liver more often have oval red cells with irregular urinalysis). ABBREVIATIONS r or ruffled membranes (burr cells). Hepatic Diseases ALP = alkaline phosphatase r r r Rarely, acanthocytic anemias can be seen in High ALT, ALP, and 𝛾-glutamyl transferase. ALT = alanine aminotransferase r r association with splenic disease alone. High bile acids, serum ammonia. PCV = packed cell volume r r r Pathogenesis not entirely clear; abnormal Possibly low albumin and serum urea RBC = red blood cell r lipid metabolism with free cholesterol loading nitrogen. WBC = white blood cell r of RBC membranes is most frequently Bilirubinuria, bilirubin crystals in urine. implicated as cause. Suggested Reading r Renal Diseases Dogs with disseminated abdominal r Christopher, MM, Lee, SE. Red cell High serum urea nitrogen, creatinine, and morphologic alterations in cats with hepatic hemangiosarcoma with liver involvement phosphorus. often have acanthocytes. r disease. Vet Clin Pathol 1994, 23:7–12. Highly variable urinalysis findings, Harvey JW. Veterinary Hematology: A SIGNALMENT including isosthenuria (urine specific gravity Diagnostic Guide and Color Atlas. China: Dogs and cats (infrequently) 1.008–1.025 in dogs; 1.008–1.035 in cats). r Elsevier, 2012, pp. 66–67. Tubular and/or protein casts. SIGNS r Ng, CY, Mills, NJ. Clinical and r Pyuria. None in most animals (usually mild to r haematological features of moderate condition). Proteinuria. hemangiosarcoma in dogs. Aust Vet J 1985, r r Detection of spiculated RBCs on peripheral Hematuria. 62:1–4. blood film can be first marker for liver, OTHER LABORATORY TESTS Rebar AH. Hemogram Interpretation for kidney, or splenic disease. None Dogs and Cats. Wilmington, DE: Gloyd r In large-breed dogs with vague signs or large IMAGING Group for Ralston Purina Co., 1998, spleen, suggests possibility of splenic or pp. 22–23. Abdominal radiographs and ultrasound— Rebar AH, Lewis HB, DeNicola DB, hepatic hemangiosarcoma. evaluate hepatic, renal, and splenic structure. CAUSES & RISK FACTORS Halliwell WH, Boon GD. Red blood cell r DIAGNOSTIC PROCEDURES fragmentation in the dog: An editorial Any disease of the liver, kidneys, or possibly Liver or kidney biopsy if indicated. review. Vet Pathol 1981, 18:415–426. spleen. r Rebar AH, MacWilliams PS, Feldman BF, The likelihood of RBC morphologic Metzger FL, Pollock RVH, Roche J. A abnormalities parallels the severity of organ Guide to Hematology in Dogs and Cats. involvement. r TREATMENT Jackson, WY: Teton NewMedia, 2002, Hemangiosarcoma involving the liver is a p. 36. frequent cause. r Focus treatment on diagnosis and treatment Tant, MS, Lumsden, JH, Jacobs, RM, et al. Observed in cats with fatty liver syndrome. of underlying hepatic, renal, or splenic Evaluation of acanthocyte count as a disease. diagnostic test for canine hemangiosarcoma. Comp Clin Path 2004, 12:174–181. Weiss, DJ, Kristensen, A, Papenfuss, N. DIAGNOSIS Quantitative evaluation of irregularly DIFFERENTIAL DIAGNOSIS MEDICATIONS speculated red cells in the dog. Vet Clin Pathol 1993, 22:117–121. Determination of renal or hepatic causes DRUG(S) Author Alan H. Rebar based on results of biochemistry profile and Variable according to underlying cause. Consulting Editor Alan H. Rebar urinalysis. CONTRAINDICATIONS/POSSIBLE CBC/BIOCHEMISTRY/URINALYSIS r INTERACTIONS Mild to moderately low PCV, RBC count, Variable according to underlying cause. and hemoglobin. JWST589-A60-51 JWST589-Tilley Printer: Yet to Come August 3, 2015 6:45 279mm×216mm

Canine and Feline, Sixth Edition 85 Anemia, Nonregenerative A

CAUSES and lymphoproliferative diseases, metastatic Nonregenerative Anemia without Other neoplasia, myelofibrosis, and osteosclerosis. Cytopenias RISK FACTORS BASICS r r r Anemia of inflammatory disease (AID)— Renal failure Inflammatory or chronic DEFINITION r r most common cause of mild nonregenerative disease Liver failure Sertoli cell tumor r r r Low RBC mass without evidence of increased anemia; can be seen within 3–10 days of Cancer Chronic blood loss Cats from r polychromasia or reticulocytosis in the infection, inflammation, tissue injury, multicat households (FeLV) Lead or arsenic peripheral blood. immune-mediated processes, and neoplasia; exposure—chronic PATHOPHYSIOLOGY increased liver production of hepcidin and r Low erythroid production or release. release of cytokines from T-lymphocytes and r Onset of anemia and its related signs macrophages lead to iron sequestration in insidious unless RBC survival is concurrently macrophages, decreased iron absorption; low DIAGNOSIS shortened by hemorrhage or hemolysis. serum iron and transferrin, increased ferritin, r decreased EPO production and function, and DIFFERENTIAL DIAGNOSIS May be caused by selective alteration in r erythropoiesis or generalized bone marrow shortened RBC lifespan. Chronic renal Regenerative anemia initially nonregenerative; injury affecting leukocytes and platelets as failure—kidneys fail to produce adequate sudden onset of signs more consistent with r EPO; uremic toxins shorten RBC lifespan well. Mechanisms for selectively altered r regenerative than nonregenerative anemia; erythropoiesis include deficient hormonal and impair response to EPO. Chronic liver exacerbation of a chronic condition may stimulation, nutritional deficiency, disease—shortened RBC survival caused by produce the appearance of an acute onset. cytokine-mediated iron sequestration, and changes in RBC membrane lipids; functional LABORATORY FINDINGS disturbed metabolism in or destruction of iron deficiency due to decreased transferrin synthesis and impaired mobilization of Disorders That May Alter Laboratory precursors; generalized bone marrow injury r Results hepatic iron. Endocrine disease—thyroid r usually caused by toxin, infection, or Lipemia can falsely elevate hemoglobin and infiltrative process. hormones and cortisol stimulate r erythropoiesis and facilitate the effect of MCHC values. Lead toxicity-increased SYSTEMS AFFECTED r NRBC may falsely elevate the WBC count. r erythropoietin. Immune-mediated Cardiovascular—heart murmur from low r destruction of precursors—pure red cell Valid If Run in Human Laboratory? blood viscosity Hemic/Lymph/Immune r r r r aplasia. Infectious destruction of precursors Dogs—yes. Cats—yes, if hematology Hepatobiliary—centrilobular degeneration (although usually > one cell line is involved), instrument uses species-specific parameters; from hypoxic injury e.g., FeLV and ehrlichiosis, Cytauxzoon felis. instruments designed strictly for human SIGNALMENT Nutritional or Mineral Deficiency/Toxicity specimens may under-count small feline r r r Varies with primary cause. Giant Iron deficiency—usually due to chronic RBCs. schnauzer, Australian shepherd dog, border external blood loss; initially regenerative, but CBC/BIOCHEMISTRY/URINALYSIS collie, beagle—congenital cobalamin as severity increases, anemia becomes CBC and Blood Smear malabsorption. r r nonregenerative. Cobalamin (vitamin B12) PCV, RBC count, and hemoglobin low. r SIGNS and/or folate deficiency—rare in dogs and Anemia usually normocytic, normochromic, General Comments cats; can be caused by dietary insufficiency, with normal MCV and MCHC. r r malabsorption, or chronic drug r Usually secondary. Signs associated with Macrocytosis (high MCV)—without administration (e.g., sulfas, methotrexate, primary disease often precede signs of anemia. polychromasia suggests nuclear maturation anticonvulsants) that inhibits folate; Historical Findings defect (cells skip a division); seen in cats with r congenital defect in cobalamin absorption in FeLV; rarely caused by vitamin B or folate Lack of energy, exercise intolerance, r 12 r giant schnauzers, border collies, Australian deficiency. Microcytosis (low inappetence, and cold intolerance. Other shepherd dogs, and beagles; can occasionally findings reflect primary condition: polyuria MCV)—suggests cytoplasmic maturation cause normocytic anemia and defect (cells undergo extra division); iron and polydipsia (e.g., CRF), paint exposure hypersegmented neutrophils; megaloblastic from remodeling old houses (e.g., lead r deficiency most common cause; in late stages, changes possible in the marrow. Disruption concurrent hypochromasia (low MCHC) poisoning), treating female dogs for of precursor metabolism—chronic lead mismating or urinary incontinence or common in dogs but not in cats; seen in toxicity and possibly high concentrations of approximately one-third of patients with feminization in male dogs (e.g., aluminum, arsenic, and cadmium inhibit hepatic insufficiency or vascular shunting. hyperestrogenism), failure to thrive observed r heme synthesis; cadmium and lead cause renal Specific RBC morphologies—schistocytes at 8–12 weeks of age (hereditary cobalamin toxicity and impaired EPO production. ± malabsorption). common with iron deficiency visibly Nonregenerative Anemia with Other hypochromic RBCs (dogs); acanthocytes with Physical Examination Findings Cytopenias liver disease; target cells with iron deficiency, r r Pallor, heart murmur (severe anemia), and Toxicities—drugs or chemicals (e.g., cancer liver disease, and hypothyroidism. r r possibly tachycardia or polypnea. Signs chemotherapeutics, chloramphenicol, Inflammatory leukogram supports AID. r reflecting primary condition: oral ulcerations phenylbutazone, trimethoprim-sulfadiazine, Thrombocytosis common in iron deficiency. r (e.g., CRF), cachexia (e.g., cancer), zonisamide, phenobarbital, griseofulvin, High number of NRBCs without organomegaly (e.g., lymphoma), methimazole, fenbendazole, albendazole, and polychromasia or disproportionate to the gastrointestinal or CNS signs (e.g., lead benzene), hormones (e.g., estrogen toxicity degree of anemia and polychromasia seen with poisoning), symmetrical alopecia (e.g., secondary to abortifacient therapy and Sertoli lead toxicity, EMH, heat stroke, and injury to r hypothyroidism and hyperestrogenism). cell tumor). Infections—FeLV, FIV, bone marrow stroma by endotoxemia or r ehrlichiosis, babesiosis, and parvoviral hypoxia. RBC or WBC precursors in infection (recovery usually precedes peripheral blood without orderly progression r development of anemia). Infiltrative to more mature forms suggest myelodysplasia r processes—myelodysplasia, myeloproliferative or myeloproliferative disease. Concurrent JWST589-A60-51 JWST589-Tilley Printer: Yet to Come August 3, 2015 6:45 279mm×216mm

86 Blackwell’s Five-Minute Veterinary Consult

A Anemia, Nonregenerative (Continued)

r r cytopenia in other cell lines without evidence Classically, iron deficiency has expanded Iron supplementation in patients with iron of marrow responsiveness (e.g., band erythron and high numbers of deficiency anemia (see Anemia, neutrophils and macroplatelets) suggests metarubricytes; absence of iron stores Iron-Deficiency). r r generalized bone marrow injury. supportive in dogs, but not cats. Increased May supplement with folic acid at rate of erythrophagocytosis suggests injury to cells 4–10 mg/kg/day. Serum Biochemistry and Urinalysis r r (e.g., immune-mediated and toxic causes). May supplement with cobalamin (vitamin CRF: high BUN and creatinine with r inadequate urine concentration (dogs, Incomplete maturation sequence suggests B12) at rate of 100–200 mg/day PO (dogs) or r < 1.030; cats, < 1.035). Liver disease: high injury to specific maturation stage (e.g., 50–100 mg/day PO (cats); parenteral 𝜇 ALT, total bilirubin, or elevated bile acids immune-mediated and toxic causes) or cyanocobalamin administration (50 g/kg or r possibly incomplete recovery from a previous 0.5–1 mg/dog SC weekly to monthly) needed suggests liver disease. Hypothyroidism: high r serum cholesterol (> 500 mg/dL). injury (recheck in 3–5 days). Disorderly in dogs with inherited cobalamin r Hypoadrenocorticism: Na/K < 23, maturation and atypical cellular morphology malabsorption. suggest myelodysplastic syndrome. lymphocytosis, and eosinophilia. r PRECAUTIONS Hypercellular marrow with increased blast OTHER LABORATORY TESTS Monitor for transfusion reactions (see Blood cells (> 20% of nucleated cells) indicates r < 𝜇 Transfusion Reactions). Reticulocyte count—value of 95,000/ L hematopoietic neoplasia; immunophenotyping < 𝜇 (dogs) or 60,000/ L (cats) (automated can identify affected cell line(s); circulating counts) accompanied by a low PCV confirms neoplastic cells may or may not be seen. r r nonregenerative anemia. Direct antiglobulin Non-marrow cells indicate metastatic test (Coombs’)—spherocytosis, neoplasia. FOLLOW-UP autoagglutination, or positive Coombs’ test Abdominal Ultrasound PATIENT MONITORING provides support for immune-mediated r r Evaluation of microcytic anemia; look for With severe anemia: PCV and blood smear destruction of erythroid precursors. Serum r iron profile—may be indicated for patients intestinal neoplasia or other source of external examination every 1–2 days. Stable animals with microcytic anemia; with iron deficiency blood loss. with chronic or slowly improving disease both serum iron and ferritin are low, while course: reevaluate every 1–2 weeks. total iron-binding capacity varies; with AID, serum iron is low but serum ferritin is high r (MCV and MCHC usually normal). Bile TREATMENT r acids measurement—may be indicated for Anemia usually resolves with resolution of MISCELLANEOUS r evaluation of microcytic anemia; high values underlying disease. Conditions associated PREGNANCY/FERTILITY/BREEDING suggest hepatic insufficiency or vascular r with severe anemia or pancytopenia often Some pregnant animals have mildly low PCV, shunting. Serum lead—indicated when carry guarded-to-poor prognosis and may caused by expanded blood volume. NRBCs are present, especially with involve long-term treatment without r SYNONYMS concurrent gastrointestinal or CNS signs; complete resolution. Metabolic value > 30 𝜇L/dL (0.3 ppm) strongly Non-responsive anemia r compensation occurs with slowly developing supports lead intoxication. Serologic nonregenerative anemia; thus mild to ABBREVIATIONS r testing—FeLV test in any cat with moderately severe anemia (PCV > 15%) ACTH = adrenocorticotropic hormone r nonregenerative anemia; Ehrlichia canis, generally requires no supportive intervention. AID = anemia of inflammatory disease r r r Anaplasma phagocytophilia, and Babesia PCR For patients with severe anemia (PCV ALT = alanine aminotransferase CNS = r assays indicated in dogs with unexplained < 10–15%), the degree of hypoxia may central nervous system CRF = chronic renal r anemia, especially when concurrent with require transfusion (e.g., 6–10 mL/kg for failure EMH = extramedullary r r thrombocytopenia. Endocrine testing— packed RBCs; 10–20 mL/kg for whole hematopoiesis EPO = erythropoietin r r when clinical signs and laboratory tests blood). Less blood may be needed in animals FeLV = feline leukemia virus FIV = feline r r suggest hypothyroidism (T4,freeT4,and with chronic anemia. Determine blood type immunodeficiency virus IL-1 = r TSH concentrations) or hypoadrenocorticism prior to transfusion to ensure compatibility. interleukin-1 MCHC = mean corpuscular r r (ACTH stimulation test). Serum cobalamin Cross match against donor blood if blood hemoglobin concentration MCV = mean r ± urine methylmalonic acid concentrations— typing reagents are not available, or if patient cell volume NRBC = nucleated red blood r puppies at risk for hereditary cobalamin requires a second transfusion more than cells PCR = polymerase chain reaction r r malabsorption. 4 days after the first transfusion. If blood TSH = thyroid stimulating hormone DIAGNOSTIC PROCEDURES volume and tissue perfusion are compromised INTERNET RESOURCES by concurrent blood loss or shock, administer Cytologic Examination of Bone Marrow r Erythrocytes: Overview, Morphology, and Core Biopsy lactated Ringer’s solution or colloids. With r Quantity; A.H. Rebar, P.S. MacWilliams, B.F. Cytologic examination of aspirate indicated chronic anemia, volume overload is a Feldman, et al.: http://www.ivis.org/ in all patients unless primary cause is apparent concern—blood products and fluids should r advances/Rebar/Chap4/chapter.asp?LA=1 (e.g., AID and CRF). Bone marrow core be given slowly. biopsy—useful in evaluation of bone marrow Suggested Reading architecture and overall cellularity; important Abram-Ogg, A. Nonregenerative anemia. In: for diagnosis of aplastic marrow or Ettinger SJ, Feldman EC, eds., Textbook of r myelofibrosis. Erythroid hypoplasia or MEDICATIONS Veterinary Internal Medicine: Diseases of the Dog and Cat, 7th ed. St Louis, MO: aplasia confirms the problem, although DRUG(S) history and other tests may be needed to Elsevier Saunders, 2010, pp. 788–797. r r determine the underlying etiology. Myeloid Erythropoietin in patients with anemia of Author Joyce S. Knoll hyperplasia and high iron stores support AID. CRF (see Anemia of Chronic Kidney Consulting Editor Alan H. Rebar Disease). JWST589-A61-52 JWST589-Tilley Printer: Yet to Come August 1, 2015 14:21 279mm×216mm

Canine and Feline, Sixth Edition 87 Anemia, Nuclear Maturation Defects (Anemia, Megaloblastic) A

CBC/BIOCHEMISTRY/URINALYSIS r In dogs, mild to moderate anemia (PCV: r 30–40%). In cats, anemia can be mild to BASICS r FOLLOW-UP severe. Anemia classically macrocytic (high r OVERVIEW mean corpuscular volume) and Monitor response to treatment by CBC r normochromic (normal mean corpuscular (weekly) and occasional bone marrow Nonregenerative anemia characterized by r arrested development of the nuclei of RBC hemoglobin concentration). However, mean collection and evaluation. Closely monitor precursors (as a result of interference with corpuscular volume and mean corpuscular FeLV-positive cats for evidence of onset of haemoglobin concentration can be normal. other signs of hematopoietic dyscrasia in the DNA synthesis) while the cytoplasm develops r normally (nuclear-cytoplasmic asynchrony). Large, fully hemoglobinized RBC; peripheral blood and bone marrow. r r Affected RBC precursors fail to divide occasional to numerous megaloblasts, Prognosis—depends on underlying cause; in particularly at the feather edge; minimal to no FeLV-positive cats, prognosis guarded; in normally and thus are larger than r corresponding normal precursors with the polychromasia. In cats with FeLV, anemia animals with drug-associated anemia, same degree of cytoplasmic maturity may occur in association with a prognosis good when use of offending drug is (hemoglobinization); because their nuclei are myelodysplastic syndrome or in conjunction interrupted. deficient in chromatin (DNA), they have a with leukemia of a different cell line. distinctive open and stippled appearance; OTHER LABORATORY TESTS these giant precursors with atypical, immature r FeLV nuclei are known as megaloblasts. Although IMAGING MISCELLANEOUS these asynchronous changes are most N/A SEE ALSO prominent in RBC precursors, WBC and r r platelet precursors are similarly affected. OTHER DIAGNOSTIC PROCEDURES Anemia, Nonregenerative Feline Leukemia Virus Infection (FeLV) SIGNALMENT Bone Marrow Biopsy r r r ABBREVIATIONS Dogs and cats. Spontaneous, clinically In dogs, usually hyperplastic, often in all cell r r r FeLV = feline leukemia virus PCV = unimportant occurrence in toy poodles lines. In cats, marrow findings are highly r r variable and may be hyper- to hypocellular. packed cell volume RBC = red blood cell (occasional). Breed predilection: giant r r r schnauzers, also border collies, Australian Maturation arrest with nuclear and WBC = white blood cell FIV = feline cytoplasmic asynchrony may be seen in all cell immunodeficiency virus shepherds, and beagles with inherited r r lines. Many megaloblastic RBC precursors cobalamin malabsorption. Defect usually r Suggested Reading acquired. may be observed. Macrophagic hyperplasia Canfield, PJ, Watson, ADJ. Investigations of SIGNS with active phagocytosis of nucleated RBCs bone marrow dyscrasia in a poodle with r and megaloblasts (common). In dogs, generally mild, usually not macrocytosis. J Comp Pathol 1989, r clinically important. In cats with 101:269–278. FeLV-associated nuclear maturation anemia, Harvey JW. Veterinary Hematology: A FeLV-related signs can be anticipated. Anemia Diagnostic Guide and Color Atlas. China: may be mild to severe. TREATMENT Elsevier, 2012, pp. 273–275. r CAUSES & RISK FACTORS Treat by targeting the underlying cause if Rebar AH, MacWilliams PS, Feldman BF, r r Metzger FL, Pollock RVH, Roche J. A Infectious—FeLV; retroviral infection the possible. Except for that occurring with FeLV in cats, megaloblastic anemia is a Guide to Hematology in Dogs and Cats. most common cause of megaloblastic anemia r Jackson, WY: Teton NewMedia, 2002, pp. in cats. FIV has been reported as a cause much relatively mild condition. Tre at mos t r patients on an outpatient basis. 57–58. less frequently. Nutritional—folic acid and Rebar AH. Hemogram Interpretation for vitamin B12 deficiencies (Giant Schnauzers Dogs and Cats. Wilmington, DE: Gloyd and other with inherited cobalamin r Group for Ralston Purina Co., 1998, p. 23. malabsorption). Toxic—phenytoin, Schalm, OW. Erythrocyte macrocytosis in methotrexate (folate antagonist), alkylating MEDICATIONS miniature and toy poodles. Can Pract 1976, agents (cyclophosphamide), plant alkaloids DRUG(S) 3(6):55–57. (vincristine), antimetabolites (azathioprine). r r Shelton, GH, Linenberger, ML, Abkowitz, Congenital—toy and miniature poodles. In animals with drug toxicity, discontinue the offending drug. JL. Hematologic abnormalities in cats r In all animals, consider supplementation seropositive for feline immunodeficiency with folic acid (4–10 mg/kg/day) or vitamin virus. J Am Vet Med Assoc 1992, 199:1353–1357. B12 (dogs, 100–200 mg/day PO; cats, 50–100 DIAGNOSIS mg/day PO). Weiss, DJ. Congenital dyserythropoiesis. In: r DIFFERENTIAL DIAGNOSIS Giant schnauzers with inherited cobalamin Weiss DJ, Wardrop KJ, eds., Schalm’s r Veterinary Hematology, 6th ed. Ames, IA: In dogs, all other mild to moderate malabsorption require parenteral treatment Wiley-Blackwell, 2010, pp. 196–198. nonregenerative anemias, including anemia of with vitamin B12 (0.5–1 mg IM weekly to Author Alan H. Rebar inflammatory disease, renal disease, and lead every few months). r Consulting Editor Alan H. Rebar poisoning. Differentiation based on the CONTRAINDICATIONS/POSSIBLE distinctive CBC and bone marrow findings r INTERACTIONS listed. In cats, FeLV infection is the primary Drugs known to cause megaloblastic anemia differential. (e.g., methotrexate and phenytoin) should be avoided in patients whose condition results from other causes. JWST589-A62-53 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:7 279mm×216mm

88 Blackwell’s Five-Minute Veterinary Consult A Anemia, Regenerative

r SIGNS (cats). In cats, some systemic diseases (e.g., r r Pallor. Weakness, exercise intolerance. diabetes mellitus, hyperthyroidism, r r Anorexia. Possible heart murmur, lymphoma) enhance Heinz body formation BASICS r tachycardia, bounding pulses. Possible but do not necessarily cause anemia. r DEFINITION jaundice and hemoglobinuria. Petechiae, Erythrocyte Parasites epistaxis, melena suggest blood loss due to r Decreased circulating RBC mass (indicated r Cats: Mycoplasma haemofelis, by low PCV, hemoglobin, and total RBC vasculitis or a platelet problem. Hematomas M. haemominutum, M. turicensis, and or cavity bleeds suggest a coagulation factor r count) accompanied by appropriate, r M. haematoparvum, Cytauxzoon felis. Dogs: deficiency. Clinical signs depend on degree compensatory increase in RBC production by r Mycoplasma haemocanis, Babesia canis, and the bone marrow (e.g., reticulocytosis in the of anemia and rapidity of onset. Rapid loss B. gibsoni. of 15–25% blood volume or acute hemolysis peripheral blood and RBC hyperplasia in the r Mechanical RBC Fragmentation bone marrow). results in shock and possible death. With r chronic anemia, compensatory increases in Caused by vasculitis, thromboembolic PATHOPHYSIOLOGY disease or disease of any vascular organ (e.g., r heart rate, and eventually heart size, lessens r Caused by blood loss or hemolysis. liver, kidney, spleen, heart). Rare cause of r RBC circulation time; hemoglobin can drop Hemolysis—caused by intrinsic RBC to as low as 50% of minimum normal value anemia unless accompanied by hemorrhage. defects (e.g., congenital RBC membrane without overt signs of hypoxia. Inherited RBC Abnormalities defects or enzyme deficiencies) or extrinsic r CAUSES PK deficiency—impaired ATP formation, factors (e.g., RBC parasites, oxidative injury, leading to premature RBC destruction; hemolysins, osmotic changes, immune- Immune Mediated r r autosomal recessive trait. PFK deficiency— mediated RBC destruction, heat stroke, and Antibodies ± complement on membrane r marked alkaline fragility caused by impaired severe hypophosphatemia. Intravascular shorten RBC lifespan. Antibodies may target synthesis of 2,3-diphosphoglycerate; hemolysis may lead to DIC. RBC membrane components or may be hemolytic episodes triggered by SYSTEMS AFFECTED directed against tumor antigens, infectious hyperventilation-induced alkalemia, especially r Cardiovascular—murmurs with marked agents, vaccines, or drugs (e.g., sulfonamides, after vigorous exercise; autosomal recessive r r anemia; tachycardia. Hemic/Lymph/ penicillins, cephalosporins, methimazole, trait. Increased RBC osmotic fragility, Immune—erythroid hyperplasia in bone amiodarone) that are either directly adherent (unknown RBC defect) leads to recurrent to RBC surface or part of immune complexes r marrow; splenic EMH; splenomegaly due to r severe anemia and splenomegaly. Feline EMH and histiocytic hyperplasia can be adherent to RBCs. Anemia is usually congenital porphyria—enzyme deficiency in feature of extravascular hemolytic anemia. regenerative, but up to 30% of cases will be heme synthetic pathway leads to r Hepatic—anoxia causes centrilobular nonregenerative due to immune-mediated accumulation of heme precursors, hemolytic destruction of erythroid precursors in bone degeneration of the liver; hemosiderosis ± r anemia and brown-red discoloration of teeth hemochromatosis possible with chronic marrow. Hemolysis may be either and bones. Siamese tend to have severe hemolytic anemia (e.g., PK-deficient dogs) intravascular, through IgM-mediated hemolytic anemia, while domestic shorthair especially following repeated transfusions. activation of complement, or extravascular, cats have a less severe autosomal dominant r through IgG-mediated phagocytosis. Renal—severe intravascular hemolysis rarely r trait that causes mild anemia. leads to renal tubular necrosis and acute renal Hemolytic antibodies are generally reactive r at body temperature; rarely cold-acting Hypophosphatemia failure. Musculoskeletal—progressive Severe hypophosphatemia, secondary to osteoclerosis seen in PK-deficient dogs. antibodies cause in vivo hemolysis and/or RBC agglutination in cooler, peripheral treatment with insulin or phosphate binders, SIGNALMENT r impairs ATP production, leading to increased r vasculature. Transfusion of a blood type B PK deficiency—basenji, beagle, cairn terrier, cat with type A blood can result in rapid, erythrocyte fragility and hemolysis. Chihuahua, dachshund, Labrador retriever, Blood Loss severe, intravascular hemolysis; neonatal r r miniature poodle, pug, West Highland white isoerythrolysis seen in kittens born to a blood Trauma Bleeding neoplasms (e.g., terrier, and American Eskimo; and Somali, type B queen mated to a blood type A tom. hemangiosarcoma, intestinal Abyssinian, and domestic shorthair cats. r r r Canine blood type DEA 1.1 can cause adenocarcinoma) Coagulopathies (e.g., PFK deficiency—English springer spaniel, warfarin poisoning, hemophilia, hemolysis in a DEA 1.1-negative dog, r American cocker spaniel, whippet, although a single incompatible transfusion thrombocytopenia) Bloodsucking parasites wachtelhund, and mixed breed dogs with r (e.g., fleas, ticks, and Ancylostoma) r can be tolerated. The newly identified blood r spaniel parentage. Marked RBC osmotic types Mik (cats) and Dal (dogs) can cause Gastrointestinal ulcers fragility—English springer spaniel and significant hemolytic transfusion reactions in Abyssinian, Somali, Siamese, and domestic r animals lacking these common RBC antigens. shorthair cats. Feline congenital Oxidant Injury porphyria—Siamese and domestic shorthair r r Oxidants can cause Heinz body formation DIAGNOSIS cats. Some dog breeds have a genetic (aggregates of oxidized hemoglobin), predisposition for heritable coagulopathies DIFFERENTIAL DIAGNOSIS eccentrocytes (oxidation of RBC membranes), such as factor VIII deficiency and von r Differentiated from nonregenerative anemia r and methemoglobinemia. Heinz bodies are Willebrand disease. Middle-aged female by high reticulocyte count. removed through extravascular hemolysis, dogs, especially American cocker spaniel, while oxidized membrane components cause LABORATORY FINDINGS English springer spaniel, Irish setter, Old r intravascular hemolysis. Oxidants include English sheepdog, poodle, and Shetland Disorders That May Alter Laboratory onions, garlic, acetaminophen (especially in sheepdog, are predisposed to immune- Results cats), zinc (from pennies minted after 1982, r mediated syndromes, such as SLE and Lipemia can cause mild in vitro hemolysis, zinc oxide ointment, and zinc bolts), acute without appreciable anemia, and may falsely immune-mediated hemolytic anemia. r copper toxicosis, benzocaine, vitamin K3 elevate MCHC. Autoagglutination may (dogs), propofol, phenolic compounds (moth falsely decrease the RBC count. r balls), skunk musk, and phenazopyridine Intraerythrocytic inclusions (e.g. basophilic JWST589-A62-53 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:7 279mm×216mm

Canine and Feline, Sixth Edition 89

(Continued) Anemia, Regenerative A

r stippling or intraerythrocyte parasites may (canine) in the peripheral blood is Hemolytic anemias—varies with cause of falsely increase automated reticulocyte count. confirmatory; false negatives and false hemolysis. r r Exercise and excitement can increase RBC positives are possible. PCR test for PK count, PCV, and reticulocyte count through deficiency: young Basenji, beagle, dachshund, splenic contraction. Toy Eskimo, West Highland white terrier, and Valid If Run in Human Laboratory? cairn breeds with persistent anemia, massive FOLLOW-UP r r reticulocytosis and a negative Coombs’ test. Dogs—yes. Cats—yes, if hematology r PATIENT MONITORING instrument uses species-specific parameters; PCR test for PFK deficiency: spaniels and r instruments designed for analysis of human whippets with recurrent hemolytic crises. Initially, monitor of RBC mass (e.g., PCV, specimens may under-count small feline DIAGNOSTIC PROCEDURES RBC count, and hemoglobin) and r morphologic features on a blood film (i.e., RBCs. Bone marrow aspirate—needed only when polychromasia) every 24 hours to evaluate CBC/BIOCHEMISTRY/URINALYSIS reticulocytosis is lacking; RBC hyperplasia r effectiveness of treatment and bone marrow r confirms regenerative response. Bone r PCV, RBC count, and hemoglobin low. responsiveness. As regeneration becomes r marrow biopsy—useful in evaluation of bone Total protein often low with blood loss apparent (rising RBC values and marrow architecture and overall cellularity; anemia and may be the only sign with acute polychromasia), recheck patients every important for confirmation of blood loss; normal PCV may be maintained 3–5 days; return to normal values occurs through transient splenic contraction. nonregenerative process. r about 14 days after acute hemorrhage but Severity of acute blood loss may be may take longer with immune-mediated r underestimated until the plasma volume has process. Following transfusion, monitor for been restored by fluid administration and/or r complications (see Blood Transfusion internal fluid shifts. RBC indices vary TREATMENT Reactions). r depending on the cause of anemia and degree Emergency if anemia is severe and develops r of regenerative response—MCV, normal to rapidly. Massive hemorrhage leads to high; MCHC, normal to low in most hypovolemic shock and anoxia; acute r patients; MCHC, artificially high with hemolysis leads to anoxia. Cage rest and MISCELLANEOUS intravascular hemolysis and hemoglobinemia. r careful observation indicated, depending on With iron deficiency, dogs may have a low SEE ALSO severity of signs. r r MCV, MCH, and MCHC; cats have a low Anemia, Heinz Body Anemia, Blood Loss Anemias r MCV but normal MCH and MCHC. r Immune-Mediated Anemia, r r r Specific RBC morphologies may suggest Traumatic blood loss leading to shock- Iron-Deficiency Babesiosis Bartonellosis crystalloid fluids can rapidly correct r r cause of hemolysis: marked spherocytosis r Cytauxzoonosis Lupus Erythematosus, r suggests immune-mediated disease (not as hypovolemia and restore circulation. RBC Systemic Zinc Toxicosis easily detected in cats whose RBCs generally replacement (packed RBCs or whole blood) < ABBREVIATIONS lack central pallor); Heinz bodies or indicated if PCV 15–20% and signs of r r ATP = adenosine triphosphate DIC = eccentrocytes suggest oxidant injury; severe hypoxia (i.e., extremely pale mucous disseminated intravascular coagulation numerous schistocytes suggest membranes, weakness, tachycardia, pounding r r EMH = extramedullary hematopoiesis microangiopathy. Agglutinated RBCs pulses, tachypnea). Initial dosage depends on r MCH = mean corpuscular hemoglobin indicate anemia is immune mediated; product selected; 6–10 mL/kg for packed r MCHC = mean corpuscular hemoglobin distinguish autoagglutination from rouleaux RBCs; 10–20 mL/kg for whole blood. Less r concentration MCV = mean cell volume by generous sample dilution with saline. blood may be needed in animals with chronic r r r PCV = packed cell volume PFK = Hemolysis may cause inflammatory anemia. Determine blood type prior to r phosphofructokinase PK = pyruvate kinase leukogram (neutrophilia with a left shift and transfusion, to ensure compatibility. Cross r r RBC = red blood cell SLE = systemic monocytosis). Acute blood loss may be match against donor blood if blood typing lupus erythematosus associated with stress leukogram (mild reagents not available, or if patient requires r second transfusion more than 4 days after first INTERNET RESOURCES neutrophilia and lymphopenia). Blood loss r may be accompanied by either transfusion. Animals with chronic blood Erythrocytes: Overview, Morphology, thrombocytopenia or rebound loss are normovolemic with increased cardiac Quantity; A.H. Rebar, P.S. MacWilliams, B.F. thrombocytosis; iron deficiency is often output, therefore transfusion volumes and Feldman, et al.: http://www.ivis.org/ accompanied by thrombocytosis. rates should be conservative to avoid cardiac advances/Rebar/Chap4/chapter.asp?LA=1. r failure. Hyperbilirubinemia and bilirubinuria Suggested Reading Hemolytic Anemias accompany marked hemolysis; Mitchell K, Krush S. Immune-mediated hemoglobinemia and hemoglobinuria seen Blood transfusion may be indicated; in haemolytic anemia and other regenerative with intravascular hemolysis. patients with immune-mediated process, anemias. In: Ettinger SJ, Feldman EC, eds., OTHER LABORATORY TESTS RBCs probably survive similarly to patient’s r Textbook of Veterinary Internal Medicine: In anemia automated absolute reticulocyte own RBCs, so transfusion should not be Diseases of the Dog and Cat, 7th ed. count (RBC count × reticulocyte %) withheld if marked signs of anemia present. St Louis, MO: Elsevier Saunders, 2010, > 60,000/휇L(cats)or> 95,000/휇L(dogs) r pp. 761–772. suggests regenerative anemia. It takes Author Joyce S. Knoll 3–5 days for bone marrow to mount a peak Consulting Editor Alan H. Rebar regenerative response, so reticulocytosis may MEDICATIONS initially be absent with blood loss or r DRUG(S) hemolysis. Direct antiglobulin test r Iron may benefit animals with chronic (Coombs’ test) indicated when immune- blood-loss anemia (see Anemia, mediated hemolytic anemia suspected; a Iron-Deficiency). positive test and evidence of spherocytosis JWST589-A03-54 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:36 279mm×216mm

90 Blackwell’s Five-Minute Veterinary Consult A Anisocoria

SIGNS IMAGING r Unequal pupil size See Table 1. r BASICS CAUSES Ultrasound—use to identify ocular, retrobulbar or jugular groove lesions. r DEFINITION Neurologic MRI—use to identify CNS lesions. See Table 1 r Asymmetric pupils CT—use to identify tympanic bulla lesions. Ocular PATHOPHYSIOLOGY DIAGNOSTIC PROCEDURES r See Table 2 r Disruption of sympathetic (causing miosis) See Table 1. RISK FACTORS r or parasympathetic (causing mydriasis) CSF tap—evaluate CNS inflammation/ N/A infection. innervation to the eye. r r ERG—evaluate retinal function. Ocular disease – numerous causes. r SYSTEMS AFFECTED Pharmacologic testing—see Figure 1; r postganglionic lesions cause denervation Nervous r DIAGNOSIS supersensitivity resulting in more rapid Ophthalmic constriction or dilation with application of GENETICS DIFFERENTIAL DIAGNOSIS r pharmacologic agents. Differentiation of pre- None Must determine which pupil is abnormal— or postganglionic lesions can be difficult if see Figure 1 and Tables 1 and 2. INCIDENCE/PREVALENCE r based solely on pharmacologic testing. Distinguish between neurologic and ocular PATHOLOGIC FINDINGS Common causes. Dependent on the underlying diagnosis GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS None N/A SIGNALMENT r OTHER LABORATORY TESTS Dog and cat r N/A TREATMENT All ages affected r No gender predisposition Dependent on underlying disease

Table 1 Neurologic lesions causing anisocoria.

Sign PLR Lesion Localization Differential List Diagnostic Test Mydriasis—Inability to No direct, present Ipsilateral optic nerve/chiasm Neuritis, neoplasia MRI/CSF tap/ERG constrict the pupil indirect Ipilateral oculomotor nerve/nucleus Encephalitis, neoplasia, trauma, MRI/CSF tap retrobulbar mass Ultrasound orbit Miosis—Inability to Present Brainstem Encephalitis, neoplasia, trauma MRI/CSF tap dilate the pupil C1-T2 myelopathy or C6-T2 Trauma, myelitis, neoplasia, IVDH (rare) MRI/myelogram/CT brachial plexus Vagosympathetic trunk Jugular venipuncture, trauma MRI/ultrasound Tympanic bulla Otitis media, neoplasia, trauma MRI/CT Trigeminal nerve Neuritis, neoplasia MRI

Table 2 Ocular diseases causing anisocoria.

Lesion Associated Signs Causes Anterior uveitis Miosis, aqueous flare, corneal edema, conjunctival hyperemia Infectious/inflammatory disease, trauma, neoplasia Glaucoma Mydriasis Primary glaucoma, secondary Sluggish/absent PLR, increased intraocular pressure, corneal edema glaucoma Neoplasm Miosis/mydriasis, iris color change Lymphoma, melanoma Posterior synechia Variable pupil shape, sluggish/absent PLR, anterior uveitis Secondary to anterior uveitis Iris atrophy Variable pupil shape, iridal thinning, sluggish PLR Old age change Iris hypoplasia Sluggish/absent PLR, irregular pupil margin, other ocular abnormalities Congenital Pharmacologic blockade Mydriasis Atropine Absent direct/consensual PLR Normal vision Spastic pupil syndrome Miosis, normal vision FeLV JWST589-A03-54 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:36 279mm×216mm

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Anisocoria

Miotic pupil in the dark Pupils dilated and equal in dark

Intact direct and indirect PLR Incomplete or absent PLR

PARASYMPATHETIC SYMPATHETIC DYSFUNCTION DYSFUNCTION

1% hydroxyamphetamine 1% phenylephrine 0.5% 0.2% Dilation physostigmine pilocarpine No dilation Delayed No Rapid No Rapid No No dilation Dilation constriction constriction constriction constriction Constriction constriction Normal eye or pre Post Normal Preganglionic Iris atrophy Normal ganglionic Post ganglionic lesion ganglionic lesion Evaluate for Normal Evaluate for lesion of the Lesion in brainstem iris, the iris or or Abnormal eye oculomotor Evaluate for oculomotor oculomotor nerve or central nerve nerve brainstem (spinal cord Evaluate disease Evaluate central, or brain), tympanic brachial plexus, brachial bulla or vagosympathetic plexus or trigeminal trunk, bulla and vago- nerve sympathetic trigeminal nerve trunk lesion

Figure 1.

r MRI = magnetic resonance imaging r PLR = pupillary light reflex MEDICATIONS MISCELLANEOUS INTERNET RESOURCES None DRUG(S) OF CHOICE ASSOCIATED CONDITIONS Dependent on underlying disease N/A Suggested Reading Cottrill NB, Differential diagnosis of CONTRAINDICATIONS AGE-RELATED FACTORS anisocoria. In: Kirk’s Current Veterinary N/A N/A Therapy, 14th ed. St Louis, MO: Saunders, PRECAUTIONS ZOONOTIC POTENTIAL 2009, pp. 1168–1174. N/A N/A Lorenz MD, Kornegay JN. Blindness, POSSIBLE INTERACTIONS PREGNANCY/FERTILITY/BREEDING anisocoria and abnormal eye movements. In: Handbook of Veterinary Neurology, 4th N/A N/A ed. St. Louis, MO: Saunders, 2004, pp. ALTERNATIVE DRUG(S) SYNONYMS 283–295. N/A None Author Heidi L. Barnes Heller SEE ALSO Consulting Editor Paul E. Miller r Anterior Uveitis—Cats Acknowledgment The author and editors r Anterior Uveitis—Dogs acknowledge the prior contribution of David r FOLLOW-UP Glaucoma Lipsitz. r Horner’s Syndrome PATIENT MONITORING r Iris Atrophy N/A r Client Education Handout Optic Neuritis and Papilledema PREVENTION/AVOIDANCE available online ABBREVIATIONS N/A r CNS = central nervous system r POSSIBLE COMPLICATIONS CSF = cerebrospinal fluid r N/A CT = computed tomography r EXPECTED COURSE AND PROGNOSIS ERG = electroretinogram r Dependent on the underlying disease FeLV = feline leukemia virus JWST589-A63-55 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:52 279mm×216mm

92 Blackwell’s Five-Minute Veterinary Consult A Anorexia

r absent in cancer patients. Exogenous and Pseudoanorexia r endogenous toxins (e.g., renal and liver Any disease causing painful or dysfunctional r failure) cause hyporexia. Any disorder that prehension, mastication, and swallowing. BASICS r decreases cerebral arousal will potentially Stomatitis, glossitis, gingivitis, pharyngitis, r DEFINITION decrease food intake. Gastroparesis and esophagitis (e.g., physical agents, caustics, The lack or loss of appetite for food; appetite associated with neoplasia, metabolic disorders, bacterial or viral infections, foreign bodies, and primary gastrointestinal disease is immune-mediated diseases, uremia). is psychological and its existence in animals is r r assumed. Hunger is physiologically aroused associated with decreased appetite. Fear, Retropharyngeal disorders (e.g., pain, and stress may decrease appetite. lymphadenopathy, abscess, hematoma, by the body’s need for food. Anorexia may be r sialocele). Dental disease or periodontal partial (hyporexia) or complete. Anorexia SYSTEMS AFFECTED r r results in decreased food intake, which then All body systems disease. Retrobulbar abscess. Oral, glossal, pharyngeal, or esophageal neoplasia. leads to weight loss. Pseudoanorexia is SIGNALMENT r associated with the inability to prehend or Neurologic disorders (e.g., rabies; swallow food rather than actual loss of Species neuropathies of cranial nerves V, VII, IX, X, Dog and cat XII; and central nervous system lesions). appetite. r PATHOPHYSIOLOGY Breed Predilections Musculoskeletal lesions (e.g., masticatory r N/A myositis, temporomandibular joint disease, The control of appetite is a complex fractures, craniomandibular osteopathy, interaction between the central nervous Mean Age and Range r myasthenia gravis, botulism, and r system and the periphery. The N/A cricopharyngeal achalasia). Salivary gland hypothalamus and brainstem contain Predominant Sex neoplasia or inflammation. peptidergic feeding-regulatory neurons that N/A act as input stations for sensory and metabolic RISK FACTORS SIGNS signals. These cell populations project to N/A several brain regions and interconnect Historical Findings r r extensively. Sensory signals that affect Refusal to eat is a common presenting complaint because pet owners strongly appetite include the odor, taste, texture, and r temperature of food as well as gastric and associate poor appetite with illness. Patients r DIAGNOSIS duodenal distention. Metabolic signals for with disorders causing dysfunction or pain of DIFFERENTIAL DIAGNOSIS hunger and satiety include a variety of the face, neck, oropharynx, and esophagus r peptides and hormones released during the may display an interest in food but cannot Perform a nutritional assessment. Gather eat. These patients are referred to as being information about the patient’s diet fasting and fed states as well as plasma r concentrations of glucose and fatty acids pseudoanorectic. Animals lacking a sense of (including all foods fed to the patient), food interacting with nutrient-specific receptors in smell (anosmia) often show no sniffing intake (current and normal) and obtain body r r r the liver and gastrointestinal tract. Leptin is behavior. Weight loss may be noted. and muscle condition scores. Elicit a primarily produced by adipocytes and acts on Physical Examination Findings thorough history regarding the patient’s r environment, changes in routine, people, or specific hypothalamic receptors to decrease Clinical signs in animals with anorexia/ other pets to help identify potential metabolism and decrease appetite. hyporexia vary depending on the underlying r r psychological etiologies. Question owners Neuropeptide Y release from the cause but may include fever, pallor, icterus, about the patient’s interest in food and ability gastrointestinal tract induces hunger and pain, changes in organ size, ocular changes, r to prehend, masticate, and swallow food. A hyperphagia, and decreases energy abdominal distention, dyspnea, muffled heart r complete physical examination is required to expenditure after food restriction. Ghrelin and lung sounds, adventitious lung sounds, determine the presence of systemic disease. produced by the stomach is a prokinetic and cardiac murmurs, and masses. Weight loss r Perform a thorough ophthalmic, dental, decreases leptin and increases neuropeptide Y and muscle wasting may be evident oropharyngeal, facial, and cervical production. ∙ Cholecystokinin and bombesin depending upon the extent and duration of r examination (sedation or anesthesia may be released from the gastrointestinal tract decreased food intake. Pseudoanorectic r required) in addition to observing the patient decrease appetite. Serotonin is an important patients commonly display weight loss, r eating to rule out pseudoanorexia. A and perhaps final mediator centrally via a halitosis, excessive drooling, difficulty in database including a complete blood count, serotonergic tract that passes near the prehending and masticating food, and r serum biochemistry panel, urinalysis, ventromedial hypothalamus. Dopaminergic odynophagia (painful swallowing). heartworm serology, retrovirus serology, tracts in the hypothalamus help regulate food CAUSES intake and are closely associated with the abdominal, thoracic and cervical imaging lateral hypothalamus (classical feeding Anorexia/Hyporexia studies, endoscopy, and histologic/cytologic r r center). Environmental factors including Almost any systemic disease process can examination of tissue/cell samples are often r required to make a definitive diagnosis. the location and timing of meals as well as cause anorexia/hyporexia. Psychological— r learned behaviors and circadian rhythms unpalatable diet, food aversion, stress, Only if the history, physical examination, alterations in routine and environment. and database strongly suggest psychologic modulate appetite and may override other r r r Pain. Toxicities and drug side-effects. anorexia should further diagnostic work-up signals for satiety and hunger. Appetite is r r Gastrointestinal disease. Acid-base be forgone; in such cases, daily contact with stimulated by aldosterone and corticosterone r r disorders. Cardiac failure. Endocrine and the pet owner is essential until the anorexia and suppressed by glucagon and somatostatin. r r r metabolic disease. Neoplasia. Infectious has resolved. Inflammatory and neoplastic disease can r disease. Immune mediated disease. cause hyporexia by releasing proinflammatory r r CBC/BIOCHEMISTRY/URINALYSIS cytokines such as interleukin-1, tumor Respiratory disease. Musculoskeletal r r r r Abnormalities vary with different necrosis factor, and interferon. The expected disease. Neurologic disease. Miscellaneous underlying diseases and causes of r upregulation of dietary intake in response to (e.g., motion sickness, high environmental pseudoanorexia and anorexia. Can be elevated energy expenditure is frequently temperature). JWST589-A63-55 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:52 279mm×216mm

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normal in patients with medical as well as POSSIBLE COMPLICATIONS r psychologic causes of anorexia. Dehydration, malnutrition, and cachexia are most likely; these exacerbate the OTHER LABORATORY TESTS MEDICATIONS r Special diagnostic tests may be necessary to underlying disease. A loss of more than DRUG(S) OF CHOICE 25–30% of body protein compromises the rule out specific diseases suggested by history, r physical examination, and preliminary tests. Diazepam is a short-acting appetite immune system and muscle strength, and stimulant with sedative properties dosed at death results from infection and/or IMAGING r r 0.1 mg/kg IV q24h or 1 mg PO q24h in cats. pulmonary failure. Feline hepatic lipidosis is Thoracic and abdominal imaging r a possible complication of anorexia in obese Oxazepam (2 mg/cat PO q12h) is a r (radiographic and ultrasound) studies are short-acting appetite stimulant and sedative. cats. Breakdown of the intestinal mucosal r often included in the minimum database to Cyproheptadine, an antihistamine with barrier is a concern in debilitated patients. detect anatomic or functional abnormalities. r antiserotonergic properties, has been used as EXPECTED COURSE AND PROGNOSIS Videofluoroscopy may be indicated to an appetite stimulant with mixed success at a Varies with underlying cause specifically evaluate pharyngeal and dose range of 0.2–0.4 mg/kg PO 10–20 esophageal function. minutes prior to feeding. r DIAGNOSTIC PROCEDURES Mirtazapine is a serotonin antagonist that is r Vary with underlying condition suspected. dosed at 3.75–7.5 mg/dog PO q24h or r 1.9 mg/cat PO q24–72h. MISCELLANEOUS Endoscopy may be useful for visualization r of the pharyngeal and esophageal structures. Analgesics may promote appetite in painful ASSOCIATED CONDITIONS conditions but their use must be balanced N/A with the potential to cause gastrointestinal AGE-RELATED FACTORS side-effects. r Metoclopramide (0.2–0.4 mg/kg SC or PO Nutritional support and glucose-containing TREATMENT fluids may be necessary to treat or prevent r q8–12h), ranitidine (2 mg/kg SC, IV, or PO The mainstay of treatment is aimed at q12h), or erythromycin (0.5–1 mg/kg PO hypoglycemia in anorectic puppies and identifying and correcting the underlying kittens. r q12h) are useful if anorexia is associated with disease. Symptomatic therapy includes gastroparesis or ileus. ZOONOTIC POTENTIAL r attention to fluid and electrolyte Antiemetics such as prochlorperazine N/A derangements, control of pain and/or nausea, (0.1–0.5 mg/kg PO q12h), maropitant (dogs: PREGNANCY/FERTILITY/BREEDING reduction in environmental stressors, and 1 mg/kg SC or 2 mg/kg PO q24h; cats: modification of the diet to improve N/A r 1 mg/kg SC or PO q24h) or metoclopramide palatability. Palatability can be improved by are useful to decrease nausea-associated SYNONYMS adding flavored toppings such as chicken and anorexia. N/A beef broth, seasoning with condiments such CONTRAINDICATIONS SEE ALSO as garlic powder, increasing the moisture, fat r See “Causes” or protein content of the food, and warming Avoid antiemetics and prokinetics if r gastrointestinal obstruction is present or ABBREVIATION the food to body temperature. When r r learned food aversion is suspected, food suspected. Drugs with sedative properties CCK = cholecystokinin should be offered cautiously and removed should be used with caution in severely debilitated animals. Suggested Reading immediately at the first signs of aversion. A Michel KE. Anorexia. In: Washabau RJ, Day PRECAUTIONS patient showing signs of aversion to its MJ, eds., Canine & Feline Gastroenterology, normal diet may accept novel foods. N/A r Elsevier Saunders, 2013, pp. 75–79. Medications the patient is receiving should POSSIBLE INTERACTIONS Remillard RL, Armstrong PJ, et al. Assisted be reviewed for possible side-effects leading to r N/A feeding in hospitalized patients: Enteral and reduced food intake. Significantly ALTERNATIVE DRUG(S) parenteral nutrition. In: Hand MS, malnourished dogs and cats are immediate Thatcher CD, Remillard RL, et al., eds., N/A candidates for assisted feeding (enteral or Small Animal Clinical Nutrition, 4th ed. parenteral feeding). Well-nourished patients Topeka, KS: Mark Morris Institute, 2000, with debilitating disease should not go pp. 351–399. without food for longer than 3–5 days before r Author Kathryn E. Michel assisted feeding is started. The decision to FOLLOW-UP Consulting Editor Stanley L. Marks institute enteral or parenteral feeding can be PATIENT MONITORING Acknowledgment The author and editors influenced by several factors. In animals with r acknowledge the prior contribution of inadequate food intake that have ≥ 10% body Body weight, body and muscle condition score assessment, and hydration Elizabeth M. Streeter. weight loss, hypoalbuminemia, poor body r condition score, evidence of muscle wasting, determination. Monitor caloric intake to and/or chronic disease processes, ensure return of appetite is sufficient to meet Client Education Handout supplemental nutrition should be considered. nutritional needs. r available online Techniques for providing enteral nutrition PREVENTION/AVOIDANCE r include coax feeding and placement of a Maximize patient comfort and wellbeing. r nasoesophageal, esophagostomy, gastrostomy, Enhance the palatability of the diet. or jejunostomy tube. Force feeding should be avoided, particularly in cats in light of the association with conditioned food aversions. JWST589-A64-56 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:57 279mm×216mm

94 Blackwell’s Five-Minute Veterinary Consult A Antebrachial Growth Deformities

decreasing as nutritional standards are closure of distal physis—may note straight r improved. Congenital agenesis of the radius limb with a widened radiocarpal or BASICS (cats and rarely dogs)—occurs infrequently; radiohumeral joint space; may note caudal results in severely bowed antebrachium and bow (recurvatum) to radius and ulna. r DEFINITION carpal subluxation. Asymmetrical closure of medial aspect of Abnormally shaped forelimbs and/or GEOGRAPHIC DISTRIBUTION distal radial physis—varus angular deformity; occasionally internal torsion and pronation. malalignments of the elbow or antebrachial N/A r carpal joints that result from maldevelopment Closure of lateral aspect of distal radial SIGNALMENT physis—valgus angular deformity; external of the radius or ulna in the growing animal. r PATHOPHYSIOLOGY Species torsion. Closure of proximal radial physis r Dog and cat with continued ulnar growth— Antebrachium—predisposed to deformities Breed Predilections malarticulation of the elbow joint; widened resulting from growth of one bone after r Skye terrier—recessive inheritable form. radiohumeral space, and proximal subluxation premature growth cessation or decreased r r Chondrodysplastic and toy breeds of the humeroulnar joint (increased humerus growth rate of the paired bone. Decreased to anconeal process space). rate of elongation in one bone behaves as a (especially basset hound, dachshund, Lhasa apso, Pekingese, Jack Russell terrier)—may be CAUSES retarding strap; the growing paired bone must r r predisposed to elbow malalignment and Trauma Developmental basis twist and curve around the short bone or r r overgrow at the elbow or carpus; causes joint incongruity. Giant breeds (e.g., Great Dane, Nutritional basis r malalignment. Normal growth—bones wolfhound)—may be induced by rapid RISK FACTORS growth owing to excessive or unbalanced r r elongate through the process of endochondral Forelimb trauma Excessive dietary nutrition, osteochondrosis, or hypertrophic ossification, which occurs in the physis; physis supplementation closure occurs when the germinal cell layer osteodystrophy. stops producing new cartilage and the existing Mean Age and Range r cartilage hypertrophies, ossifies, and is Traumatic—any time during the active r r remodeled into bone. Hereditary—may be a growth phase. Elbow malarticulations— DIAGNOSIS component of common elbow joint during growth; may not be recognized until malalignment in many chondrodysplastic secondary arthritic changes become severe, DIFFERENTIAL DIAGNOSIS r r breeds (e.g., basset hound and Lhasa apso). occasionally at several years of age. Elbow dysplasia Fragmented medial r r Osteochondrosis or dietary coronoid process Ununited anconeal Predominant Sex r r oversupplementation—possibly associated N/A process Panosteitis Flexor tendon with retardation of endochondral ossification r SIGNS contracture Hypertrophic osteodystrophy (retained cartilaginous cores) in giant-breed CBC/BIOCHEMISTRY/URINALYSIS r General Comments dogs. Hypertrophic osteodystrophy— r Longer-limbed dogs—angular deformities N/A juvenile growth syndrome with physeal and r periosteal inflammation that may impede generally more common. Shorter-limbed OTHER LABORATORY TESTS r dogs—tend to develop more severe joint N/A growth. Trauma—most common cause; if r germinal cell layer of the physis is damaged, malalignments. Age at the time of IMAGING r new cartilage production and bone elongation premature closure—affects relative degree of Damage to growth potential of the are stopped. Commonly occurs with fractures deformity and joint malarticulation; dogs physis—commonly cannot be seen at the involving the distal ulnar or radial growth with more growth potential remaining tend to time of trauma; usually 2–4 weeks before r plates. A crushing-type fracture (Salter-Harris develop more severe deformity. radiographically apparent. Standard type V) may not be detected on radiographs Historical Findings r craniocaudal and mediolateral radiographic of the injured antebrachium, and angular Traumatic—progressive limb angulation or views—include entire elbow joint; from deformity only becomes evident over time lameness 3–4 weeks after injury; owner may mid-humerus proximally extend to digits due to lack of growth of the affected bone. not be aware of causative event. distally; take same series for comparison to r r SYSTEMS AFFECTED Developmental elbow malalignments— normal contralateral limb. Degree of Musculoskeletal insidious onset of lameness in one or both angular deformities and relative shortening— GENETICS forelimbs; most apparent after exercise. determined by comparing relative lengths of r radius and ulna within the deformed pair to Skye terriers—reported as a recessive Physical Examination Findings r r Premature Distal Ulnar Closure the normal contralateral pair. Degree of inheritable trait. Chondrodysplastic breeds r (dogs)—disturbed endochondral ossification Results in three deformities of the distal torsional deformity—determined by results in asynchronous growth of the paired radius—lateral deviation (valgus), cranial comparing position of the elbow and carpus on same view, i.e., lateral projection of elbow bone system, resulting in altered growth and bowing (procurvatum), and external torsion ◦ resulting in supination of the manus. and 45 oblique of carpus on same view angular deformity. Affected dogs are r predisposed to elbow malalignment. Relative shortening of limb length indicates torsional deformity. Cross-sectional compared to the contralateral normally imaging and creation of models using INCIDENCE/PREVALENCE r stereolithography is useful for full r growing limb. Caudolateral subluxation of r Traumatic—may occur in up to 10% of the radiocarpal joint and malarticulation of appreciation of the deformity. Elbow and actively growing dogs that sustain injuries of the elbow joint—may occur; causes lameness carpal joints—evaluate for malalignment the antebrachium; uncommon in cats. r and painful joint restriction. anddegenerative change.. Presence of Elbow malalignment syndrome ± angular Premature Radial Physeal Closure degenerative change is associated with less r deformity (chondrodysplastic dog breeds)— Affected limb—significantly shorter than optimal outcome following surgical r r fairly common and can be bilateral. Clinical the normal contralateral. Severity of treatment. Elbow joint—evaluate for abnormality in affected individuals is variable. lameness—depends on degree of joint associated ununited anconeal process and r r Nutritionally induced—incidence malarticulation. Complete symmetrical fragmented medial coronoid process. JWST589-A64-56 JWST589-Tilley Printer: Yet to Come August 3, 2015 7:57 279mm×216mm

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DIAGNOSTIC PROCEDURES correct to minimize arthritis development N/A (primary cause of lameness); obtain optimal PATHOLOGIC FINDINGS joint alignment via dynamic proximal ulnar MISCELLANEOUS Cartilage of abnormal growth plate often osteotomy (use triceps brachii muscle traction and joint pressure) or shortening longer bone ASSOCIATED CONDITIONS replaced with bone. Angular deformity can r r (radial or ulnar ostectomy as indicated). Osteochondrosis Hypertrophic occur due to retained cartilage core r r (osteochondrosis) of the ulna. Significant limb length discrepancies— osteodystrophy Un-united anconeal process distraction osteogenesis; osteotomy of the AGE-RELATED FACTORS shortened bone is progressively distracted at the rate of 1 mm/day with an external fixator The younger the patient at the time of system to create new bone length. traumatically induced physeal closure, the TREATMENT more severe the deformity and APPROPRIATE HEALTH CARE malarticulation. r Genetic predisposition—do not breed. ZOONOTIC POTENTIAL r Traumatic physeal damage—not seen at MEDICATIONS r N/A time of injury; revealed 2–4 weeks later. In DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING young (< 6 months) animals, surgical treatment is generally recommended as soon Anti-inflammatory drugs—symptomatic N/A as possible following diagnosis. Treatment treatment of osteoarthritis SYNONYMS may require multiple surgical procedures. CONTRAINDICATIONS Radius curvus NURSING CARE Corticosteroids—do not use owing to ABBREVIATIONS potential systemic side effects and cartilage r N/A HOD = hypertrophic osteodystrophy damage seen with long-term use. r r ACTIVITY = = PRECAUTIONS OCD osteochondrodysplasia UAP Exercise restriction—reduces joint ununited anconeal process Warn client of possible gastrointestinal upset malalignment damage; slows arthritic Suggested Reading progression. associated with chronic anti-inflammatory Balfour RJ, Boudrieau RJ, Gores BR. T-plate DIET therapy. r POSSIBLE INTERACTIONS fixation of distal radial closing wedge Decrease nutritional supplementation in osteotomies for treatment of angular limb giant-breed dogs—slows rapid growth; may N/A r ALTERNATIVE DRUG(S) deformities in 18 dogs. Vet Surg 2000, reduce incidence. Avoid excess weight— 29:207–217. helps control arthritic pain resulting from Neutraceuticals (e.g., chondroitin sulfate and Dismukes DI, Fox DB, Tomlinson JL, joint malalignment and overuse. glucosamine)—may help minimize cartilage Essman SC. Use of radiographic measures CLIENT EDUCATION damage and osteoarthritis development, but r and three-dimensional computed Discuss heritability in chondrodysplastic not proven. r tomographic imaging in surgical correction breeds. Explain that damage to physeal of an antebrachial deformity in a dog. J Am growth potential is not apparent at time of Vet Med Assoc 2008, 232(1):68–73. forelimb trauma and that the diagnosis is FOLLOW-UP Fox DB. Radius and ulna. In Tobias KM, often made 2–4 weeks following an injury. r Johnston SA, eds. Veterinary Surgery Small Discuss the importance of joint PATIENT MONITORING Animal. St. Louis, MO: Elsevier Saunders, r malalignment and resultant osteoarthritis as Postoperative—depends on surgical 2012, pp. 760–784. r r primary causes of lameness. Emphasize that treatment. Periodic checkups—evaluate Fox DB, Tomlinson JL. Principles of angular early surgical treatment leads to a better arthritic status and anti-inflammatory therapy. r limb deformity correction. In Tobias KM, prognosis. Depending on the patient’s age, PREVENTION/AVOIDANCE Johnston SA, eds. Veterinary Surgery Small r treatment may involve multiple procedures. Selective breeding of susceptible breeds. Animal. St. Louis, MO: Elsevier Saunders, r SURGICAL CONSIDERATIONS Avoid dietary oversupplementation in 2012, pp. 657–668. r Premature distal ulnar physeal closure in a rapidly growing giant-breed dogs. Fox DB, Tomlinson JL, Cook JL, Breshears patient < 5–6 months of age (significant POSSIBLE COMPLICATIONS LM. Principles of uniapical and biapical amount of radial growth potential Routinely seen with various osteotomy radial deformity correction using dome remaining)—treated with partial ulnar fixation techniques (e.g., infection, non-union osteotomies and the center of rotation of ≤ ◦ ostectomy, valgus deformities 25 :may of osteotomy, fixator pin tract inflammation, angulation methodology in dogs. Vet Surg improve and may not require additional undercorrection). 2006, 35(1):67–77. surgery; young patients and those with more EXPECTED COURSE AND PROGNOSIS QuinnMK,ErhartN,JohnsonAL,Schaeffer severe deformities: often require a second r DJ. Realignment of the radius in canine r Generally, best results seen with early antebrachial growth deformities treated with definitive correction after maturity. Radial diagnosis and surgical treatment—minimizes or ulnar physeal closure in a mature patient r corrective osteotomy and bilateral (Type II) osteoarthritis. Premature ulnar closure— external fixation. Vet Surg 2000, 29: (limited or no growth potential) requires tends to be easier to manage than premature definitive deformity correction, joint 558–563. r closure of the radial growth plates. Prognosis Author Spencer A. Johnston realignment, or both. Deformity is dependent on severity of the deformity, correction—may be accomplished with a Consulting Editor Walter C. Renberg joint congruity, and presence of degenerative Acknowledgment The author and editors variety of osteotomy techniques; may be joint disease. The prognosis worsens with stabilized with several different internal or r acknowledge the prior contribution of increasing severity. Limb lengthening by Peter K. Shires. external fixation devices; must correct both distraction osteogenesis— requires extensive torsional and angular deformities; performed r postoperative management by the veterinarian at the point of greatest curvature. Joint and owner; high rate of complications. Client Education Handout available malalignment (particularly elbow)—must online JWST589-A65-57 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:3 279mm×216mm

96 Blackwell’s Five-Minute Veterinary Consult A Anterior Uveitis—Cats

inflammatory cells adherent to corneal associated with ulcers is either localized to, or endothelium; most notable ventrally. most severe at, site of ulcer; ocular discharge r BASICS Aqueous flare and cells—cloudiness of often thicker and more copious than with aqueous humor due to increased protein uveitis; discomfort may be alleviated by r DEFINITION content and suspended cellular debris; best topical anesthetic. Horner’s syndrome— r Inflammation of the anterior uveal tissues, visualized with a bright, narrow beam of miosis, enophthalmos, and nictitans including iris (iritis), ciliary body (cyclitis), or light shined through anterior chamber. protrusion are similar in both conditions, but r r both (iridocyclitis). May be associated with Ciliary flush—injection of deep perilimbal Horner’s is non-painful with no ocular r concurrent posterior uveal and retinal anterior ciliary vessels. Deep corneal discharge; ptosis with Horner’s is inflammation (choroiditis; chorioretinitis). vascularization—circumcorneal distribution distinguished from blepharospasm, as the r r May be unilateral or bilateral. (brush border). Miosis and/or resistance to latter is an active process; minor conjunctival r PATHOPHYSIOLOGY pharmacologic dilation. Iridal swelling— hyperemia may be noted with Horner’s, but r r Increased permeability of the blood-aqueous may be generalized or nodular. Reduced cornea and anterior chamber are clear; clinical IOP is consistent with anterior uveitis but is signs of Horner’s syndrome resolve following barrier related to infectious, immune- r mediated, neoplastic, traumatic, or other not a uniform finding. Posterior synechia— topical application of ophthalmic 1–10% adhesions between posterior iris and anterior phenylephrine. causes; allows entrance of plasma proteins and r blood cellular components into aqueous lens surface. Fibrin in anterior chamber. CBC/BIOCHEMISTRY/URINALYSIS r r r humor. Disruption of blood-aqueous barrier Hypopyon or hyphema—accumulations of CBC—often normal; changes may be white blood cells or red blood cells, present related to underlying disease. is initiated and maintained by numerous r chemical mediators, including histamine, respectively, in the anterior chamber; usually Biochemistry—often normal; most settles horizontally in ventral aspect of prostaglandins, leukotrienes, serotonin, r common abnormality in cats with uveitis is kinins, and complement. chamber but may be diffuse. Chronic elevated serum proteins (usually due to changes may include rubeosis iridis, iridal r SYSTEMS AFFECTED polyclonal gammopathy). Urinalysis—often r r hyperpigmentation, secondary cataract, lens normal; changes may be present related to Ophthalmic. Other systems may also be luxation, pupillary seclusion, iris bombe,´ underlying disease. affected by underlying disease process. secondary glaucoma, and phthisis bulbi. OTHER LABORATORY TESTS INCIDENCE/PREVALENCE CAUSES r r r r FeLV serum titers. FIV serum titers. r r Relatively common condition. Tr ue Infectious—mycotic (Blastomyces spp., Coronavirus titers—not specific for FIP but incidence/prevalence unknown. Cryptococcus neoformans; Coccidiodes immitis; may influence the index of suspicion for this r GEOGRAPHIC DISTRIBUTION Histoplasma capsulatum); protozoal disease. Toxoplasma gondii IgM and IgG Geographic location may affect incidence of (Toxoplasma gondii; Leishmania infantum); titers performed on serum and/or aqueous r certain infectious causes of uveitis. bacterial (Bartonella spp., Mycobacterium spp. humor. Bartonella spp. serology, PCR SIGNALMENT or any bacterial septicemia); viral (FIV, FeLV, (serum or aqueous humor) and/or blood feline coronavirus; FHV-1); parasitic culture. Species (ophthalmomyiasis; ocular larval migrans). r IMAGING Cat Idiopathic—lymphocytic-plasmacytic r r Thoracic radiography—may show evidence Mean Age and Range uveitis. Immune-mediated—reaction to lens of causative disease process (e.g., infiltrates r r proteins (due to cataract or lens trauma). Mean age 7–9 years. Anyagemaybe r related to infectious disease; evidence of Neoplastic—primary ocular tumors (esp. r affected. metastatic neoplastic disease). Ocular diffuse iris melanoma, ocular sarcoma); Predominant Sex ultrasound—indicated if opacity of ocular metastasis to uveal tract (esp. lymphoma). Males/neutered males more commonly r media precludes direct examination; may Metabolic—hyperlipidemia; hyperviscosity; affected than females. r reveal intraocular neoplasm or retinal systemic hypertension. Miscellaneous— SIGNS detachment. trauma (blunt or penetrating); ulcerative Historical Findings keratitis; corneal stromal abscess; toxemia of DIAGNOSTIC PROCEDURES r r Cloudy eye—due to corneal edema, any cause. Tonometry—low IOP consistent with r aqueous flare, hypopyon, etc. Painful eye— RISK FACTORS uveitis; elevated IOP indicates glaucoma (primary disease or secondary to uveitis). manifest by blepharospasm, photophobia, or None specific; immune suppression and r rubbing eye; usually less pronounced than in Ocular centesis—if retinal detachment is r geographic location may increase incidence of present, cytology of subretinal aspirate may dogs. Red eye—due to conjunctival certain infectious causes of uveitis. hyperemia and ciliary flush; less pronounced reveal causative agents; anterior chamber r than in dogs in most cases. Vision loss— centesis may be performed for Toxoplasma variable. gondii or Bartonella IgM and IgG titers on Physical Examination Findings aqueous humor. DIAGNOSIS PATHOLOGIC FINDINGS Importance of a thorough physical r examination in cats presenting with uveitis DIFFERENTIAL DIAGNOSIS Gross—see physical examination findings. r r cannot be overstated. Conjunctivitis—redness limited to Histopathologic—corneal edema; Ophthalmic Findings peripheral corneal deep stromal r conjunctival hyperemia (i.e., no ciliary flush); Ocular discomfort—manifest by vascularization; keratic precipitates; preiridal r ocular discharge usually thicker and more blepharospasm and photophobia Ocular copious than in uveitis; discomfort may be fibrovascular membrane; peripheral anterior r discharge—usually serous; sometimes mucoid synechia; posterior synechia; entropion or r alleviated by topical anesthetic. Glaucoma— to mucopurulent. Conjunctival elevated IOP is most consistent distinguishing ectropion uveae; leukocyte accumulation in hyperemia—bulbar and palpebral conjunctiva iris, ciliary body, sclera, choroid (lymphocytic- r feature of this disease; others may include both usually affected. Corneal edema— dilated pupil, Haab’s striae, and buphthalmos. plasmacytic, suppurative, or granulomatous r r diffuse; mild to severe. Keratic Ulcerative keratitis—corneal fluorescein infiltrates, depending on etiology); secondary precipitates—multifocal aggregates of staining will detect ulcers; corneal edema cataract; with posterior segment involvement JWST589-A65-57 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:3 279mm×216mm

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r r r in inflammatory process, cyclitic membrane; required. Indicated only in severe cases as Secondary cataract. Lens luxation. r r vitreal traction bands and retinal detachment one-time injection, followed by topical and/or Retinal detachment. Phthisis bulbi. r may be present. Lymphoplasmacytic systemic anti-inflammatories. EXPECTED COURSE AND PROGNOSIS infiltrate of iris and ciliary body (either diffuse Systemic r r Guarded prognosis for affected eyes. or nodular) is most common histopathologic Prednisone 1–3 mg/kg/day initially; taper r Depends on underlying disease and response r finding. dose after 7–10 days. Use only if systemic to treatment. Cats with treatable underlying infectious causes of uveitis have been ruled disease (e.g., toxoplasmosis) are more likely to out. have a favorable ophthalmic outcome than Nonsteroidal Anti-inflammatory Drugs those with idiopathic lymphocytic- TREATMENT Topical r plasmacytic uveitis or untreatable underlying APPROPRIATE HEALTH CARE Flurbiprofen—apply 2–4 times daily, condition (e.g., FIP, FIV). r depending on severity of disease. Outpatient medical management generally r sufficient. Diclofenac—apply 2–4 times daily, ACTIVITY depending on severity of disease. Systemic MISCELLANEOUS No changes indicated in most cases. r Meloxicam 0.2 mg/kg IV, SC, PO once, AGE-RELATED FACTORS DIET then 0.05 mg/kg IV, SC, PO q24h for 2 days, r Youngercatsmorelikelytobediagnosed No changes indicated. then 0.025 mg/kg q24–48h. Due to potential r renal effects, limit duration of use to 4 days. with infectious etiology. Older cats at higher CLIENT EDUCATION r r Robenacoxib 1 mg/kg PO once daily; limit risk of idiopathic lymphocytic-plasmacytic Inform of potential systemic diseases r uveitis and intraocular neoplastic causes. causing ophthalmic signs and emphasize duration of use to 3 days. Ketoprofen 1 mg/ ZOONOTIC POTENTIAL importance of appropriate diagnostic testing. kg PO q24h; limit duration of use to 5 days. r r r None in most cases. Some forms of In addition to symptomatic uveitis Topical Mydriatic/Cycloplegic r systemic infection causing uveitis may pose a treatment, treatment of underlying disease Atropine sulfate 1%—apply 1–4 times slight risk to immunocompromised owners. (when possible) is paramount to a positive daily, depending on severity of disease. Use r outcome. Inform of potential complications lowest frequency adequate to maintain dilated PREGNANCY/FERTILITY/BREEDING and emphasize compliance with treatment pupil and ocular comfort; taper medication as Avoid systemic corticosteroids. Because of and follow-up recommendations that will condition resolves. Ointment is preferred over systemic absorption, topical corticosteroids reduce the likelihood of complications. solution in cats as it causes less salivation. may also pose a risk, especially with frequent SURGICAL CONSIDERATIONS CONTRAINDICATIONS application. r r r None in most cases. Specific instances Avoid the use of miotic medications (e.g., SYNONYM requiring surgical intervention include pilocarpine), including topical prostaglandins Iridocyclitis (e.g., latanoprost), in the presence of uveitis. removal of ruptured lenses and surgical r SEE ALSO management of secondary glaucoma. Topical and subconjunctival corticosteroids r r r Horner’s Syndrome Red Eye Chronic uveitis leading to secondary are absolutely contraindicated in the presence r ABBREVIATIONS glaucoma commonly necessitates enucleation of ulcerative keratitis. Corticosteroids r r r FeLV = feline leukemia virus FHV-1 = of affected globes. Enucleation is (especially systemic) should be avoided in cats r feline herpesvirus type 1 FIP = feline recommended in cats with uveitis related to with systemic hypertension. Avoid systemic r infectious peritonitis FIV = feline diffuse iris melanoma or other primary NSAIDs in cats with renal disease. r intraocular tumors. PRECAUTIONS immunodeficiency virus IOP = intraocular Owing to concern for secondary glaucoma, pressure topical atropine should be used judiciously Suggested Reading and IOP should be monitored periodically. Cullen C, Webb A. Ocular manifestations of MEDICATIONS POSSIBLE INTERACTIONS systemic diseases. Part 2: The cat. In: Gelatt DRUG(S) Systemic corticosteroids and nonsteroidal KN, ed., Veterinary Ophthalmology, 5th Corticosteroids anti-inflammatory drugs should not be used ed. Ames, IA: Wiley-Blackwell, 2013, pp. 1978–2036. Topical concurrently. r Martin C. Anterior uvea and anterior Prednisolone acetate 1%—apply 2–8 times chamber. In: Ophthalmic Disease in daily, depending on severity of disease; taper Veterinary Medicine. London: Manson medication as condition resolves. r Publishing, 2010, pp. 298–336. Dexamethasone 0.1%—apply 2–8 times FOLLOW-UP Miller P. Uvea. In: Maggs DJ, Miller PE, Ofri daily, depending on severity of disease; taper PATIENT MONITORING r R, Slatter’s Fundamentals of Veterinary medication as condition resolves. Other Recheck in 3–7 days, depending on severity Ophthalmology, 5th ed. St. Louis, MO: topical corticosteroids (e.g., betamethasone, of disease. IOP should be monitored at Elsevier Saunders, 2013, pp. 220–246. hydrocortisone) are considerably less effective recheck to detect secondary glaucoma. Stiles J. Feline ophthalmology. In: Gelatt KN, in the treatment of intraocular inflammation. r Frequency of subsequent rechecks dictated by ed., Veterinary Ophthalmology, 5th ed. Taper treatment frequency as condition severity of disease and response to treatment. Ames, IA: Wiley-Blackwell, 2013, improves; stopping topical corticosteroids POSSIBLE COMPLICATIONS pp. 1477–1559. abruptly may result in rebound of ocular Author Ian P. Herring inflammation. Systemic Complications Consulting Editor Paul E. Miller Subconjunctival Occur as a result of the systemic etiology of r Triamcinolone acetonide 4 mg by the uveitis. subconjunctival injection. Ophthalmic Complications Client Education Handout r r Methylprednisolone 4 mg by Secondary glaucoma—common available online r subconjunctival injection. Often not complication of chronic uveitis in cats. JWST589-A66-58 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:12 279mm×216mm

98 Blackwell’s Five-Minute Veterinary Consult A Anterior Uveitis—Dogs

r eye. Ocular discharge—usually serous; sometimes mucoid to mucopurulent. r BASICS Conjunctival hyperemia—bulbar and DIAGNOSIS palpebral conjunctiva both usually affected. r DEFINITION Corneal edema—diffuse; mild to severe. DIFFERENTIAL DIAGNOSIS r r r Inflammation of the anterior uveal tissues, Keratic precipitates—multifocal aggregates Conjunctivitis—redness limited to including iris (iritis), ciliary body (cyclitis), or of inflammatory cells adherent to corneal conjunctival hyperemia (i.e., no ciliary flush); r endothelium; most notable ventrally. both (iridocyclitis). May be associated with r ocular discharge usually thicker and more concurrent posterior uveal and retinal Aqueous flare and cells—cloudiness of copious than in uveitis; discomfort may be inflammation (choroiditis; chorioretinitis). aqueous humor due to increased protein alleviated with application of topical r r May be unilateral or bilateral. content and suspended cellular debris; best anesthetic. Glaucoma—elevated IOP is PATHOPHYSIOLOGY visualized with a bright, narrow beam of most consistent feature of this disease; others r light shined through anterior chamber. may include dilated pupil, Haab’s striae, and Increased permeability of the blood-aqueous r r Ciliary flush—injection of deep perilimbal buphthalmos. Lens luxation—corneal barrier related to infectious, immune- r anterior ciliary vessels. Deep corneal edema may be localized to site of lens contact mediated, traumatic, or other causes allows vascularization—circumcorneal distribution with endothelium or may be diffuse as a result entrance of plasma proteins and blood cellular r (brush border). Miosis and/or resistance to of associated uveitis and/or glaucoma; lens components into aqueous humor. r r pharmacologic dilation. Iridal swelling. luxation is highly breed associated. Disruption of blood-aqueous barrier is r r Reduced IOP is consistent with uveitis but Ulcerative keratitis—corneal fluorescein initiated and maintained by numerous r is not a uniform finding. Posterior staining will detect ulcers; corneal edema chemical mediators, including histamine, synechia—adhesions between posterior iris associated with ulcers is either localized to, or prostaglandins, leukotrienes, serotonin, r and anterior lens surface. Fibrin in anterior most severe at, site of ulcer; ocular discharge kinins, and complement. r chamber. Hypopyon or hyphema— often thicker and more copious than with SYSTEMS AFFECTED accumulations of white blood cells or red uveitis; discomfort may be partially alleviated r r r Ophthalmic. Other systems may also be blood cells, respectively, in the anterior by topical anesthetic. Corneal endothelial affected by underlying disease process. chamber; usually settles horizontally in dystrophy or degeneration—diffuse corneal ventral aspect of chamber but may be diffuse. INCIDENCE/PREVALENCE r edema is present, but IOP is normal; r r Chronic changes may include rubeosis conjunctival hyperemia and signs of ocular Relatively common condition. Tr ue r incidence/prevalence unknown. iridis, iridal hyperpigmentation, secondary discomfort are generally absent. Horner’s cataract, lens luxation, pupillary seclusion, iris GEOGRAPHIC DISTRIBUTION syndrome—miosis, enophthalmos, and bombe,´ secondary glaucoma, and phthisis nictitans protrusion are similar in both Geographic location may affect incidence of bulbi. conditions, but Horner’s is non-painful with certain infectious causes of uveitis. CAUSES no ocular discharge; ptosis with Horner’s is SIGNALMENT r Infectious—mycotic (Blastomyces distinguished from blepharospasm as the Species dermatitidis, Cryptococcus neoformans, latter is an active process; minor conjunctival Dog Coccidiodes immitis, Histoplasma capsulatum); hyperemia may be noted with Horner’s, but cornea and anterior chamber are clear; clinical Breed Predilections protozoal (Toxoplasma gondii, Neospora r r caninum, Leishmania donovani); rickettsial signs of Horner’s syndrome resolve following None for most causes. Uveitis associated topical application of 1–10% phenylephrine. with iridociliary cysts in golden retriever (Ehrlichia canis, Rickettsia rickettsii); bacterial (a.k.a. golden retriever uveitis, pigmentary (Leptospira spp., Bartonella spp., Brucella CBC/BIOCHEMISTRY/URINALYSIS r uveitis). Increased incidence of canis, Borrelia burgdorferi, any bacterial Often normal; changes related to underlying uveodermatologic syndrome in Siberian septicemia); algal (Prototheca spp.); viral disease may be present. husky, Akita, Samoyed, and Shetland (adenovirus, distemper, rabies, herpes); OTHER LABORATORY TESTS parasitic (ocular filariasis, ocular larval r sheepdog. r Serology for infectious diseases listed under migrans). Immune-mediated—reaction to Mean Age and Range “Causes” may be appropriate, depending on r r lens proteins (due to cataract or lens trauma); Any age may be affected. Mean age in index of suspicion for infectious etiology. uveodermatologic syndrome; post-vaccinal r uveodermatologic syndrome—2.8 years. Clinical signs raising the suspicion of r reaction to canine adenovirus vaccine; r systemic disease including lethargy, pyrexia, Mean age in golden retriever uveitis— vasculitis. Neoplastic—primary ocular weight loss, coughing, lymphadenopathy, etc., 8.6 years. tumors (especially uveal melanoma, warrant serology for infectious diseases. SIGNS iridociliary adenoma/adenocarcinoma); IMAGING Historical Findings metastasis to uveal tract (lymphosarcoma r r r Red eye—due to conjunctival hyperemia most common). Metabolic— Thoracic radiography may show evidence of r hyperlipidemia; hyperviscosity; systemic causative disease process (e.g., systemic and ciliary flush. Cloudy eye—due to r r corneal edema, aqueous flare, hypopyon, etc. hypertension. Miscellaneous—idiopathic; mycoses; metastatic neoplasia). Abdominal r Painful eye—manifest by blepharospasm, trauma; pigmentary uveitis of golden ultrasound may be warranted if suspicion for r r photophobia, or rubbing eye. Vision loss— retrievers; ulcerative keratitis; corneal stromal metastatic neoplastic disease is high. Ocular variable. abscess; scleritis; lens instability/luxation; ultrasound is indicated if opacity of ocular media precludes direct examination; may Physical Examination Findings dental/periodontal disease; toxemia. RISK FACTORS reveal intraocular neoplasm or retinal The importance of a thorough physical detachment. examination in dogs presenting with uveitis None specific; immune suppression and DIAGNOSTIC PROCEDURES cannot be overstated. geographic location may increase incidence of r Ophthalmic Findings certain infectious causes of uveitis; breed Tonometry—low IOP consistent with r Ocular discomfort—manifest by predispositions should be considered. uveitis; elevated IOP indicates glaucoma (primary disease or secondary to uveitis). blepharospasm, photophobia, and rubbing r Lymph node aspirates—if enlarged nodes JWST589-A66-58 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:12 279mm×216mm

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r are palpable, aspiration for cytology is Dexamethasone 0.1%—apply 2–8 times r indicated. Ocular centesis—if retinal daily, depending on severity of disease; taper detachment is present, cytology of subretinal medication as condition resolves. r FOLLOW-UP aspirate may reveal causative agents; anterior Other topical corticosteroids (e.g., chamber centesis is generally unrewarding. betamethasone, hydrocortisone) are PATIENT MONITORING PATHOLOGIC FINDINGS considerably less effective in the treatment of Recheck in 3–7 days, depending on severity r intraocular inflammation. Gross—see “Physical Examination r of disease. IOP should be monitored at r Findings.” Histopathologic—corneal Taper treatment frequency over several recheck to detect secondary glaucoma. edema; peripheral corneal deep stromal weeks as condition improves; stopping topical Frequency of subsequent rechecks dictated by vascularization; keratic precipitates; preiridal corticosteroids abruptly may result in severity of disease and response to treatment. fibrovascular membrane; peripheral anterior rebound of ocular inflammation. POSSIBLE COMPLICATIONS Subconjunctival r synechia; posterior synechia; entropion or r Triamcinolone acetonide 4–6 mg by Many systemic complications, including ectropion uveae; leukocyte accumulation in death, may occur due to systemic etiology of subconjunctival injection. r iris, ciliary body, sclera, choroid (lymphocytic, r uveitis. Ophthalmic complications include plasmacytic, suppurative, or granulomatous Methylprednisolone 3–10 mg by subconjunctival injection. secondary cataract, secondary glaucoma, lens infiltrates, depending on etiology); secondary r Often not required. luxation, retinal detachment, phthisis bulbi. cataract; with posterior segment involvement r EXPECTED COURSE AND PROGNOSIS in inflammatory process, cyclitic membrane; Indicated only in severe cases as one-time vitreal traction bands and retinal detachment injection followed by topical and/or systemic Extremely variable; depends on underlying may be present. anti-inflammatories. disease and response to treatment. Systemic r Prednisone 0.5–2.2 mg/kg/day initially; taper dose after 7–10 days. r TREATMENT Use only if systemic infectious causes of MISCELLANEOUS uveitis have been ruled out. APPROPRIATE HEALTH CARE ZOONOTIC POTENTIAL Nonsteroidal Anti-inflammatory Drugs None in most cases. Some forms of systemic Outpatient medical management is generally Topical sufficient. r infection causing uveitis may pose a slight risk Less effective than topical corticosteroids. to immune-compromised owners. NURSING CARE r Flurbiprofen—apply 2–4 times daily, PREGNANCY/FERTILITY/BREEDING None depending on severity of disease. r Avoid systemic corticosteroids. Because of ACTIVITY Diclofenac—apply 2–4 times daily, r possibility of systemic absorption, topical No changes indicated in most cases. depending on severity of disease. r Systemic corticosteroids may also pose risk, especially Reduced exposure to bright light may r with frequent application in small dogs. alleviate discomfort. Do not use concurrently with systemic corticosteroids; avoid in the presence of SYNONYMS DIET hyphema. Iridocyclitis r No changes indicated. Carprofen 2.2 mg/kg PO q12h or SEE ALSO CLIENT EDUCATION 4.4 mg/kg PO q24h. r Red Eye r Tepoxalin 10 mg/kg PO q24h. Inform of potential systemic diseases r ABBREVIATIONS causing ophthalmic signs and emphasize Meloxicam 0.2 mg/kg PO q24h. r r r = = importance of appropriate diagnostic testing. Firocoxib 5 mg/kg PO q24h. IOP intraocular pressure NSAID r nonsteroidal anti-inflammatory drug In addition to symptomatic uveitis Topical Mydriatic/Cycloplegic r treatment, treatment of underlying disease Atropine sulfate 1%—apply 1–4 times Suggested Reading (when possible) is paramount to a positive r daily, depending on severity of disease. Use Cullen C, Webb A. Ocular manifestations of outcome. Inform of potential complications lowest frequency adequate to maintain dilated systemic diseases. Part 1: The dog. In: Gelatt and emphasize compliance with treatment pupil and ocular comfort; taper medication as KN, ed., Veterinary Ophthalmology, 5th and follow-up recommendations that will condition resolves. ed. Ames, IA: Wiley-Blackwell, 2013, reduce the likelihood of complications. CONTRAINDICATIONS pp. 1897–1977. r SURGICAL CONSIDERATIONS Avoid the use of miotic medications (e.g., Hendrix D. Diseases and surgery of the None in most cases. Specific instances pilocarpine, demecarium bromide), including canine anterior uvea. In: Gelatt KN, ed., requiring surgical intervention include topical prostaglandins (e.g., latanoprost), in Veterinary Ophthalmology, 5th ed. Ames, r removal of ruptured lenses, removal of the presence of uveitis. Topical and IA: Wiley-Blackwell, 2013, pp. 1146–1198. cataracts causing uveitis (if prognosis for subconjunctival corticosteroids are Martin C. Anterior uvea and anterior r successful surgery is otherwise favorable), and contraindicated in ulcerative keratitis. Avoid chamber. In: Ophthalmic Disease in surgical management of secondary glaucoma. systemic corticosteroids in dogs with systemic Veterinary Medicine. London: Manson hypertension or systemic infections. Publishing, 2010, pp 298–336. PRECAUTIONS Miller P. Uvea. In: Maggs DJ, Miller PE, Ofri R, Slatter’s Fundamentals of Veterinary MEDICATIONS Out of concern for secondary glaucoma, Ophthalmology, 5th ed. St. Louis, MO: topical atropine should be used judiciously Elsevier Saunders, 2013, pp. 220–246. DRUG(S) OF CHOICE and IOP should be monitored periodically. Author Ian P. Herring Corticosteroids POSSIBLE INTERACTIONS Consulting Editor Paul E. Miller Topical Systemic corticosteroids and NSAIDS should r not be used concurrently. Prednisolone acetate 1% apply 2–8 times Client Education Handout daily, depending on severity of disease; taper ALTERNATIVE DRUG(S) available online medication as condition resolves. N/A JWST589-A67-59 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:14 279mm×216mm

100 Blackwell’s Five-Minute Veterinary Consult A Antidepressant Toxicosis—SSRIs and SNRIs

r Mean Age and Range Testing for SSRIs/SNRIs can be performed, Any age can be affected. but the tests are not clinically useful. r BASICS SIGNS Note: venlafaxine will give a false positive for PCP on many urine drug screens. Historical Findings DEFINITION r DIAGNOSTIC PROCEDURES r Agitation or lethargy r Toxicity secondary to the overdose of a Dilated pupils There are no diagnostic tests to confirm r selective serotonin reuptake inhibitor (SSRI), Vomiting serotonin syndrome. r serotonin and norepinephrine reuptake Tre mor s r inhibitor (SNRI) or co-ingestion of two types Hypersalivation of serotonergic drugs. r r Diarrhea r SSRIs include citalopram (Celexa), Seizures r TREATMENT escitalopram (Lexapro), fluoxetine (Prozac), Nystagmus fluvoxamine (Luvox), paroxetine (Paxil), APPROPRIATE HEALTH CARE Physical Examination Findings r sertraline (Zoloft), vilazodone (Viibryd), r Emesis (if asymptomatic and recent Agitation vortioxetine (Brintellix). SNRIs include r ingestion) or gastric lavage (if large number of Ataxia desvenlafaxine (Pristiq), duloxetine r pills ingested). Mydriasis r (Cymbalta), levomilnacipran (Fetzima), r Activated charcoal with cathartic (if severe Tre mor s milnacipran (Ixel, Savella), tofenacin (Elamol, r signs are expected, may need to repeat due to Vomiting Tofacine), and venlafaxine (Effexor). r long half-life). Disorientation PATHOPHYSIOLOGY r Hyperthermia NURSING CARE r r SSRIs and SNRIs are antidepressants that Vocalization IV fluids to help maintain blood pressure and r inhibit reuptake of serotonin, a Depression body temperature, and to protect kidneys r neurotransmitter involved in aggression, Tachycardia from myoglobinuria. r anxiety, appetite, depression, migraine, pain, Hypotension CLIENT EDUCATION r and sleep. The SNRIs also inhibit the Diarrhea r If animal appears blind, sight should return. reuptake of norepinephrine. Blindness r r Excessive stimulation of serotonin receptors Seizures r can occur by enhanced serotonin synthesis, Hypersalivation r increased presynaptic serotonin release, Death inhibition of serotonin uptake into the MEDICATIONS CAUSES presynaptic neuron, inhibition of serotonin r DRUG(S) OF CHOICE metabolism, or serotonin agonism. Serotonin SSRI/SNRI overdose—accidental exposure, r Agitation: syndrome is characterized in humans as a inappropriate administration, or therapeutic ◦ Phenothiazines (acepromazine combination of symptoms that include at use. r 0.025–0.05 mg/kg IV, titrate up as needed). least three of the following: myoclonus, Ingestion of an SSRI/SNRI along with ◦ Cyproheptadine (dog, 1.1 mg/kg; cat, mental aberration, agitation, hyperreflexia, another class of medications that increases 2–4 mg PO q4–6h or can be given rectally tremors, diarrhea, ataxia, or hyperthermia. serotonin (TCAs, MAOIs, novel r if vomiting). Toxic dosage varies widely among antidepressants, tramadol, fentanyl, ◦ Benzodiazepines (diazepam 0.5–2 mg/kg commonly available SSRIs and SNRIs and are meperidine, amphetamines, cocaine, IV) (see “Precautions”). not well defined in veterinary medicine. dextromethorphan, 5-HTP, buspirone, r Tremors: methocarbamol (50–150 mg/kg SYSTEMS AFFECTED bupropion, triptans, LSD). r RISK FACTORS IV, titrate up but do not exceed Cardiovascular—decreased vascular tone r 330 mg/kg/day). Animals on a serotonergic drug. (hypotension), increased heart rate and stroke r CONTRAINDICATIONS volume (tachycardia). Underlying liver or kidney disease. Cats are r r High risk of serotonin syndrome: other Gastrointestinal—increased smooth muscle attracted to venlafaxine and will eat multiple SSRIs, SNRIs, MAOIs, TCAs, contractility (vomiting, diarrhea). capsules. r amphetamines, 5-HTP, clarithromycin, Nervous—stimulation (agitation, dextromethorphan, lithium, St. John’s wort. restlessness, seizures) and altered mental status r Low risk of serotonin syndrome: tramadol, (vocalization, disorientation). r fentanyl, amantadine, bupropion, Neuromuscular—autonomic dysfunction DIAGNOSIS carbamazepine, codeine. (hyperactivity) and neuromuscular DIFFERENTIAL DIAGNOSIS PRECAUTIONS hyperactivity (hyperreflexia, myoclonus, r r tremors). Toxicologic: TCAs, MAOIs, metaldehyde, Benzodiazepines (e.g., diazepam) are r Ophthalmic—increased autonomic lead, ethylene glycol, hops, anticholinergics, reported by some sources to exacerbate function (mydriasis). antihistamines. serotonin syndrome and their use for r r Respiratory—increased bronchial smooth Non-toxicologic: meningitis e.g., (rabies, SSRI/SNRI toxicosis is not universally muscle contraction (dyspnea). canine distemper), neoplasia, heat stroke, recommended. malignant hyperthermia. INCIDENCE/PREVALENCE POSSIBLE INTERACTIONS CBC/BIOCHEMISTRY/URINALYSIS r Second most common human prescription r Decreased metabolism of SSRIs/SNRIs: medication toxicosis (after cardiac CBC/biochemistry: no changes are cimetidine, diuretics, quinidine, lithium. expected. r medications). r Increased levels of medications (decreased Urinalysis: myoglobinuria secondary to SIGNALMENT metabolism): theophylline, coumadin, rhabdomyolysis may be seen. digoxin. Species OTHER LABORATORY TESTS r Dogs and cats Blood gas: metabolic acidosis may be seen. JWST589-A67-59 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:14 279mm×216mm

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Suggested Reading Pugh CM, Sweeney JT, Bloch CP, et al. FOLLOW-UP MISCELLANEOUS Selective serotonin reuptake inhibitor (SSRI) toxicosis in cats: 33 cases PATIENT MONITORING AGE-RELATED FACTORS (2004–2010). J Vet Emerg Crit Care 2013, Blood pressure, heart rate, urine color: Young and elderly animals are more at risk for 23(5):565–570. monitor hourly, then less frequently as the developing serious toxicosis. Thomas DE, Lee JA, Hovda LR. animal remains stable. PREGNANCY/FERTILITY/BREEDING Retrospective evaluation of toxicosis from selective serotonin reuptake inhibitor PREVENTION/AVOIDANCE SSRIs and SNRIs can cause increased litter r antidepressants: 313 dogs (2005–2010). J Keep medications out of the reach of mortality and possible birth defects. Vet Emerg Crit Care 2012, 22(6):674–681. animals. r ABBREVIATIONS Wismer TA. Antidepressant drug overdoses in Follow label directions when giving r 5-HTP = 5-hydroxytryptophan dogs. Vet Med 2000, 95(7):520–525. serotonergic drugs to animals. r MAOI = monoamine oxidase inhibitor r Author Tina Wismer POSSIBLE COMPLICATIONS PCP = phencyclidine (angel dust) r Consulting Editor Lynn R. Hovda Renal failure secondary to myoglobinuria SNRI = serotonin and norepinephrine from rhabdomyolysis. DIC secondary to reuptake inhibitor r hyperthermia. SSRI = selective serotonin reuptake EXPECTED COURSE AND PROGNOSIS inhibitor r r Prognosis is good in most cases, with TCA = tricyclic antidepressant recovery in 12–24 hours. r Patients that present in status epilepticus or with severe hyperthermia have a guarded prognosis. JWST589-A68-60 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:20 279mm×216mm

102 Blackwell’s Five-Minute Veterinary Consult A Antidepressant Toxicosis—Tricyclic

r Predominant Sex Serum TCA levels—can be used to None determine if exposure has occurred. BASICS SIGNS IMAGING General Comments N/A DEFINITION r r Signs can occur at therapeutic doses. DIAGNOSTIC PROCEDURES r Toxicity secondary to the acute or chronic Signs of toxicosis can occur within 30–60 r ingestion of a tricyclic antidepressant (TCA). ECG to monitor for arrhythmias r minutes or be delayed by several hours. r TCA medications include amitriptyline, Blood pressure monitoring Historical Findings amoxapine, clomipramine, desipramine, r PATHOLOGIC FINDINGS doxepin, imipramine, maprotiline (tetracyclic Evidence of accidental consumption of the No specific lesions expected owner’s or another pet’s medication antidepressant), nortriptyline, protriptyline, r CNS depression (lethargy, ataxia) trimipramine, and many others. r Vocalization PATHOPHYSIOLOGY r Vomiting or hypersalivation r r TCAs block the reuptake of norepinephrine, Panting TREATMENT r dopamine, and serotonin at the neuronal Agitation or restlessness APPROPRIATE HEALTH CARE r membrane. They also have anticholinergic Tachypnea or dyspnea r r Outpatient—not recommended for activity and are thought to have membrane Tre mor s r symptomatic patients, patients with cardiac stabilizing effects on the myocardium Seizures (particularly inhibiting fast sodium channels disease, or patients ingesting greater than a Physical Examination Findings therapeutic dose of TCAs. in the ventricular myocardium). They can also r r CNS depression or stimulation Inpatient—asymptomatic: have slight alpha-adrenergic blocking activity r Tachycardia ◦ Decontamination with emesis (less than and antihistaminic effects. r r Mydriasis 15 minutes of exposure time), gastric lavage TCAs are rapidly and well absorbed across r Hypothermia in large exposures, and activated charcoal. the digestive tract. They can decrease GI r Hypertension ◦ Monitor at a clinic for a minimum of motility and delay gastric emptying, resulting r Pallor 6 hours after exposure. in delayed drug absorption. r r r Cyanosis Inpatient—symptomatic: stabilize the CV Lipophilic, protein bound, and well r Hyperthermia and CNS systems and provide supportive distributed across all tissues. r r Arrhythmias care. They are metabolized by the liver and r Hypotension undergo enterohepatic recirculation. The r NURSING CARE Urinary retention r inactive metabolites are eliminated in the r Fluid therapy—restore hydration due to urine. Constipation vomiting, regulate blood pressure when CAUSE hypotension is noted. SYSTEMS AFFECTED r r Thermoregulation as needed. Nervous—increased dopamine, serotonin, Accidental exposure, inappropriate r and norepinephrine levels in the CNS administration, or therapeutic use. Enema with warm water if not defecating contribute to CNS signs. RISK FACTORS within 6–12 hours. r r Cardiovascular—anticholinergic effects and Concurrent use of other antipsychotic DIET inhibition of norepinephrine reuptake medication NPO if vomiting r contribute to tachycardia; alpha adrenergic Pre-existing cardiac disease CLIENT EDUCATION r blockade, cardiac membrane stabilization, and With a prescribed TCA, instruct client to decreased cardiac contractility contribute to monitor for adverse or idiosyncratic effects, hypotension and arrhythmias. r and to stop the medication and contact the Gastrointestinal—anticholinergic effects DIAGNOSIS clinic if they occur. may cause ileus and delayed gastric emptying. r r DIFFERENTIAL DIAGNOSIS Prevent exposure to non-prescribed Ophthalmic—anticholinergic effects can r medication. cause pupillary dilation. Toxicity caused by other antipsychotic r SURGICAL CONSIDERATIONS Renal/Urologic—anticholinergic effects medication, stimulant substances (e.g., may cause urinary retention. amphetamines, cocaine, methylxanthines, or N/A GENETICS pseudoephedrine) or substances capable of Species and individual differences in causing cardiac arrhythmias (e.g., quinidine, propranolol, albuterol, digoxin). absorption, metabolism, and elimination can r be significant. Non-toxicologic differentials include MEDICATIONS hyperkalemia, cardiac ischemia, DRUG(S) OF CHOICE INCIDENCE/PREVALENCE cardiomyopathy, and other diseases of cardiac Incidence is unknown. Decontamination conduction. r SIGNALMENT CBC/BIOCHEMISTRY/URINALYSIS Emesis within 15 minutes of ingestion only if asymptomatic; induce emesis with either Species Expected to be normal hydrogen peroxide (dog, 1–2 mL/kg PO) or Dogs and cats OTHER LABORATORY TESTS r apomorphine (dog/cat, 0.03–0.05 mg/kg IV, Breed Predilections Blood gases—metabolic acidosis may be IM, or 0.1 mg/kg SC, or 0.25 mg instilled in None noted. conjunctiva of eye). r r Mean Age and Range OTC urine drug screen for TCAs—can be Gastric lavage under anesthesia may be None used to determine if exposure has occurred; considered with large exposures. not useful in determining degree of toxicity. JWST589-A68-60 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:20 279mm×216mm

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r After emesis (or if > 15 minutes of POSSIBLE INTERACTIONS PREGNANCY/FERTILITY/BREEDING r exposure), administer activated charcoal TCAs increase risk of hyperthermia, TCAs cross the placenta and be found in (1–2 g/kg PO) with a cathartic such as seizures, and death with use of MAOIs. breast milk; the significance of this is not r sorbitol (70% sorbitol at 3 mL/kg) or sodium Sympathomimetic and anticholinergic known at this time. sulfate (0.25 tsp/5 kg) if no diarrhea. medications increase the risk for arrhythmias r SEE ALSO Repeat one-half dose of activated charcoal or cardiac effects from TCAs. r r Antidepressant Toxicosis—SSRIs and in 4–6 hours if patient is still symptomatic. Levothyroxine increases the risk for SNRIs Other arrhythmias when used with TCAs. r r Poisoning (Intoxication) Therapy Cyproheptadine: dogs, 1.1 mg/kg q8h PO ALTERNATIVE DRUG(S) ABBREVIATIONS or rectally; cats, 2–4 mg/cat q12–24h PO or r N/A CNS = central nervous system rectally; used for treatment of serotonin r CV = cardiovascular syndrome. r r ECG = electrocardiogram 20% intravenous lipid emulsion-prevents r GI = gastrointestinal lipophilic TCAs from reaching the site of r FOLLOW-UP MAOI = monoamine oxidase inhibitor action by acting as a sequestrant in an r OTC = over-the-counter expanded plasma lipid phase; 1.5 mL/kg IV PATIENT MONITORING r r TCA = tricyclic antidepressant bolus followed by 0.25 mL/kg/min IV CRI Acid-base status—monitor for acidosis and INTERNET RESOURCES for 1 hour. Can repeat bolus every 3–5 if implementing sodium bicarbonate therapy. r r http://www.aspcapro.org/poison minutes as needed up to 3 mL/kg, not to Blood pressure—monitor until r exceed a total dose of 8 mL/kg. asymptomatic. http://www.petpoisonhelpline.com/ r r Sodium bicarbonate—used to maintain ECG—monitor until asymptomatic. Suggested Reading blood pH at 7.55; if not monitoring acid-base PREVENTION/AVOIDANCE Gwaltney-Brant S. Antidepressants: Tricyclic status, start with 2–3 mEq/kg IV over 15–30 Keep medications out of reach of pets. antidepressants. In: Plumlee KH, ed., minutes in a symptomatic patient. r POSSIBLE COMPLICATIONS Clinical Veterinary Toxicology. St. Louis, Diazepam 0.5–1 mg/kg IV, repeat if MO: Mosby, 2004, pp. 286–288. necessary; for agitation or seizures. Pulmonary edema can occur secondary to r aggressive fluid therapy. Gwaltney-Brant S, Meadows I. Use of Acepromazine 0.02 mg/kg IV, repeat if intravenous lipid emulsions for treating necessary; for agitation or mild hypertension. EXPECTED COURSE AND PROGNOSIS r r certain poisoning cases in small animals. Vet Phenobarbital—as needed for seizure Due to the variable half-lives of the different Clin North Am Small Anim Pract 2012, control. TCAs, signs can last 24 hours or longer. r 42:251–262. CONTRAINDICATIONS The prognosis is generally good in patients Johnson LR. Tricyclic antidepressant r exhibiting mild to moderate signs. Atropine should not be used because TCAs r toxicosis. Vet Clin North Am Small Anim have anticholinergic effects that are The prognosis is guarded in patients Pract 1990, 20:393–403. exacerbated by atropine. exhibiting severe signs such as seizures, Volmer PA. Recreational drugs: Tricyclic r Magnesium sulfate should not be used as a arrhythmias, or hypotension that are poorly antidepressants. In: Peterson ME, Talcott cathartic. Ileus or reduced GI motility will responsive to therapy. PA, eds., Small Animal Toxicology, 2nd ed. enhance absorption of magnesium and may St. Louis, MO: Saunders Elsevier, 2006, result in magnesium toxicity. pp. 303–306. r Beta-blockers (e.g., propranolol, atenolol) Wismer TA. Antidepressant drug overdoses in should not be used for tachycardia because of MISCELLANEOUS dogs. Vet Med 2000, 95:520–525. their potential to exacerbate hypotension. Author Cristine L. Hayes r ASSOCIATED CONDITIONS Do not induce emesis in a patient already Consulting Editor Lynn R. Hovda showing clinical signs. Serotonin syndrome may occur as a result of PRECAUTIONS TCA ingestion. AGE-RELATED FACTORS N/A None JWST589-A69-61 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:23 279mm×216mm

104 Blackwell’s Five-Minute Veterinary Consult A Aortic Stenosis

r (dogs), supravalvular aortic stenosis (cats), Newfoundland dogs are overrepresented for and dynamic LVOT obstruction (cats). combined patent ductus arteriosus and SAS. r BASICS GEOGRAPHIC DISTRIBUTION Volume overload of PDA can cause a N/A relative aortic stenosis and be difficult to DEFINITION distinguish from PDA with mild SAS. SIGNALMENT A narrowing of the left ventricular outflow CAUSES r r tract (LVOT) that restricts blood flow leaving Species Congenital heart disease. Secondary to the ventricle. It is most commonly congenital, Dog and Cat valvular change as with aortic valve r often heritable. The lesion is most commonly Breed Predilections endocarditis or calcification. Dynamic or subvalvular in dogs, but may be valvular or The Newfoundland, golden retriever, fixed LVOT obstruction in some cats with supravalvular (more often in cats). rottweiler, Bouvier des Flanders, Dogue de hypertrophic (obstructive) cardiomyopathy. r Subvalvular aortic stenosis (SAS) in dogs is Bordeaux, German shepherd, and boxer have A component of complex congenital heart caused by fibrous tissue manifested as the highest incidence of SAS and a familial disease as with some cases of mitral valve nodules, a ridge, ring or tunnel-like lesion. component or heritability is reported. dysplasia. SAS may be associated with other defects Increased risk is also described for English RISK FACTORS including mitral valve dysplasia. bulldog, American Staffordshire terrier, bull r r Familial history of SAS. SAS predisposes PATHOPHYSIOLOGY Terrier, English bulldog, Great Dane, and r to aortic valve endocarditis. Aortic valve Samoyed. No breed predilection is reported Restriction to outflow generates pressure endocarditis predisposes to valvar aortic for cats. r overload of the LV. Degree of obstruction is stenosis. HCM predisposes cats to fixed or related to severity of secondary changes. Left Mean Age and Range dynamic LVOT obstruction. ventricular pressure overload causes thickened Clinical signs may be seen at any age. LV walls, resulting in diminished blood Although often inherited, SAS becomes supply relative to muscle demand and identifiable during the first few weeks to myocardial ischemia. This may result in months of life as the subvalvular lesion DIAGNOSIS arrhythmogenesis and if severe or infarcted, progresses. Full phenotype is appreciated by mechanical dysfunction. The restriction to 1yearofage. DIFFERENTIAL DIAGNOSIS blood flow causes high velocity, turbulent flow Predominant Sex The systolic murmur must be differentiated across the valve, which may cause endothelial N/A from other causes of similar murmurs. damage, lead to aortic insufficiency (AI) and SIGNS Innocent or physiologic murmurs are predisposing to endocarditis. SAS may lead to commonly ausculted in athletic dogs, or with chamber enlargement, distortion of the mitral Historical Findings anemia, fever, stress or excitement. Pulmonic valve annulus and mitral regurgitation with a Many dogs with SAS show no clinical signs stenosis, tetralogy of Fallot, and atrial septal possible sequela of left-sided congestive heart and have no relevant historical findings. defects cause a similar murmur. Weak pulses failure. Sudden death is common with severe Historical findings are related to disease may also occur with conditions that reduce SAS and may be secondary to arrhythmias or severity and may include syncope, exercise cardiac output such as heart failure, infarction. intolerance, sudden death, and signs due to cardiomyopathy, and severe pulmonic SYSTEMS AFFECTED CHF such as respiratory distress and/or stenosis. Other obstruction to flow may cause r coughing when severe. Cardiovascular—LV pressure overload reduced pulse quality, such as aortic Physical Examination Findings thromboembolism or rarely aortic leading to arrhythmias, syncope, sudden r death, heart failure, endocarditis Systolic left basilar ejection murmur; may coarctation/tubular hypoplasia. r Respiratory—possible pulmonary edema radiate to the apex, right side of the thorax, CBC/BIOCHEMISTRY/URINALYSIS r with CHF Multisystemic—possible due to include the carotid arteries and if very loud Typically within normal limits the cranium. A precordial thrill may be low cardiac output or endocarditis OTHER LABORATORY TESTS GENETICS palpable. Murmur intensity is loosely correlated to severity of stenosis. As the Genetic testing for the mutation associated SAS is inherited in the Newfoundland, golden disease worsens during early life, some may with Newfoundland SAS is a breeding tool to retriever, rottweiler and Dogue de Bordeaux. have absence of or a quiet murmur that reduce frequency in this breed. A mutation in the phosphatidylinositol- develops to a more characteristic finding by IMAGING binding clathrin assembly protein gene r 1year. Diastolic murmur may be present Thoracic Radiography (PICALM) is reported in Newfoundlands; a r with significant AI. The combination of this Mild disease may be radiographically silent. screening test is available. Dominant diastolic murmur with the systolic ejection r inheritance patterns are proposed with LV hypertrophy may be subtle as pressure murmur is a to-and-fro murmur. overload causes concentric hypertrophy. incomplete penetrance responsible for the r r r r Arrhythmias may be ausculted. Pulse Left heart enlargement. Prominent aortic disease appearing to skip generations. More deficits may be appreciated, often associated r r root and/or widened mediastinum. Lung than one gene or modifying genes may be with ventricular arrhythmias. Weak pulses involved. fields typically normal unless CHF with may be appreciated that are late or slow to rise pulmonary venous distention and interstitial INCIDENCE/PREVALENCE with severe SAS (pulsus parvus et tardus). r to alveolar infiltrates. SAS is one of the most common congenital Tachypnea, respiratory distress and crackles Echocardiography heart defects of dogs. It is reported as second may occur with CHF. r Findings are variably present and associated most common, but difficulty in diagnosing General Comments r mild disease may underestimate true caseload. r with disease severity. Ridge, ring, nodule, or Boxers have a relatively small aorta tunnel-like narrowing below the aortic valve Aortic stenosis has been reported as a small compared to other breeds, which can be r r with SAS. Thickened LV free wall or contributor of feline congenital heart disease, difficult to distinguish from mild SAS. Bull r about 6%. Approximately 2 out of 1,000 dogs interventricular septum. Aortic valve terriers are overrepresented for combined thickening and increased echogenicity with and 0.2 per 1,000 cats evaluated at veterinary mitral valve dysplasia and SAS. r teaching hospitals are diagnosed with SAS valvar stenosis. Mitral regurgitation and JWST589-A69-61 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:23 279mm×216mm

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thickening of valve leaflet possible. Alert owners to the risks of sudden death, POSSIBLE COMPLICATIONS r Post-stenotic dilatation of the aorta. CHF and increased anesthetic risk. Ventricular arrhythmias, syncope, myocardial r Hyperechoic myocardium associated with infarction, sudden death, AI, mitral r SURGICAL CONSIDERATIONS ischemia. AI with secondary LV chamber No surgical or interventional technique has regurgitation, endocarditis. enlargement and volume overload if r been shown to extend life beyond medical EXPECTED COURSE AND PROGNOSIS significant. Left atrial enlargement may be therapy. Balloon valvuloplasty or combined Mildly affected dogs may have a normal seen with significant valve regurgitation. r > cutting and traditional balloon valvuloplasty lifespan and quality without therapy. Severely Elevated LVOT flow velocity ( 2.4 m/s), may acutely reduce the pressure gradient and affected dogs have limited lifespans and with acceleration proximal to the stenosis and temporarily alleviate some clinical signs. typically succumb to sudden death or CHF. turbulent flow distal to the obstruction and r However, the effects are not shown to be In one study the average lifespan for dogs with valve. Transvalvular pressure gradient beneficial beyond those achieved with severe SAS on atenolol was about 4.5 years. estimated by the LVOT flow velocity (4 × beta-blockers. Currently, data does not flow velocity squared). Estimated gradients of support surgery or intervention. 25–49 mmHg are considered mild; 50–79 mmHg moderate, and ≥ 80mmHg r MISCELLANEOUS severe. With myocardial failure the estimated pressure gradient may be falsely low. ASSOCIATED CONDITIONS r MEDICATIONS Effective valve orifice, if calculated, is Increased risk of infective endocarditis reduced. DRUG(S) OF CHOICE r AGE-RELATED FACTORS DIAGNOSTIC PROCEDURES Beta adrenergic blockers are advocated with SAS is not immediately apparent at birth but r ECG may show changes consistent with LV moderate to severe SAS, particularly with appears over few weeks to months of life. hypertrophy (tall R waves, widened QRS ventricular arrhythmias, syncope or ECG evidence of ischemia. They may reduce PREGNANCY/FERTILITY/BREEDING complexes, left axis deviation); signs of Contraindicated myocardial ischemia (ST segment deviation or myocardial oxygen demand, eliminate or slurring). Ventricular arrhythmias may occur protect against ventricular arrhythmias, and SYNONYMS and contribute to syncope or sudden death. reduce heart rate. Atenolol is most common Subaortic stenosis, discrete subaortic stenosis. r (dogs, 0.5–1.5 mg/kg PO q12h; cats Holter monitoring may be used to quantify r SEE ALSO 6.25 mg/cat PO q12–24h). Therapy for r arrhythmia severity and therapeutic response. Congestive Heart Failure, Left-Sided ventricular arrhythmias, CHF, atrial r r PATHOLOGIC FINDINGS Endocarditis, Infective Cardiomyopathy, fibrillation or endocarditis may be required. r Hypertrophic—Cats Cardiomyopathy, Findings vary with severity but typically CONTRAINDICATIONS include LV concentric or mixed (if significant Hypertrophic—Dogs AI) hypertrophy. A subvalvular lesion of dense Beta blockers are contraindicated in animals ABBREVIATIONS with bronchoconstriction such as asthmatic r r fibrous tissue is seen with variable. Myocardial AI = aortic insufficiency CHF = cats. Starting beta-blockers with CHF is r ischemia, necrosis and replacement fibrosis congestive heart failure HCM = contraindicated and continued use in patients r may be evident. Post–stenotic dilatation of hypertrophic cardiomyopathy ECG = that develop CHF is controversial. r the aorta and associated valvular endothelial electrocardiogram LV = left ventricle r damage and sometimes left atrial enlargement PRECAUTIONS LVOT = left ventricular outflow tract r r r is reported. Beta-blockers are negatively impact cardiac PDA = patent ductus arteriosus SAS = output and starting low doses with gradual r subvalvular aortic stenosis uptitration is warranted. Positive inotropes INTERNET RESOURCES may worsen a fixed obstruction and are used with caution when treating CHF. N/A TREATMENT r Anesthetic drugs that cause hypotension, Suggested Reading APPROPRIATE HEALTH CARE arrhythmias or cardiac depression should be Kienle RD, Thomas WP, Pion PD. The Therapy is limited prior to the onset of avoided with severe SAS. natural clinical history of canine congenital complications and aimed at preventing POSSIBLE INTERACTIONS subaortic stenosis. J Vet Intern Med 1994, clinical signs and avoiding sudden death. N/A 8(6):423–431. NURSING CARE Meurs KM, Lehmkuhl LB, Bonagura JD. ALTERNATIVE DRUGS Aimed at relieving symptoms and r Survival times in dogs with severe Carvedilol (dogs, 0.5–1.5mg/kg PO q12h) complications such as arrhythmias, syncope r subvalvular aortic stenosis treated with Metoprolol tartrate (dogs, 0.5–1.5mg/kg and CHF. balloon valvuloplasty or atenolol. J Am Vet PO q12h) ACTIVITY Med Assoc 2005, 227(3):420–424. Stern JA, White SN, Lehmkuhl LB, et al. A Restriction is warranted with severe disease; single codon insertion in PICALM is exertion may increase incidence of associated with development of familial arrhythmias, syncope and sudden death. FOLLOW-UP subvalvular aortic stenosis in Newfoundland DIET PATIENT MONITORING dogs. Hum Genet 2014, Modest salt restriction with CHF. Monitor by ECG, Holter monitor, thoracic 133(9):1139–1148. CLIENT EDUCATION radiography, and echocardiography. Author Joshua A. Stern SAS is considered an inherited disease; Treatment of complications such as CHF and Consulting Editors Larry P. Tilley and affected animals should not be bred. Owners arrhythmias may necessitate additional Francis W.K. Smith, Jr. should be counseled on the risk of monitoring for renal/electrolyte, blood endocarditis and appropriate antibiotics for pressure, and rhythm disturbances. Client Education Handout any wounds, infections or surgical procedures. PREVENTION /AVOIDANCE available online N/A JWST589-A70-62 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:26 279mm×216mm

106 Blackwell’s Five-Minute Veterinary Consult A Aortic Thromboembolism

study. In dogs, no breed predilection has been identified in the USA. A European study BASICS suggested that Cavalier King Charles Spaniels DIAGNOSIS may be overrepresented. DEFINITION Mean Age and Range DIFFERENTIAL DIAGNOSIS Aortic thromboembolism results from a Age distribution is 1–20 years. The median Hind limb paresis secondary to other causes thrombus or blood clot that is dislodged age is approximately 8–9 years in cats. In such as spinal neoplasia, trauma, myelitis, within the aorta, causing severe ischemia to dogs, the median age is 8–10 years. fibrocartilaginous infarction, or intervertebral the tissues served by that segment of aorta. Predominant Sex disc protrusion. These conditions resulting in spinal cord injury present with signs of upper PATHOPHYSIOLOGY Males > females (2:1) in cats. In dogs, no sex r motor neuron disease, whereas ATE patients ATE is commonly associated with predilection in dogs in the USA. A European present with signs of lower motor neuron myocardial disease in cats, most commonly study suggested a male predilection. disease. hypertrophic cardiomyopathy. It is theorized SIGNS that abnormal blood flow (stasis) and a CBC/BIOCHEMISTRY/URINALYSIS The presence of the 5 “P’s” is helpful to r High creatine kinase as a result of muscle hypercoagulable state contribute to the remember the classic clinical signs associated formation of a thrombus within the left injury. with ATE: Pain, Paralysis or Paresis, r High aspartate aminotransferase and alanine atrium. The blood clot is then embolized Pulselessness, Pallor, and Poikilothermic aminotransferase as a result of muscle and distally to the aorta. The most common site of (cold). liver injury. embolization is the caudal aortic trifurcation r Historical Findings Hyperglycemia secondary to stress. (hind legs). Other less common sites include r r the front leg, kidneys, gastrointestinal tract, or Acute onset paralysis and pain are the most Mild increases in blood urea nitrogen and cerebrum. common complaints in cats. Vocalization and creatinine due to low cardiac output and r anxiety are also common. possible renal emboli. ATE in dogs typically is associated with r r neoplasia, sepsis, infectious endocarditis, Lameness or a gait abnormality, typically of Electrolyte derangements, due to low output Cushing’s disease, protein-losing nephropathy, several week duration, is more common in and muscle damage, such as hypocalcemia, dogs. or other hypercoagulable states. However, in r hyponatremia, hyperphosphatemia and one recent retrospective study, no concurrent Tachypnea or respiratory distress is hyperkalemia are not uncommon. commonincats. r condition was identified in 58% of dogs. r CBC and urinalysis changes are SYSTEMS AFFECTED About 15% of cats may vomit prior to ATE. non-specific. r Physical Examination Findings Cardiovascular—the majority of affected r OTHER LABORATORY TESTS cats have advanced heart disease and left heart Usually paraparesis or paralysis of the rear Routinely available coagulation profiles failure. legs with signs of lower motor neuron injury. typically do not reveal significant r Nervous/Musculoskeletal—severe ischemia Less commonly, monoparesis of a front leg. In abnormalities because the hypercoagulability dogs, the majority are paretic and ambulatory. to the muscles and nerves served by the r results from hyperaggregable platelets. In the Absent or diminished femoral pulses. segment of occluded aorta causes variable r dog, thromboelastrography may suggest a Pain upon palpation of the legs. pain and paresis. Gait abnormalities or r hypercoagulable state with a clot strength paralysis results in the leg or legs involved. Gastrocnemius muscle often becomes firm (increased maximum amplitude) or shortened several hours after embolization. GENETICS r clotting time (decreased R). Cyanotic or pale nail beds and foot pads. r IMAGING Hypertrophic cardiomyopathy, a common Tachypnea/dyspnea and hypothermia are associated disease, is likely heritable. Radiographic Findings commonincats. r Additionally, a family of domestic shorthair r Cardiomegaly is common in cats. Since commonly associated with heart r cats with remodeled hypertrophic disease in cats, a cardiac murmur, Pulmonary edema and/or pleural effusion in cardiomyopathy who all died of ATE has been approximately 50% of cats. arrhythmias, or gallop sound may be present. r reported. CAUSES Rarely, a mass is seen in the lungs, INCIDENCE/PREVALENCE r suggestive of neoplasia. Cardiomyopathy (all types) r r Prevalence is not known in the general Hyperthyroidism Echocardiographic Findings r r population of cats. In two large studies of cats Neoplasia In cats, changes consistent with r with hypertrophic cardiomyopathy, 12–16% Sepsis (dogs) cardiomyopathy. Hypertrophic r presented with signs of ATE. In two Hyperadrenocorticism (dogs) cardiomyopathy is most common, followed r retrospective studies of cats with ATE, Protein-losing nephropathy (dogs) by restrictive or unclassified cardiomyopathy 11–25% of cats had previous evidence of and then dilated cardiomyopathy. RISK FACTORS r heart disease. Most cases (> 50%) have severe left atrial r r Rare in dogs. In the cat, cardiomyopathy is a risk factor. enlargement (i.e., left atrial to aortic ratio Cardiomyopathic cats with a markedly GEOGRAPHIC DISTRIBUTION of ≥ 2). enlarged left atrium, spontaneous r N/A A left atrial thrombus or spontaneous echocardiographic contrast (smoke), or an echocardiographic contrast (smoke) may be SIGNALMENT intracardiac thrombus observed on an seen. Species echocardiogram are at a higher risk for development of ATE. Abdominal Ultrasonographic Findings Cat, rarely dog r r In the dog, hypercoagulable conditions, May be able to identify the thrombus in the Breed Predilections caudal aorta. such as neoplasia, sepsis, endocarditis, protein r Mixed-breed cats are most commonly losing nephropathies, or Typically not necessary to reach a diagnosis affected. Abyssian, Birman, and ragdoll hyperadrenocorticism are risk factors. in the cat but often needed to reach a purebred cats were overrepresented in one diagnosis in the dog. JWST589-A70-62 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:26 279mm×216mm

Canine and Feline, Sixth Edition 107

(Continued) Aortic Thromboembolism A

Advanced Diagnostic Imaging frequent re-evaluations and an indoor the activated partial thromboplastin time r Nonselective or CT angiography should lifestyle. approximately two-fold. r r identify a negative filling defect in the caudal Most cats that survive an initial episode will Aspirin is theoretically beneficial during and aorta representing the thrombus. recover complete function to the legs; after an episode of thromboembolism because r Typically not necessary to reach a diagnosis. however, if ischemia was severe and of its antiplatelet effects. The dose in cats isan DIAGNOSTIC PROCEDURES prolonged, sloughing of parts of the distal 81 mg tablet PO q48–72h. Vomiting and Electrocardiography extremities or persistent neurologic deficits diarrhea are not uncommon. Some specialists r Sinus rhythm and sinus tachycardia most may result. In one study, approximately 15% advocate a mini dose of 5 mg/cat q72h. common. Less common rhythms include of cats had permanent neuromucscular Antithrombotic dose recommendations for atrial fibrillation, ventricular arrhythmias, abnormalities after surviving the initial dogs range from 0.5 to 2 mg/kg q24h. Always embolic event. give aspirin with food. supraventricular arrhythmias, and sinus r r bradycardia. Based on 3 small retrospective studies in Buprenorphine in the cat is useful and r dogs, the prognosis is generally poor but may widely available drug used for analgesia and Left ventricular enlargement pattern and 휇 left ventricular conduction disturbances (left be better in dogs presenting with chronic (vs. sedation at a dose of 5–20 g/kg IV, SC, or in anterior fascicular block) are common. acute) lameness and dogs treated cheek pouch q6–8h. For stronger analgesia, appropriately with warfarin. use fentanyl or hydromorphone. PATHOLOGIC FINDINGS r r SURGICAL CONSIDERATIONS Acepromazine may be cautiously used for its Thrombus typically is identified at the r sedative and vasodilatory properties at a dose caudal aortic trifurcation. Surgical embolectomy typically is not r of 0.01–0.02 mg SC q8–12h. Occasionally, a left atrial thrombus is seen. recommended because these patients are high r r risk for surgery because of severe heart disease. Warfarin, a vitamin K antagonist, is the Emboli of the kidneys, gastrointestinal tract, r anticoagulant most widely used in humans cerebrum, and other organs also may be seen. Rheolytic thrombectomy has been used with limited success in a small number of cats and has been proposed for prevention of with ATE. re-embolization in cats surviving an initial episode. The initial dose is 0.25–0.5 mg/cat PO q24h or 0.05–0.2 mg/kg PO q 24h in the TREATMENT dog. Overlap with heparin therapy for 3 days. The dose is then adjusted to prolong the APPROPRIATE HEALTH CARE MEDICATIONS prothrombin time approximately two times Initially, cats with ATE should be treated as DRUG(S) OF CHOICE its baseline value or to attain an international inpatients because many have concurrent r normalized ratio of 2 to 3. Long-term congestive heart failure and require injectable Thrombolytic therapy (e.g., tissue plasminogen activator [TPA]) is used management with warfarin can be challenging drugs, in addition to being in considerable because of frequent monitoring and dose pain and distress. extensively in humans and infrequently in cats and dogs. These drugs are expensive and carry adjustments in addition to bleeding NURSING CARE complications. In one study, dogs treated r a significant risk for bleeding complications; Fluid therapy is cautiously used as most cats to date, they have not demonstrated improved appropriately with warfarin had a better clinical outcome. have advanced myocardial disease. If in treatment efficacy and thus are rarely used in r congestive heart failure, IV fluid therapy may general practice. TPA is theorized to be more Low molecular weight heparin has recently not be necessary. been proposed for the long-term prevention r beneficial if given early, ideally, within the first Supplemental oxygen therapy or 6 hours of the event. of feline ATE. LMWH has a more predictable r thoracocentesis may be beneficial if in Clopidogrel is an antiplatelet aggregation relationship between dose and response than congestive heart failure. warfarin and does not need monitoring or r drug. One may choose to give a loading dose Initially, minimally handle the affected legs. of clopidogrel for treatment of an acute dose adjustments. It also has a lower risk of However, as reperfusion occurs, physical embolic event. The loading dose in the cat is bleeding complication. The main therapy (passive extension and flexion of the 75 mg/cat PO once and then maintenance disadvantage of LMWH is high drug cost and legs) may speed full recovery. the injectable route of administration. The r dose starting 24h later is 18.75 mg/cat Do not perform venipuncture on the (one-fourth of 75 mg tablet) PO q24h. The two LMWHs that have been used in feline affected legs. ATE are: dalteparin (100–150 units/kg SC r loading dose in the dog is approximately These animals may have difficulty posturing 10 mg/kg once and then a maintenance dose q8–24h) and enoxaparin (1 mg/kg SC to urinate and may need to have their of 1 mg/kg q24h. When compared to aspirin, q12–24h). Best dose unknown. LMWH bladders expressed to prevent overdistention clopidogrel was superior in preventing usually started q24h due to cost. Some studies or urine scald. re-embolization, resulting improved survival suggest q6h dosing necessary for stable blood ACTIVITY times in cats that had survived an ATE. levels, but may increase bleeding risk. r Restrict activity and stress Unfractionated heparin is the preferred CONTRAINDICATIONS DIET anticoagulant drug in general practice for N/A initial management of feline ATE. Heparin PRECAUTIONS Initially, most cats are anorexic. Tempt these has no effect on the established clot; however, r Anticoagulant therapy with heparin, cats with any type of diet to keep them eating it prevents further activation of the warfarin, or the thrombolytic drugs may cause and avoid hepatic lipidosis. coagulation cascade. In either a cat or dog, bleeding complications. CLIENT EDUCATION give an initial dose of 100–200 units/kg IV r r Avoid a nonselective beta-blocker such as Short- and long-term prognosis is poor in and then 200–300 units/kg SC q8h. propranolol as it may enhance peripheral both dogs and cats. Alternatively, heparin can be administered as a r vasoconstriction. Most cats will re-embolize. Most cats that CRI, if there is concern about adequate survive an initial episode will be on some type bioavailability via the SC route, at a dose of of anticoagulant therapy that may require 25–35 units/kg/h. Titrate the dose to prolong JWST589-A70-62 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:26 279mm×216mm

108 Blackwell’s Five-Minute Veterinary Consult

A Aortic Thromboembolism (Continued)

r POSSIBLE INTERACTIONS In two large studies, ∼ 60% of cats were Suggested Reading Warfarin may interact with other drugs, euthanized or died during the initial Alwood AJ, Downend AB, Brooks MB, et al. which may enhance its anticoagulant effects. thromboembolic episode. Long-term Anticoagulant effects of ALTERNATIVE DRUG(S) prognosis varies between 2 months to several low-molecular-weight heparins in healthy N/A years; however, the average is a few months cats. J Vet Intern Med 2007, 21:378–387. with treatment. Predictors of poorer prognosis Cole SG, Drobatz KJ. Emergency include hypothermia (< 99◦F) and congestive management and critical care. In: Tilley LP, heart failure. One study demonstrated a Smith FWK, Oyama MA, Sleeper MM, median survival time of 77 days in cats with eds., Manual of Canine and Feline FOLLOW-UP congestive heart failure and 223 days in cats Cardiology, 4th ed. St. Louis, MO: PATIENT MONITORING without congestive heart failure. Predictors of Saunders Elsevier, 2008, pp. 342–355. r ECG monitoring while the cat is in hospital better prognosis include normothermia, single Gonc¸alves R, Penderis J, Chang YP, et al. is helpful to detect reperfusion injury and leg affected, and presence of motor function Clinical and neurological characteristics of hyperkalemia related ECG changes. on initial exam. aortic thromboembolism in dogs. J Small r r Monitoring electrolytes and renal In dogs, the disease is rare and prognosis in Anim Pract 2008, 49:178-184. parameters periodically may be helpful to general is also poor. One study suggested a Lake-Bakaar, GA, Johnson EG, Griffiths LG. optimize management of the cardiac disease. better prognosis if the dog had chronic Aortic thrombosis in dogs: 31 cases r clinical signs and if treated with warfarin. (2000-2010). J Am Vet Med Assoc 2012, Examine the legs frequently to assess clinical r response. Initially, APTT should be Recurrence of ATE is common. 241:910–915. performed once daily to titrate the heparin Laste NJ, Harpster NK. A retrospective study dose. of 100 cats with feline distal aortic r If warfarin is used, PT or INR is measured thromboembolism: 1977–1993. J Am Anim approximately 3 days after initiation of MISCELLANEOUS Hosp Assoc 1995, 31:492–500. Smith CE, et al. Use of low molecular weight therapy and then weekly until the desired ASSOCIATED CONDITIONS anticoagulant effect is reached. Thereafter, heparin in cats: 57 cases (1999–2003). J Am measure three to four times yearly or when See “Causes” and “Risk Factors” Vet Med Assoc 2004, 225:1237–1241. drug regimen is altered. AGE-RELATED FACTORS Smith SA. Feline arterial thromboembolism: An update. Vet Clin North Am Small Anim PREVENTION/AVOIDANCE N/A Pract 2004, 34:1245–1271. ZOONOTIC POTENTIAL Because of the high rate of re-embolization, Smith SA. Arterial thromboembolism in cats: prevention with either clopidogrel, aspirin, None Acute crisis in 127 cases (1992–2001) and warfarin, or LMWH is strongly PREGNANCY/FERTILITY/BREEDING long-term management with low dose recommended. N/A aspirin in 24 cases. J Vet Intern Med 2003, POSSIBLE COMPLICATIONS 17:73–83. r SYNONYMS Bleeding with the anticoagulant therapy. r Winter RL, Sedacca CD, Adams A, Orton r Saddle thromboembolism r EC. Aortic thrombosis in dogs: Permanent neurologic deficits or muscular Systemic thromboembolism abnormalities in the hind limbs may arise presentation, therapy, and outcome in 26 SEE ALSO with prolonged ischemia. r cases. J Vet Cardiol 2012, 14:333–342. r Cardiomyopathy, Dilated—Cats Recurrent congestive heart failure or sudden r Author Teresa C. DeFrancesco death. Cardiomyopathy, Hypertrophic—Cats Consulting Editors Larry P. Tilley and r r Reperfusion injury and death usually Cardiomyopathy, Restrictive—Cats Francis W.K. Smith, Jr. associated with hyperkalemic arrhythmias. ABBREVIATIONS r EXPECTED COURSE AND PROGNOSIS APTT = activated partial thromboplastin Client Education Handout r time Expected course is days to weeks for full r available online ATE = aortic thromboembolism recovery of function to the legs. r r CRI = constant rate infusion Prognosis, both short term and long term, is r ECG = electrocardiogram poor in cats. r INR = international normalized ratio r LMWH = low molecular weight heparin r PT = prothrombin time JWST589-A71-63 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:29 279mm×216mm

Canine and Feline, Sixth Edition 109 Apudoma A

r r Increased BUN secondary to Omeprazole—a proton pump inhibitor; the gastrointestinal bleeding most potent inhibitor of gastric acid secretion r Hypoproteinemia available; highly effective and expensive. BASICS r r Electrolyte abnormalities with chronic Sucralfate—adheres to ulcerated gastric OVERVIEW vomiting mucosa and protects it from acid; promotes r Tumors of endocrine cells that are capable OTHER LABORATORY TESTS healing by binding pepsin and bile acids and r of amine precursor uptake and Serum gastrin concentration normal or stimulating local prostaglandins. decarboxylation and secretion of peptide high-normal in patients with gastrinoma. CONTRAINDICATIONS/POSSIBLE hormones; the tumors are named after the Treatment with H2 antagonists or proton INTERACTIONS hormone they secrete. r pump inhibitors increases serum Because sucralfate may be less effective in an APUD cells are generally found in the concentrations of gastrin and could lead to alkaline environment, and may reduce the gastrointestinal tract and CNS. r false-positive diagnosis of gastrinoma, but absorption of other drugs, it should be given Gastrin- and pancreatic polypeptide- withdrawal of these drugs results in return of 1–2 hours prior to antacid drugs. secreting tumors are discussed here; gastrin concentrations to baseline in dogs insulinoma and glucagonoma are discussed without gastrinoma. separately. r r Provocative test of gastrin secretion— Hypergastrinemia from gastrin-secreting increased gastrin concentration after FOLLOW-UP tumors causes gastritis and duodenal intravenous calcium gluconate or secretin hyperacidity, which can cause gastric administration suggests gastrinoma; see PATIENT MONITORING r ulceration, esophageal dysfunction from Appendix II for protocol and interpretation. Physical examination and clinical signs are chronic reflux, and intestinal villous atrophy. r IMAGING the most useful measures of treatment High concentration of pancreatic effectiveness and disease progression. polypeptide also causes gastric hyperacidity Abdominal ultrasound sometimes r demonstrates a pancreatic mass but is usually Gastroscopy can monitor progression of and its consequences. gastritis but is not necessary. normal. r SIGNALMENT Abdominal radiography or ultrasound may r DIAGNOSTIC PROCEDURES Gastrinoma—rare in dogs and cats; age r detect development of abdominal masses. Endoscopy with gastric and duodenal range 3–12 years, mean 7.5 years (dogs). EXPECTED COURSE AND PROGNOSIS r biopsy. r Pancreatic polypeptide—extremely rare in r Difficult to predict. dogs. Aspirate any detectable masses because of r suspicion of mast cell disease. Patients with gastrinoma have been SIGNS r controlled on medical management for r If no detectable masses exist, examine a Vomiting months to years. r buffy coat smear for mast cells. r Weight loss No cure available. r PATHOLOGIC FINDINGS Anorexia r r Diarrhea Endoscopic biopsy reveals gastrointestinal r Lethargy, depression ulceration. r r Polydipsia Histopathologic examination of pancreatic r MISCELLANEOUS Melena tumors reveals findings consistent with islet r Abdominal pain cell tumor but not specific for hormone type. SEE ALSO r r Hematemesis Immunocytochemical staining can aid in Gastroduodenal Ulceration/Erosion r Hematochezia the specific diagnosis. ABBREVIATIONS r r Fever Histopathologic examination also can reveal r metastasis to liver and regional lymph nodes. APUD = amine precursor uptake and CAUSES & RISK FACTORS decarboxylation r CNS = central nervous system Unknown r NSAID = nonsteroidal anti-inflammatory TREATMENT drug r Tell owner that most APUDomas are Suggested Reading DIAGNOSIS malignant and have metastasized by the time Hughes SM. Canine gastrinoma: a case study DIFFERENTIAL DIAGNOSIS of diagnosis and that long-term control is and literature review of therapeutic options. r N Z Vet J 2006, 54(5):242–247. Other conditions associated with often difficult. r Lurye JC, Behrend EN. Endocrine tumors. hypergastrinemia, gastric hyperacidity, and Aggressive medical management can Vet Clin North Am Small Anim Pract 2001, gastrointestinal ulceration sometimes palliate signs for months to years. r r 31(5):1083–1110, ix–x. Uremia Surgical exploration and excisional biopsy of r Parente NL, Bari Olivier N, Refsal KR, Hepatic failure a pancreatic mass are important both r diagnostically and therapeutically. Johnson CA. Serum concentrations of Drug-induced ulceration (e.g., NSAIDs or r gastrin after famotidine and omeprazole steroids) Medical management is useful for gastric r administration to dogs. J Vet Intern Med Inflammatory gastritis hyperacidity. r 2014, 28(5):1465–1470. Stress-induced ulceration r Zerbe CA. Islet cell tumors secreting insulin, Mast cell disease pancreatic polypeptide, gastrin, or glucagon. CBC/BIOCHEMISTRY/URINALYSIS r MEDICATIONS In: Kirk RW, Bonagura JD, eds., Current Normal or reflect the chronic effects of Veterinary Therapy XI. Philadelphia: DRUG(S) general disease r r Saunders, 1992, pp. 368–375. Iron-deficiency anemia secondary to Histamine H2-receptor antagonists— Author Thomas K. Graves gastrointestinal bleeding cimetidine, ranitidine, and famotidine; Consulting Editor Deborah S. Greco decrease acid secretion by gastric parietal cells. JWST589-A72-64 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:31 279mm×216mm

110 Blackwell’s Five-Minute Veterinary Consult A Arteriovenous Fistula and Arteriovenous Malformation

CAUSES & RISK FACTORS newer treatment options. Coils or devices are r AVMs are rare; frequently a congenital often sufficient for treatment of AVF; AVMs r BASICS lesion. Acquired AVFs typically result from typically require glue embolization, as closure local damage to vasculature secondary to of the nidus is required for complete cure. OVERVIEW trauma, surgery, venipuncture, perivascular Potential advantages include less invasive injection, or tumor. treatment and intravascular access to remote Abnormal, low-resistance connections r between an artery and vein which bypass a lesions. AVMs and AVFs may recur. In some capillary bed; arteriovenous malformations animals, surgical removal of the affected limb (AVM) are typically congenital and involve a or organ (e.g., amputation, liver lobectomy) vascular nidus, or complex of communicating DIAGNOSIS may be necessary. vessels, while arteriovenous fistulae (AVF) are DIFFERENTIAL DIAGNOSIS often acquired direct connections. Large r The lesion may look like a mass if AVMs and AVFs allow a significant fraction r of the total cardiac output to bypass the peripherally located (limb, ear). Other MEDICATIONS differentials include an aneurysm or false capillary bed. The resulting increase in cardiac r aneurysm. Atypical clinical findings, DRUG(S) output may lead to circulatory volume r overload and congestive heart failure (CHF). depending on location, may suggest other Concurrent medical treatment depends on The anatomic location of AVMs is variable, disease processes; AVF or AVM may be a late the site of the lesion and secondary clinical diagnostic consideration. features. most often reported in the liver of dogs. The r location of AVFs is also variable, occurring CBC/BIOCHEMISTRY/URINALYSIS Medical treatment for CHF or other organ frequently in the limbs or at the site of May reflect damage to systems in the vicinity dysfunction may be required before surgery. previous surgery/trauma. of the lesion, i.e., biochemical abnormalities CONTRAINDICATIONS/POSSIBLE SIGNALMENT suggesting hepatic, renal, or other organ INTERACTIONS r r Dog and cat (rare in both). No specific dysfunction are possible. Avoid excessive fluid administration; animals age, breed, or sex predilections known, OTHER LABORATORY TESTS with these lesions are often volume though AVMs are typically seen in younger N/A overloaded. animals. IMAGING SIGNS Thoracic Radiographic Findings Historical Findings r Cardiac enlargement and pulmonary Animals with AVF often have a history of FOLLOW-UP r overcirculation in some animals with trauma to the affected area. Owner may hemodynamically significant lesions. Postoperative reevaluation is needed to notice a warm, non-painful swelling at the r Ultrasonographic Findings determine whether the AVM or AVF has site. Other findings depend on the lesion r AVM and AVF appear as cavernous, recurred and if organ dysfunction has location (e.g., ascites with hepatic AVM). r r vascular structures. Doppler ultrasound may normalized. The shunt may cause local organ demonstrate high-velocity, turbulent flow dysfunction. within the lesion. Physical Examination Findings r Cross-sectional Imaging Vary and depend on location of the r Computed tomography or magnetic MISCELLANEOUS AVM/AVF. Signs of CHF (e.g., coughing, resonance angiography can aid in the SEE ALSO dyspnea, tachypnea, exercise intolerance) may diagnosis, particularly when imaged with develop in animals with long-standing disease Congestive Heart Failure, Left-Sided r contrast injection to highlight the vascular and high blood flow. Bounding pulses may ABBREVIATIONS anatomy. r r be present because of high ejection volume AVF = arteriovenous fistula AVM = and rapid runoff through the AVM/AVF. Angiography r r arteriovenous malformation CHF = Continuous murmur (bruit) at the site Selective angiography defines the lesion and congestive heart failure caused by turbulent blood flow through the may be necessary for definitive diagnosis. This r lesion. Cautious compression of the artery is performed at the time of intervention, if Suggested Reading proximal to the lesion abolishes the bruit. transcatheter therapy is pursued. Placement of Fox PR, Petrie J-P, Hohenhaus AE. Peripheral When blood flow is high, this compression the catheter close to the lesion and rapid vascular disease. In: Ettinger SJ, Feldman may also elicit an immediate reflex decrease in injection is necessary; high-volume blood flow EC, eds., Textbook of Veterinary Internal r heart rate (Branham’s sign). Edema, dilutes the contrast medium quickly. Medicine, 6th ed. St. Louis: Elsevier, 2005. ischemia, and congestion of organs and tissues DIAGNOSTIC PROCEDURES Author BrianA.Scansen caused by high venous pressure in the Consulting Editors Larry P. Tilley and r N/A proximity of the lesion. If the lesion is on a Francis W.K. Smith, Jr. limb, pitting edema, lameness, ulceration, Acknowledgment The author and editors r scabbing, and gangrene may result. Lesions acknowledge the prior contribution of Donald J. Brown. near vital organs may cause signs associated TREATMENT with organ failure such as ascites (liver), r seizures (brain), paresis (spinal cord), and Surgery can be difficult and labor-intensive dyspnea (lung). and may require blood transfusion, though is the traditional treatment for r clinically-significant lesions. Transcatheter therapies with coils, devices, or glue represent JWST589-A73-65 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:33 279mm×216mm

Canine and Feline, Sixth Edition 111 Arteriovenous Malformation of the Liver A

r Hepatofugal portal flow (away from the liver)—through APSS. r Renomegaly. BASIC DIAGNOSIS r Urolithiasis: urinary bladder or renal pelvis. r OVERVIEW DIFFERENTIAL DIAGNOSIS Rule out portal thrombosis (luminal filling r r Intrahepatic arteriovenous (AV) CNS signs—infectious disorders (e.g., defect, abrupt blood flow termination). malformations (also referred to as AV fistulae) distemper); toxicity (e.g., lead); Radiographic Contrast Angiography r are communications between proper hepatic hydrocephalus; idiopathic epilepsy; metabolic Not indicated in most cases. r arteries and intrahepatic portal veins; this disorders (e.g., hypoglycemia, hypokalemia or Venous portography—only confirms APSS. r anatomic union results in hepatofugal (away hyperkalemia); HE (e.g., acquired liver disease Hepatic arteriography—required to confirm from the liver) splanchnic circulation. or PSVA). r r AV communication (celiac trunk or anterior Blood flows directly from a hepatic artery Abdominal effusion:—pure transudate mesenteric artery contrast injection). into portal vasculature retrograde into the (ascites; protein-losing nephropathy, Multi-Sector CT vena cava through multiple acquired protein-losing enteropathy, liver disease); Non-invasive contrast imaging of hepatic portosystemic shunts (APSS). modified transudate (congenital cardiac r vasculature; arterial and venous phases; Associated with ascites. malformations, right-sided heart failure, r 3-dimensional reconstruction illustrates AV Uncommon, usually congenital, but may be pericardial tamponade, supradiaphragmatic malformation, large liver lobe, atrophied liver. acquired (surgical injury, trauma, neoplasia). vena caval obstruction, neoplasia, portal vein thrombosis); hemorrhage. Echocardiography SIGNALMENT r r Rule out right-sided heart disease, pericardial Dogs,lesscommonincats Portal hypertension—chronic hepatic r disease, and vena caval occlusion. Age-related presentation (congenital): disease, ductal plate malformations/congenital DIAGNOSTIC PROCEDURES < 2years hepatic fibrosis, non-cirrhotic or idiopathic r r No sex or breed predilection portal hypertension, cirrhosis, portal thrombi. Multi-sector CT and exploratory CBC/BIOCHEMISTRY/URINALYSIS laparotomy. SIGNS r r Erythrocyte microcytosis (APSS), target cells Liver biopsy—collect samples from affected r General Comments Hypoalbuminemia with normal or low and unaffected liver lobes; “normal” liver often Vague or acute illness; present for signs caused serum globulins; ALP and ALT activity demonstrates severe vascular arterialization by portal hypertension and APSS: ascites and normal or moderately increased; variable low (more severe than associated with PSVA). hepatic encephalopathy (HE). BUN and hypocholesterolemia, and anicteric r Historical Findings Hyposthenuria or isosthenuria r r Dogs may have a normal transition to Ammonium biurate crystalluria growth foods, unlike PSVA that demonstrate OTHER LABORATORY TESTS TREATMENT HE. r r Coagulation tests—variable, may be APPROPRIATE HEALTH CARE May have an acute onset of ascites or HE. r normal; low protein C activity reflects APSS. Vague signs include: lethargy, anorexia, r Inpatient— Treat HE and ascites prior to Total serum bile acids—preprandial values vomiting, diarrhea, weight loss, polydipsia, surgical approach or percutaneous selective variable, postprandial values increased; classic dementia, abdominal distention, and uroliths acrylamide embolization. shunting pattern. causing obstructive uropathy. r NURSING CARE Plasma ammonia—usually increased, r Physical Examination Findings inferred by ammonium biurate crystalluria. Diet—restrict nitrogen intake to ameliorate r r Lethargic, poor body condition, ascites; Peritoneal fluid—pure transudate (total HE and hyperammonemia; restrict sodium to attenuate ascites formation. enlarged liver lobe containing the AV protein < 2.5 g/dL) or modified transudate. r HE—resolve endoparasitism, electrolyte malformation; rarely palpated on initial IMAGING examination. and hydration disturbances, treat infections, r Radiography Rarely, bruit auscultated over AV r initiate treatments to alter enteric uptake and Abdominal effusion malformation. r formation of HE toxins (see Hepatic Microhepatia or normal sized liver due to Encephalopathy). CAUSES & RISK FACTORS r enlarged lobe with AV malformation r r Ascites—mobilize by restricting activity and Usually congenital vascular malformations Renomegaly r sodium intake and instituting dual diuretic (single or multiple vessels) reflecting failed Normal thorax therapy (furosemide and spironolactone); differentiation of common embryologic Abdominal Ultrasonography reserve therapeutic abdominocentesis for anlage. r r Abdominal effusion tense ascites impairing ventilation, nutrition, Rare: secondary to abdominal trauma, r Liver lobe with AV malformation—large sleep, or recumbent posture; (see Portal inflammation, neoplasia, surgical Hypertension, Portosystemic Shunting, interventions, or diagnostic procedures (e.g., compared to most other liver lobes that are atrophied due to portal hypoperfusion. Acquired, and below). liver biopsy). r r Tortuous anechoic tubules represent AV SURGICAL CONSIDERATIONS Portal hypertension—reflects arterialization r of valveless portal system—establishing APSS. structure with unidirectional pulsating or Resection of liver lobe containing AV turbulent flow on color-flow Doppler. r malformation is complicated by coexistence Hepatic artery and/or portal vein branches of additional hepatic vascular malformations; may appear tortuous. clinical cure possible but unlikely. JWST589-A73-65 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:33 279mm×216mm

112 Blackwell’s Five-Minute Veterinary Consult

A Arteriovenous Malformation of the Liver (Continued)

r Percutaneous selective acrylamide vascular Gastrointestinal Hemorrhage EXPECTED COURSE AND PROGNOSIS r r embolization; complicated by risk of Histamine type-2 receptor antagonists Prognosis fair if patient survives surgical thromboembolism of additional vasculature; (famotidine 0.5–2 mg/kg PO, IV, or SC resection of AV malformation or temporary improvement; but treatment may q12–24h); or HCl pump inhibitors embolization. r be curative. (omeprazole 1.0 mg/kg/24h PO or Most patients require indefinite nutritional r Multiple microscopic vascular pantoprazole 1 mg/kg/24h IV [omeprazole and medical management (HE, ascites) malformations continue portal hypertension may induce p450 cytochrome-associated drug because of coexisting microscopic vascular and APSS. interactions and may have a 24–48h delay malformations across the liver; APSS persists r Do not ligate APSS nor band the vena cava. onset of action]; some clinicians recommend requiring continued management of HE. chronic treatment to minimize gastrointestinal bleeding and ulceration that may be chronic problems). r MEDICATIONS Gastroprotectant—sucralfate: MISCELLANEOUS 0.25–1.0 g/10 kg PO q8–12h; titrate to DRUG(S) SEE ALSO effect, beware of drug interactions as r Ascites Hepatic Encephalopathy sucralfate may bind other medications, r Hepatic Encephalopathy See Hepatic Encephalopathy reducing bioavailability. r r Hypertension, Portal Ascites Eliminate endoparasitism. r r Portosystemic Shunting, Acquired Restrict sodium intake. CONTRAINDICATIONS r r Portosystemic Vascular Anomaly, Furosemide (0.5–2 mg/kg PO IM or IV Avoid drugs dependent on hepatic Congenital q12–24h)—combine with spironolactone. biotransformation or first pass hepatic r ABBREVIATIONS Spironolactone (0.5–2 mg/kg PO q12h)— extraction (reduced by APSS) or that react r APSS = acquired portosystemic shunt double initial dose as loading dose once. with GABA-benzodiazepine receptors because r r GABA = 𝛾-aminobutyric acid Chronic diuretic therapy— individualized of propensity for HE. r HE = hepatic encephalopathy to response, 4- to 7-day assessment intervals r used to titrate dose to response, avoiding PSVA = portosystemic vascular anomalies hydration, electrolyte, and HE complications. Author Sharon A. Center r Diuretic-resistant ascites— may require FOLLOW-UP Consulting Editor Sharon A. Center therapeutic abdominocentesis; to initiate diuresis. PATIENT MONITORING r Vasopressin V2 receptor antagonists newly Biochemistry—initially monthly until available may control ascites accumulation. stabilized after surgery or AV malformation (See Portosystemic Shunting, Acquired.) embolization, thereafter quarterly; monitor Bleeding Tendencies for hypoalbuminemia, infection, optimization See Coagulopathy of Liver Disease of HE management and control of ammonium biurate crystalluria. JWST589-A74-66 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:52 279mm×216mm

Canine and Feline, Sixth Edition 113 Arthritis (Osteoarthritis) A

r r Cat—90% of cats over 12 years of age had lameness. Neurologic conditions causing r evidence of DJD on radiographs. Clinical lameness or decreased activity/weakness. problems are more prevalent in larger, OTHER LABORATORY TESTS BASICS r overweight, and very active animals. Coombs’ test, ANA, and rheumatoid factor DEFINITION r Primary DJD is rare. may help to rule out immune-mediated r Osteoarthritis or degenerative joint disease is SIGNALMENT arthritis. Serum titers for Borrelia, Ehrlichia, the progressive and permanent deterioration Species and Rickettsia to evaluate for infectious of the articular cartilage of diarthrodial Dog and cat arthritis. (synovial) joints due to primary (idiopathic) Mean Age and Range IMAGING and secondary causes. r r Radiographic changes—include joint PATHOPHYSIOLOGY Secondary DJD due to congenital disorders r (OCD, hip dysplasia) seen in immature capsular distention, osteophytosis, DJD is initiated by mechanical stress— animals; some present with DJD signs when enthesiophytosis, soft-tissue thickening, and r traumatic injury, instability, abnormal older (hip and elbow dysplasia). Secondary narrowed joint spaces; in severely affected conformation, abnormal activity, etc. r to trauma—any age. patients: subchondral sclerosis, and Metalloproteinases, serine proteases, and intra-articular calcified bodies (joint mice). SIGNS r cysteine protease enzymes are released from Radiographic severity often does not Historical Findings r damaged chondrocytes, causing collagen r correlate with clinical severity. Stress degradation and loss of collagen cross-linking Dogs—decreased activity level, unwilling to r radiography may identify underlying in cartilage. Collagen synthesis is altered, perform certain tasks; intermittent lameness instability and accentuate joint incongruity resulting in decreased collagen/proteoglycan or stiff gait that slowly progresses; possible (e.g., distraction index, passive hip laxity of interaction and reduced hydrophyllic matrix history of joint trauma, OCD, or the coxofemoral joint is predictive of hip r r properties. Cartilage matrix is further developmental disorders; may be exacerbated DJD). Bone nuclear scintigraphy can assist by exercise, long periods of recumbency, and compromised by increased breakdown of r in localizing subtle DJD. proteoglycans and manufacture of cold weather. Cats—overt lameness may not r DIAGNOSTIC PROCEDURES poorer-quality proteoglycans. Nitric oxide is be seen. May have difficulty grooming, r released, which mediates cartilage breakdown jumping onto furniture, or accessing the litter Arthrocentesis and synovial fluid analysis— box; increased irritability. cell counts are normal or slightly increased and supports chronic inflammation. < Chondrocyte apoptosis is facilitated by ( 2,000–5,000 cells/mL) predominantly r Physical Examination Findings mononuclear (macrophages) and occasional cyclooxygenase-2 enzymes. Synovial r r Stiff-legged or altered gait (e.g., bunny synovial lining cells. Bacterial culture of membrane inflammation results in decreased hopping in hip dysplasia) or non-use of leg. r r r synovial fluid—negative. Biopsy of synovial viscosity of the synovial fluid, reducing Decreased range of motion. Crepitus. r r tissue to rule out neoplasia or lubrication. Poorer-quality synovial fluid Joint swelling (effusion and/or thickening of reduces oxygen and nutrient supply to the r r immune-mediated arthritides (lymphocytic r the joint capsule). Joint pain. Joint plasmacytic synovitis, SLE). chondrocytes. Subchondral bone becomes instability. sclerotic, worsening loading qualities of the PATHOLOGIC FINDINGS r CAUSES r bone and overlying cartilage. Pain of DJD r r Fibrillation or erosion of articular cartilage. r results from stimulation of pain receptors in Primary—no known cause. Secondary— Eburnation and sclerosis of subchondral r the tendons, ligament, subchondral bone, and results from an initiating cause: abnormal bone. Thickening and fibrosis of the joint r r joint capsule. The result of these processes is wear on normal cartilage (e.g., joint capsule. Synovial fluid can be grossly progressive cartilage degradation ranging from instability, joint incongruity, trauma to normal to thin and watery, usually increased r fibrillation to deep fissuring of cartilage. cartilage or supporting soft tissues) or normal volume. Synovial villous hypertrophy and r Full-thickness cartilage loss can eventually wear on abnormal cartilage (e.g., hyperplasia. Osteophytes and r occur. Periarticular fibrosis occurs to reduce osteochondral defects). enthesiophytes at joint capsule attachments r joint motion (and pain), leading to poorer RISK FACTORS and adjacent to the joint. Neovascularization r vascularity of the synovial membrane. Working, athletic, and obese dogs place or pannus in severe cases over joint surfaces. r r Osteophytes and enthesiophytes develop more stress on their joints. Dogs with around and within the joint to increase the disorders that affect collagen or cartilage r load-bearing surface area. These changes (Cushing’s disease, diabetes mellitus, reduce functionality and may eventually lead hypothyroidism, hyperlaxity, prolonged, TREATMENT to ankylosis. steroids). APPROPRIATE HEALTH CARE SYSTEMS AFFECTED r r Medical—usually tried initially. Surgical Musculoskeletal—diarthrodial joints options—to improve joint geometry or GENETICS r r DIAGNOSIS remove bone-on-bone contact areas. Primary DJD is rare. Dogs—causes of NURSING CARE secondary DJD are varied, including hip and DIFFERENTIAL DIAGNOSIS r r Physical therapy—very beneficial. elbow dysplasias, osteochondrosis dissecans, r Neoplastic (synovial sarcoma; rarely, Maintaining or increasing joint motion— patellar luxations, congenital shoulder r chondrosarcoma; osteosarcoma). Septic passive range of motion exercises, massage, luxation, Legg-Perthes, and cranial cruciate r r arthritis (caused by bacteria; spirochetes; L swimming. Pain management—cold and ligament rupture. Cats—causes of r forms in cats; Mycoplasma; Rickettsia; heat therapy. Muscle tone/strengthening— secondary DJD are patellar luxation, hip Ehrlichia; viruses, such as feline calicivirus; r swimming (aerobic exercise with minimal dysplasia, and arthropathy. fungi, and protozoa). Immune-mediated r weight bearing); controlled leash walks up INCIDENCE/PREVALENCE arthritis (erosive vs. non-erosive). Other r hills or on soft surfaces, such as sand or dry or Dog—very common; 20% of dogs older musculoskeletal conditions that cause underwater treadmill. than 1 year have some degree of DJD. JWST589-A74-66 JWST589-Tilley Printer: Yet to Come August 3, 2015 8:52 279mm×216mm

114 Blackwell’s Five-Minute Veterinary Consult

A Arthritis (Osteoarthritis) (Continued)

r r ACTIVITY Adequan—clinical study in dogs with hip anti-inflammatory drug OCD = r Limited to a level that minimizes aggravation dysplasiam; 4.4 mg/kg IM every 3–5 days for osteochondrodysplasia PSGAGs = r of clinical signs. 8 injections had a positive, temporary effect. polysulfated glycosaminoglycans SLE = r DIET Cosequin—trials showed positive effects. systemic lupus erythematosus r Weight reduction for obese patients— CONTRAINDICATIONS r Suggested Reading decreases stress placed on arthritic joints. NSAIDs must not be given with steroids. r r Aragon CL, Hofmeister EH, Budsberg SC. Omega n-6 and n-3 fatty acids decrease the Acetaminophen must not be given to cats. Systematic review of clinical trials of production of certain prostaglandins and PRECAUTIONS treatments for osteoarthritis in dogs. J Am r modulate inflammation. NSAIDs—may cause gastric ulceration. Vet Med Assoc 2007, 230(4):514–521. r CLIENT EDUCATION COX-2 selective drugs may interfere with Baime MJ. Glucosamine and chondroitin r r Medical therapy is palliative and the liver function. When switching NSAIDs— sulphate did not improve pain in r condition is likely to progress. Discuss wait 3 days for washout before starting new osteoarthritis of the knee. Evid Based Med treatment options, activity level, and diet. drug. 2006, 11(4):115. Beale BS, Goring RL. Degenerative joint SURGICAL CONSIDERATIONS POSSIBLE INTERACTIONS r disease. In: Bojrab MJ, ed., Disease Arthrotomy—used to remove aggravating Steroids and NSAIDS Mechanisms in Small Animal Surgery. causes (e.g., fragmented coronoid process, ALTERNATIVE DRUG(S) Philadelphia: Febiger, 1993, pp. 727–736. un-united anconeal process, osteochondral r r r Free-radical scavengers. Glucocorticoids— Budsberg SC, Bartges JW. Nutrition and flaps). Arthroscopy—used to diagnose and inhibit inflammatory mediators and osteoarthritis in dogs: Does it help? Vet Clin remove aggravating causes; flushing the joint r cytokines; however, chronic use delays healing North Am Small Anim Pract 2006, may be beneficial. Reconstructive and initiates damage to articular cartilage; 36(6):1307–1323. procedures—used to eliminate joint potential systemic side effects documented; Glass GG. Osteoarthritis. Dis Mon 2006, instability and correct anatomic problems r goal is low-dose (dogs, 0.5–2 mg/kg; cats, 52(9):343–362 (human review). r (patella luxation, angular deformity). Joint 2–4 mg/kg) q48h. Prednisone—initial dose Hampton T. Efficacy still uncertain for removal—femoral head and neck ostectomy, r 1–2 mg/kg PO q24h for dogs and 4 mg/kg widely used supplements for arthritis. J Am r temperomandibular joint arthroplasty. Joint PO q24h for cats. Triamcinolone Med Assoc 2007 297(4):351–352. replacement—total hip replacement is widely hexacetonide—intra-articular injection of Herrero-Beaumont G, Ivorra JA, et al. used, total elbow replacement still r 5 mg in dogs showed a protective and Glucosamine sulfate in the treatment of experimental. Joint fusion (arthrodesis)—in therapeutic effect in one model. knee osteoarthritis symptoms: A selected chronic cases and for joint instability, randomized, double-blind, complete or partial; carpus, hock: generally placebo-controlled study using excellent outcome; shoulder, elbow, stifle,: less acetaminophen as a side comparator. predictable outcome. FOLLOW-UP Arthritis Rheum 2007, 56(2):555–567. Johnston SJ. Osteoarthritis joint anatomy, PATIENT MONITORING physiology and pathobiology. Vet Clin Clinical deterioration—indicates need to North Am 1997, 27:699–723. MEDICATIONS change drug selection or dosage; may indicate Mlacnik E, Bockstahler BA, Muller M, DRUG(S) OF CHOICE need for surgical intervention. Tetrick MA, Nap RC, Zentek J. Effects of PREVENTION/AVOIDANCE caloric restriction and a moderate or intense NSAIDs r Early identification of predisposing causes and physiotherapy program for treatment of Inhibit prostaglandin synthesis through lameness in overweight dogs with cyclooxygenase enzymes. prompt treatment to help reduce progression r of secondary conditions, e.g., surgical removal osteoarthritis. J Am Vet Med Assoc 2006, Deracoxib (3–4 mg/kg PO q24h, 229(11):1756–1760. chewable). of osteochondral lesions. r Pederson NC. Joint diseases of dogs and cats. Carprofen (2.2 mg/kg PO q12h or q24h). EXPECTED COURSE AND PROGNOSIS r r r In: Ettinger SJ, ed., Textbook of Veterinary Meloxicam (load 0.2 mg/kg PO, then Slow progression of disease likely. Some Internal Medicine, 5th ed. Philadelphia: 0.1 mg/kg PO q24h: liquid). form of medical or surgical treatment usually r Saunders, 2000, pp. 1862–1886. Tepoxalin (load 20 mg/kg, then 10 mg/kg allows a good quality of life. Van Der Kraan PM, Van Den Berg WB. PO q24h). r Osteophytes: Relevance and biology. Cats—meloxicam (0.1 mg/kg PO q24h: Osteoarthritis Cartilage 2007, liquid) or robenacoxib (1 mg/kg PO q24h for 15(3):237–244. 3 days). MISCELLANEOUS Author Walter C. Renberg Consulting Editor Walter C. Renberg Chondroprotective/Regenerative SYNONYMS Supplements r r Acknowledgment The author and editors r Degenerative arthritis Degenerative joint Supply PSGAG molecules to repair and r r acknowledge the prior contribution of Peter regenerate cartilage. disease Osteoarthritis Osteoarthrosis K. Shires. r Host of products, many with little production oversight so effects vary widely. ABBREVIATIONS r r r Glucosamine and chondroitin sulfate— ANA = antinuclear antibody COX-2 = Client Education Handout r injectable Adequan, oral Cosequin, oral cyclooxygenase-2 DJD = degenerative joint available online r MSM, mixtures (e.g., Glycoflex II, SynFlex). disease NSAID = nonsteroidal JWST589-A75-67 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:2 279mm×216mm

Canine and Feline, Sixth Edition 115 Arthritis, Septic A

r r Decreased range of motion Elevated WBC count—> 80% neutrophils r Local lymphadenopathy with > 40,000/mm3 (normal joint fluid r Fever < 10% neutrophils and < 3,000/mm3) BASICS r CAUSES Neutrophils may show degenerative changes DEFINITION r Aerobic bacterial organisms—most (chromatolysis, vacuolation, nuclear swelling, loss of segmentation) Pathogenic microorganisms within the closed common: staphylococci, streptococci, r space of one or more synovial joints coliforms and Pasteurella Neutrophils with phagocytosed bacteria— r PATHOPHYSIOLOGY Anaerobic organisms—most common: definitive diagnosis or bacteria in the synovial r fluid Usually caused by contamination associated Propionibacterium, Peptostreptococcus, Fusobacterium and Bacteroides Synovial Fluid Culture with traumatic injury (e.g., a direct r r Spirochete—Borrelia burgdorferi Positive culture is definitive but not penetrating injury such as bite, gunshot r Mycoplasma necessary for diagnosis. wound, foreign object), a sequela to surgery, r r arthrocentesis or joint injection, Fungal agents—Blastomyces, Cryptococcus, Must be collected aseptically; requires heavy and Coccidioides sedation or general anesthesia. hematogenous spread of microorganisms r r Rickettsial—Anaplasma, Ehrlichia, Rickettsia Place fluid sample in aerobic and anaerobic from a distant septic focus, or less commonly r the extension of primary osteomyelitis Leishmania culturettes and in blood culture medium. r r r Primary sources of hematogenous Feline calicivirus Use 1:9 dilution of synovial fluid to blood culture media. infection—urogenital, integumentary RISK FACTORS r r Culturette samples—cultured immediately (including ears and anal sacs), respiratory, Predisposing factors for hematogenous upon arrival to the laboratory. cardiac, and gastrointestinal systems infection—diabetes mellitus; r Blood culture medium—re-culturing after SYSTEMS AFFECTED hypoadrenocorticism (Addison’s disease); 24 hours of incubation increases accuracy by immunosuppression Musculoskeletal—usually affects one joint r 50% and is the preferred method. Penetrating trauma to the joint including r GENETICS Mycoplasma, bacterial L-forms and protozoa surgery r require specific culture procedures—contact N/A Existing osteoarthritis or other joint damage r laboratory prior to sample collection. INCIDENCE/PREVALENCE Intra-articular injection, particularly if Other Relatively uncommon cause of monoarticular steroid injected r arthritis in dogs and cats Synovial biopsy—to rule out immune- GEOGRAPHIC DISTRIBUTION mediated joint disease; no more effective than incubated blood culture medium for growing May be an increased incidence in Lyme bacterial organisms. DIAGNOSIS r disease-endemic areas Blood and urine cultures if hematogenous SIGNALMENT DIFFERENTIAL DIAGNOSIS source is suspected. r Species Osteoarthritis PATHOLOGIC FINDINGS r r Most common in dogs Trauma r r r Synovium—thickened; discolored; often Rare in cats Immune-mediated arthropathy r very proliferative Postvaccinal transient polyarthritis r Breed Predilections r Histology—evidence of hyperplastic Greyhound polyarthritis Any. Medium to large breeds—most r synoviocytes Feline progressive polyarthritis r commonly German shepherds, Dobermans, r Increased numbers of neutrophils, Crystal-induced joint disease and Labrador retrievers. r macrophages, and fibrinous debris Synovial sarcoma r Mean Age and Range Cartilage—loss of proteoglycan, destruction CBC/BIOCHEMISTRY/URINALYSIS of articular surface, pannus formation Any age; usually between 4 and 7 years. r Hematogenous: more common in immature Hemogram—inflammatory left shift in some cases animals. r Other results normal Predominant Sex Male OTHER LABORATORY TESTS TREATMENT SIGNS Serologic testing for specific pathogens APPROPRIATE HEALTH CARE IMAGING r General Comments Inpatient—initial stabilization; initiate Radiography systemic antibiotic therapy as soon as fluid is Always consider the diagnosis in patients with r acute, monoarticular lameness associated with Early disease—may reveal thickened and obtained for bacterial culture; consider joint soft tissue swelling, heat, and pain. dense periarticular tissues; may see evidence drainage/lavage as soon as possible to minimize intra-articular injury. Historical Findings of synovial effusion. Often difficult to r r diagnose early disease radiographically. Identify and treat source if hematogenous Lameness—acute onset most common, but r spread is suspected. can present as chronic lameness Late disease—reveals bone destruction, r r Outpatient—long-term management. Lethargy osteolysis, irregular joint space, discrete r NURSING CARE Anorexia erosions, and periarticular osteophytosis. r May report previous trauma—dog bite, DIAGNOSTIC PROCEDURES Alternating heat and cold packing—beneficial penetrating injury, prior surgery or other Synovial Fluid Analysis in promoting increased blood flow and r invasive procedure of the joint Increased volume decreased swelling. r Turbid fluid ACTIVITY Physical Examination Findings r r Decreased viscosity Restricted until resolution of symptoms Monoarticular lameness, rarely polyarticular r r Decreased mucin clot reaction Joint pain and swelling—commonly carpus, r DIET stifle, hock, shoulder, or cubital joint Make slides immediately; if additional fluid r N/A Localized joint heat is obtained, place in EDTA tube JWST589-A75-67 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:2 279mm×216mm

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A Arthritis, Septic (Continued)

CLIENT EDUCATION ALTERNATIVE DRUG(S) ABBREVIATION r Discuss probable cause. N/A NSAIDs = nonsteroidal anti-inflammatory r Warn client about the need for long-term drugs antibiotics and the likelihood of residual INTERNET RESOURCES degenerative joint disease. N/A SURGICAL CONSIDERATIONS FOLLOW-UP r Suggested Reading Acute disease with minimal radiographic PATIENT MONITORING Bennett D, Taylor DJ. Bacterial infective changes—joint drainage and lavage via needle r If drainage and irrigation catheters have arthritis in the dog. J Small Anim Pract arthrocentesis, arthroscopic lavage or been placed—may be removed after 4–6 days 1988, 29:207–230. arthrotomy. An irrigation catheter or after reassessment of synovial fluid Benzioni H, Shahar R, Yudelevitch S, (ingress/egress) can be placed in larger joints. r cytology. Milgram J. Bacterial infective arthritis of the Chronic disease—may require open r Duration of antibiotic therapy—2 weeks coxofemoral joint in dogs with hip arthrotomy with debridement of the following resolution of clinical signs. Total dysplasia. Vet Comp Orthop Traumatol synovium and copious lavage; if appropriate, treatment may be 4–8 weeks or longer 2008, 21:262–266. an irrigation catheter (ingress/egress) may be depending on clinical signs and pathogenic Clements DN, Owen MR, Mosely JR, et al. placed to lavage the joint postoperatively. r organism. Retrospective study of bacterial infective Lavage—use warmed physiologic saline or r Persistent synovial inflammation without arthritis in 31 dogs. J Small Anim Pract lactated Ringer’s solution (2–4 mL/kg q8h) viable bacterial organisms (dogs)—may be 2005, 46:171–176. until effluent is clear. Do not add caused by antigenic bacterial fragments or Ellison RS. The cytologic examination of povidone/iodine or chlorhexidine to lavage antigen antibody deposition. synovial fluid. Semin Vet Med Surg Small fluid. r r Systemic corticosteroid therapy (after joint Anim 1988, 3:133–139. Effluent fluid—cytologically monitored sepsis has been resolved) and aggressive Fitch RB, Hogan TC, Kudnig ST. daily for existence and character of bacteria physical therapy—may be needed to Hematogenous septic arthritis in the dog: and neutrophils. r maximize normal joint dynamics. results of five patients treated nonsurgically Removal of catheters—when effluent fluid with antibiotics. J Am Anim Hosp Assoc has no bacteria and the neutrophils are PREVENTION/AVOIDANCE 2003, 39:563–566. cytologically healthy. If clinical signs recur, early (within 24–48 r Hodgin EC, Michaelson F, Howerth EW. Arthroscopy allows for visual assessment of hours) treatment provides the greatest benefit. Anaerobic bacterial infections causing articular cartilage, lavage and biopsy, and is a POSSIBLE COMPLICATIONS osteomyelitis/arthritis in a dog. J Am Vet less invasive method of thorough joint lavage r Chronic disease—severe degenerative joint Med Assoc 1992, 201:886–888. than arthrotomy. r disease Luther JF, Cook JL, Stoll MR. Arthroscopic Recent reports suggest there may be no r Recurrence of infection exploration and biopsy for diagnosis of difference between combined medical and r Limited joint range of motion septic arthritis and osteomyelitis of the surgical management and medical r Generalized sepsis coxofemoral joint in a dog. Vet Comp management alone. r Osteomyelitis Orthop Traumatol 2005, 18:47–51. EXPECTED COURSE AND PROGNOSIS Machevsky AM, Read RA. Bacterial septic r Acutely diagnosed disease (within 24–48 arthritis in 19 dogs. Aust Vet J 1999, hours) responds well to antibiotic therapy. 77:233–237. r MEDICATIONS Delayed diagnosis or resistant or highly MacWilliams PS, Friedrichs KR. Laboratory DRUG(S) OF CHOICE virulent organisms—guarded to poor evaluation and interpretation of synovial r Pending culture susceptibility data— prognosis. fluid. Vet Clin Small Anim 2003, bactericidal antibiotics, such as 33:153–178. first-generation cephalosporin or Montgomery RD, Long IR, Milton JL. amoxicillin-clavulanic acid, preferred. Comparison of aerobic culturette, synovial r Choice of antimicrobial drugs—primarily MISCELLANEOUS membrane biopsy, and blood culture depends on in vitro determination of medium in detection of canine bacterial ASSOCIATED CONDITIONS susceptibility of microorganisms; toxicity, arthritis. Vet Surg 1989, 18:300–303. frequency, route of administration and N/A Nord KD, Dore DD, Deeney VF, et al. expense also considered; most penetrate the AGE-RELATED FACTORS Evaluation of treatment modalities for septic arthritis with histologic grading and analysis synovium well; need to be given for a N/A minimum of 4–8 weeks. of levels of uronic acid, neutral protease, r ZOONOTIC POTENTIAL NSAIDs—may help decrease pain and and interleukin-1. J Bone Jt Surg 1995, N/A inflammation. 77:258–265. PREGNANCY/FERTILITY/BREEDING Author Sherisse A. Sakals CONTRAINDICATIONS N/A Consulting Editor Walter C. Renberg Avoid fluorinated quinolones in pediatric Acknowledgment The author and editors SYNONYMS patients; they induce cartilage lesions r acknowledge the prior contribution of Infectious arthritis experimentally. r Spencer A. Johnston. PRECAUTIONS Joint ill SEE ALSO Failure to respond to conventional antibiotic r Osteomyelitis Client Education Handout therapy—may indicate anaerobic disease or r other unusual cause (fungal, spirochete). Polyarthritis, Immune-mediated available online POSSIBLE INTERACTIONS N/A JWST589-A76-68 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:7 279mm×216mm

Canine and Feline, Sixth Edition 117 Ascites A

IMAGING r Thoracic and abdominal radiography is sometimes helpful. BASICS DIAGNOSIS r Ultrasonography of the liver, spleen, DEFINITION DIFFERENTIAL DIAGNOSIS pancreas, kidney, bladder, and abdomen can often determine cause. The escape of fluid, either transudate or Differentiating Abdominal Distension r exudate, into the abdominal cavity between without Effusion Stages of ascites: r ◦ the parietal and visceral peritoneum. Organomegaly—hepatomegaly, Stage I: minimal ascites. Detected by PATHOPHYSIOLOGY splenomegaly, renomegaly, and hydrometra. ultrasound only. r ◦ r Abdominal neoplasia. Stage II: moderate ascites. Abdominal Ascites can be caused by the following: r ◦ Pregnancy. distention visible and/or noted on CHF and associated interference in r Bladder distension. ballottement. venous return r ◦ ◦ Obesity. Stage III: significant ascites. Marked Depletion of plasma proteins associated r Gastric dilatation. abdominal distention. Patient with inappropriate loss of protein from uncomfortable, possibly with labored renal or gastrointestinal disease—protein- Differentiating Diseases r breathing. losing nephropathy or enteropathy, Transudate—nephrotic syndrome, cirrhosis respectively of liver, right-sided CHF, hypoproteinemia, DIAGNOSTIC PROCEDURES ◦ Obstruction of the vena cava or portal and ruptured bladder. Ascitic Fluid Evaluation r vein, or lymphatic drainage due to Exudate—peritonitis, abdominal neoplasia, Exfoliative cytologic examination and neoplastic occlusion and hemorrhage. bacterial culture and antibiotic sensitivity— ◦ Overt neoplastic effusion CBC/BIOCHEMISTRY/URINALYSIS remove approximately 3–5 mL of abdominal ◦ r Peritonitis—infective or inflammatory Neutrophilic leukocytosis occurs in patients fluid via aseptic technique. ◦ Electrolyte imbalance, especially Transudate with systemic infection. r hypernatremia r Clear and colorless. Albumin is low in patients with impaired r ◦ Liver cirrhosis. Protein < 2.5 g/dL. liver synthesis, gastrointestinal loss, or renal r Specific gravity < 1.018. SYSTEMS AFFECTED loss. r r r < 3 Cardiovascular Cholesterol is low in patients with impaired Cells 1,000/mm —neutrophils and r Gastrointestinal liver synthesis. mesothelial cells. r Modified Transudate Hemic/Lymph/Immune r r Liver Enzymes Red or pink; may be slightly cloudy. Renal/Urologic r r Low to normal in patients with impaired Protein 2.5–5 g/dL. SIGNALMENT liver synthesis. r > r r Specific gravity 1.018. Dogs and cats High in patients with liver inflammation, r < 3 r Cells 5,000/mm —neutrophils, No species or breed predisposition hyperadrenocorticism, gallbladder mesothelial cells, erythrocytes, and SIGNS obstruction, and chronic passive congestion. lymphocytes. r Episodic weakness Total and Direct Bilirubin Exudate (Non-septic) r r r Lethargy Low to normal in patients with impaired Pink or white; cloudy. r r Abdominal fullness liver synthesis. Protein 2.5–5 g/dL. r r r Abdominal discomfort when palpated High in patients with biliary obstruction Specific gravity > 1.018. r r 3 Dyspnea from abdominal distension or caused by tumor, gallbladder distension, or Cells 5,000–50,000/mm —neutrophils, associated pleural effusion obstruction. mesothelial cells, macrophages, erythrocytes, r Anorexia BUN and Creatinine and lymphocytes. r r Vomiting High in patients with renal failure. Exudate (Septic) r r r Weight gain BUN low in patients with impaired liver Red, white, or yellow; cloudy. r r Scrotal or penile edema synthesis or hyperadrenocorticism. Protein > 4.0 g/dL. r r > Groaning when lying down Glucose Specific gravity 1.018. r 3 CAUSES Low in patients with impaired liver synthesis. Cells 5,000–100,000/mm —neutrophils, r Nephrotic syndrome mesothelial cells, macrophages, erythrocytes, r OTHER LABORATORY TESTS Cirrhosis of liver r lymphocytes, and bacteria. r To detect hypoproteinemia—protein Right-sided CHF Hemorrhage r electrophoresis and immune profile. r Hypoproteinemia r Red; spun supernatant clear and sediment r To detect proteinuria—urinary red. Ruptured bladder < r r protein:creatinine ratio (normal 0.5:1). Protein > 5.5 g/dL. Peritonitis r r r To detect liver ascites—analysis of serum Specific gravity 1.007–1.027. Abdominal neoplasia r r ascites albumin gradient. Cells consistent with peripheral blood. Abdominal hemorrhage r RISK FACTORS Does not clot. N/A JWST589-A76-68 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:7 279mm×216mm

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A Ascites (Continued)

Chyle management (e.g., patient with splenic r Pink, straw, or white. tumor: tumor removed, abdominal bleeding r Protein 2.5–7 g/dL. controlled, blood transfusion administered). r MISCELLANEOUS Specific gravity 1.007–> 1.040. r LARGE-VOLUME PARACENTESIS < 3 r AGE-RELATED FACTORS Cells 10,000/mm —neutrophils, Stage III treatment. r mesothelial cells, and large population of Pretreat patient with hetastarch (6%) @ N/A small lymphocytes. r 1–2 mL/kg for 2 hours. PREGNANCY/FERTILITY/BREEDING Other—fluid in tube separates into r Abdominal tap (paracentesis), until N/A cream-like layer when refrigerated; fat drainage slows. r SYNONYMS droplets stain with Sudan III. Post-treat patient with hetastarch (6%) @ Pseudochyle Abdominal effusion r 1–2 mL/kg for 4 hours. White. SEE ALSO r r Protein > 2.5 g/dL. Cirrhosis and Fibrosis of the Liver r r Specific gravity 1.007–1.040. Congestive Heart Failure, Right-Sided r r Cells < 10,000/mm3—neutrophils, MEDICATIONS Hypoalbuminema mesothelial cells, and small lymphocytes. r r Nephrotic Syndrome Other—fluid in tube does not separate into DRUG(S) OF CHOICE r ABBREVIATIONS cream-like layer when refrigerated; does not Patients with liver insufficiency or CHF = congestive heart failure stain with Sudan III. CHF—restrict sodium and give a diuretic Urine combination of hydrochlorothiazide Suggested Reading r Clear to pale yellow. (2–4 mg/kg q12h PO) and spironolactone Kramer RE, Sokol RJ, Yerushalmi B, Liu E, r Protein > 2.5 g/dL. (1–2 mg/kg q12h PO); if control is MacKenzie T, Hoffenberg EJ, Narkewicz r Specific gravity> 1– 1.040. inadequate, furosemide (1–2 mg/kg q8h PO) MR. Large-volume paracentesis in the r Cells 5,000–50,000/mm3—neutrophils, can be substituted for the thiazide with management of ascites in children. J Ped erythrocytes, lymphocytes, and macrophages. spironolactone continued; must monitor Gastro Nutr 2001; 33:245–249. r Other—if the urinary bladder ruptured serum potassium concentration to prevent Lewis LD, Morris ML Jr, Hand MS. Small < potassium imbalances. Animal Clinical Nutrition, 3rd ed. Topeka, 12 hours before, urinary glucose and r protein could be negative; if bladder ruptured Patients with hypoproteinemia, nephrotic KS: Mark Morris Associates, 1987. > 12 hours before, urine becomes a dialysis syndrome, and associated ascitic fluid Li MK. Management of ascites. Hong Kong medium with ultrafiltrate of plasma, and accumulation—can treat as above with the Med Di 2009, 14:27–29. urine contains glucose and protein. addition of hetastarch (6% hetastarch in Runyon BA. Management of adult patients 0.9% NaCl); administer an IV bolus (dogs, with ascites due to cirrhosis. Hepatol 2004, Bile r 20 mL/kg; cats, 10–15 mL/kg) slowly over 39:1–16. Slightly cloudy and yellow. r ∼ 1 hour; hetastarch increases plasma oncotic Gompf RE. The history and physical Protein > 2.5 g/dL. r pressure and pulls fluid into the intravascular examination. In: Smith FWK, Tilley LP, Specific gravity > 1.018. r space for up to 24–48 hours. Oyama MA, Sleeper MM, eds., Manual of 3 r Cells 5,000–750,000/mm —neutrophils, Systemic antibiotic therapy is dictated by Canine and Feline Cardiology, 5th ed. erythrocytes, macrophages, and lymphocytes. r bacterial identification and sensitivity testing St. Louis, MO: Saunders Elsevier, 2015 Other—bilirubin confirmed by urine in patients with septic exudate ascites. (in press). dipstick; non-icteric patient may have Kumar KS, Srikala D. Ascites with right heart gallbladder rupture, biliary tree leakage, or failure in a dog: diagnosis and management. rupture in the proximal bowel. J Adv Vet Anim Res 2014, 1(3):140–144. FOLLOW-UP Pradham, MS, Dakshinkar, NP, Waghaye UG, Bodkhe AM. Successful treatment of PATIENT MONITORING ascites of hepatic origin in dog. Vet World r TREATMENT Varies with the underlying cause. 2008, 1(1):23. r r Can design treatment on an outpatient Check sodium, potassium, BUN, creatinine, Saravanan M, Sharma K, Kumar M, basis, with follow-up or inpatient care, and weight fluctuations periodically if the Vijaykumar H, Mondai DB. Analysis of depending on physical condition and patient is maintained on a diuretic. serum ascites albumin gradient test in ascitic underlying cause. POSSIBLE COMPLICATIONS dogs. Vet World 2012, 5(5):285–287. r If patients are markedly uncomfortable Aggressive diuretic administration may cause Author Jerry A. Thornhill when lying down or become more dyspneic hypokalemia, which could predispose to Consulting Editors Larry P. Tilley and with stress, consider removing enough ascites metabolic alkalosis and exacerbation of Francis W.K. Smith, Jr. to reverse these signs. hepatic encephalopathy in patients with r Dietary salt restriction may help control underlying liver disease; alkalosis causes a shift Client Education Handout transudate fluid accumulation due to CHF, from NH4 to NH3. available online cirrhosis, or hypoproteinemia. r For exudate ascites control, address the underlying cause; corrective surgery is often indicated, followed by specific therapeutic JWST589-A77-69 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:21 279mm×216mm

Canine and Feline, Sixth Edition 119 Aspergillosis, Nasal A

ulceration, facial asymmetry, loss of nasal the frontal sinus if the opening of the airflow—sino-orbital disease in cats. nasofrontal duct is destroyed by fungal r CAUSES infection. Rigid rhinoscopy—examination BASICS r No underlying cause identified, although of the nasal cavity alone; good visualization is DEFINITION preexisting foreign body or trauma is possible due to large airspaces caused by r r Nasal disease caused by Aspergillus spp., occasionally implicated. Likely due to turbinate lysis; excessive mucus and bleeding r can make full examination difficult. primarily A. fumigatus. Saprophytic fungus inhalation of a large bolus of fungus that is r that is ubiquitous in the environment. r Visualization of fungal plaques (white, r ubiqutous in the environment. Species— Opportunistic pathogen. most commonly A. fumigatus in dogs, A. felis yellow, black, or light-green) on the mucosa of the nasal cavity and/or frontal sinus PATHOPHYSIOLOGY in cats others—A. niger, A. flavus. r r confirms fungal infection. Sinuscopy—may Inhalation of fungus leads to disease in the RISK FACTORS be required to confirm the diagnosis in dogs nasal cavity and frontal sinus with destruction Unknown that lack nasal plaques. of turbinates, formation of plaque lesions, and overproduction of mucus causing clinical PATHOLOGIC FINDINGS r r signs of nasal disease. Rarely may be Biopsies obtained of affected area under associated with underlying foreign body or direct rhinoscopic visualization using cup r DIAGNOSIS r previous trauma. Causes a locally aggressive biopsy instruments. Samples immersion- and invasive disease but does not result in DIFFERENTIAL DIAGNOSIS fixed in buffered 10% formalin, routinely r r r r systemic mycosis. Confined to nasal cavity Foreign body Oronasal fistula processed. Evidence supportive of a r r and frontal sinus—sinonasal form (most Lymphoplasmacytic rhinitis Neoplasia diagnosis of aspergillosis—identification of r r common in dogs). Can result in sino-nasal Nasopharyngeal polyp, nasal tumor, or septate, branching hyphae and conidia on or sino-orbital disease in cats. cryptococcus—cats only histopathology. Surrounding inflammation is commonly neutrophilic or SYSTEMS AFFECTED CBC/BIOCHEMISTRY/URINALYSIS lymphoplasmacytic, rarely eosinophilic. r r r Respiratory—nasal cavity, sinus, orbit (cats, Often normal Possible inflammatory Blind biopsies in an unaffected area of the rare in dogs) leukogram nasal cavity can result in a false diagnosis of GENETICS OTHER LABORATORY TESTS inflammation. Unknown Serology r INCIDENCE/PREVALENCE Detects fungi-specific serum antibodies. r Unknown, but a common diagnosis in dogs AGID—commercially available; 98% with nasal discharge in many locations. specificity, 67% sensitivity in dogs; 43% TREATMENT GEOGRAPHIC DISTRIBUTION sensitivity in cats. Serial serology does not APPROPRIATE HEALTH CARE appear to correlate with clinical status. Worldwide r ELISA—88% sensitivity, 97% specificity in Overnight hospitalization advised after topical r SIGNALMENT dogs, 90% sensitivity in cats. Counter- treatment or surgery. Species immunoelectrophoresis—85% specificity in NURSING CARE r Dog and cat (less common) dogs. Serum galactomannan—unreliable. Maintain the nares free of nasal discharge. Breed Predilections Culture ACTIVITY r r Dogs—dolichocephalic and mesocephalic Tissue fungal culture of affected area; r Restriction of activity is not required if no breeds Cats—brachycephalic breeds may be visualized biopsy sample taken from a region bleeding is documented. of suspected fungal growth showed 100% overrepresented r DIET Mean Age and Range specificity, 81% sensitivity in dogs. Culture r N/A Dogs—predominantly young to of nasal discharge is less specific and r CLIENT EDUCATION middle-aged Cats—no predilection insensitive. r IMAGING Dogs—inform client that multiple topical Predominant Sex treatments are usually necessary to cure the Computed Tomography None identified r r disease; follow-up with rhinoscopy is highly Imaging method of choice. Cavitated r SIGNS r recommended to ensure resolution. No turbinate lysis. Thickening of the mucosa r established protocols for treatment in cats. Historical Findings along the nasal turbinates. Frontal sinus r r SURGICAL CONSIDERATIONS Unilateral or bilateral nasal discharge— proliferative mass effect. Soft tissue mass in typically mucoid, mucopurulent, or the choana or nasopharynx—cats. Endoscopic Debridement serosanguinous but may be primarily r r r r Necessary for evaluation of the cribriform Extensive curettage and removal of fungal epistaxis. Sneezing. Typically chronic r plate before topical antifungal treatment. material from the nose and frontal sinus are signs—several months. Many patients will Skull Radiography essential to allow efficacy of topical have been treated with antibiotics for a r medication. possible bacterial infection before Intraoral dorsoventral radiograph of the nasal cavity shows turbinate lysis. Trephination of the Frontal Sinus presentation with variable response. r r Rostrocaudal or skyline frontal sinus view Can be required for dogs with frontal sinus Physical Examination Findings r r may show increased soft tissue density in the involvement. Performed using a Jacob’s Unilateral or bilateral nasal discharge. r r r frontal sinus. Cannot evaluate cribriform chuck and intramedullary pin. Allows direct Increased nasal airflow on the affected side. r plate. visualization of the frontal sinus with a rigid Depigmentation with ulceration of the nasal r DIAGNOSTIC PROCEDURES rhinoscope and local debridement of fungal planum—∼40% of dogs. Facial pain. r r plaques. Allows for lavage and topical Ipsilateral mandibular lymphadenopathy. Rhinoscopy r r treatment of the area using a red rubber Stertor, exophthalmos, hard palate Flexible rhinoscopy in dogs allows catheter. examination of the nasopharynx and possibly JWST589-A77-69 JWST589-Tilley Printer: Yet to Come August 26, 2015 11:21 279mm×216mm

120 Blackwell’s Five-Minute Veterinary Consult

A Aspergillosis, Nasal (Continued)

Surgical Debridement and Exenteration PRECAUTIONS than previously thought and can occur years r r r Used in some cats with sino-orbital disease. Topical clotrimazole and enilconazole are after supposedly successful therapy. The caustic to all mucosal surfaces—protective prognosis for cats with sinonasal aspergillosis gear (gloves, goggles) should be worn by all is better than with the sino-orbital form. r staff that are in close contact. Enilconazole MEDICATIONS can be associated with tissue swelling and upper airway obstruction. DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) MISCELLANEOUS Topical Clotrimazole or Enilconazole Enilconazole Therapy r ASSOCIATED CONDITIONS r Also active in the vapor phase. 1-hour infusion into nasal cavity under N/A anesthesia. Combined Clotrimazole Irrigation and ZOONOTIC POTENTIAL r Depot Therapy Treatment is usually performed during the r There are no documented cases of human same anesthesia as diagnostics. Clotrimazole (1%) is flushed through a infection from an affected dog or cat. r trephine hole in the frontal sinus over Treatment of choice in dogs; reported PREGNANCY/FERTILITY/BREEDING efficacy 85–89% with multiple treatments. 5 minutes; 50 mL in each side in dogs r > 10kg;25mLineachsideindogs< 10 kg. N/A Foley catheters are used to occlude the nares r and nasopharynx. Clotrimazole cream (1%) is then introduced SYNONYMS r Dose—Clotrimazole: 1 gram in 100 mL of into the front sinuses; 20 g in each side in None dogs > 10 kg, 10 g in each side in dogs polyethylene glycol 200 (1% solution) evenly r ABBREVIATIONS < 10 kg. Reported efficacy similar to topical r r divided between two 60 mL syringes slowly AGID = agar gel immunodiffusion CT = clotrimazole or enilconazole alone (86%). r infused over 1 hour into each side for large computed tomography ELISA = dogs; if trephination is used, divide the enzyme-linked immunosorbent assay amount between the nasal cavity and sinus on the same side; less volume in smaller dogs. Suggested Reading Enilconazole: 100 mL of 1%, 2%, or 5% FOLLOW-UP Barrs VR, Talbot JJ. Feline aspergillosis. Vet solution. Clin North Am 2014, 44(1):51–73. r PATIENT MONITORING Dog is placed in dorsal recumbency with Friend E, Anderson DM, White RAS. Dogs Combined clotrimazole irrigation and depot head turned to each side every 15 minutes r during the infusion. Monitor clinical signs, although reduction therapy for canine nasal aspergillosis. J r of clinical signs does not establish resolution Small Anim Pract 2006, 47(6):312–315. Dog is placed in sternal recumbency with r head down at the end of the procedure to of disease. Follow-up rhinoscopy is Mathews KG, Davidson AP, Koblik PD, et al. drain all medication from the nasal cavity. recommended in all cases to establish Comparison of topical administration of r Has been used in cats without orbital response to treatment, regardless of clinical clotrimazole through surgically placed signs—histopathology and culture can help versus nonsurgically placed catheters for involvement in combination with oral r antifungal therapy with varying success. establish response. Serial serology (AGID) treatment of nasal aspergillosis in dogs: 60 appears not to correlate with clinical status. cases (1990–1996). J Am Vet Med Assoc Systemic Therapy r r Antifungal triazole drugs should be Repeat CT scan should be considered for 1998, 213:501–506. considered if the cribriform plate is not intact; reassessment of the cribriform plate before McLellan GJ, Aquino SM, Mason DR, Myers repeat topical treatment if a worsening clinical RK. Use of posaconazole in the also used as primary therapy in some cats. r r signs are seen. Monitor liver enzymes in management of invasive orbital aspergillosis Can also be used in combination with r topical therapy. animals on triazole therapy. Monitor renal in a cat. J Am Anim Hosp Assoc 2006, r May be cost-prohibitive. parameters in animals on Amphotericin B. 42:302–307. r Cats Pomrantz JS, Johnson LR, Nelson RW, Itraconazole 5 mg/kg PO q12h in dogs with r Monitor clinical signs for improvement or Wisner ER. Comparison of serologic a reported efficacy of 60–70%; 10 mg/kg PO r q24h in cats. resolution. Monitor liver enzymes in evaluation via agar gel immunodiffusion r r Voriconazole 5 mg/kg PO q12h; efficacy as animals on triazole therapy. Monitor renal and fungal culture of tissue for diagnosis of sole therapy has not been established, parameters in animals on Amphotericin B. nasal aspergillosis in dog. J Am Vet Med Assoc 2007, 230:1319–1323. neurotoxicity in cats. PREVENTION/AVOIDANCE r Author Jill S. Pomrantz Posaconazole: dogs, 5–10 mg/kg PO N/A q12–24h, cats, 5 mg/kg PO q24h or divided Consulting Editor Lynelle R. Johnson POSSIBLE COMPLICATIONS q12h; efficacy as sole therapy has not been r established. Topical therapy—monitor after treatment r Fluconazole is not recommended due to for any complications such as swelling of oropharynx, neurologic signs, infection/ resistance. r swelling of trephine site. Triazoles can cause CONTRAINDICATIONS anorexia and can be hepatotoxic. r r Breach in the cribriform plate can allow Amphotericin B can be nephrotoxic. contact of antifungal medication with brain EXPECTED COURSE AND PROGNOSIS resulting in neurologic signs and possible r r death. Sino-orbital disease necessitates the Studies have shown an 87% response rate to topical therapy in dogs after one to three use of systemic therapy. Amphotericin B r should be considered. treatments. A newer study showed that recurrence or reinfection is more common JWST589-A78-70 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:23 279mm×216mm

Canine and Feline, Sixth Edition 121 Aspergillosis, Systemic A

r Cats Culture on Sabouraud’s dextrose agar r Usually nonspecific signs (e.g., lethargy, (requires 5–7 days). r depression, vomiting, and diarrhea). Antibody serology (agar gel BASICS r Ocular—exophthalmos. immunodiffusion, and ELISA) support the OVERVIEW CAUSES & RISK FACTORS diagnosis but is insensitive for diagnosis of r r disseminated aspergillosis. Opportunistic fungal infection caused by Caused by Aspergillus species, most r Aspergillus spp., common molds that are commonly A. terreus or A. deflectus, Galactomannan antigen ELISA (urine or ubiquitous in the environment, forming A. fumigates, A. niger, A. flavipes, and serum) good sensitivity (89%) and specificity numerous spores in dust, straw, grass A. alabamensis also associated. A. felis recently (89%) in one small study. Pulmonary and clippings, and hay. ocular infections have lower sensitivity. False r reported to cause fungal rhinosinusitis in cats, Disseminated disease does not appear to be disseminated disease in dogs, and pulmonary positive in dogs treated with Plasmalyte or related to the nasal form of the disease, aspergillosis in humans. with other mycotic infections (Penicillium, r although one report of a dog developing German shepherds and immunosuppressed Paecilomyces, Cladosporidium, Geotrichum, Histoplasma, Cryptococcus). fungal osteomyelitis 6 months after treatment animals at higher risk. r for nasal aspergillosis raises the possibility. r Cats—test for FeLV and FIV. r Geographic/environmental conditions— Disseminated disease—usually A. terreus or may be a factor, as some regions have a higher IMAGING A. deflectus, r incidence (e.g., California, Louisiana, Radiographic Findings r Portal of entry not definitively established Michigan, Georgia, Florida, and Virginia in Spinal views may show end-plate lysis, but possibly through the respiratory tract or the United States; Western Australia; attempted bony intervertebral bridging, and gastrointestinal tract, with subsequent Barcelona; and Milan). lysis of vertebral bodies consistent with hematogenous spread. r r Cats—associated with FIP, FePLV, FeLV, discospondylitis; productive and destructive Most commonly affects intervertebral discs, FIV, diabetes mellitus, and lesions of the vertebral bodies. r bones, thoracic lymph nodes, lung and renal immunosuppressant use. Bony proliferation, lysis and periosteal pelvis. May affect respiratory reaction typical of osteomyelitis of the (bronchopulmonary) only, or rarely, cornea or diaphyseal region of long bones. r ear canal only. Pulmonary involvement rare, mixed SIGNALMENT DIAGNOSIS interstitial/alveolar pattern, enlarged sternal Dogs and/or tracheobronchial lymph nodes, pleural r DIFFERENTIAL DIAGNOSIS Morecommonindogsthanincats. effusion; productive and destructive lesions of r German shepherds, and less so Rhodesian Bacterial osteomyelitis/discospondylitis; sternebrae. Pulmonary cavitary lesions in dogs ridgebacks, overrepresented but reported spinal neoplasia; intervertebral disc disease; with chronic pulmonary localization. skeletal neoplasia; bacterial pyelonephritis; sporadically in many breeds; average age Ultrasonographic Findings bacterial pneumonia; other causes of r 3 years (range 2–8 years); females three times Kidneys—most common site to detect more likely to develop disease as males. vestibular signs/seizures; other causes of uveitis (see Anterior Uveitis—Cats, Anterior changes; changes seen include renal pelvis Cats dilation ± echogenic debris within pelvis; loss r Uveitis—Dogs). Persians—marginally increased incidence. of corticomedullary distinction; renal r CBC/BIOCHEMISTRY/URINALYSIS Disseminated cases mostly affect the lungs r distortion and mottled appearance of the Nonspecific. and/or gastrointestinal tract. r parenchyma; dilation of proximal ureter; Dogs—mature neutrophilic leukocytosis SIGNS renalomegaly; nodules or masses; with eosinophilia and monocytosis. One third hydronephrosis. Dogs r r have normocytic, normochromic Spleen—hypoechoic, lacy, sharply May develop acutely or slowly over a period nonregenerative anemia. Cats—may have demarcated areas with no doppler signal of several months, usually terminally ill when nonregenerative anemia and leukopenia. r suggestive of infarct are most significant first presenting. r Biochemistry—may see high globulins, finding in spleen; other findings include Lameness—fungal osteomyelitis causing ALP, ALT, amylase, creatinine, phosphate, nodules/masses, mottled parenchyma, splenic pronounced swelling and discharging, fistulus BUN, and calcium. r venous thrombosis. tracts. r r Urinalysis—may see isosthenuria, Other—abdominal lymphadenomegaly; Neurologic—fungal discospondylitis hematuria, pyuria, and possible fungal hyphae diffuse hepatic hypoechogenicity, ascites, or causing paraparesis, paraplegia, spinal pain. in the sediment; detection of the fungal evidence of venous thrombosis. Central signs—vestibular signs, seizures, hyphae can be improved by allowing the MRI Findings hemiparesis, mental dullness, ataxia, vision sample to incubate at room temperature for Useful for further defining brain lesions in impairment, circling.. 24–48 hours; sediment samples may be r animals with CNS signs; changes similar to Renal involvement—polyuria/polydipsia, examined unstained as wet preparations or other infectious and non-infectious hematuria. may be air dried and stained with Diff-Quick r ◦ inflammatory brain diseases. May help to Respiratory—cough, hemoptysis, increased (the hyphae branch at 45 and stain purple). identify subtle vertebral lesions in dogs with respiratory effort. r OTHER LABORATORY TESTS discospondylitis. Reproduction—pyometra. r r Methods of detection include: cytology, DIAGNOSTIC PROCEDURES Cardiac—pericarditis, ascites due to right culture and histopathology. sided failure, arrhythmias. r Area to collect sample relies on clinical r Definitive diagnosis by fungal culture from presentation but may include CSF tap, joint Gastrointestinal—abdominal distension, normally sterile body fluids and tissues, e.g., anorexia. aspirates, intervertebral disc space aspirates, r urine, bone, CSF, blood, lymph node, pleural Ocular—uveitis, chorioretinitis, hyphema, abdominocentesis/thoracocentesis, aspirate of effusions, intervertebral disc aspirates, kidney, panopthalmitis. various organs (spleen, liver, kidney) or lymph r spleen. Urine culture positive in Nonspecific—fever, weight loss, weakness, nodes. approximately 50% of dogs. vomiting, and lymphadenopathy. JWST589-A78-70 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:23 279mm×216mm

122 Blackwell’s Five-Minute Veterinary Consult

A Aspergillosis, Systemic (Continued)

r PATHOLOGIC FINDINGS New triazoles: voriconazole, posaconazole r Hyphae usually visualized, special stains and ravuconazole all have activity against assist organism detection. Aspergillus. Some dogs treated with r MISCELLANEOUS Focal osteomyelitis with multiple pale voriconazole or posaconazole have gone into granulomas in kidneys, spleen, lymph node, remission for many months. Aspergillus spp. ZOONOTIC POTENTIAL myocardium, pancreas, and liver. resistant to fluconazole. r r None Microscopic granulomas can be found in Terbinifine (5–10 mg/kg PO q24h) used ABBREVIATIONS lungs, eyes, thyroid, uterus, brain, and alone or in combination with triazoles has r ALP = alkaline phosphatase prostate and contain numbers of septate, been used to treat resistant infections in r ALT = alanine transaminase branching hyphae that may have humans. r r BUN = blood urea nitrogen characteristic lateral branching aleuriospores. 𝛽-glucan synthase inhibitors caspofungin, r r CSF = cerebrospinal fluid Occasionally pulmonary congestion or GI micafungin, anidulafungin—limited clinical r = mucosal reddening and erosions. information in dogs but efficacious in invasive ELISA enzyme-linked immunosorbent r assay Best visualized with periodic acid-Schiff, aspergillosis in humans. r r FeLV = feline leukemia virus Gomori’s methenamine silver, or Crocott’s Combination therapy with flucytosine r FePLV = feline panleukopenia virus stain. (dogs, 25–50 mg/kg PO q6h) and r FIP = feline infectious peritonitis amphotericin B may prove successful, but no r FIV = feline immunodeficiency virus published reports. r MRI = magnetic resonance imaging CONTRAINDICATIONS/POSSIBLE TREATMENT INTERACTIONS Suggested Reading r Maddison JE, Page SW, Church DB. Small Amphotericin B—contraindicated in dogs DOGS Animal Clinical Pharmacology, 2nd ed. r with pre-existing renal compromise or failure; Treatment rarely curative; severely ill dogs Edinburgh: Saunders, 2008, pp. 186–197. amphotericin B lipid complex significantly are recognized to have poor prognosis. May Sykes, JE. Canine and Feline Infectious reduced nephrotoxicity. halt progression of clinical signs. r Diseases. Philadelphia: Saunders, 2014, r Oral azoles—nausea, intermittent anorexia, Fluid therapy—indicated by the degree of pp. 639–647. liver enzyme elevation. renal compromise and azotemia. r Author Hannah N. Pipe-Martin r Combination of flucytosine and Pulmonary lobectomy followed by systemic Consulting Editor Stephen C. Barr amphotericin B—cutaneous drug eruptions antifungals has been successful in dogs with Acknowledgment The author and editors in dogs. cavitary lesions without evidence of r acknowledge the prior contributions of Tania Avoid midazolam and cisapride with dissemination. N. Davey. azoles—fatal drug reactions noted in humans. CATS r Hepatotoxicity and ulcerative dermatitis Disseminated—likely difficult to treat; more likely to occur at doses of 10 mg/kg/day Client Education Handout limited data. or higher. Discontinue itraconazole if adverse available online effects occur. May be able to reinstitute at lower dose once side effects have resolved. MEDICATIONS DRUG(S) r Combination itraconazole 5–10 mg/kg PO FOLLOW-UP q24h (can be divided) and amphotericin B Disseminated—monitor serial radiographs (dogs, 2–3 mg/kg IV 3 days per week for a every 1–2 months, renal function, and urine total of 9–12 treatments, to cumulative dose cultures; prognosis poor, especially in German of 24–27 mg/kg) —treatment of choice. r shepherds. Itraconazole as monotherapy has achieved long-term remission in a small number of dogs. JWST589-A79-71 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:25 279mm×216mm

Canine and Feline, Sixth Edition 123 Aspirin Toxicosis A

r Other causes of liver failure, including CONTRAINDICATIONS/POSSIBLE acetaminophen, iron, metaldehyde, and INTERACTIONS BASICS blue-green algae N/A CBC/BIOCHEMISTRY/URINALYSIS OVERVIEW r Cats—prone to Heinz body formation r r Given for its antipyretic, analgesic, Hyponatremia and hypokalemia anti-inflammatory, and antiplatelet effects. r r Anemia, hypoproteinemia, elevated liver FOLLOW-UP Aspirin inhibits cyclooxygenase, reducing enzymes, elevated white blood cell count r Maintaining renal function and acid-base the synthesis of prostaglandins and OTHER LABORATORY TESTS thromboxanes. balance is vital. r r r Gastric irritation and hemorrhage can Initial respiratory alkalosis followed by Severe acid-base disturbances, severe occur; dogs are especially sensitive. metabolic acidosis dehydration, toxic hepatitis, bone marrow r r Repeated doses can produce gastrointestinal High ketones and pyruvic, lactic, and depression, and coma are poor prognostic ulceration and perforation. amino acid levels indicators. r r Toxic hepatitis, metabolic acidosis, and Decreased sulfuric and phosphoric acid anemia can occur, especially in cats. renal clearance SIGNALMENT DIAGNOSTIC PROCEDURES Cats and less commonly dogs Salicylic acid concentrations in serum or urine MISCELLANEOUS r SIGNS Be sure that history of “aspirin” medication r Depression does not refer to other available pain r Anorexia medications. r TREATMENT r Vomiting—vomitus may be blood-tinged Question owner about any pre-existing r r Tachypnea Inpatient—following general principles of painful condition that may have prompted r Hyperthermia poisoning management the aspirin administration. r r Muscular weakness and ataxia Induced gastric emptying—gastric lavage or r Suggested Reading induced emesis Ataxia, coma, seizures, and death in 1 or r Plumb DC. Aspirin. In: Plumb DC, ed., more days Correction of acid-base balance— Plumb’s Veterinary Drug Handbook, 7th CAUSES & RISK FACTORS continuous intravenous fluids; assisted ed. Ames, IA: Wiley-Blackwell, 2011, r ventilation and supplemental oxygen for Owners employing human dosage pp. 83–87. severely-affected animals guidelines to medicate cats and dogs. r Talcott PA, Gwaltney-Brant SM. r Whole blood transfusions for severe cases of Cats have a decreased ability to conjugate Nonsteroidal antiinflammatories. In: hemorrhage and hypotension salicylate with glycine and glucuronic acid r Peterson ME, Talcott PA, eds. Small Animal Peritoneal dialysis, hemodialysis, or charcoal due to a deficiency in glucuronyl transferase. Toxicology, 3rd ed. St. Louis, MO: Elsevier, r hemoperfusion—advanced procedures Half-life increases with dosage—cats, 2013, pp. 698–700. 22–27 hours for 5–12 mg/kg and Author Lisa A. Murphy approximately 44 hours for 25 mg/kg; dogs, Consulting Editor Lynn R. Hovda 7.5 hours; responsible for higher risk in cats. Acknowledgment The author and editors Elimination is slower in neonatal and geriatric MEDICATIONS acknowledge the prior contribution of patients. Frederick W. Oehme. r DRUG(S) Patients with hypoalbuminemia may be at r No specific antidote available. higher risk of toxicity because aspirin is highly r Activated charcoal— 1–2 g/kg PO. protein bound to plasma albumin. r Sodium bicarbonate 1 mEq/kg IV alkalinizes urine; must closely monitor acid-base status. r Gastrointestinal protectants—sucralfate and DIAGNOSIS a H2 blocker or proton pump inhibitor; DIFFERENTIAL DIAGNOSIS misoprostol for patients at higher risk for r gastrointestinal hemorrhage. Ethylene glycol or alcohol r Anticoagulant rodenticides JWST589-A80-72 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:29 279mm×216mm

124 Blackwell’s Five-Minute Veterinary Consult A Asthma, Bronchitis—Cats

r Physical Examination Findings Pulmonary lobar arterial enlargement is r Severely affected cats present with suspicious for heartworm disease. open-mouth breathing, tachypnea, and BASICS r Echocardiography cyanosis. Increased tracheal sensitivity is r Useful to document heartworm disease or DEFINITION common. Chest auscultation may reveal secondary pulmonary hypertension. r crackles and/or expiratory wheezes, but can be Chronic bronchitis—inflammation in the r DIAGNOSTIC PROCEDURES airways (bronchi and bronchioles) lacking a normal. Labored breathing with an specific etiology; chronic daily cough of abdominal push on expiration, increase in Transoral Tracheal Wash greater than 2 months in duration. expiratory effort. Use a sterile endotracheal tube and r Asthma—acute or chronic airway CAUSES polypropylene catheter to collect airway fluids at the level of the carina. inflammation associated with increased Triggers of airway inflammation unknown airway responsiveness to various stimuli, Bronchoscopy RISK FACTORS r airway narrowing due to smooth muscle r Allows visualization of trachea and bronchi. hypertrophy or constriction, reversibility of Cigarette smoke, poor environmental Excessive amounts of thick mucus are hygiene, dusty cat litter, hair sprays, and air airway constriction, and presence of r common with bronchitis. Mucosa of the eosinophils, lymphocytes, and mast cells fresheners can exacerbate disease. Use of airways is typically hyperemic and edematous. r potassium bromide—implicated in causing within the airways. Bronchitis is thought to Cytology of TOTW or BAL signs of bronchitis/asthma in some cats. r result in airflow obstruction due to airway Eosinophils and neutrophils are most r remodeling while asthma is associated with prominent cell types. Up to 20% airway constriction; however, clinically the eosinophils on BAL cytology can be found in r two disease processes can appear similar. No normal cats. A mixed inflammatory cell physical examination findings or biomarkers DIAGNOSIS population occurs in about 21% of cats. can distinguish between the two syndromes, DIFFERENTIAL DIAGNOSIS Bacterial Cultures although reversal of airflow obstruction r r following administration of a beta-agonist is Rule out infectious pneumonia Quantitated cultures recommended; (Mycoplasma, Toxoplasma, bacterial or fungal suggestive of the asthmatic form of disease. r positive cultures frequently encountered but pneumonia). Consider Dirofilaria immitis bacterial colony counts > 100–300 cfu/mL PATHOPHYSIOLOGY r r and primary lung parasites (Aelurostrongylus uncommon with bronchitis. Specific Lower airway inflammation likely results abstrusus, Capillaria aerophilia, Paragonimus Mycoplasma culture often needed. from inhalation of irritant substances. r kellicotti).Morecommoninsouthernand Biopsy Bronchiolar smooth muscle constriction— midwest US, and in outdoor and hunting cats Keyhole biopsy—can differentiate between reversible spontaneously or with treatment. r r in some geographic regions. Primary or idiopathic pulmonary fibrosis, neoplasia and Increase in mucosal goblet cells, mucus metastatic neoplasia can have similar clinical r bronchitis if needed. production, and edema of bronchial wall and radiographic appearance. Clinical r PATHOLOGIC FINDINGS associated with inflammation. Excessive presentation of idiopathic pulmonary fibrosis mucus can cause bronchiolar obstruction, Hyperplasia/hypertrophy of goblet cells, r may appear similar to feline bronchitis. atelectasis, or bronchiectasis. Smooth CBC/BIOCHEMISTRY/URINALYSIS hypertrophy of airway smooth muscle, muscle hypertrophy implies chronicity— epithelial erosion, and inflammatory r ∼ usually not reversible. Chronic Frequently normal, 40% of cats with infiltrates. inflammation leads to airway remodeling and bronchial disease have peripheral eosinophilia. OTHER LABORATORY TESTS irreversible airflow obstruction. r SYSTEMS AFFECTED Fecal exams—flotation for Capillaria, r r Respiratory Cardiac—pulmonary sedimentation for Paragonimus, Baermann for TREATMENT Aelurostrongylus. False-negative tests common. hypertension rarely r APPROPRIATE HEALTH CARE Heartworm antigen and antibody testing, r GEOGRAPHIC DISTRIBUTION particularly if coughing occurs in conjunction Remove patient from environment that r r Worldwide. with vomiting. Radioallergosorbent testing exacerbates disease. Hospitalize for acute SIGNALMENT or intradermal skin testing—no correlation respiratory distress. Species between skin allergies and respiratory disease NURSING CARE Cat currently documented. Oxygen therapy, bronchodilators, and IMAGING Breed Predilections sedatives in an acute crisis. Minimize Siamese overrepresented Radiography manipulation in order to lessen stress and r oxygen needs of the animal. Mean Age and Range Classically, diffuse bronchial wall thickening; interstitial or patchy alveolar ACTIVITY Any age; more common between 2 and r patterns also possible. Severity of 8years Usually self-limited by patient. radiographic changes does not necessarily DIET Predominant Sex correlate with clinical severity or duration, Calorie restriction for obese cats. One study showed females overrepresented and normal radiographs can be found. SIGNS r CLIENT EDUCATION Hyperinflation of lung fields—flattened and r Most causes are chronic and progressive. Historical Findings caudally displaced diaphragm, increased r r Coughing, tachypnea, labored breathing or distance between the heart and diaphragm, Do not discontinue medical therapy when r wheezing. Signs are typically episodic and extension of lungs to the first lumbar clinical signs have resolved—subclinical vertebrae thought to reflect inflammation is common and can lead to can be acute or chronic. r bronchoconstriction. Collapse of right progression of disease. Lifelong medication and environmental changes usually necessary. middle lung lobe due to mucus plugging and r atelectasis reported in 11% of cases. Some clients can be taught to give JWST589-A80-72 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:29 279mm×216mm

Canine and Feline, Sixth Edition 125

(Continued) Asthma, Bronchitis—Cats A

terbutaline subcutaneously and corticosteroid q12h. Initial albuterol dose is 20 𝜇g/kg PO Change furnace and air-conditioner filters on injections at home for a crisis situation. q12h; can increase to 50 𝜇g/kg PO q8h. a regular basis. Consider dust-free litters. Inhaled Bronchodilators r POSSIBLE COMPLICATIONS r Albuterol—preferred inhalant Acute episodes can be life-threatening. r bronchodilator, effect lasts less than 4 hours. Right-sided heart disease rarely develops as a MEDICATIONS Long-term use of traditional racemic form of result of long-term bronchitis. inhaled albuterol (R and S-enantiomers) has DRUG(S) OF CHOICE EXPECTED COURSE AND PROGNOSIS been associated with worsened airway r Emergency Treatment inflammation. Enantiomer specific Long-term therapy should be expected. r r Oxygen and a parenteral bronchodilator. R-albuterol should be used if the drug is Most cats do well if recurrence of clinical signs is carefully monitored and medical Injectable terbutaline (0.01 mg/kg IV or SC); needed in moderately to severely affected cats r repeat if no clinical improvement (decrease in (q12–24h) or during respiratory distress. therapy appropriately adjusted. Afewcats will be refractory to treatment; these carry a respiratory rate or effort) in 20–30 minutes. Anthelminthics r r much worse prognosis. A sedative can aid in decreasing anxiety Empirical therapy is indicated for cats with (butorphanol tartrate at 0.2–0.4 mg/kg IV or clinical signs of bronchial disease and IM, buprenorphine at 0.01 mg/kg IV or IM, eosinophilic airway cytology in an appropriate or acepromazine at 0.01–0.05 mg/kg SC). geographic location. r r A short-acting parenteral corticosteroid may Consider fenbendazole, ivermectin, or MISCELLANEOUS also be required. Dexamethasone sodium praziquantel. ASSOCIATED CONDITIONS phosphate (0.1–0.25 mg/kg, IV or SC). Can Antibiotics repeat if no improvement noted within Cor pulmonale can be a sequela to chronic Use based on a positive quantitative culture 20–30 minutes. lower airway disease. and susceptibility testing or Mycoplasma PREGNANCY/FERTILITY/BREEDING Long-Term Management isolation. Corticosteroids Glucocorticoids are contraindicated in the r CONTRAINDICATIONS Decrease inflammation. pregnant animal. Bronchodilators should be r Oral treatment is preferred over injectable Beta-2 antagonists (e.g., propranolol) are used with caution. for closer monitoring of dose and duration. contraindicated because of their ability to SYNONYMS r block sympathetically mediated Prednisolone: 0.5–1 mg/kg PO q12h. Begin Allergic bronchitis, asthmatic bronchitis, bronchodilation. to taper dose (50% each week) after feline lower airway disease, extrinsic asthma, 1–2 weeks if clinical signs have improved. PRECAUTIONS r eosinophilic bronchitis. Maintenance therapy = 0.5–1 mg/kg PO Long-term use of steroids increases risk of SEE ALSO q24–48h. development of diabetes mellitus and r r r r Heartworm Disease—Cats Respiratory Longer-acting parenteral steroids (Vetalog predisposes to immunosuppression. Use of Parasites or Depomedrol) should be reserved only for corticosteroids in cats may precipitate r ABBREVIATIONS situations where owners are unable to congestive heart failure. Beta agonists could r BAL = bronchoscopy/bronchoalveolar administer oral or inhaled medication on a cause tachycardia and exacerbate underlying r lavage MDI = metered-dose inhaler routine basis. cardiac disease. r Inhaled Corticosteroids PU/PD = polyuria/polydipsia r ALTERNATIVE DRUG(S) Requires a form-fitting facemask, spacer, INTERNET RESOURCES Leukotriene receptor blockers and inhibitors r and metered-dose inhaler (MDI). Veterinary of generation: no evidence to support use. www.Aerokat.com: for ordering facemasks brand: Aerokat (Trudell Medical). and spacers for inhalant therapy. r Anti-serotonin and antihistamine drugs: no r The most common corticosteroid used asan evidence to support use. Immunotherapy: no www.fritzthebrave.com: source for clients to MDI is fluticasone propionate (Flovent). clinical evidence to support use at this time. research use of inhaled medications. 110-𝜇g Flovent MDI is recommended (1–2 actuations, 7–10 breaths q12h). In one study, Suggested Reading use of 44-𝜇g Flovent decreased BAL CohnLA,DeClueAE,CohenRL,Reinero eosinophil counts in cats with experimentally CR. Effects of fluticasone propionate dosage induced lower airway disease. FOLLOW-UP in an experimental model of feline asthma. r Flovent is used for long-term control of PATIENT MONITORING J Feline Med Surg 2010, 12(2):91–96. r Kirschvink J, Leemans J, Delvaux F, et al. airway inflammation. Takes 10–14 days to Owners should report any increase in Inhaled fluticasone reduces bronchial reach peak effect; use oral steroids coughing, sneezing, wheezing, or respiratory responsiveness and airway inflammation in concurrently during this time. distress. Medications should be increased r cats with mild chronic bronchitis. J Feline Results in some suppression of the appropriately or additional therapy initiated if r Med Surg 2006, 8(1):45–54. hypothalamic-pituitary axis but systemic side clinical signs worsen. Follow-up radiographs Authors Carrie J. Miller and Lynelle R. effects appear to be limited. may be helpful to detect onset of new disease. r Johnson Bronchodilators Owner should watch for signs of PU/PD r Consulting Editor Lynelle R. Johnson Methylxanthines: sustained-release that could indicate diabetes mellitus or renal theophylline formulations recommended, and disease. Monitor blood glucose and urine pharmacokinetics can vary greatly. Only cultures. generic currently available. Dose at Client Education Handout PREVENTION/AVOIDANCE 15–20 mg/kg PO once daily in the evening. available online r Beta-2 agonists (terbutaline, albuterol)— Eliminate any environmental factors that can reverse smooth muscle constriction. Oral trigger a crisis situation (see “Risk Factors”). terbutaline dose is 1/4 of a 2.5 mg tablet JWST589-A81-73 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:31 279mm×216mm

126 Blackwell’s Five-Minute Veterinary Consult A Astrocytoma

characteristics highlighted in specific increase in hepatic enzymes on serum r sequences. biochemical panel. CBC and platelet count DIAGNOSTIC PROCEDURES is recommended 7–10 days after BASICS r r Neurologic exam. Ophthalmic exam. chemotherapy and immediately before each OVERVIEW r r r dose of chemotherapy to monitor r MRI. CSF analysis. Tumor biopsy for r Glial cell neoplasm, most commonly definitive diagnosis, when specific myelosuppression. Chemotherapy has the affecting the brain and rarely the spinal cord. potential to be synergistic with radiation r r antineoplastic treatment is sought (surgery, Neoplastic cells are of astrocytic origin. It curative-intent radiation therapy, therapy. Timely specialty to a referral center is the most common intra-axial (situated experimental therapies). with neurosurgery, radiation therapy, and inside of the brain parenchyma) intracranial medical oncology capabilities is important for neoplasm of dogs but is rarely diagnosed in patients seeking more than palliative care. r cats. Tumors are often located in the pyriform area of the temporal lobe, the TREATMENT cerebral hemispheres, the thalamus, r r r hypothalamus, or midbrain. Biologic Surgery. Radiation therapy can be very FOLLOW-UP behavior of this tumor is dictated by the effective in improving neurologic signs. r PATIENT MONITORING histopathologic grade (I–IV, from best to Chemotherapy with lomustine, r worst prognosis) and anatomic involvement. procarbazine, or temozolomide might exert Blood phenobarbital concentration should r r Tumors typically do not penetrate the cytoreductive activities. Anti-inflammatory be assessed after 7–10 days of treatment, with dosing with corticosteroids to reduce modifications to dosages for achieving target ventricular system or metastasize outside of r r the cranial vault. peritumoral edema. Consultation with a plasma concentrations. Serial MRIs should be considered for documenting response if SIGNALMENT neurosurgeon and a radiation oncologist is r r multimodality therapy is used. Serial CBC Dog—often brachycephalic breeds > 5years essential for the appropriate patient management. and platelet counts should be performed to of age; no sex predilection reported. r > monitor myelotoxicity associated with Cat—usually 9 years; no sex or breed chemotherapy. predilection reported. EXPECTED COURSE AND PROGNOSIS SIGNS r r r MEDICATIONS Long-term prognosis—guarded. Median Location and growth kinetic dependent survival after chemotherapy plus medical r r r DRUG(S) Seizures Behavioural changes Apathy management may be up to 7 months. r towards normal activities including eating, Seizure Control Median survival after radiation therapy has playing, and societal interactions r r r Status epilepticus—diazepam (0.5–1 mg/kg been reported to be as high as 12 months. Disorientation Loss of conscious r IV, up to three times to achieve effect); if no proprioception Cranial nerve abnormalities r r response to diazepam, use pentobarbital Head muscle atrophy Upper motor (5–15 mg/kg IV slowly to effect). r neuron tetraparesis Long-term management—phenobarbital MISCELLANEOUS (1–4 mg/kg PO q12h) with or without adjuvant potassium bromide (20 mg/kg PO SEE ALSO r q24h). Seizures (Convulsions, Status Epilepticus)— r DIAGNOSIS Tumor Control Cats Seizures (Convulsions, Status r DIFFERENTIAL DIAGNOSIS Timely consultation with a neurosurgeon is Epilepticus)—Dogs r of paramount importance for the appropriate ABBREVIATIONS Other primary tumors arising from tissues r r r r management of the patient. Radiation CSF = cerebrospinal fluid CT = of the central nervous system Metastatic r neoplasia with brain tropism such as therapy may be effective, and consultation computed tomography MRI = magnetic r hemangiosarcoma Granulomatous with a radiation oncologist is recommended. resonance imaging r meningoencephalitis Trauma Stereotactic radiosurgery or intensity r r Suggested Reading Cerebrovascular infarction Meningitis modulated radiation therapy may be considered as first-line treatment options. Bentley RT, Ober CP, Anderson KL, Feeney CBC/BIOCHEMISTRY/URINALYSIS r Chemotherapy may be effective for treating DA, Naughton JF, Ohlfest JR, O’Sullivan Usually unremarkable dogs. Potential drugs that may exert MG, Miller MA, Constable PD, Pluhar GE. OTHER LABORATORY TESTS measurable anticancer effects include CCNU Canine intracranial gliomas: relationship between magnetic resonance imaging CSF analysis may show albumin-cytologic (60–70 mg/m2 PO every 3 weeks) or temozolomide (100–120 mg/m2 PO q24h for criteria and tumor type and grade. Vet J dissociation (high protein with low number of r 5daysevery3weeks). Prednisone (1 mg/kg 2013, 198(2):463–471. nucleated cells). The CSF analysis is indicated Stoica G, Levine J, Wolff J, Murphy K. to exclude infectious etiology, not to diagnose q24h), may be effective in reducing peritumoral edema and improving the Canine astrocytic tumors: a comparative astrocytoma. review. Vet Pathol 2011, 48(1):266–275. IMAGING neurologic signs. Patients may need to be on r steroids long term, even after the definitive Troxel MT, Vite CH, Van Winkle TJ, et al. MRI of brain is ideal for mass lesion treatment of the tumor. Feline intracranial neoplasia: Retrospective confirmation, as it is superior to CT scanning review of 160 cases (1985–2001). J Vet for detecting lesions in the middle and caudal CONTRAINDICATIONS/POSSIBLE Intern Med 2003, 17:850–859. fossae. Additionally, MRI is more sensitive INTERACTIONS Author Nick Dervisis r than CT for detection infarcts, bleeding, and r Prednisone and phenobarbital may cause Consulting Editor Timothy M. Fan edema. Brain MRI may be useful in polyphagia, polydipsia, and polyuria. Acknowledgment The author and editors r establishing a tentative differential diagnosis Phenobarbital may cause sedation for up to acknowledge the prior contribution of of a glial tumor, based on tumor 2 weeks after initiation of treatment, and Wallace B. Morrison. 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Canine and Feline, Sixth Edition 127 Astrovirus Infection A

CBC/BIOCHEMISTRY/URINALYSIS PREVENTION/AVOIDANCE N/A Isolate infected cats during acute disease. OTHER LABORATORY TESTS POSSIBLE COMPLICATIONS BASICS r Electron microscopy of feces—identify Secondary intestinal viral and bacterial OVERVIEW astrovirus particles. infections. r An uncommon intestinal viral infection Difficult to isolate in the laboratory. EXPECTED COURSE AND PROGNOSIS characterized by enteritis and diarrhea. r IMAGING Illness usually < 1 week. SIGNALMENT r r N/A Mortality—appears low. Cats r r DIAGNOSTIC PROCEDURES Prognosis—good. No known breed, sex, or age predilection r None If diarrhea persists, investigate other causes. SIGNS r PATHOLOGIC FINDINGS Small bowel diarrhea often green and watery. None described; similar to mild enteritis, r Kittens show more severe signs. rotavirus, or coronavirus enteritis. r MISCELLANEOUS May be severe and acute enough to cause ZOONOTIC POTENTIAL dehydration and anorexia. CAUSES & RISK FACTORS Sequence analysis of human and animal r TREATMENT astroviruses suggests human-to-animal A small, non-enveloped, RNA virus of the r transmission does not occur. genus Astrovirus. Control diarrhea. r r Details of the incidence, prevalence, and Reestablish fluid and electrolyte balance. Suggested Reading predisposing factors unknown. Barr MC, Olsen CW, Scott FW. Feline viral diseases. In: Ettinger SJ, Feldman EC, eds., Veterinary Internal Medicine. Philadelphia: MEDICATIONS Saunders, 1995, pp. 409–439. DIAGNOSIS Lukashov VV, Goudsmit J. Evolutionary DRUG(S) relationships among Astroviridae. J Gen DIFFERENTIAL DIAGNOSIS No specific antiviral drugs. Virol 2002, 83:1397–1405. r Many causes of gastroenteritis Author Fred W. Scott r CONTRAINDICATIONS/POSSIBLE Food allergy Consulting Editor StephenC.Barr r INTERACTIONS Toxin ingestion r Inflammatory bowel disease None r Neoplasia r Intestinal parasites r Viral infections—panleukopenia, rotavirus, enteric coronavirus, enteric calicivirus FOLLOW-UP r Bacterial infections—salmonellosis, PATIENT MONITORING coliforms r Monitor fluid and electrolytes. Protozoal infections—Giardia, cryptosporidiosis JWST589-A83-75 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:38 279mm×216mm

128 Blackwell’s Five-Minute Veterinary Consult A Ataxia

r Bilateral vestibular involvement, peripheral Vestibular—Central Nervous System r or central in origin, has characteristic Infectious—FIP; canine distemper virus; exaggerated head motion with often poor to rickettsial diseases. BASICS r absent physiologic nystagmus. Inflammatory, idiopathic, DEFINITION Cerebellar immune-mediated—granulomatous r r A sign of sensory dysfunction that produces The cerebellum regulates, coordinates, and meningoencephalomyelitis, incoordination of the limbs, head, and/or modulates motor activity. meningoencephalomyelitis of unknown r origin. trunk. Proprioception is normal because the r r Nutritional—thiamine deficiency. Three clinical types—sensory ascending proprioceptive pathways to the r (proprioceptive), vestibular, and cerebellar; all cortex are intact; weakness does not occur Toxic—metronidazole. produce changes in limb coordination, but because the upper motor neurons are intact. Vestibular—Peripheral Nervous System r r vestibular and cerebellar ataxia also produce Inadequacy in the performance of motor Infectious—otitis media interna; Cryptococcus granuloma (cats). changes in head and neck movement. activity; strength preservation; no r PATHOPHYSIOLOGY proprioceptive deficits. Inflammatory—nasopharyngeal (middle r ear) polyps (cats). Sensory (Proprioceptive) Affected animal shows uncoordinated motor r r activity of limbs, head, and neck; hypermetria; Idiopathic—geriatric vestibular disease Proprioceptive pathways in the spinal cord dysmetria; head tremors; intention tremors; (dogs); idiopathic vestibular syndrome (cats). (i.e., fasciculus gracilis, fasciculus cuneatus, r and truncal sway. Menace responses may be Metabolic—hypothyroidism. and spinocerebellar tracts) relay limb and r absent without visual dysfunction. Neoplastic—squamous cell carcinoma, trunk position to the brain. bone tumors. r SYSTEMS AFFECTED r When the spinal cord is slowly compressed, Traumatic. proprioceptive deficits are usually the first Nervous—spinal cord (and brainstem and Spinal Cord r signs observed, because these pathways are cortex), cerebellum, vestibular system. Degenerative—degenerative myelopathy located more superficially in the white matter SIGNALMENT (old German shepherd, Welsh corgi). r and their larger sized axons are more Any age, breed, or sex Vascular—fibrocartilaginous embolic susceptible to compression than are other myelopathy. SIGNS r tracts. r Anomalous—hemivertebrae; dens r Important to define the type of ataxia to Generally accompanied by weakness owing hypoplasia with atlantoaxial subluxation- localize the problem. to early concomitant upper motor neuron r luxation; Chiari-like malformation; cervical Only one limb involved—consider a involvement; weakness not always obvious spondylomyelopathy; spinal sub-arachnoid lameness problem. early in the course of the disease. r diverticulum; other spinal cord and vertebral r Only hind limbs affected—likely a spinal Ataxia can occur with spinal cord, malformation. cord disorder affecting the spinocerebellar r brainstem, and cerebral lesions; mild to absent Neoplastic—primary bone tumors; multiple tracts. with unilateral brainstem lesions, and subtle r myeloma and metastatic tumors that infiltrate All or both ipsilateral limbs affected— to absent with unilateral cerebral lesion. the vertebral body; meningioma; others. cervical spinal cord, or cerebellar localization. r Vestibular r Infectious—discospondylitis; myelitis. Head tilt and/or nystagmus—vestibular r r Traumatic—intervertebral disc herniation; Changes in head and neck position are localization. relayed through the vestibulo-cochlear nerve fracture or luxation; atlantoaxial to the brainstem. CAUSES subluxation-luxation. r Neurologic Metabolic Vestibular receptors or the nerve in the r Anemia inner ear are considered part of the peripheral Cerebellar r r Polycythemia nervous system, whereas nuclei in the Degenerative—abiotrophy (Kerry blue r brainstem are part of the central nervous terrier, Gordon setter, rough-coated collie, Electrolyte disturbances—especially system. Australian kelpie, Airedale, Bernese mountain hypokalemia, hypocalcemia, and r Localize the vestibular signs to peripheral or dog, Finnish harrier, Brittany spaniel, border hypoglycemia Miscellaneous central vestibular nervous system because collie, beagle, Samoyed, wirehaired fox terrier, r prognosis and rule-outs differ for these two Labrador retriever, Great Dane, chow chow, Drugs—acepromazine; antihistamines; antiepileptic drugs locations. Rhodesian ridgeback, domestic shorthair r r Respiratory compromise Both locations of vestibular disease cause cats); storage diseases often have r various degrees of disequilibrium with cerebellomedullary involvement. Cardiac compromise—reverse PDA, aortic r ensuing vestibular ataxia. Anomalous—hypoplasia secondary to thromboembolism r Affected animal leans, tips, falls, or even perinatal infection with panleukopenia virus RISK FACTORS r rolls toward the side of the lesion; (cats); malformed cerebellum due to Intervertebral disc disease—dachshund, accompanied by head tilt. herpesvirus infection (newborn puppies); poodle, cocker spaniel, and beagle. r r Central vestibular signs usually have arachnoid or epidermoid cyst located near Cervical spondylomyelopathy—Doberman changing types of nystagmus or vertical fourth ventricle. pinscher and Great Dane. r r nystagmus; somnolence, stupor, or coma (due Neoplastic—any CNS tumor (primary or Fibrocartilaginous embolism—young, to involvement of the nearby ascending secondary) localized to the cerebellum. large-breed dogs and miniature schnauzers. r r reticular activating system); multiple cranial Infectious—canine distemper virus; FIP; Dens hypoplasia and atlantoaxial luxation— nerve signs; proprioceptive deficits and and any other CNS infection affecting the small-breed dogs, poodles. quadriparesis or hemiparesis. cerebellum. r r r Chiari-like malformation—Cavalier King Peripheral vestibular signs do not include Inflammatory, idiopathic, Charles spaniel, small-breed dogs. changes in mental status, vertical nystagmus, immune-mediated—granulomatous proprioceptive deficits, quadriparesis or meningoencephalomyelitis. r hemiparesis. 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r CT or MRI—if cerebellar disease SEE ALSO r suspected;. MRI superior to CT. See specific causes r r Abdominal ultrasonography—if hepatic, Cerebellar Degeneration DIAGNOSIS r renal, adrenal, or pancreatic dysfunction Head Tilt r DIFFERENTIAL DIAGNOSIS suspected. Paralysis r Differentiate the types of ataxia. DIAGNOSTIC PROCEDURES ABBREVIATIONS r r Differentiate from other disease processes Cerebrospinal fluid—helps confirm nervous CNS = central nervous system r that can affect gait—musculoskeletal, system etiology. CT = computed tomography r metabolic, cardiovascular, respiratory. FIP = feline infectious peritonitis r r Musculoskeletal disorders—typically MRI = magnetic resonance imaging produce lameness, pain, and a reluctance to INTERNET RESOURCES move; degenerative joint disease signs often improve with increased movements. TREATMENT https://www.vetlearn.com/_preview?_cms.fe r r Systemic illness and endocrine, Usually outpatient, depending on severity .previewId=1f98fff0-caa9-11e1-aa85-00505 cardiovascular, and metabolic disorders—can and acuteness of clinical signs. 6ad4736&WT.mc_id=newsletter%3BPV0 r cause intermittent ataxia, especially of the Exercise—decrease or restrict if ataxia 7111 pelvic limbs; with fever, weight loss, originates from spinal cord disease. r Suggested Reading murmurs, arrhythmias, hair loss, or collapse Client should monitor gait for increasing CherubiniGB,LowrieM,AndersonJ.Pelvic with exercise, suspect a non-neurologic cause; dysfunction or weakness; if paresis worsens or limb ataxia in the older dog. In Pract 2008, obtain minimum data from hemogram, paralysis develops, other testing is warranted. r 30:386–391. biochemistry, and urinalysis. Avoid drugs that could contribute to the r Davies C, Shell L. Neurological problems. In: Head tilt or nystagmus—likely vestibular problem; may not be possible in patients on Common Small Animal Medical Diagnoses: localization. antiepileptic drugs for seizures. r An Algorithmic Approach. Philadelphia: Intention tremors of the head or Saunders, 2002, pp. 36–59. hypermetria—likely cerebellar localization. r Lowrie M. Vestibular disease: anatomy, All four limbs affected—lesion is in the physiology, and clinical signs. Compend cervical spinal cord, cerebellum or is MEDICATIONS Contin Educ Vet 2012, 34:E1–5. multifocal to diffuse. Penderis J. The wobbly cat. Diagnostic and r DRUG(S) OF CHOICE Only pelvic limbs affected—lesion is therapeutic approach to generalised ataxia. anywhere below the second thoracic vertebra. Not recommended until the source or cause J Fel Med Surg 2009, 11:349–359. CBC/BIOCHEMISTRY/URINALYSIS of the problem is identified. Rossmeisl JH Hr. Vestibular disease in dogs Normal unless metabolic cause (e.g., and cats. Vet Clin North Am Small Anim hypoglycemia, electrolyte imbalance, anemia, Pract 2010, 40:81–100. polycythemia). Author Linda G. Shell OTHER LABORATORY TESTS FOLLOW-UP Consulting Editor Joane M. Parent r Hypoglycemia—determine serum insulin PATIENT MONITORING concentration on sample that has low glucose Periodic neurologic examinations to assess Client Education Handout value; low glucose and higher than expected condition. available online insulin value suggest insulin-secreting tumor. r POSSIBLE COMPLICATIONS Anemia—differentiate as nonregenerative or r Spinal cord—progression to weakness and regenerative on the basis of the reticulocyte possibly paralysis count. r r Hypoglycemia—seizures Electrolyte imbalance—correct the r Cerebellar disease—head tremors and problem; see if ataxia resolves. r bobbing Antiepileptic drugs—if being administered, r Brainstem disease—stupor, coma, death evaluate serum concentration for toxicity. IMAGING r Spinal radiography, myelography, CT or MRI—if spinal cord dysfunction suspected. r MISCELLANEOUS Bullae radiography—if peripheral vestibular disease suspected; CT or MRI superior; for AGE-RELATED FACTORS inner ear disease, MRI superior to CT. N/A r Thoracic radiography—for older patients and patients suspected to have neoplasia or systemic fungal infection. JWST589-A84-76 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:40 279mm×216mm

130 Blackwell’s Five-Minute Veterinary Consult A Atherosclerosis

CBC/BIOCHEMISTRY/URINALYSIS r Hypercholesterolemia r Hyperlipidemia BASICS r FOLLOW-UP High BUN and creatinine r r OVERVIEW High liver enzymes Monitor T4 concentration 4–6 hours Thickening of the inner arterial wall in OTHER LABORATORY TESTS post-administration after the first 6 weeks of r treatment and adjust dosage accordingly. association with lipid deposits. Chronic Low T and T . r r 3 4 arterial change characterized by loss of High values for alpha-2 and beta fractions Monitor blood triglyceride and cholesterol levels. elasticity, luminal narrowing, and on protein electrophoresis. r Monitor ECG for conduction disturbances proliferating and degenerative lesions of the IMAGING intima and media. and ST segment changes. SIGNALMENT Radiography r Thoracic and abdominal radiographs may Rare in dogs. r reveal cardiomegaly and hepatomegaly. Not described in cats. r Higher prevalence in miniature schnauzer, DIAGNOSTIC PROCEDURES MISCELLANEOUS Doberman pinscher, poodle, and Labrador Electrocardiography r ASSOCIATED CONDITIONS retriever. Conduction abnormalities and notched r r Hypothyroidism Geriatric patients (> 9 years). QRS complexes. r r Diabetes Atrial fibrillation. r SIGNS r Mitral valve disease (myxomatous) ST segment elevation or depression with r Historical Findings Glomerulonephritis r myocardial infarction. None in some animals AGE-RELATED FACTORS r Lethargy > r Geriatric patients ( 9 years) Anorexia r SEE ALSO Weakness r Myocardial Infarction Dyspnea TREATMENT r Collapse r INTERNET RESOURCES r Treat the underlying disorder and clinical Vomiting www.vetgo.com/cardio r signs (e.g., dyspnea if congestive heart failure Diarrhea develops). r Suggested Reading Physical Examination Findings Diet—low-fat diet, weight loss program, r Drost WT, Bahr RJ, Henay GA, Campbell Dyspnea and high soluble fiber intake to control r GA. Aortoiliac thrombus secondary to a Irregular rhythm hyperlipidemia. r mineralized arteriosclerotic lesion. Vet Heart failure r Radiol Ultrasound 1999, 40:262–266. Disorientation r Hamlen HJ. Sinoatrial node arteriosclerosis in Blindness r two young dogs. J Am Vet Med Assoc 1994, Circling r MEDICATIONS 204:751. Coma r DRUG(S) Hess RS, Kass PH, Van Winkle JV. Episodic lameness r Association between diabetes mellitus, CAUSES & RISK FACTORS Treat conduction disturbances and hypothyroidism or hyperadrenocorticism r arrhythmias if clinically indicated. Severe hypothyroidism r and atherosclerosis in dogs. J Vet Intern r Thyroid replacement if hypothyroidism is Increasing age Med 2003, 17:489–494. r confirmed. Hyperlipidemia in miniature schnauzers r Kidd L, Stepien RL, Amrheiw DP. Clinical r Antihypertensive therapy if hypertension is findings and coronary artery disease in dogs Male gender (male dogs may have documented. predisposition) r and cats with acute and subacute myocardial r Blood cholesterol-reducing medications if High total cholesterol necrosis: 28 cases. J Am Anim Hosp Assoc r hyperlipidemic. Diabetes r 2000, 36:199–208. r Tre at di abe t e s . Glomerulonephritis Liu SK, Tilley LP, Tappe JP, Fox PR. Clinical CONTRAINDICATIONS/POSSIBLE and pathologic findings in dogs with INTERACTIONS atherosclerosis: 21 cases (1970–1983). J Am N/A Vet Med Assoc 1986, 189:227–232. Ross R. Atherosclerosis and inflammatory DIAGNOSIS disease. N Engl J Med. 1999; 340:115–126. DIFFERENTIAL DIAGNOSIS Author Larry P. Tilley Arteriosclerosis Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr. JWST589-A85-77 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:42 279mm×216mm

Canine and Feline, Sixth Edition 131 Atlantoaxial Instability A

r Toy-breed dogs—at risk for congenital monitored until they are capable of malformation of the dens. maintaining normal head and neck carriage. BASICS OVERVIEW r Results from malformation or disruption of DIAGNOSIS TREATMENT the articulation between the first and second r DIFFERENTIAL DIAGNOSIS Prior to treatment, consultation with a cervical vertebrae (atlas and axis, respectively); r causes spinal cord compression. Differential diagnoses are consistent with board-certified neurologist or surgeon should r be pursued. AA instability can result in spinal cord various causes of cervical myelopathies, r trauma or compression at the junction including: Improper treatment can lead to irreversible ◦ deterioration in neurologic function. between the atlas and axis—may cause neck Other congenital malformation. ◦ pain and/or varying degrees of general Trauma. MEDICAL ◦ r proprioceptive (GP) ataxia /upper motor Meningitis or meningomyelitis (i.e., Neck brace (splint) to stabilize the cervical neuron (UMN) tetraparesis, tetraplegia (with infectious or non-infectious [granulomatous vertebral column in extension. or without nociception), and death from meningoencephalomyelitis]). ◦ Fiberglass cast material is positioned ◦ respiratory arrest. Fibrocartilaginous embolic myelopathy. ventrally from the rostral aspect of ◦ Disk herniation. Etiology mandible to the xiphoid and incorporated r ◦ Neoplasia. Congenital: anomaly of the dens (aplasia, into bandage material, which immobilizes CBC/BIOCHEMISTRY/URINALYSIS the head and neck. hypoplasia, or malformation [dorsal ◦ angulation] of the dens) and its ligamentous Normal Strict exercise restriction (cage attachments. IMAGING confinement) for a minimum of 8 weeks. r ◦ Acquired: may be a consequence of r Frequent bandage/splint changes are Plain radiography of the cervical vertebral needed. traumatic injury. r column: Adjunctive medication (see below). SIGNALMENT ◦ Lateral view—caudal and dorsal r Overall Prognosis Congenital—toy-breed dogs (Yorkshire displacement of the axis in relationship to r terrier, miniature or toy poodle, Chihuahua, the atlas, resulting in an increased distance Successful outcome observed in 62.5% of dogs. Pekingese, and Pomeranian). between vertebrae. r r Age at onset—usually before 12 months of ◦ Ventral dorsal or oblique view—may Improved prognosis was associated with an reveal absence, hypoplasia, or malformation acute onset and short duration of clinical age. < r (dorsal angulation) of the dens. signs ( 30 days). Uncommon in larger-breed dogs, dogs r r > 1yearold,andcats. Cross-sectional imaging: Surgery is recommended to treat animals r No sex predilection. ◦ MRI. that fail to improve or experience recurrence ◦ of signs following medical treatment. SIGNS Diagnosis based on observation of caudal r and dorsal displacement of the axis in SURGERY Intermittent or progressive ambulatory r relationship to the atlas as evidenced by the Treatment of choice in the majority of cases. tetraparesis, usually with neck pain—most r following features of the atlantoaxial Surgical approach; ventral method is common. r articulation: (1) Dorsal: displacement of the preferred. Neurologic signs vary from mild to r spinous process of the axis; (2) Ventral: Ventral approach—variety of methods: moderate GP/UMN ambulatory tetraparesis increased size of the occipito-atlas-axis joint ◦ Transarticular pinning or lag screw to non-ambulatory GP/UMN tetraparesis, or cavity. technique; ventral tips of the pins tetraplegia depending on degree of spinal cord ◦ Allows identification of spinal cord incorporated in polymethylmethacrylate to compression and secondary pathology (i.e., compression. edema, hemorrhage, or gliosis). prevent pin migration. r ◦ Allows recognition of secondary spinal ◦ Transarticular pinning and ventral cortical Animals may have only neck pain without cord pathology such as edema, hemorrhage, concurrent neurologic deficits. screws or K-wires in the bodies of the atlas r or gliosis, which may impact prognosis. ± Episodes of collapse secondary to weakness. r and axis K-wires applied longitundinally r Computed tomography: and wired to the screws; screw heads and Abnormal postural reactions with spinal ◦ May provide detailed visualization of bony reflexes that are normal to exaggerated with K-wires are incorporated in structures, which allows for the creation of polymethylmethacrylate to provide fixation. normal to increased muscle tone in all four r three-dimensional reconstructed image to Dorsal approach—use wire or synthetic limbs. r help surgical planning. Acute death may occur when accompanied r suture material to fix the spinous process of Precautions: the axis to the dorsal arch of the atlas; by trauma and respiratory arrest ◦ Proper positioning will require sedation or (uncommon). provides less rigid fixation and may be general anesthesia. associated with greater implant failure. CAUSES & RISK FACTORS ◦ r r Sedation or general anesthesia carries Strict exercise restriction is required for the Usually caused by abnormal development of significant risk for iatrogenic trauma. first month postoperatively, followed bya the dens and/or ligamentous support ◦ Care needs to be exercised when gradual return to activity over an additional structures, resulting in subluxation of the positioning animals. month. atlantoaxial joint. ◦ r r AVOID EXCESSIVE FLEXION OF Adjunctive medication (see below). Fracture of the axis. r r THE NECK!! Overall prognosis ranges from 63% to 91% Clinical signs often occur as a result of mild ◦ Flexion may exacerbate compression, success: improved prognosis was associated or insignificant trauma (e.g., jumping or which may worsen clinical signs or cause with young (< 24 months) dogs, duration of playing). < r death due to spinal cord trauma. clinical signs 10 months, and mild Clinical signs may be exacerbated by activity ◦ To protect against neck flexion during neurologic deficits. such as flexion of the neck. recovery, affected animals should be closely JWST589-A85-77 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:42 279mm×216mm

132 Blackwell’s Five-Minute Veterinary Consult

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r r Complications: All dogs should be reevaluated at 1 and Havig ME, Cornell KK, Hawthorne JC, ◦ Failure to improve/worsening of 3 months (postoperatively or after neck brace McDonnell JJ, Selcer BA. Evaluation of neurologic deficits. removal) and monthly until neurologic nonsurgical treatment of atlantoaxial ◦ Implant failure/infection. deficits resolve or remain static over subluxation in dogs: 19 cases (1992–2001). ◦ Respiratory—respiratory arrest, dyspnea, 2–3 months. J Am Vet Med Assoc 2005, r cough, and aspiration pneumonia. More frequent rechecks may be needed for 227(2):257–262. ◦ Death. dogs experiencing complications or McCarthy RJ, Lewis DD, Hosgood G. recurrence of signs. Atlantoaxial subluxation in dogs. Compend r Untreated animals may experience Contin Educ Pract Vet 1995, 17:215–226. deterioration in neurologic function, Platt SR, Chambers JN, Cross A. A modified MEDICATIONS catastrophic acute spinal cord trauma, ventral fixation for surgical management of respiratory arrest, and death. atlantoaxial subluxation in 19 dogs. Vet DRUG(S) r Surg 2004, 33(4):349–354. Anti-inflammatory medication: Sanders SG, Bagley RS, Silver GM, Moore ◦ Corticosteroids: prednisone M, Tucker RL. Outcomes and 0.5–1.0 mg/kg PO divided twice daily for MISCELLANEOUS complications associated with ventral 2 weeks, followed by a tapering regime. r screws, pins, and polymethyl methacrylate Suggested protocol following initial dose: Rehabilitation may play a significant role in for atlantoaxial instability in 12 dogs. J Am 0.5 mg/kg PO daily for 5 days, followed by the ultimate neurologic functional level of the Anim Hosp Assoc 2004, 40:204–210. patient. 0.5 mg/kg PO every other day for 5 days. r Schulz KS, Waldron DR, Fahie M. ◦ NSAID: 1- to 4-week course. Rehabilitation should only be considered in Application of ventral pins and r > Analgesia: dogs 30 days postoperatively or after neck polymethylmethacrylate for the ◦ Tramadol 2.0–4.0 mg/kg PO q6–8h. brace (splint) removal. management of atlantoaxial instability: ◦ Gabapentin 10–20 mg/kg PO q6–8h. ABBREVIATIONS Results in nine dogs. Vet Surg 1997, ◦ r Pregabalin 3–4 mg/kg (begin with GP = general proprioceptive 26(4):317–325. r 2 mg/kg) PO q8–12h. MRI = magnetic resonance imaging Shires PK. Atlantoaxial instability. In: Slatter r CONTRAINDICATIONS/POSSIBLE NSAID = nonsteroidal anti-inflammatory D, ed., Textbook of Small Animal Surgery, drug 3rd ed. Philadelphia: Saunders, 2003. INTERACTIONS r r Tomlinson J. Surgical conditions of the Corticosteroid—use caution when given in UMN = upper motor neuron cervical spine. Semin Vet Med Surg Small conjunction with medical treatment; may INTERNET RESOURCES Anim 1996, 11(4):225–234. reduce pain, resulting in increased activity http://www.acvs.org/AnimalOwners/Health Authors Mathieu M. Glassman and andspinalcordtrauma. Conditions/SmallAnimalTopics/Atlantoaxial r Marc Kent Avoid NSAIDs in combination with Instability/. Consulting Editor Walter C. Renberg corticosteroids in all patients—increases risk Suggested Reading of life-threatening gastrointestinal Beaver DP, Ellison GW, Lewis DD. Risk hemorrhage. factors affecting the outcome of surgery for atlantoaxial subluxation in dogs: 46 cases (1978–1998). J Am Vet Med Assoc 2000, 216(7):1104–1109. FOLLOW-UP Fossum TW, Hedlund CS, Johnson AL, et al. r Dogs treated medically require frequent Small Animal Surgery. St. Louis: (weekly) bandage changes for associated soft Mosby-Year Book, 1997. tissue trauma. JWST589-A86-78 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:50 279mm×216mm

Canine and Feline, Sixth Edition 133 Atopic Dermatitis A

Breed Predilections r Canine—any breed, including mongrels; recognized more frequently in certain breeds BASICS r DIAGNOSIS or families (can vary geographically). United DEFINITION States—Boston terrier, boxer, cairn terrier, DIFFERENTIAL DIAGNOSIS r r A genetically predisposed hypersensitivity Chinese Shar-Pei, cocker spaniel, Dalmatian, Adverse food reaction—may cause identical reaction to normally innocuous substances. English bulldog, English and Irish setter, symptoms; may occur concurrently with r French bulldog, American pit bull terrier, atopic dermatitis; differentiation is made by Manifests as an inflammatory, chronically r relapsing, non-contagious and pruritic skin Lhasa apso, miniature schnauzer, pug, noting response to hypoallergenic diet. Flea Sealyham terrier, Scottish terrier, West bite different lesion distribution and response disease. r PATHOPHYSIOLOGY Highland white terrier, wirehaired fox terrier, to flea control. Sarcoptic mange—causes r Labrador retriever, and golden retriever. severe pruritus of the ventral chest, lateral Atopic dermatitis (AD) has a multifactorial r Feline—none reported. elbows, lateral hocks, and pinnal margins; etiology involving genetic, structural, and r differentiation by multiple skin scrapings immunologic factors. Classical theory Mean Age and Range r and/or complete response to a trial of describes the pathway through which Canine—mean age at onset 1–3 years; range r miticidal therapy. Secondary pyoderma— susceptible animals become sensitized to 3 months–6 years; signs may be mild the first follicular papules, pustules, crusts, and environmental allergens producing year but usually progress and become r epidermal collarettes. Secondary yeast allergen-specific IgE, followed by mast cell clinically apparent before 3 years of age. r infections—erythematous, scaly, crusty, degranulation upon re-exposure to allergens Feline—6 months to 2 years. greasy, and malodorous body folds and via epicutaneous absorption (extrinsic AD). Predominant Sex r intertriginous areas; differentiation by A subset of AD patients does not have None reported demonstration of numerous budding yeast increased allergen-specific IgE (intrinsic AD). r r SIGNS organisms on skin cytology. Contact Current focus on the pathogenesis of AD dermatitis (allergic or irritant)—severe includes abnormalities in barrier function and General Comments r r erythema and pruritus of the feet and thinly T-cell dysregulation or imbalance. Barrier Pruritus—itching, scratching, rubbing, r haired areas of the flank and axillae. function impairment, shown as increased licking. Most cutaneous changes caused by transepidermal water loss and decreased self-induced trauma; primary lesions usually CBC/BIOCHEMISTRY/URINALYSIS fillagrin expression, in affected dogs has been unrecognized. Eosinophilia—rare in dogs without r Historical Findings concurrent flea infestations; common in cats. demonstrated. Acute lesions of AD are r r Facial, pedal, or axillary pruritus Early age characterized by increased TH2 lymphocyte r DIAGNOSTIC PROCEDURES of onset History in related individuals r activity while TH1 cytokines predominate in r r Diagnosis of AD is made by history, May be initially seasonal Recurring skin or chronic lesions. Thus aH T 2:TH1 imbalance r physical examination, and ruling out of r ear infection Temporary response to in AD has been proposed. Recently, aberrant r differential diagnoses; not by either serologic regulatory T-cell function has been reported. glucocorticosteroids Symptoms r r r or intradermal allergy testing. Greatest Following repeat epicutaneous absorption of progressively worsen with time Feline—face treatment success noted when allergens, mast cell degranulation results in and neck pruritus immunotherapy is based on results of both the release of histamine, proteolytic enzymes, Physical Examination Findings serum and intradermal testing. cytokines, chemokines, and other chemical r r Areas most commonly affected—interdigital Serologic Allergy Tests mediators. Bacterial superantigens, r spaces, carpal and tarsal areas, muzzle, Measures the amount of allergen-specific auto-antigens released via keratinocyte periocular region, axillae, groin, and pinnae. r IgE antibody in the patient’s serum. damage, and Malassezia may play a role in Lesions—vary from none to broken hairs or r perpetuating the inflammation. Advantages over IDT—availability; hair salivary discoloration to erythema, papules, coat does not require clipping; sedation is not SYSTEMS AFFECTED and, alopecia, to crusts, hyperpigmentation, r r r r required. Disadvantages—cannot Ophthalmic Respiratory Skin/Exocrine lichenification. The skin may become distinguish between allergic and normal GENETICS excessively oily or dry seborrhea, and patients; frequent false-positive or r hyperhidrotic (apocrine sweating). r false-negative reactions; limited number of Dogs—inherited predisposition; Secondary bacterial and yeast skin infections r allergens tested; inconsistent assay validation, polygenetic with environmental influences (common). Chronic relapsing otitis externa. important for disease development. r quality control, and reliability (may vary with r Conjunctivitis, blepharitis, and rhinitis may the laboratory used); a subset of AD patients Cats—inherited predisposition less clear. occur. INCIDENCE/PREVALENCE does not have elevated levels of circulating r CAUSES allergen-specific IgE. r r Canine—true prevalence is unknown; Pollens (grasses, weeds, and trees) Mold estimated at 3–15% of the canine population. r Intradermal Test (Preferred) r spores (indoor and outdoor) Malassezia r r r Small amounts of test allergen are injected Feline—unknown; generally believed to be House dust and storage mites Animal lower than that for dogs. r intradermally causing localized reactions; dander Insects wheal formation is measured and evaluated GEOGRAPHIC DISTRIBUTION r RISK FACTORS subjectively. Advantages—more r Canine—recognized worldwide; local Temperate environments with long allergy physiologically-appropriate determination of environmental factors (temperature, seasons and high pollen and mold spore allergens for immunotherapy; potentially r humidity, and flora) influence the seasonality, levels. Concurrent pruritic dermatoses, such higher success rate of immunotherapy versus severity, and duration of signs. allergens chosen based on serum testing. as flea bite hypersensitivity and adverse food r SIGNALMENT reaction (summation effect). Disadvantages—results more difficult to Species interpret in cats owing to the relatively small Dogs and cats wheals produced; requires sedation and clipping a small patch of hair coat; false JWST589-A86-78 JWST589-Tilley Printer: Yet to Come August 3, 2015 9:50 279mm×216mm

134 Blackwell’s Five-Minute Veterinary Consult

A Atopic Dermatitis (Continued)

positive and false negative reactions may tapered to the lowest dosage that adequately pruritus, self-trauma, development of r occur. controls pruritus. Prednisolone bacterial folliculitis, and possible adverse drug r r PATHOLOGIC FINDINGS (0.25–0.5 mg/kg PO q48h). Cats—oral reactions. Once an acceptable level of steroids or very infrequent control is achieved, examine patient every Skin biopsy—rule out other differential r diagnoses; results not pathognomonic; methylprednisolone acetate by injection 3–12 months. CBC, serum chemistry acanthosis, mixed mononuclear superficial (2–4 mg/kg). profile, and urinalysis with culture— Antihistamines recommended every 3–12 months for patients perivascular dermatitis, sebaceous gland r Less effective than corticosteroids. on chronic corticosteroid, cyclosporine or metaplasia, with secondary superficial r bacterial folliculitis. Dogs—hydroxyzine (1–2 mg/kg PO q12h), Oclacitinib therapy. chlorpheniramine (0.2–0.4 mg/kg PO q12h), PREVENTION/AVOIDANCE r diphenhydramine (2.2 mg/kg PO q12h), If offending allergens have been identified fexofenadine (2–5 mg/kg PO q12–24h), and through allergy testing, avoidance may help to TREATMENT clemastine (0.04–0.10 mg/kg PO q12h). reduce the level of pruritus; this is seldom r r APPROPRIATE HEALTH CARE Cats—chlorpheniramine (0.5 mg/kg PO possible. Minimizing other sources of q12h); efficacy estimated at 10–50%. pruritus (e.g., flea infestation, adverse food Outpatient Oclacitinib reaction, and secondary skin infection) ACTIVITY Oclacitinib Apoquel (0.4–0.6 mg/kg q12h for permits better response to therapy. Avoid offending allergens when possible 14 days then q24h). Dogs—effective in POSSIBLE COMPLICATIONS r DIET controlling pruritus associated with chronic Secondary bacterial folliculitis or Malassezia r Diets rich in essential fatty acids may be atopic dermatitis. Onset time and response dermatitis. Concurrent flea bite beneficial similar to glucocorticoids. Long-term safety hypersensitivity and/or adverse food reaction. CLIENT EDUCATION and efficacy undetermined. EXPECTED COURSE AND PROGNOSIS r r Explain the inheritable and progressive PRECAUTIONS Not life-threatening unless intractable r r r nature of the condition. Rarely goes into Cyclosporine—may affect glucose pruritus results in euthanasia. Degree of r homeostasis; may increase incidence of remission and cannot be cured. Ongoing r pruritus usually worsens and the duration of therapy may be necessary to maintain quality urinary tract infection. Corticosteroids—use signs last longer each year without r of life. judiciously in dogs to avoid iatrogenic intervention. Some cases spontaneously hyperglucocorticism and associated problems, resolve. aggravation of pyoderma, and induction of r demodicosis. Antihistamines—can produce MEDICATIONS drowsiness, and rarely anorexia, vomiting, DRUG(S) OF CHOICE diarrhea, increased pruritus; use with caution MISCELLANEOUS in patients with cardiac arrhythmias. r ASSOCIATED CONDITIONS Immunotherapy (Hyposensitization) Oclacitinib—not for use in dogs under r r r Flea bite hypersensitivity Adverse food Subcutaneous or sublingual administration 1 year of age; insufficient long-term r of gradually increasing doses of the causative reaction/food hypersensitivity Bacterial r experience. r r allergens to reduce sensitivity. Allergen POSSIBLE INTERACTIONS folliculitis Malassezia dermatitis Otitis selection—based on allergy test results, externa Concurrent use of cyclosporine and patient history, and/or knowledge of local AGE-RELATED FACTORS r ketoconazole permits a 50% dose reduction of exposure. Immunotherapy formulation Severity worsens with age procedures and administration protocols are each drug ALTERNATIVE DRUG(S) PREGNANCY/FERTILITY/BREEDING not standardized and vary widely between r r r Corticosteroids—contraindicated during clinicians. Preferred treatment in most cases; Frequent bathing (once to twice weekly) in r especially indicated when it is desirable to cool water with antipruritic shampoos is very pregnancy Affected animals should not be beneficial and should be strongly encouraged. used for breeding avoid or reduce the amount of corticosteroids r required to control signs, when signs last Fatty acids: 𝜔-3 (eicosapentaenoic acid SYNONYMS r r longer than 4–6 months per year, or when 66 mg/kg/day) may be more effective than Atopy Canine atopic disease non-steroid forms of therapy are ineffective. 𝜔-6 (linoleic acid 130 mg/kg/day) fatty acids. r r SEE ALSO Successfully reduces pruritus in 60–80% of Tricyclic antidepressants: dog—(doxepin r r Flea Bite Hypersensitivity and Flea Control dogs and cats. Response is slow, requiring at 1–2 mg/kg PO q12h; or amitriptyline r r Food Reactions, Dermatologic Otitis least 3 months and up to 1 year for full effect. 1–2 mg/kg PO q12h); overall effectiveness is r Externa and Media Pyoderma unclear; not extensively studied in the cat. Cyclosporine r r Gabapentin (dogs, 10–30 mg/kg q6–12h; ABBREVIATION Cyclosporine, modified (name brand r cats, 3–8 mg/kg q6–8h) Pentoxifylline IDT = intradermal test preferred—Atopica 5 mg/kg/day) effective in r controlling pruritus associated with chronic 10 mg/kg q8–12h. Topical triamcinolone r Suggested Reading atopic dermatitis. Response is similar to that spray 0.015% can be used over large body r Miller WH, Griffin CE, Campbell KL. Muller of glucocorticosteroids. Slow onset of surfaces to control pruritus with minimal side r & Kirk’s Small Animal Dermatology, 7th activity (1–4 weeks). Many patients can be effects. ed. St. Louis, MO: Elsevier Mosby, 2013. adequately controlled with less frequent r Author Alexander H. Werner dosing (every 2–4 days). Patient monitoring r Consulting Editor Alexander H. Werner is recommended. Drug blood level FOLLOW-UP monitoring recommended in cats. Client Education Handout Corticosteroids PATIENT MONITORING r r available online May be given for short-term relief and to Examine patient every 2–8 weeks when a r r break the itch-scratch cycle. Should be new course of therapy is started. Monitor JWST589-A04-79 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:0 279mm×216mm

Canine and Feline, Sixth Edition 135 Atrial Fibrillation and Atrial Flutter A

conduction properties of the AV junctional CAUSES r r tissue and alter conduction of subsequent Chronic valvular disease Cardiomyopathy r r electrical impulses; electrical impulses are Congenital heart disease Digoxin toxicity BASICS r r conducted through the AV junction Idiopathic Ventricular preexcitation (atrial DEFINITION irregularly, producing an irregular ventricular flutter) r r Atrial fibrillation—rapid, irregularly rhythm. Atrial flutter—probably originates irregular supraventricular rhythm. Two forms from one site of reentry that moves recognized: primary atrial fibrillation, an continuously throughout the atrial uncommon disease that occurs mostly in large myocardium and frequently and regularly DIAGNOSIS dogs with no underlying cardiac disease, and stimulates the AV node. When the atrial rate DIFFERENTIAL DIAGNOSIS secondary atrial fibrillation, which occurs in becomes sufficiently fast, the refractory period r Frequent atrial (supraventricular) premature dogs and cats secondary to underlying cardiac of the AV node exceeds the cycle length (P to r r depolarizations Supraventricular tachycardia disease. Atrial flutter is similar to atrial P interval) of the SVT, and some atrial r fibrillation, but the atrial rate is generally depolarizations are blocked from traversing with AV block Multifocal atrial tachycardia slower and is characterized by saw-toothed the AV node (functional second-degree AV (irregular) flutter waves in the baseline of the ECG.The block). CBC/BIOCHEMISTRY/URINALYSIS ventricular response is generally rapid but SYSTEMS AFFECTED N/A may be regular or irregular. Cardiovascular OTHER LABORATORY TESTS ECG FEATURES Loss of atrial contraction may result in N/A Atrial Flutter decreased stroke volume and cardiac output IMAGING r depending on heart rate; high heart rate may r Atrial rhythm usually regular; rate Echocardiography and radiography may r result in deterioration in myocardial function approximately 300–400 bpm. Pwaves characterize type and severity of the (tachycardia-induced myocardial failure). usually discerned as either discrete P waves or underlying cardiac disease; moderate to severe r r a “saw-toothed” baseline. Ventricular GENETICS left atrial enlargement common. Typically rhythm and rate generally depend on the No breeding studies available normal in patients with primary atrial atrial rate and AV nodal conduction, but are SIGNALMENT fibrillation, although mild left atrial generally regular or regularly irregular and r Species enlargement may accompany the rapid. Conduction pattern to the ventricles hemodynamic alterations imposed by the Dog and cat is variable—in some cases every other atrial arrhythmia. depolarization produces a ventricular Breed Predilections DIAGNOSTIC PROCEDURES depolarization (2:1 conduction ratio), giving a Large- and giant-breed dogs are more prone regular ventricular rhythm; other times the to primary atrial fibrillation. A baseline 24-hour Holter is recommended to conduction pattern appears random, giving determine if the arrhythmia is chronic or Mean Age and Range paroxysmal. If it is chronic, drug therapy is an irregular ventricular rhythm that can N/A mimic atrial fibrillation. indicated. Predominant Sex Secondary Atrial Fibrillation r N/A No P waves present—baseline may be flat or may have small irregular undulations (“f” SIGNS waves); some undulations may look like P General Comments TREATMENT r r waves. Ventricular rate high—usually Generally relate to the underlying disease APPROPRIATE HEALTH CARE 180–240 bpm in dogs and > 220 bpm in cats. process and/or CHF rather than the r r Patients with fast (secondary) atrial Interval between QRS complexes is arrhythmia itself, but previously stable r fibrillation are treated medically to slow the irregularly irregular; QRS complexes usually animals may decompensate. Patients with ventricular rate. Converting the atrial appear normal. primary atrial fibrillation are generally fibrillation to sinus rhythm would be ideal, Primary Atrial Fibrillation asymptomatic but may demonstrate mild but such attempts in patients with severe Similar to secondary atrial fibrillation except exercise intolerance. underlying heart disease or left atrial ventricular rate usually in the normal range. Historical Findings r r enlargement are generally futile because of a PATHOPHYSIOLOGY Coughing/dyspnea/tachypnea. Exercise low success rate and high rate of recurrence. r r r Atrial fibrillation—caused by numerous intolerance. Rarely syncope. Dogs with Consider electrical cardioversion to sinus small reentrant pathways creating a rapid primary atrial fibrillation are typically rhythm for a dog with primary atrial asymptomatic. fibrillation and only mild structural heart (> 500 depolarizations/minute) and r Physical Examination Findings disease. Patients with primary atrial disorganized depolarization pattern in the r atria that results in cessation of atrial On auscultation, patients with atrial fibrillation may be converted back to normal fibrillation have an erratic heart rhythm that sinus rhythm. The success rate depends on contraction. Depolarizations continuously r sounds like “tennis shoes in a dryer.” First chronicity. Patients that have been in atrial bombard the AV nodal tissue, which acts as a > filter and does not allow all depolarizations to heart sound intensity in atrial fibrillation is fibrillation for 4 months generally have a conduct to the ventricles. Many atrial variable; second heart sound only heard on lower success rate and a higher rate of beats with effective ejection, not on every recurrence. In these patients, rate control, if depolarizations activate only a part of the atria r beat. Third heart sounds (gallop sounds) necessary, is the recommended treatment. because the rapid rate renders portions of the r r atria refractory, and thus they cannot reach may be present. Patients with atrial Electrical (DC) cardioversion—application fibrillation have pulse deficits and variable of a transthoracic electrical shock at a specific the AV junction. Other atrial impulses r penetrate into the AV junctional tissue but are pulse quality. Signs of CHF often present time in the cardiac cycle; requires special not robust enough to penetrate the entire (e.g., cough, dyspnea, cyanosis). equipment, trained personnel, and general length. Blocked impulses affect the anesthesia. Using a monophasic defibrillator: Start with 4 J/kg; if no conversion occurs, JWST589-A04-79 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:0 279mm×216mm

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Figure 1. Atrial flutter with 2:1 conduction at ventricular rate of 330/minute ina dog with an atrial septal defect. This supraventricular tachycardia was asso- ciated with a Wolff-Parkinson-White pattern. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore: Williams & Wilkins, 1992, with permission.)

increase dose by 50 J and repeat until a max SURGICAL CONSIDERATIONS the heart rate remains high, check the digoxin of 360 J. Using a biphasic defibrillator: Start N/A level and adjust the dose to bring the level with 1 to 2 J/kg; if no cardioversion occurs, into the therapeutic range. If the heart rate increase dose by 50 J and repeat until max of remains high, consider adding a calcium r 360 J. For atrial flutter, conversion to sinus channel blocker or a 𝛽-adrenergic blocker. r rhythm can be done by drug therapy, MEDICATIONS Diltiazem—initially administered at a dose electrical cardioversion, or rapid atrial pacing of 0.5 mg/kg PO q8h, then titrated up to a (transvenous pacing electrode). DRUG(S) OF CHOICE maximum of 1.5 mg/kg PO q8h or until an r Digoxin, 𝛽-adrenergic blockers, esmolol, adequate response is obtained. NURSING CARE r As indicated for CHF. and calcium channel blockers (diltiazem) are Therapy for atrial fibrillation is aimed at frequently used to slow conduction through suppressing the atrial reentry circuit using ACTIVITY the AV node; definition of an adequate heart sotalol, amiodarone, or procainamide. The Restrict activity until tachycardia is rate response varies among clinicians, but in conversion to normal sinus rhythm is usually controlled. dogs is generally 140–160 bpm. unsuccessful. r DIET For atrial flutter, therapy is aimed at Cats r Mild to moderate sodium restriction if CHF. suppressing the atrial re-entry circuit using Diltiazem (1–2.5 mg/kg PO q8h) or CLIENT EDUCATION sotlalol, amiodarone or procainamide. atenolol (6.25–12.5 mg/cat PO q12–24h) are r Dogs the drugs of choice in most cats. Secondary atrial fibrillation and atrial flutter r r is usually associated with severe underlying Digoxin—maintenance oral dose If the heart rate is not sufficiently slowed heart disease; goal of therapy is to lower heart 0.005–0.01 mg/kg PO q12h; to achieve a with these drugs or if myocardial failure is r 𝜇 rate and control clinical signs. Sustained therapeutic serum concentration more rapidly, present, digoxin (5 g/kg PO q24–48h) can conversion to sinus rhythm is unlikely with the maintenance dose can be doubled for the be added. secondary atrial fibrillation. first day. If digoxin is administered alone and

Figure 2. “Coarse” atrial fibrillation in a dog with patent ductus arteriosus. The f waves are prominent. (From: Tilley LP.Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore: Williams & Wilkins, 1992, with permission.) JWST589-A04-79 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:0 279mm×216mm

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CONTRAINDICATIONS accurate means for assessing the need for to control heart rate in dogs with atrial r Digoxin, diltiazem, propranolol, and heart rate control and/or the efficacy of fibrillation using 24-hour ambulatory atenolol should not be used in patients with medical therapy for heart rate control. electrocardiographic (Holter) recordings. r preexisting AV block. Use of calcium POSSIBLE COMPLICATIONS J Vet Intern Med 2004, 18(5):779. channel blockers in combination with beta Worsening of cardiac function with onset of Kittleson MD. Electrocardiography. In: blockers should be avoided because clinically arrhythmia. Kittleson MD, Kienle RD, eds., Small significant bradyarrhythmias and/or AV block Animal Cardiovascular Medicine. St Louis, EXPECTED COURSE AND PROGNOSIS can develop. r MO: Mosby, 1998, pp. 72–94. PRECAUTIONS Secondary atrial fibrillation—associated Kraus MS, Gelzer ARM, Moise S. Treatment r with severe heart disease, so a guarded-to- Calcium channel blockers and 𝛽-adrenergic r of cardiac arrhythmias and conduction poor prognosis. Primary atrial fibrillation disturbances. In: Smith FWK, Tilley LP, blockers, both negative inotropes, should be with normal ultrasound findings—generally a used cautiously in animals with myocardial Oyama MA, Sleeper MM, eds., Manual of r good prognosis. failure. Using high-dose oral quinidine for Canine and Feline Cardiology, 5th ed. St. conversion into sinus rhythm carries a risk of Louis, MO: Saunders Elsevier, 2015 (in quinidine toxicity (e.g., hypotension, press). weakness, ataxia, and seizures)— Tilley LP, Smith FWK, Jr. administration of diazepam intravenously MISCELLANEOUS Electrocardiography. In: Smith FWK, Tilley LP, Oyama MA, Sleeper MM, eds., Manual controls seizures; other signs abate within ABBREVIATIONS r r of Canine and Feline Cardiology, 5th ed. St. several hours of discontinuing quinidine AV = atrioventricular CHF = congestive r Louis, MO: Saunders Elsevier, 2015 administration. heart failure ECG = electrocardiogram r (in press). POSSIBLE INTERACTIONS SVT = supraventricular tachycardia Tilley LP, Smith, F.W. Essentials of Quinidine raises the digoxin level, generally Suggested Reading Electrocardiography. Interpretation and necessitating a digoxin dose reduction. Bright JM, Brunnen J. Chronicity of atrial Treatment, 4th ed. Ames, IA: Wiley fibrillation affects duration of sinus rhythm Blackwell Publishing, 2016 (in preparation). after transthoracic cardioversion of dogs Author Larry P. Tilley with naturally occurring atrial fibrillation. Consulting Editors Larry P. Tilley and FOLLOW-UP J Vet Intern Med 2008, 22(1):114–119. Francis W.K. Smith, Jr. Acknowledgment The author and editors PATIENT MONITORING Gelzer R.M., Kraus M.S.. Management of r r atrial fibrillation. Vet Clin North Am Small acknowledge the prior contribution of Monitor heart rate and ECG closely. As Anim Pract 2004, 34:1127–1144. Richard D. Kienle. heart rates in the hospital and those measured Gelzer A.R.M., Kraus M.S., Moise N.S., on the surface ECG may be inaccurate (due Pariaut R., Charter M.E., Renaud-Farrell S. to patient anxiety and other environmental Client Education Handout Assessment of antiarrhythmic drug efficacy factors), Holter monitoring provides a more available online JWST589-A05-80 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:3 279mm×216mm

138 Blackwell’s Five-Minute Veterinary Consult A Atrial Premature Complexes

r valvular insufficiency; may also be observed in Toxemias r dogs or cats with any atrial disease. Drug toxicity (e.g., digitalis) r r BASICS May not cause hemodynamic problems; the Normal variation in aged animals clinical significance relates to their frequency, DEFINITION timing relative to other complexes, and the underlying clinical problems. Premature atrial beats that originate outside r the sinoatrial node and disrupt the normal Can presage more serious rhythm DIAGNOSIS sinus rhythm for 1 or more beats disturbances (e.g., atrial fibrillation, atrial DIFFERENTIAL DIAGNOSIS ECG FEATURES flutter, or atrial tachycardia). r Marked sinus arrhythmia. r SYSTEMS AFFECTED r Heart rate usually normal; rhythm irregular Ventricular premature complexes when ′ Cardiovascular due to the premature P wave (called a P aberrant ventricular conduction follows an wave) that disrupts the normal P wave GENETICS APC. rhythm (Figure 1). N/A r ′ CBC/BIOCHEMISTRY/URINALYSIS Ectopic P wave—premature; configuration INCIDENCE/PREVALENCE differs from that of the sinus P waves and may N/A be negative, positive, biphasic, or Not documented OTHER LABORATORY TESTS superimposed on the previous T wave. SIGNALMENT r N/A QRS complex—premature; configuration Species IMAGING usually normal (same as that of the sinus Dog and cat complexes). If the P′ wave occurs during the Echocardiography and Doppler ultrasound Breed Predilections refractory period of the AV node, ventricular may reveal the type and severity of the Small-breed dogs conduction does not occur (non-conducted underlying heart disease. ′ Mean Age and Range DIAGNOSTIC PROCEDURES APCs), so no QRS complex follows the P r Geriatric animals, except those with Electrocardiography wave. If there is partial recovery in the AV r node or intraventricular conduction systems, congenital heart disease Holter monitor to quantify APC frequency the P′ wave is conducted with a long P′–R SIGNS and event monitor/Holter ECG to correlate interval or with an abnormal QRS Historical Findings symptoms with rhythm. r configuration (aberrant conduction). The No signs PATHOLOGIC FINDINGS r more premature the complex, the more CHF Atrial enlargement; other features vary marked the aberration. r r Coughing and dyspnea depending on underlying cause. ′ r In the P–QRS relationship, the P –R Exercise intolerance r interval is usually as long as, or longer than, Syncope the sinus P′–R interval. r Physical Examination Findings A non-compensatory pause—when the r Irregular heart rhythm TREATMENT R–R interval of the two normal sinus r Cardiac murmur complexes enclosing an APC is less than the r APPROPRIATE HEALTH CARE Gallop rhythm r R–R intervals of three consecutive sinus r Treat animal as inpatient or outpatient. Signs of CHF r complexes—usually follows an APC (Figure Treat the underlying CHF, cardiac disease, 2). The ectopic atrial impulse discharges the CAUSES & RISK FACTORS r or other causes. sinus node and resets the cycle. Chronic valvular disease r NURSING CARE PATHOPHYSIOLOGY Congenital heart disease r Usually not necessary; varies with underlying r Cardiomyopathy Mechanisms—an increase in automaticity r cause. Atrial myocarditis of atrial myocardial fibers or a single reentrant r Electrolyte disorders ACTIVITY circuit. r r Neoplasia Restrict if symptomatic. May be normal finding in aged dogs; r commonly seen in dogs with atrial Hyperthyroidism enlargement secondary to chronic mitral

Figure 1. APCs in a dog. P′ represents the premature complex. The premature QRS resembles the basic QRS. The upright′ P wave is superimposed on the T wave of the preceding complex. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.) JWST589-A05-80 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:3 279mm×216mm

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Figure 2. APCs in bigeminy in a cat under general anesthesia. The second complex of each pair is an APC, where the first is a sinus complex. The abnormality inrhythm disappeared after the anesthetic was stopped. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.)

DIET CONTRAINDICATIONS AGE-RELATED FACTORS No modifications unless required for Negative inotropic agents (e.g., propranolol) Typically occurs in geriatric dogs management of underlying condition (i.e., should be avoided in animals with CHF. PREGNANCY/FERTILITY/BREEDING low-salt diet). PRECAUTIONS CLIENT EDUCATION N/A Use digoxin, diltiazem, atenolol, or SYNONYMS APCs may not cause hemodynamic propranolol cautiously in animals with abnormalities; may be precursors of serious underlying atrioventricular block or Atrial extrasystoles, atrial premature arrhythmias. hypotension. contractions, atrial premature impulses SURGICAL CONSIDERATIONS POSSIBLE INTERACTIONS SEE ALSO N/A N/A Supraventricular Tachycardia ABBREVIATIONS ALTERNATIVE DRUG(S) r APC = atrial premature complex N/A r AV = atrioventricular r MEDICATIONS CHF = congestive heart failure DRUG(S) OF CHOICE INTERNET RESOURCES Treat CHF and correct any electrolyte or FOLLOW-UP www.vetgo.com/cardio. acid/base imbalances. PATIENT MONITORING Suggested Reading Dogs Jackson BL, Lehmkuhl LB, Adin DB. Heart r Monitor heart rate and rhythm with serial Digoxin (0.005–0.01 mg/kg PO q12h, ECG. rate and arrhythmia frequency of normal cats compared to cats with asymptomatic maintenance dosage), diltiazem PREVENTION/AVOIDANCE (0.5–1.5 mg/kg PO q8h), or atenolol hypertrophic cardiomyopathy. J Vet (0.25–1 mg/kg PO q12h) are used to treat N/A Cardiology 2014, 16:215–225. clinically significant arrhythmias. POSSIBLE COMPLICATIONS Keene B, Smith FWK, Tilley LP, Hansen B. r Digoxin—treatment of choice; also Frequent APCs may further diminish cardiac Rapid Interpretation of Heart Sounds, indicated to treat the cardiac decompensation output in patients with underlying heart Murmurs, Arrhythmias, and Lung Sounds: that is usually present. A Guide to Cardiac Auscultation in Dogs r disease and worsen clinical symptoms. CHF is treated with appropriate dosage of EXPECTED COURSE AND PROGNOSIS and Cats. 3rd ed. CD-ROM and Manual. diuretic, angiotensin converting enzyme Philadelphia: Elsevier, 2015. Even with optimal antiarrhythmic drug inhibitor, and pimobendan; appropriate Tilley LP, Smith FWK, Jr. therapy some animals have an increased management of CHF may reduce APC Electrocardiography. In: Smith FWK, Tilley frequency of APCs or deteriorate to more frequency. LP, Oyama MA, Sleeper MM, eds., Manual severe arrhythmia as the underlying disease Cats of Canine and Feline Cardiology, 5th ed. St. r progresses. Cats with hypertrophic cardiomyopathy— Louis, MO: Saunders Elsevier, 2015 (in diltiazem (1–2.5 mg/kg PO q8h) or atenolol press). (6.25–12.5 mg PO q12–24h). Author Larry P. Tilley r Consulting Editors Larry P. Tilley and Cats with dilated cardiomyopathy—digoxin MISCELLANEOUS (one-fourth of a 0.125 mg digoxin tablet Francis W.K. Smith, Jr. q24h or q48h). ASSOCIATED CONDITIONS Acknowledgment The author and editors acknowledge the prior contribution of Naomi None L. Burtnick.

Client Education Handout available online JWST589-A06-81 JWST589-Tilley Printer: Yet to Come September 5, 2015 12:9 279mm×216mm

140 Blackwell’s Five-Minute Veterinary Consult A Atrial Septal Defect

r r Signs related to generalized cyanosis may Treatment of polycythemia (right-to-left occur with right-to-left shunting. shunting) if clinically indicated. Historical Findings SURGICAL THERAPY BASICS r Clinical signs related to concurrent heart Open heart surgery under cardiopulmonary OVERVIEW r disease or cyanosis; exercise intolerance, bypass- direct surgical closure using patch Congenital defect in which the interatrial syncope, cough, and dyspnea. graft. r septum fails to develop normally, resulting in Physical Examination Findings Pulmonary artery banding as palliative r communication between the atria. Unknown Soft systolic murmur over the pulmonic measure to limit left-to-right shunting. cause; genetic basis suspected. Acquired ASD valve due to relative pulmonic stenosis CATHETER-BASED THERAPY secondary to atrial rupture reported in dogs (increased blood flow across a normal r ® with degenerative mitral valve disease. Amplatzer atrial septal occluder (ASO) r pulmonic valve). Comprises 0.7–3.7% of congenital heart r device delivered percutaneously through the < Rarely a diastolic murmur over the tricuspid jugular vein for secundum-type defects; defects in dogs and 10% of congenital heart valve due to relative tricuspid stenosis. r requires adequate atrial diameter, ostium defects in cats. Significantly higher incidence Split S2 (fixed) due to delayed closure of the (37.7%) noted in a more recent study. diameter, ASD rim tissue, and vessel size for r pulmonic valve. r venous access. 3 major types of ASD classified based on the Cyanosis with right-to-left shunting. r location of the defect within the interatrial r Hybrid procedure involving surgical access Ascites and jugular vein distension with to right atrium, transatrial delivery of ASO septum: ostium primum ASD (most apical right heart failure. portion of septum, adjacent to the device, and active device fixation under inflow atrioventricular valves), ostium secundum occlusion reported. ASD (central portion of the septum, region of fossa ovalis), and sinus venosus ASD (upper portion of septum, junction of cranial vena DIAGNOSIS cava). CBC/BIOCHEMISTRY/URINALYSIS FOLLOW-UP r r Secundum ASD with left-to-right shunting Typically normal. PATIENT MONITORING is most common (98.7% in one study of dogs r Polycythemia in some patients with Recheck when decompensation or other and cats). r right-to-left shunting. Ostium primum ASDs typically large; may clinical signs develop. IMAGING EXPECTED COURSE AND PROGNOSIS be component of atrioventricular (AV) canal r defect. Radiographic Findings Dependent on defect size and co-existing r r None with small defects. abnormalities. Sinus venosus ASDs typically located at the r r junction of the cranial vena cava (less Right-sided heart enlargement and Small, isolated defects unlikely to cause pulmonary overcirculation with significant clinical signs. commonly the caudal vena cava) and right r atrium. Right pulmonary veins may be shunting. Defects > 12 mm more likely to cause heart directed at the right atrium through the Echocardiographic Findings failure. r defect. May be associated with anomalous Right atrial and/or right ventricular dilation r pulmonary venous connections of some or all Septal dropout (not artifactual septal pulmonary veins. dropout in the region of the fossa ovalis) r r Isolated ASDs typically shunt left-to-right. Shunting across ASD by color-flow or MISCELLANEOUS Magnitude of flow dependent on size spectral Doppler r ABBREVIATIONS (ostium) of defect, relative systemic and Increased pulmonic flow velocity r r ASD = atrial septal defect pulmonary resistance, and relative compliance Dilation of the pulmonary trunk r CHF = congestive heart failure of the ventricles. Small defects allowing atria OTHER to maintain normal differential pressure are Electrocardiography Suggested Reading termed restrictive. Large defects more likely to r Bonagura JD, Lehmkuhl LB. Congenital Usually normal. cause significant left-to-right shunting and r heart disease. In: Fox PR, Sisson D, Moise Right atrial and ventricular enlargement volume overload to the right heart and ND, eds., Textbook of Canine and Feline (tall P wave, right axis deviation, deep S waves pulmonary vessels. Development of secondary Cardiology, 2nd ed. Philadelphia: Saunders in lead II). pulmonary hypertension can lead to reverse r 1999, pp. 471–535. Arrhythmias and intraventricular (right-to-left) shunting, termed Eisenmenger’s Chetboul V, Charles V, Nicolle A, et al. conduction disturbances possible. physiology. ASDs may occur with concurrent Retrospective study of 156 atrial septal defects; conditions increasing right atrial defects in dogs and cats (2001–2005). J Vet pressure (i.e., pulmonic stenosis, tricuspid Med Assoc 2006, 53(4):179–184. valve dysplasia, tricuspid valve stenosis) can Gordon SG, Miller MW, Roland RM, et al. also cause balanced or reverse shunting. TREATMENT Transcatheter atrial septal defect closure SIGNALMENT with the Amplatzer atrial septal occluder in r GENERAL Dog and cat r 13 dogs: short- and mid-term outcome. J r Long-term prognosis for small ASDs is Various breeds affected; higher prevalence in good; treatment is not typically required. Vet Intern Med 2009, 23(5):995–1002. boxer and standard poodle r Author Sandra P. Tou r Large ASDs with hemodynamically No sex predisposition significant shunting and right-sided Consulting Editors Larry P. Tilley and SIGNS enlargement warrant closure. Francis W.K. Smith, Jr. General Comments MEDICAL THERAPY r r Most commonly asymptomatic (73.7% in Standard treatment of CHF (furosemide, one study). r pimobendan, ACE inhibitor). Severe cases may present with signs of CHF. JWST589-A07-82 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:13 279mm×216mm

Canine and Feline, Sixth Edition 141 Atrial Standstill A

Mean Age and Range PATHOLOGIC FINDINGS Most animals with persistent atrial standstill Persistent Atrial Standstill r BASICS are young; animals with hypoadrenocorticism Greatly enlarged and paper-thin atria; are usually young to middle-aged. usually biatrial involvement, although one DEFINITION Predominant Sex case of only left atrial involvement was ECG rhythm characterized by absence of P reported. Hypoadrenocorticism more common in r waves; condition can be temporary (e.g., females (69%). Severe scapular and brachial muscle wasting associated with hyperkalemia or in some dogs. SIGNS r drug-induced), terminal (e.g., associated with Marked fibrosis, fibroelastosis, chronic Historical Findings severe hyperkalemia or dying heart), or r mononuclear cell inflammation, and steatosis Vary with underlying cause. persistent. r throughout the atria and interatrial septum. Lethargy common; syncope may occur. ECG Features r Patients with persistent atrial standstill may Persistent Atrial Standstill r show signs of congestive heart failure. P waves absent. r < Physical Examination Findings Heart rate usually slow ( 60 bpm). r TREATMENT r Vary with underlying cause. Rhythm regular with supraventricular type r APPROPRIATE HEALTH CARE QRS complexes. Bradycardia common. r r Heart rate does not increase with atropine Patients with persistent atrial standstill may Persistent Atrial Standstill administration. have skeletal muscle wasting of the Not life-threatening condition; animal can be Hyperkalemic Atrial Standstill antebrachium and scapula. treated as an outpatient. r Heart rate normal or slow. CAUSES Hyperkalemic Atrial Standstill r r Rhythm regular or irregular. Hyperkalemia. Potentially life-threatening; often requires r r QRS complexes tend to be wide and Atrial disease, often associated with atrial aggressive treatment. become wider as the potassium level rises; distension (e.g., cats with cardiomyopathy). r NURSING CARE with severe hyperkalemia (potassium Atrial myopathy (persistent atrial standstill). > 10 mEq/L), the QRS complexes are Aggressive fluid therapy with 0.9% saline RISK FACTORS often required to correct hypovolemia and replaced by a smooth biphasic curve. r r Hyperkalemic atrial standstill lower serum potassium levels (see Heart rate may increase slightly with r Hypoadrenocorticism Hyperkalemia) in patients with hyperkalemic atropine. r Conditions leading to obstruction or atrial standstill. PATHOPHYSIOLOGY rupture of the urinary tract r ACTIVITY Persistent Atrial Standstill Oliguric or anuric renal failure Restrict activity in patients with persistent Caused by an atrial muscular dystrophy; atrial standstill and signs of CHF or syncope. skeletal muscle involvement common. DIET Hyperkalemic Atrial Standstill N/A Generally occurs with serum potassium levels DIAGNOSIS > CLIENT EDUCATION 8.5 mEq/L; value influenced by serum DIFFERENTIAL DIAGNOSIS sodium and calcium levels and acid-base r Persistent Atrial Standstill Slow atrial fibrillation status. Hyperkalemic patients with atrial r Clinical signs generally improve after Sinus bradycardia with small P waves lost in standstill have sinus node function, but pacemaker implantation; signs of CHF may the baseline impulses do not activate atrial myocytes; thus, develop, and weakness and lethargy may the associated rhythm is termed a CBC/BIOCHEMISTRY/URINALYSIS persist even after heart rate and rhythm are sinoventricular rhythm. Since the sinus node Persistent Atrial Standstill corrected with the pacemaker. is functional, an irregular rhythm may be due Normal SURGICAL CONSIDERATIONS to sinus arrhythmia. Hyperkalemic Atrial Standstill r Persistent Atrial Standstill SYSTEMS AFFECTED Hyperkalemia. r Implant permanent ventricular pacemaker to Cardiovascular Hyponatremia and sodium:potassium ratio regulate rate and rhythm. < 27 if atrial standstill secondary to GENETICS Hyperkalemic Atrial Standstill hypoadrenocorticism. None r Hyperkalemia secondary to urinary tract Azotemia and hyperphosphatemia with INCIDENCE/PREVALENCE obstruction or rupture may require surgery. hypoadrenocorticism, renal failure, and Rare rhythm disturbance rupture or obstruction of the urinary tract. GEOGRAPHIC DISTRIBUTION OTHER LABORATORY TESTS None ACTH stimulation test if MEDICATIONS SIGNALMENT hypoadrenocorticism suspected DRUG(S) OF CHOICE Species IMAGING Dog and cat Echocardiogram and electromyography if Persistent Atrial Standstill Breed Predilections persistent atrial standstill suspected— Treat with diuretics and ACE inhibitor (e.g., Persistent atrial standstill—most common in cardiomegaly and depressed contractility may enalapril or benazepril) if CHF develops. be seen. Hyperkalemic Atrial Standstill English springer spaniels; other breeds r occasionally affected. DIAGNOSTIC PROCEDURES Treat the underlying cause (e.g., oliguric renal failure, hypoadrenocorticism). Skeletal muscle biopsy in animals with r persistent atrial standstill. Aggressive fluid therapy with 0.9% saline and possibly sodium bicarbonate or insulin JWST589-A07-82 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:13 279mm×216mm

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A Atrial Standstill (Continued)

Figure 1. Atrial stand still in a dog with a potassium of 9 mEq/L. Note the absence of P waves and wide QRS complexes.

POSSIBLE COMPLICATIONS SYNONYMS with dextrose as discussed under CHF in patients with persistent atrial Silent atrial Hyperkalemia. r standstill SEE ALSO Calcium gluconate—counters the cardiac r EXPECTED COURSE AND PROGNOSIS Digoxin Toxicity effects of hyperkalemia; can be used in r Hyperkalemia life-threatening situations to reestablish a Persistent Atrial Standstill r Hypoadrenocorticism (Addison’s Disease) sinus rhythm while instituting treatment to Clinical signs generally improve after r lower potassium concentration. pacemaker implantation. Signs of CHF may Urinary Tract Obstruction CONTRAINDICATIONS develop, and weakness and lethargy persist ABBREVIATIONS r even after heart rate and rhythm are corrected ACE = angiotensin converting enzyme Avoid potassium-containing fluids or r with the pacemaker. There may be persistence ACTH = adrenocorticotropic hormone medications that increase potassium r of signs related to muscular dystrophy. CHF = congestive heart failure concentration in hyperkalemic patients. r PRECAUTIONS Hyperkalemic Atrial Standstill ECG = electrocardiogram Long-term prognosis is excellent if underlying Diuretics lower preload and may worsen Suggested Reading cause can be corrected and hyperkalemia weakness in dogs with persistent atrial Kittleson MD. Electrocardiography. In: reversed. standstill and CHF unless a pacemaker has Kittleson MD, Kienle RD, eds., Small been implanted. Animal Cardiovascular Medicine. St. Louis, POSSIBLE INTERACTIONS MO: Mosby, 1998, pp. 72–94. Kraus MS, Gelzer ARM, Moise S. Treatment N/A MISCELLANEOUS of cardiac arrhythmias and conduction ALTERNATIVE DRUG(S) ASSOCIATED CONDITIONS disturbances. In: Smith FWK, Tilley LP, N/A Oyama MA, Sleeper MM, eds., Manual of Diseases causing hyperkalemia (e.g., Canine and Feline Cardiology, 5th ed. St. hypoadrenocorticism, urethral obstruction or Louis, MO: Saunders Elsevier, 2015 (in urinary tract tear, acidosis, and drugs). press). FOLLOW-UP AGE-RELATED FACTORS Tilley LP, Smith FWK, Jr. Persistent atrial standstill—usually diagnosed Electrocardiography. In: Smith FWK, Tilley PATIENT MONITORING r in young animals; hypoadrenocorticism— LP, Oyama MA, Sleeper MM, eds., Manual Monitor ECG during treatment of usually diagnosed in young to middle-aged of Canine and Feline Cardiology, 5th ed. St. hyperkalemia and periodically in animals with animals. Louis, MO: Saunders Elsevier, 2015 (in a permanent ventricular pacemaker. r ZOONOTIC POTENTIAL press). Monitor electrolytes in patients with None Author Francis W.K. Smith, Jr. hyperkalemic atrial standstill. Consulting Editors Larry P. Tilley and r PREGNANCY/FERTILITY/BREEDING Monitor patients with persistent atrial Francis W.K. Smith, Jr. standstill for signs of CHF. N/A PREVENTION/AVOIDANCE Client Education Handout N/A available online JWST589-A87-83 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:15 279mm×216mm

Canine and Feline, Sixth Edition 143 Atrial Wall Tear A

r commonly observed. Possible history of effusion identified may be relatively small as blunt trauma. the pericardium remains inelastic due to the BASICS Physical Examination Findings acute nature of the bleed; a characteristic r r r linear, hyperechoic blood clot may be seen Collapse. Tachycardia. Weak arterial r DEFINITION r within the pericardial sac. The actual tear is r pulses or pulsus paradoxus. Pale, muddy, or Endocardial splitting is a linear defect ashen mucous membranes; prolonged CRT. often not identified though an associated r thrombus is occasionally visualized within the limited to the endocardial layer of the atrium Other signs of significant cardiac disease r (typically the left atrium) resulting from (e.g., murmur, gallop rhythm, arrhythmia, left atrium. Cardiac tamponade is evidenced distension of the atrial wall beyond its elastic cough, or dyspnea) are typically present. by diastolic collapse of the right atrium r r r limits. An atrial tear may result if the split Signs of right heart failure (e.g., ascites and and/or ventricle. Signs of advanced mitral extends through the myocardium and jugular venous distension) may also be seen in endocardiosis, including mitral valve r epicardium, resulting in a full thickness defect some patients. Heartsoundsmaybe thickening and prolapse, moderate to severe in the atrial wall and hemorrhage into the muffled, or if a murmur was heard before the mitral regurgitation, moderate to severe left pericardial space. atrial wall tear occurred, it may be reduced in atrial enlargement and often one or more PATHOPHYSIOLOGY intensity. ruptured chordae tendineae. r Endocardial splitting typically results from CAUSES DIAGNOSTIC PROCEDURES increased left atrial volume and pressure r r Electrocardiographic Findings Mitral valve endocardiosis Chordae r r secondary to severe mitral regurgitation and r Sinus tachycardia Atrial or ventricular tendinae rupture Cardiac neoplasia, most r mechanical trauma from the regurgitant jet; r arrhythmias Possible dampened QRS commonly hemangiosarcoma Chest trauma r r primary endocardial degeneration may also r complexes Electrical alternans ST-segment r Cardiac catheterization r play a role. If the split is incomplete, fibrin RISK FACTORS abnormalities Possible left ventricular or left may seal the defect temporarily; this either r atrial enlargement pattern Severe mitral regurgitation, left atrial heals as a linear depression in the endocardial r enlargement. May be precipitated by an PATHOLOGIC FINDINGS surface or subsequently extends through the r episode of excitement, stress, or activity. Endocardial splitting is noted grossly as a myocardium resulting in a complete left atrial r pale linear depression in the atrial r tear. A left atrial tear results in peracute endocardium. Atrial wall tears appear as full bleeding into the pericardial sac and severe, thickness defects extending through the atrial life-threatening hemodynamic compromise r DIAGNOSIS endocardium, myocardium and epicardium; secondary to acute cardiac tamponade. If a an associated thrombus may or may not be tear occurs in the interatrial septum, an DIFFERENTIAL DIAGNOSIS present. The caudolateral aspect of the left acquired atrial septal defect may form. r r Other causes of acute cardiovascular atrium is most commonly affected, with many r Tearing of either atrium may also rarely collapse or syncope Pericardial effusion from tears occurring at the atrio-auricular junction. r occur secondary to blunt trauma, or other causes (e.g., neoplastic and idiopathic) Hemorrhagic pericardial effusion or r r iatrogenically during pericardiocentesis. Heart failure Severe cardiac arrhythmias pericardial thrombus are seen with acute tears. r SYSTEMS AFFECTED Mitral endocardiosis characterized by r r CBC/BIOCHEMISTRY/URINALYSIS r Cardiovascular Respiratory Anemia is uncommon unless thickened mitral valve leaflets with rolled edges; chordae tendinae rupture may be seen; INCIDENCE/PREVALENCE pericardiocentesis is performed since volume r Atrial tear is a rare cause of hemorrhagic of blood loss is relatively small. atrial jet lesions are possible. Cardiomegaly r r pericardial effusion in the dog encompassing Hypoproteinemia is common. Elevations with severe left atrial enlargement expected. approximately 2% of pericardial effusion in serum lactate, metabolic acidosis. r cases. Increased ALT, AST in some patients. r SIGNALMENT Prerenal azotemia; hyponatremia or other electrolyte derangements may be seen. TREATMENT Species OTHER LABORATORY TESTS APPROPRIATE HEALTH CARE Dog; uncommon in cat r Breed Predilections NT-proBNP and TnI levels may be elevated. If a left atrial tear is strongly suspected, r Same as endocardiosis breeds; more IMAGING perform pericardiocentesis only if the effusion is causing symptomatic, life-threatening common in small- to medium-sized dogs. Radiographic Findings r r cardiac tamponade, since further hemorrhage Poodle, dachshund, cocker spaniel, and Moderate to severe left atrial enlargement is r into the pericardial sac or exsanguination may Shetland sheepdog may be overrepresented. expected. Comparison with previous r r occur once pericardial fluid is removed. If If trauma is the cause, any breed may be thoracic radiographs may show rounding and pericardiocentesis is performed, remove only represented. further enlargement of cardiac silhouette; enough fluid to improve clinical signs. characteristic globoid cardiac silhouette r Mean Age and Range Pericardiocentesis will likely be difficult associated with pericardial effusion may be Middle-aged to older dogs are predisposed. r given the small volume of effusion typically more obvious on the DV view. Interstitial to SIGNS identified, severe cardiac enlargement, and the alveolar pulmonary infiltrates if concomitant r small size of most dogs with left atrial rupture; Historical Findings left-sided CHF is present. Small volume r ultrasound guidance and continuous ECG Acute onset of weakness and collapse that pleural effusion, ascites, hepatomegaly, and r monitoring are highly recommended. Best may progress quickly to respiratory or large caudal vena cava may be seen due to practices for management of left atrial tears cardiopulmonary arrest; episode may follow a right-sided CHF. period of increased excitement or activity. have not been clearly established; however, r Echocardiographic Findings History of long-standing cardiac disease r aggressive medical management to lower left Pericardial effusion is evidenced bya with signs of CHF described in most patients. atrial pressure using afterload and preload r hypoechoic space between the heart and reducers is recommended based on the Acute worsening of cough or dyspnea are r pericardial sac; the volume of pericardial author’s clinical experience. If a fibrin clot JWST589-A87-83 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:15 279mm×216mm

144 Blackwell’s Five-Minute Veterinary Consult

A Atrial Wall Tear (Continued)

forms over the defect, the patient may or hypertensive animals to reduce regurgitant POSSIBLE COMPLICATIONS r stabilize and recover. fraction and lower left atrial pressure. Even if the tear seals, the patient is prone to r Diuretics should be used cautiously if further tears because of underlying cardiac NURSING CARE r r Administer oxygen to dogs with dyspnea or needed to treat dyspnea associated with disease. Most dogs have or will develop signs of hemodynamic instability. concomitant congestive heart failure (e.g., concurrent CHF. r Administer IV fluids or blood products only 1–2 mg/kg of furosemide IV as needed); signs EXPECTED COURSE AND PROGNOSIS if evidence of hypovolemia is present; most of left-sided congestive heart failure may Prognosis for survival is guarded to poor; dogs remain in a volume overloaded state and worsen as cardiac tamponade resolves due to however, some animals can do well for several further intravascular volume expansion will augmentation of preload; more aggressive months or longer with close monitoring, diuretic therapy may then be required. increase left atrial pressure and potentially r exercise restriction and optimal medical worsen tamponade. Pimobendan (0.2–0.3 mg/kg PO q12h) management of cardiac disease. may result in a further reduction in left atrial ACTIVITY pressure though studies have not specifically Strict cage rest in the acute period should be examined its use in the setting of left atrial followed by chronic exercise restriction. rupture and the author typically delays CLIENT EDUCATION starting inotropes for several days so as not to MISCELLANEOUS Left atrial tear typically accompanies disrupt stability of the fibrin clot. ASSOCIATED CONDITIONS r r r advanced cardiac disease and chronic medical Once the patient is stable, ACE inhibitors Chronic valvular disease CHF r therapy will be necessary; though the (e.g., enalapril 0.5 mg/kg q12–24h) should be Mainstem bronchial compression implemented for chronic management of prognosis is guarded for surviving the acute SYNONYMS event some dogs with left atrial tear have lived accompanying heart failure. r r Atrial rupture Atrial splitting more than a year after the incident. PRECAUTIONS r SEE ALSO SURGICAL CONSIDERATIONS Aggressive fluid therapy is not warranted in r r r Atrial Septal Defect Atrioventricular Valve Exploratory thoracotomy may be these patients; further volume expansion may r (Myxomatous) Disease Congestive Heart considered if hemorrhage persists or recurs increase left atrial pressure, worsen cardiac r r tamponade, and contribute to hemodynamic Failure Pericardial Effusion Syncope but should be undertaken cautiously given the r compromise. Best practices for management ABBREVIATIONS advanced state of cardiac disease typically r r of left atrial tear have not been clearly ACE = angiotensin converting enzyme present. Transcatheter septal puncture and r r established; the choice of whether to perform ALT = alanine aminotransferase AST = balloon tear of the fossa ovalis may also be r considered to decompress the left atrium; pericardiocentesis, and whether to administer aspartate aminotransferase CHF= however, right heart failure or hypoxemia due preload and/or afterload reducers should be Congestive heart failure to right-to-left shunting may result. made based on assessment of the volume INTERNET RESOURCES status, blood pressure and clinical stability of James Buchanan Cardiology Library: the patient. http://www.vin.com/MEMBERS/CMS/Misc/ POSSIBLE INTERACTIONS Default.aspx?id=7703. MEDICATIONS Sodium nitroprusside should never be administered concurrently with Suggested Reading DRUG(S) OF CHOICE Peddle GD, Buchanan JW. Acquired atrial r phosphodiesterase-V inhibitors (e.g., Atrial tears occur secondary to elevated left sildenafil or tadalafil) due to the potential for septal defects secondary to rupture of the atrial pressure; thus medical therapy should be life-threatening systemic hypotension. atrial septum in dogs with degenerative focused on lowering of left atrial pressures in mitral valve disease. J Vet Cardiol 2010, order to reduce continued hemorrhage into 12:129–134. the pericardial space and permit fibrin clot Reineke EL, Burkett DE, Drobatz KJ. Left formation at the site of the tear; this may be atrial rupture in dogs: 14 cases accomplished with preload (e.g., diuretics, FOLLOW-UP (1990–2005). J Vet Emerg Crit Care 2008, nitroglycerin paste) and/or afterload reducers PATIENT MONITORING 18:158–164. (arterial vasodilators). r Rush JR, Cunningham SM. Chronic valvular r Recommend close monitoring of respiratory Preload and afterload reduction must be rate and effort, mucous membrane color and heart disease in dogs. In: Bonagura JD, undertaken cautiously to avoid worsening of CRT, pulse quality, and heart rate; blood Twedt DC, eds., Kirk’s Current Veterinary hemodynamic compromise. Therapy XV. St. Louis, MO: Saunders r pressure monitoring is recommended if Afterload reduction may be achieved by arterial vasodilators are implemented. Elsevier, 2014, pp. 784–794. r conservative doses of sodium nitroprusside; a Follow-up examination with Sadanaga KK, MacDonald MJ, Buchanan low starting CRI dose of 0.5–1 𝜇g/kg/min is echocardiography helps determine resolution JW. Echocardiography and surgery in a dog recommended to achieve a decrease in LA of pericardial effusion and resorption of an with left atrial rupture and r pressure without precipitating significant atrial or pericardial clot. Close follow-up hemopericardium. J Vet Intern Med 1990, hypotension; blood pressure monitoring is every 2–3 months thereafter is recommended 4:216–221. recommended and the dose may be uptitrated for repeat pericardial fluid checks and Author Suzanne M. Cunningham as necessary every 15–30 minutes up to a medication adjustments as deemed Consulting Editors Larry P. Tilley and maximum of 10 𝜇g/kg/min to achieve an appropriate. Francis W.K. Smith, Jr. improvement in clinical signs and/or a PREVENTION/AVOIDANCE reduction in blood pressure of 10–15 mmHg. r Alternatively, amlodipine may be started at Recommend avoidance of strenuous physical 0.1–0.2 mg/kg PO q24h; chronic amlodipine activity and excitement. therapy may be implemented in normotensive JWST589-A08-84 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:19 279mm×216mm

Canine and Feline, Sixth Edition 145 Atrioventricular Block, Complete (Third Degree) A

r INCIDENCE/PREVALENCE Other congenital heart defects r Not documented Lyme disease r BASICS GEOGRAPHIC DISTRIBUTION Chagas disease N/A DEFINITION r SIGNALMENT All atrial impulses are blocked at the AV junction; atria and ventricles beat Species DIAGNOSIS independently. A secondary “escape” Dog and cat DIFFERENTIAL DIAGNOSIS pacemaker site (junctional or ventricular) Breed Predilections r stimulates the ventricles. r Advanced second-degree AV block r Cocker spaniel—can have idiopathic r Atrial rate normal. fibrosis. Atrial standstill r r r Idioventricular escape rhythm slow. Pug and Doberman pinscher—can have Accelerated idioventricular rhythm ECG Features associated sudden death, AV conduction CBC/BIOCHEMISTRY/URINALYSIS r r Ventricular rate slower than the atrial rate defects, and bundle of His lesions. Abnormal serum electrolytes (e.g., hyperkalemia, hypokalemia) possible. (more P waves than QRS complexes)— Mean Age and Range r ventricular escape rhythm (idioventricular) Geriatric animals, except congenital heart High WBC with left shift in animals with usually < 40 bpm; junctional escape rhythm disease patients. Median age for cats— bacterial endocarditis. (idiojunctional) 40–60 bpm in dogs and 14 years. OTHER LABORATORY TESTS 60–100 bpm in cats. r r Predominant Sex High serum digoxin concentration if AV P waves—usually normal configuration Intact female dogs block is due to digoxin toxicity. (Figure 1). r r SIGNS Lyme titer and accompanying clinical signs QRS complex—wide and bizarre when if AV block due to Lyme disease. pacemaker located in the ventricle, or in the Historical Findings r IMAGING lower AV junction in a patient with bundle Exercise intolerance r branch block; normal when escape pacemaker Weakness or syncope Echocardiography and Doppler ultrasound to r in the lower AV junction (above the Occasionally, CHF assess cardiac structure and function. DIAGNOSTIC PROCEDURES bifurcation of the bundle of His) in a patient Physical Examination Findings r r without bundle branch block. Bradycardia Electrocardiography r r r No conduction between the atria and the Variable third and fourth heart sounds His bundle electrogram to determine the ventricles; P waves have no constant r site of the AV block. Variation in intensity of the first heart r relationship with QRS complexes; P–P and sounds Long-term (Holter) ambulatory recording if r R–R intervals relatively constant (except for a Signs of CHF AV block is intermittent. r sinus arrhythmia). Intermittent “cannon” A waves in jugular PATHOLOGIC FINDINGS PATHOPHYSIOLOGY venous pulses Degeneration or fibrosis of the AV node and Slow ventricular escape rhythms (< 40 bpm) CAUSES & RISK FACTORS its bundle branches, associated with result in low cardiac output and eventual Isolated congenital defect endocardial and myocardial fibrosis and r heart failure, often when animal is excited or Idiopathic fibrosis organized endomyocarditis. r exercised, since demand for greater cardiac Infiltrative cardiomyopathy (amyloidosis or output is not satisfied. As the heart fails, signs neoplasia) r increase with mild activity. Hypertrophic cardiomyopathy in cats r SYSTEMS AFFECTED Digitalis toxicity TREATMENT r Hyperthyroidism in cats Cardiovascular r APPROPRIATE HEALTH CARE Myocarditis GENETICS r r Endocarditis Temporary or permanent cardiac Canbeanisolatedcongenitaldefect r Electrolyte disorder pacemaker—only effective treatment in r Myocardial infarction symptomatic patients.

Figure 1. Complete heart block. The P waves occur at a rate of 120, independent of the ventricular rate of 50. The QRS configuration is a right bundle branchblockpattern. The regular rate and stable QRS indicate that the rescuing focus is probably near the AV junction. (From: Tilley LP.Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.) JWST589-A08-84 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:19 279mm×216mm

146 Blackwell’s Five-Minute Veterinary Consult

A Atrioventricular Block, Complete (Third Degree) (Continued)

Figure 2. Complete heart block in a cat. The P waves rate is 240/minute, independent of the ventricular rate of 48/minute. QRS configuration is a left bundlebranch block pattern. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.)

r Carefully monitor asymptomatic patients CONTRAINDICATIONS ABBREVIATIONS r without a pacemaker for development of Avoid digoxin, xylazine, acepromazine, beta AV = atrioventricular r clinical signs. blockers (e.g., propranolol and atenolol), and CHF = congestive heart failure r calcium channel blockers (e.g., verapamil and ECG = electrocardiogram NURSING CARE r = Cage rest prior to pacemaker implantation; diltiazem); ventricular antiarrhythmic agents WBC white blood cell when the pulse generator is put into a are dangerous because they suppress lower INTERNET RESOURCES subcutaneous pocket, a non-constricting escape foci. www.vetgo.com/cardio PRECAUTIONS bandage is required around the ventral neck Suggested Reading or abdomen for 3–5 days to prevent seroma Vasodilators—may cause hypotension in Bright JM. Pacemaker therapy. In: Smith formation or pacemaker movement. animals with complete AV block; monitor FWK, Tilley LP, Oyama MA, Sleeper MM, closely if used, especially prior to pacemaker ACTIVITY eds., Manual of Canine and Feline implantation. Restrict if symptomatic Cardiology, 5th ed. St. Louis, MO: DIET Saunders Elsevier, 2015 (in press). No modifications unless required to manage Kellum HB, Stepien RL. Third-degree underlying condition (e.g., low-salt diet). atrioventricular block in 21 cats FOLLOW-UP (1997–2004). J Vet Intern Med 2006, CLIENT EDUCATION r PATIENT MONITORING 20:97–103. Temporary or permanent cardiac r Schrope DP, Kelch WJ. Signalment, clinical pacemaker—only effective treatment in Monitor—pacemaker function with serial ECGs. signs, and prognostic indicators associated symptomatic patients. r r Radiographs—following pacemaker with high-grade second or third-degree Asymptomatic patients without a atrioventricular block in dogs: 124 cases pacemaker—must be carefully monitored for implantation, to confirm the position of the lead and generator. (January 1, 1997–December 31, 1997). development of clinical signs. J Am Vet Med Assoc 2006, 228:1710–1717. SURGICAL CONSIDERATIONS PREVENTION/AVOIDANCE Tilley LP, Smith FW. Essentials of r Most patients—at high anesthetic N/A Electrocardiography. Interpretation and cardiopulmonary risk; usually paced POSSIBLE COMPLICATIONS Treatment, 4th ed. Ames, IA: Wiley preoperatively with a temporary external Pulse generators—broad range of clinical life; Blackwell Publishing, 2016 (in preparation). pacemaker system. Author Larry P. Tilley r pacemaker replacement necessary when The small size of cats makes pacemaker battery is depleted, pulse generator Consulting Editors Larry P. Tilley and implantation more difficult than in dogs. malfunction occurs, or exit block develops; Francis W.K. Smith, Jr. pacemaker leads can become dislodged and Acknowledgment The author and editors infected. acknowledge the prior contribution of Naomi EXPECTED COURSE AND PROGNOSIS L. Burtnick. MEDICATIONS Poor long-term prognosis if no cardiac DRUG(S) OF CHOICE pacemaker implanted, especially when the Client Education Handout r animal has clinical signs. Cats can sometimes available online Treatment with drugs—usually of no value. > Traditionally used to treat complete AV block: survive 1year. atropine, isoproterenol, corticosteroids, and dobutamine. r Intravenous isoproterenol infusion may help increase the rate of the ventricular escape MISCELLANEOUS rhythm to stabilize hemodynamics. r ASSOCIATED CONDITIONS If CHF—diuretic and vasodilator therapy None may be needed before pacemaker implantation. JWST589-A09-85 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:24 279mm×216mm

Canine and Feline, Sixth Edition 147 Atrioventricular Block, First Degree A

r Mean Age and Range Myocarditis (especially Trypanosoma cruzi, r May occur in young, otherwise healthy dogs Borrelia burgdorferi, Rickettsia rickettsii). r as a manifestation of high vagal tone. Infiltrative diseases (tumors, amyloid). BASICS r r Intra-atrial conduction delay involving the Atropine administered intravenously may DEFINITION right atrium may be seen with congenital briefly prolong the PR interval. Refers to a delay in conduction that occurs heart disease, especially atrioventricular septal RISK FACTORS defects. between atrial and ventricular activation. r Any condition or intervention that raises ECG Features May be noted in aged patients with vagal tone r degenerative conduction system disease, Rate and rhythm—usually normal. r particularly cocker spaniels and dachshunds. Usually there are regularly occurring normal r Persian cats of any age with high vagal tone P waves and QRS complexes (Figures 1 and in cats of any age with hypertrophic and 2). r cardiomyopathy. DIAGNOSIS Prolonged, consistent PR intervals—dogs, > 0.13 sec; cats, > 0.09 sec (Figures 1 and 2). SIGNS DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY Historical Findings P waves superimposed upon preceding T r r waves because of first-degree AV block should Virtually never causes clinical signs. Most animals are asymptomatic. r r be differentiated from bifid T waves. May become a more severe AV conduction If drug-induced, may have a history of disturbance in some animals. clinical signs related to drug toxicity— CBC/BIOCHEMISTRY/URINALYSIS r r Normally the PR interval tends to shorten anorexia, vomiting, and diarrhea with Serum electrolytes—hypokalemia and with rapid heart rates. digoxin; weakness with calcium channel hyperkalemia may predispose to AV r blockers or 𝛽-adrenergic antagonists. conduction disturbances. May be the result of intra-atrial conduction r delay (prolongation of the PA interval on Physical Examination Findings Leukocytosis—may be noted with bacterial r surface ECG and simultaneous His bundle Normal—unless also signs of more endocarditis or myocarditis. electrogram) or delay of conduction within generalized myocardial disease, drug toxicity, OTHER LABORATORY TESTS r the AV node itself (prolongation of the AH or non-cardiac disease. Serum digoxin concentration—may be interval on His bundle electrogram). CAUSES high. r r SYSTEMS AFFECTED May occur in normal animals. T. cruzi, B. burgdorferi, R. rickettsii titers— r may be high. Cardiovascular Enhanced vagal stimulation resulting from r GENETICS non-cardiac diseases—usually accompanied T4—may be high in cats if associated with thyrotoxic myocardial disease. N/A by sinus arrhythmia, sinus arrest, and/or Mobitz type I second-degree AV block. IMAGING INCIDENCE/PREVALENCE r Pharmacologic agents (e.g., digoxin, Echocardiographic examination—may reveal 𝛽 Common -adrenergic antagonists, calcium channel hypertrophic or infiltrative myocardial GEOGRAPHIC DISTRIBUTION blocking agents, propafenone, amiodarone, disorder. 𝛼 None 2-adrenergic agonists, parasympathomimetic DIAGNOSTIC PROCEDURES SIGNALMENT agents [bethanechol, physostigmine, pilocarpine] and severe procainamide or May be needed to identify causes of high Species quinidine toxicity). vagal tone—upper airway disease, cervical and r Dog and cat Degenerative disease of the conduction thoracic masses, gastrointestinal disorders, Breed Predilections system. and high intraocular pressure. r American cocker spaniel, dachshund, Hypertrophic cardiomyopathy. PATHOLOGIC FINDINGS brachycephalic dogs, Persian cats Variable—depend on underlying cause

Figure 1. Lead II ECG rhythm strip recorded from a cat with hypertrophic cardiomyopathy. There is sinus bradycardia (120 bpm) and first-degree atrioventricular conduction block. The PR interval is 0.12 second (paper speed = 50 mm/s). JWST589-A09-85 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:24 279mm×216mm

148 Blackwell’s Five-Minute Veterinary Consult

A Atrioventricular Block, First Degree (Continued)

Figure 2. Lead II ECG rhythm strip recorded from a dog showing sinus tachycardia (175 bpm) and first-degree atrioventricular conduction block. Because the heartrateis rapid, P waves are superimposed on the downslope of the preceding T waves. The PR interval exceeds 0.16 second (paper speed = 50 mm/s).

PRECAUTIONS PREGNANCY/FERTILITY/BREEDING Drugs with vagomimetic action (e.g., digoxin, N/A TREATMENT bethanechol, physostigmine, pilocarpine) may SEE ALSO potentiate first-degree block. r APPROPRIATE HEALTH CARE Atrioventricular Block, Complete (Third r POSSIBLE INTERACTIONS Remove or treat underlying cause(s). Degree) r N/A r Hospitalization may be necessary to manage Atrioventricular Block, Second Degree— ALTERNATIVE DRUG(S) Mobitz I the underlying cause (e.g., cardiomyopathy, r gastrointestinal disease, airway disease). N/A Atrioventricular Block, Second Degree— Mobitz II NURSING CARE ABBREVIATIONS N/A r AV = atrioventricular r ACTIVITY FOLLOW-UP ECG = electrocardiogram Unrestricted; unless restriction required for an r T4 = thyroxine underlying condition. PATIENT MONITORING DIET Except in healthy young animals, monitor Suggested Reading ECG to detect any progression in conduction Kittleson MD. Electrocardiography. In: No modifications or restrictions unless disturbance. Kittleson MD, Kienle RD, eds., Small required to manage an underlying condition. PREVENTION/AVOIDANCE Animal Cardiovascular Medicine. St. Louis, CLIENT EDUCATION MO: Mosby, 1998, pp. 72–94. N/A Generally unnecessary Miller MS, Tilley LP, Smith FWK, Fox PR. POSSIBLE COMPLICATIONS SURGICAL CONSIDERATIONS Electrocardiography. In: Fox PR, Sisson D, N/A Moise NS, eds., Textbook of Canine and None unless required to manage an EXPECTED COURSE AND PROGNOSIS Feline Cardiology. Philadelphia: Saunders, underlying condition. r Depends on underlying cause. 1999,pp. 67–106. r Prognosis usually excellent if no significant Tilley LP, Smith FWK, Jr. underlying disease is present. Electrocardiography. In: Smith FWK, Tilley LP, Oyama MA, Sleeper MM, eds., Manual MEDICATIONS of Canine and Feline Cardiology, 5th ed. St. DRUG(S) OF CHOICE Louis, MO: Saunders Elsevier, 2015 (in press). Medications used only if needed to manage MISCELLANEOUS an underlying condition. Authors Francis W.K. Smith, Jr and Larry P. ASSOCIATED CONDITIONS Tilley CONTRAINDICATIONS r None Consulting Editors Larry P. Tilley and Avoid hypokalemia—increases sensitivity to Francis W.K. Smith, Jr. vagal tone; may potentiate AV conduction AGE-RELATED FACTORS delay. PR interval—tends to lengthen with r Avoid drugs likely to impair impulse advancing age Client Education Handout conduction further (calcium channel blocking ZOONOTIC POTENTIAL available online agents, 𝛽-adrenergic antagonists, 𝛼 None 2-adrenergic agonists, amiodarone, propafenone). JWST589-A10-86 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:30 279mm×216mm

Canine and Feline, Sixth Edition 149 Atrioventricular Block, Second Degree—Mobitz I A

r Mean Age and Range Type II second-degree AV block (no r Usually occurs in young, otherwise healthy variation in PR intervals). dogs as a manifestation of high vagal tone. BASICS r CBC/BIOCHEMISTRY/URINALYSIS Occasionally occurs in older dogs with Hypokalemia may predispose to AV DEFINITION abnormally strong vagal tone. r conduction disturbances Rarely noted in old dogs with degenerative Second-degree AV block refers to failure of OTHER LABORATORY TESTS one or more P waves but not all P waves to be conduction system disease. conducted. Mobitz Type I second-degree AV SIGNS Serum digoxin concentration—may be high IMAGING block occurs when AV transmission is Historical Findings r progressively delayed prior to a blocked Most animals are asymptomatic. N/A r Pwave. If drug-induced, owner may report signs of DIAGNOSTIC PROCEDURES ECG Features r r drug toxicity—anorexia, vomiting, and May be necessary to identify specific causes PR interval—becomes progressively longer diarrhea with digoxin; weakness with calcium of enhanced vagal tone (e.g., upper airway prior to the appearance of a P wave that is not channel blockers or 𝛽-adrenergic antagonists. disease, cervical and thoracic masses, followed by a QRS complex (Figure 1). r r If heart rate is abnormally slow, syncope or gastrointestinal disorders, and high Heart rate and QRS morphology—usually weakness may occur. intraocular pressure). normal. r r Physical Examination Findings Atropine response test—administer r Often cyclical. May be normal unless signs of 0.04 mg/kg atropine IM and repeat ECG in PATHOPHYSIOLOGY more-generalized myocardial disease or 20–30 minutes; may be used to determine r Frequently associated with high resting non-cardiac disease are present. whether AV block is due to vagal tone; r vagal tone and sinus arrhythmia in dogs. Intermittent pauses in the cardiac rhythm. resolution of AV block with atropine supports r r vagal cause. Generally not pathologic or First heart sound may become progressively r hemodynamically significant. softer, followed by a pause. Electrophysiologic studies are generally r r This type of AV block usually results from An audible S4 may be heard unaccompanied unnecessary but will confirm this type of conduction delay within the AV node itself by S1 and S2 when block occurs. second-degree AV block if surface ECG is equivocal. (rather than delay in other segments of the AV CAUSES r PATHOLOGIC FINDINGS conducting system) and is characterized by a Occasionally noted in normal animals. r progressive increase in AH interval with Enhanced vagal stimulation resulting from Generally, no gross or histopathologic eventual block between the A and H non-cardiac diseases—usually accompanied findings deflections on a His bundle recording. by sinus arrhythmia, sinus arrest. r SYSTEMS AFFECTED Pharmacologic agents—digoxin, Cardiovascular 𝛽 -adrenergic antagonists, calcium channel GENETICS blocking agents, propafenone, amiodarone, TREATMENT 𝛼 N/A 2-adrenergic agonists, opioids. APPROPRIATE HEALTH CARE RISK FACTORS r INCIDENCE/PREVALENCE Treatment usually unnecessary r Radiotelemetry studies have shown that this Any condition or intervention that enhances Treat or remove underlying cause(s) arrhythmia occurs in 64% of healthy adult vagal tone. NURSING CARE dogs and 100% of healthy puppies Generally unnecessary 8–12 weeks of age. ACTIVITY GEOGRAPHIC DISTRIBUTION DIAGNOSIS Unrestricted N/A DIET SIGNALMENT DIFFERENTIAL DIAGNOSIS r Modifications or restrictions only to manage Non-conducted P waves from Species an underlying condition. supraventricular premature impulses or Dog; uncommon in cat supraventricular tachycardias should be CLIENT EDUCATION Breed Predilections distinguished from second-degree AV block. Explain that any treatment is directed N/A toward reversing or eliminating an underlying cause.

Figure 1. Lead II ECG strip recorded from a dog with Mobitz type I, second-degree AV block. The PR intervals become progressively longer with the longestals PRinterv preceding non-conducted P waves (typical Wenkebach phenomenon) (paper speed = 50 mm/s). JWST589-A10-86 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:30 279mm×216mm

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SURGICAL CONSIDERATIONS POSSIBLE COMPLICATIONS Kittleson MD. Electrocardiography. In: N/A except to manage an underlying N/A Kittleson MD, Kienle RD, eds., Small condition Animal Cardiovascular Medicine. St. Louis, MO: Mosby, 1998, pp. 72–94. Mangrum JM, DiMarco JP. The evaluation MISCELLANEOUS and management of bradycardia. N Engl J MEDICATIONS Med 2000, 342:703–709. ASSOCIATED CONDITIONS Tilley LP. Essentials of Canine and Feline DRUG(S) N/A Electrocardiography, 3rd ed. Baltimore, Only as needed to manage an underlying AGE-RELATED FACTORS MD: Williams & Wilkins, 1992. condition N/A Tilley LP, Smith FWK, Jr. Electrocardiography. In: Smith FWK, Tilley CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING LP, Oyama MA, Sleeper MM, eds., Manual Drugs with vagomimetic action (e.g., digoxin, N/A bethanechol, physostigmine, pilocarpine) may of Canine and Feline Cardiology, 5th ed. St. SYNONYMS Louis, MO: Saunders Elsevier, 2015 (in potentiate block. r Wenckebach periodicity press). PRECAUTIONS r Wenckebach phenomenon Authors Francis W.K. Smith, Jr. and Larry P. Hypokalemia increases the sensitivity to vagal SEE ALSO Tilley tone and may potentiate AV conduction r Consulting Editors Larry P. Tilley and Atrioventricular Block, Complete (Third delay. Francis W.K. Smith, Jr. Degree) POSSIBLE INTERACTIONS r Acknowledgment The authors and editors Atrioventricular Block, First Degree r acknowledge the prior contribution of Janice N/A Atrioventricular Block, Second Degree— McIntosh Bright. Mobitz II ABBREVIATIONS r AV = atrioventricular Client Education Handout FOLLOW-UP r ECG = electrocardiogram available online PATIENT MONITORING Suggested Reading Typically not necessary Branch CE, Robertson BT, Williams JC. PREVENTION/AVOIDANCE Frequency of second-degree atrioventricular N/A heart block in dogs. Am J Vet Res 1975, 36:925–929. JWST589-A11-87 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:33 279mm×216mm

Canine and Feline, Sixth Edition 151 Atrioventricular Block, Second Degree—Mobitz II A

r SYSTEMS AFFECTED Degenerative change within the cardiac r Cardiovascular. conduction system—replacement of AV r BASICS Central nervous or musculoskeletal systems nodal cells and/or Purkinje fibers by fibrotic if inadequate cardiac output. and adipose tissue in old cats and dogs. r DEFINITION GENETICS Pharmacologic agents (e.g., digoxin, 𝛽 Second-degree AV block refers to failure of May be heritable in pugs -adrenergic antagonists, calcium channel blocking agents, propafenone, 𝛼 -adrenergic one or more P waves but not all P waves to be INCIDENCE/PREVALENCE 2 conducted. Mobitz Type II second-degree AV agonists, muscarinic cholinergic agonists, or Unknown severe procainamide or quinidine toxicity). block occurs when one or more P waves are r blocked without a preceding progressive delay GEOGRAPHIC DISTRIBUTION Infiltrative myocardial disorders (neoplasia, amyloid). in AV transmission. N/A r ECG Features SIGNALMENT Endocarditis (particularly involving the r aortic valve). One or more P waves not followed by a r Species Myocarditis (viral, bacterial, parasitic, QRS complex; PR interval is constant but Dog and cat idiopathic). may be either normal or consistently r Breed Predilections Cardiomyopathy (especially in cats). prolonged (Figure 1). r r Trauma. Ventricular rate—usually slow. American cocker spaniel, pug, dachshund, r r Atropine administered intravenously may Fixed ratio of P waves to QRS complexes Airedale terrier, Doberman pinscher. cause a brief period of first- or second-degree may occur (e.g., 2:1, 3:1, 4:1 AV block). Mean Age and Range r heart block before increasing the heart rate. High-grade (advanced) second-degree AV Generally occurs in older animals RISK FACTORS block is characterized by two or more Predominant Sex consecutive blocked P waves. N/A Any condition or intervention that enhances r vagal tone In second-degree AV block with a 2:1 SIGNS conduction ratio or higher, it is impossible to Historical Findings observe prolongation of the PR interval r before the block, so a designation of Mobitz is Presenting complaint may be syncope, collapse, weakness, or lethargy. not appropriate. r DIAGNOSIS r Some animals are asymptomatic. QRS complexes may appear normal but r Animals may show signs of the underlying DIFFERENTIAL DIAGNOSIS may also be wide or have an abnormal r morphology due to aberrant intraventricular disease process. High-grade (advanced) form must be conduction or to ventricular enlargement. Physical Examination Findings distinguished from complete AV block. r r r Abnormally wide QRS complexes may ± weakness. Non-conducted P waves arising from r indicate serious, extensive cardiac disease. Bradycardia common. refractoriness of the conduction system r PATHOPHYSIOLOGY May be intermittent pauses in the cardiac during supraventricular tachycardias must be r differentiated from pathologic conduction Rare in healthy animals. rhythm. r r block. May be hemodynamically important when An S4 may be audible in lieu of the ventricular rate is abnormally slow. normally expected heart sounds (i.e., S1, S2) CBC/BIOCHEMISTRY/URINALYSIS r when the block occurs. r Frequently progresses to complete AV r Serum electrolytes—hypokalemia and If associated with digoxin intoxication, there hyperkalemia may predispose to AV. block, particularly when accompanied by r wide QRS complexes. may be vomiting, anorexia, and diarrhea. Conduction disturbances. r r r Typically this type of AV block results from May be other abnormalities reflecting the Leukocytosis—may be noted with bacterial underlying etiology. endocarditis or myocarditis. conduction delay within the AV node itself r (rather than delay in another segment of the CAUSES Electrolyte abnormalities (e.g., severe r AV conducting system) that is characterized Heritable in pugs. hypokalemia, hyperkalemia, or r by normal or prolonged AH intervals with Enhanced vagal stimulation from hypercalcemia) may predispose to AV intermittent block between A and H non-cardiac diseases. block. deflections on a His bundle electrogram).

Figure 1. Lead II ECG rhythm strip recorded from a dog with both first- and second-degree atrioventricular block. The second-degree AV block is high grade withboth2:1 and 3:1 block resulting in variation in the RR intervals. The PR interval for the conducted beats is prolonged but constant (0.28 second) (paper speed = 25 mm/s). JWST589-A11-87 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:33 279mm×216mm

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OTHER LABORATORY TESTS r Serum digoxin concentration—may be high. r MEDICATIONS MISCELLANEOUS High T4 in cats—if associated with hyperthyroidism. DRUG(S) OF CHOICE ASSOCIATED CONDITIONS r r High arterial blood pressure—if associated Atropine (0.02–0.04 mg/kg IV, IM) or May be noted in cats with primary or with hypertensive heart disease. 𝜇 r glycopyrrolate (5–10 –g/kg IV, IM) may be secondary myocardial disease. Positive Borrelia, Rickettsia, or Trypanosoma used short term if positive atropine response. r AGE-RELATED FACTORS cruzi titers—if associated with one of these Chronic anticholinergic therapy infectious agents. N/A r (propantheline 0.5–2 mg/kg PO q8–12h or Blood cultures may be positive in patients hyoscyamine 3–6 𝜇g/kg q8h)—indicated for ZOONOTIC POTENTIAL with vegetative endocarditis. symptomatic patients if improved AV N/A IMAGING conduction with atropine response test. PREGNANCY/FERTILITY/BREEDING r 𝜇 Echocardiographic examination may reveal Isoproterenol (0.04–0.09 g/kg/minute IV N/A 𝜇 structural heart disease (e.g., endocarditis, to effect) or dopamine (2–5 g/kg/minute IV SEE ALSO neoplasia, or cardiomyopathy). to effect) may be administered in acute, r life-threatening situations to enhance AV Atrioventricular Block, Complete (Third DIAGNOSTIC PROCEDURES Degree) r conduction and/or accelerate an escape focus. r Atropine response test—administer Atrioventricular Block, Second Degree— CONTRAINDICATIONS 0.04 mg/kg atropine IM and repeat ECG in r Mobitz I 20–30 minutes; may be used to determine Drugs with vagomimetic action (e.g., ABBREVIATIONS digoxin, bethanechol, physostigmine, r whether AV block is due to high vagal tone. AV = atrioventricular r pilocarpine) may potentiate block. r Electrophysiologic testing is generally r ECG = electrocardiogram Avoid drugs likely to impair impulse r unnecessary but can be done to confirm this T = thyroxine type of AV block if surface ECG findings are conduction further or depress a ventricular 4 equivocal. escape focus (e.g., procainamide, quinidine, Suggested Reading lidocaine, calcium channel blocking agents, PATHOLOGIC FINDINGS Kittleson MD. Electrocardiography. In: r 𝛽-adrenergic blocking agents). Kittleson MD, Kienle RD, eds., Small Variable—depend on underlying cause. r PRECAUTIONS Animal Cardiovascular Medicine. St. Louis, Old animals with degenerative change of MO: Mosby, 1998, pp. 72–94. the conduction system may have focal Hypokalemia—increases sensitivity to vagal Mangrum JM, DiMarco JP. The evaluation mineralization of the interventricular septal tone and may potentiate AV conduction and management of bradycardia. N Engl J crest visible grossly; chondroid metaplasia of delay. Med 2000, 342:703–709. the central fibrous body and increased fibrous POSSIBLE INTERACTIONS Podrid PJ, Kowey PR. Cardiac connective tissue in the AV bundle is noted N/A Arrhythmia—Mechanisms, Diagnosis, and histopathologically. ALTERNATIVE DRUG(S) Management. Baltimore, MD: Williams & N/A Wilkins, 1995. Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Baltimore, TREATMENT MD: Williams & Wilkins, 1992. APPROPRIATE HEALTH CARE FOLLOW-UP Tilley LP, Smith FW. Essentials of r Electrocardiography. Interpretation and Treatment—may be unnecessary if heart PATIENT MONITORING rate maintains adequate cardiac output. Treatment, 4th ed. Ames, IA: Wiley r Frequent ECG because often progresses to Positive dromotropic interventions are Blackwell Publishing, 2016 (in preparation). complete (third-degree) AV block. indicated for symptomatic patients. Tilley LP, Smith FWK Jr. r Treat or remove underlying cause(s). PREVENTION/AVOIDANCE Electrocardiography. In: Smith FWK, Tilley N/A LP, Oyama MA, Sleeper MM, eds., Manual NURSING CARE of Canine and Feline Cardiology, 5th ed. St. POSSIBLE COMPLICATIONS Generally unnecessary Louis, MO: Saunders Elsevier, 2015 ACTIVITY Prolonged bradycardia may cause secondary (in press). congestive heart failure or inadequate renal Cage rest advised for symptomatic patients. Authors Larry P. Tilley and Francis W.K. perfusion. DIET Smith, Jr. EXPECTED COURSE AND PROGNOSIS Consulting Editors Larry P. Tilley and Modifications or restrictions only to manage Variable—depends on cause. If degenerative Francis W.K. Smith, Jr. an underlying condition. disease of the cardiac conduction system, Acknowledgment The editors acknowledge CLIENT EDUCATION the prior contribution of Janice McIntosh r often progresses to complete (third-degree) Need to seek and specifically treat AV block. Bright. underlying cause. r Pharmacologic agents may not be effective long term. Client Education Handout SURGICAL CONSIDERATIONS available online Permanent pacemaker may be required for long-term management of symptomatic patients. JWST589-A89-88 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:37 279mm×216mm

Canine and Feline, Sixth Edition 153 Atrioventricular Valve Dysplasia A

GENETICS gallop heart sounds. Silent tricuspid Tricuspid valve dysplasia is inherited as an regurgitation is well documented in cats and BASICS autosomal recessive trait in Labrador is attributable to a large regurgitant orifice retrievers. Heritability and pattern of and laminar regurgitant flow. Distention and DEFINITION inheritance not established in other breeds. pulsation of the external jugular veins may be r A congenital malformation of the mitral or INCIDENCE/PREVALENCE evident. Evidence of right heart tricuspid valve apparatus. These are common congenital cardiac failure—ascites and, more rarely, peripheral PATHOPHYSIOLOGY anomalies in cats (17% of reported congenital edema with severe malformations. r Atrioventricular valve dysplasia can result in cardiac defects in one study). Less frequently valvular insufficiency, valvular stenosis, or diagnosed in dogs. dynamic outflow tract obstruction, depending SIGNALMENT DIAGNOSIS on the anatomic abnormality. AVVD may Species occur alone or in association with Dog and cat DIFFERENTIAL DIAGNOSIS abnormalities of the ipsilateral outflow tract r Breed Predilections With the noted exception of the age of (e.g., valvular or subvalvular aortic or r Tricuspid valve dysplasia—increased risk for onset, congenital AV valvular insufficiency pulmonic stenosis). It is not uncommon for resembles acquired degenerative AV valve mitral and tricuspid valve dysplasia to occur Labrador retriever, German shepherd dog, r Great Pyrenees, possibly Old English insufficiency with respect to historical together in the same patient. Valvular r findings, physical examination abnormalities, insufficiency results in dilation of the sheepdog. Also common in cat. Mitral valve r dysplasia—increased risk in bull terrier, and clinical sequelae. The right-sided ipsilateral atrium, eccentric hypertrophy of murmur of tricuspid insufficiency is the associated ventricle, and, if sufficiently Newfoundland, Labrador retriever, Great Dane, golden retriever, Dalmatian, and sometimes confused with the right-sided severe, signs of CHF. Cardiomyopathy of murmur of a ventricular septal defect. chronic volume overload and elevated atrial Siamese cat. Perhaps the most common r congenital heart defects of cats. Mitral valve Ascites caused by silent tricuspid pressures are the end result culminating in regurgitation or tricuspid valve stenosis is pulmonary congestion if the mitral valve is malformations often are noted in cats with hypertrophic cardiomyopathy. often attributed to pericardial effusion, affected and systemic congestion if the hepatic disease, or obstruction of the caudal r r tricuspid valve is affected. Valvular stenosis Mean Age and Range vena cava. Dogs and cats with cor results in atrial dilation and hypertrophy and, Variable; signs are most often manifest within triatriatum share many of the clinical features r when severe, hypoplasia of the receiving the first few years after birth. of AV valve stenosis. There is no certain way ventricle. Tricuspid valve stenosis results in Predominant Sex to distinguish mitral valve dysplasia elevated right atrial pressure and systemic Males are more likely to evidence heart failure. producing outflow tract obstruction and the congestion if pressures exceed 15–20 mmHg. SIGNS obstructive form of cardiomyopathy. If the Right-to-left shunting may occur if there is an obstruction can be abolished with a beta Historical Findings atrial septal defect or patent foramen ovale. r blocker and left ventricular hypertrophy Mitral valve stenosis results in elevated Exercise intolerance is the most common resolves, it is likely that the primary problem in dogs and cats with AV valve pulmonary capillary pressure and pulmonary r abnormality was mitral valve dysplasia. edema if pressures exceed 25–30 mmHg. dysplasia. Abdominal distention, weight loss, and stunting may be observed with IMAGING Pulmonary hypertension is a common r complicating condition in animals with mitral severe tricuspid valve dysplasia. Labored Radiographic Findings r respiration is common in dogs or cats with Mitral Valve Dysplasia valve stenosis. Outflow tract obstruction r r may develop from defects that translocate the mitral valve dysplasia. Syncope and collapse Left atrial and left ventricular enlargement anterior leaflet to a position closer to the if critical mitral or tricuspid valve stenosis, with valvular insufficiency. Isolated left atrial interventricular septum. Concentric left severe outflow tract obstruction, an associated enlargement with valvular stenosis. Mild left arrhythmia, or heart failure from AV valvular atrial enlargement with dynamic outflow ventricular hypertrophy develops in r proportion to the severity of the obstruction. insufficiency. obstruction. Evidence of left heart SYSTEMS AFFECTED Physical Examination Findings failure—distended pulmonary veins, r Cardiovascular—inflow obstruction due to Mitral Valve Dysplasia interstitial or alveolar edema in severe cases. r Tricuspid Valve Dysplasia valvular stenosis and chronic volume overload A holosystolic murmur is heard over the r from valvular insufficiency result in elevated cardiac apex on the left. With severe disease Right atrial and right ventricular pulmonary (left AV valve) or systemic (right the murmur is accompanied by a thrill or enlargement with valvular insufficiency. AV valve) venous pressures. Signs of low gallop heart sounds. A soft diastolic murmur Cardiac silhouette may appear globoid with cardiac output develop if the lesion is may be present in the same location in pronounced enlargement. Isolated right atrial enlargement with valvular stenosis. sufficiently severe. Concentric left ventricular animals with mitral stenosis but many r hypertrophy develops secondary to dynamic affected animals have no audible murmur. A Evidence of right heart failure—dilated r outflow obstruction. Respiratory— systolic ejection murmur that intensifies with caudal vena cava, hepatosplenomegaly, or pulmonary edema may develop secondary to exercise or excitement is audible in animals ascites in severe cases. with dynamic outflow tract obstructions. Echocardiography mitral stenosis or mitral valve insufficiency. r Evidence of left heart failure—tachypnea, Mitral Valve Dysplasia Pulmonary hypertension is a common r complication in animals with mitral stenosis. increased respiratory efforts, pulmonary Valvular insufficiency results in left atrial r Neurologic—collapse and loss of crackles, and cyanosis in animals with severe dilation and eccentric hypertrophy of the left consciousness, most often during physical defects. ventricle. The papillary muscles are typically Tricuspid Valve Dysplasia flattened and displaced dorsally. Chordae exertion, may occur with severe disease due to r low cardiac output and hypotension. Collapse A holosystolic murmur is heard over the tendineae are often short and thickened. in animals with dynamic outflow obstruction cardiac apex on the right. With severe disease Doppler echocardiography demonstrates a is most often due to ventricular arrhythmia. the murmur is accompanied by a thrill or high velocity retrograde systolic transmitral jet JWST589-A89-88 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:37 279mm×216mm

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and modestly increased transmitral inflow accompanied by a variety of arrhythmias, POSSIBLE COMPLICATIONS r r velocities. Mitral stenosis results in left atrial particularly atrial premature beats, Congestive heart failure—left-sided with dilation while the left ventricular dimensions supraventricular tachycardia, or atrial mitral valve dysplasia; right-sided with r are normal or small. The valve leaflets are fibrillation. tricuspid valve dysplasia. Collapse or r often thickened, relatively immobile, and syncope with exercise. Paroxysmal often fused. Doppler echocardiography supraventricular tachycardia or atrial demonstrates a high velocity transmitral fibrillation with severe disease. diastolic jet with a reduced EF slope. There TREATMENT EXPECTED COURSE AND PROGNOSIS r may also be evidence of concurrent mitral Depends on severity of underlying defect APPROPRIATE HEALTH CARE r insufficiency and/or secondary pulmonary Guarded to poor with serious defects hypertension. Exclude the possibility of cor Inpatient treatment required for CHF. r triatriatum sinister. Dynamic left ventricular CLIENT EDUCATION outflow obstruction is characterized by Owners should be informed of heritability systolic motion of the anterior mitral valve and advised against breeding. leaflet toward the interventricular septum, MISCELLANEOUS DIET increased LV outflow tract velocities, and ASSOCIATED CONDITIONS Sodium-restricted if overt or pending CHF. r concentric left ventricular hypertrophy. Mitral valve dysplasia commonly Tricuspid Valve Dysplasia SURGICAL CONSIDERATIONS r r accompanies valvular or subvalvular aortic Valvular insufficiency results in right atrial Valve repair or replacement is available in a r r stenosis as well as TVD. Tricuspid valve dilation and eccentric hypertrophy of the few centers. Balloon valvuloplasty is dysplasia commonly accompanies pulmonic right ventricle. The papillary muscles and sometimes effective for valvular stenosis. stenosis as well as MVD. chordae tendineae may be fused, creating a PREGNANCY/FERTILITY/BREEDING curtain-like appearance of the tricuspid valve. Doppler echocardiography demonstrates a Should be avoided—heritable defect and possibility of causing decompensated or high velocity retrograde systolic trans- MEDICATIONS tricuspid jet and modestly increased worsening heart failure. r transtricuspid inflow velocities. Tricuspid DRUG(S) OF CHOICE SEE ALSO r r stenosis results in right atrial dilation with Mitral or tricuspid dysplasia with Congestive Heart Failure, Left-Sided r normal or small right ventricular dimensions. insufficiency—diuretics, angiotensin Congestive Heart Failure, Right-Sided The valve leaflets do not open completely. converting enzyme inhibitors, and ABBREVIATIONS Doppler echocardiography demonstrates a pimobendan (0.3 mg/kg q12h) for patients r r AV = atrioventricular AVVD = high velocity diastolic trans-tricuspid jet with with imminent or overt congestive heart r atrioventricular valve dysplasia CHF = a reduced EF slope. There may be evidence of failure. Furosemide (2–4 mg/kg q12–24h), r congestive heart failure ECG = concurrent tricuspid valve insufficiency enalapril (0.5 mg/kg q12h) are used to control r electrocardiogram MVD = mitral valve and/or right-to-left shunting across a patent congestion. Digoxin (2–4 𝜇g/kg q12h) is used r dysplasia TVD = tricuspid valve dysplasia foramen ovale or associated atrial septal to control supraventricular tachyarrhythmias. r defect. Exclude the possibility of cor Mitral or tricuspid stenosis—diuretics to Suggested Reading triatriatum dexter. control edema. Furosemide (2–4 mg/kg Bonagura JD, Lehmkuhl LB. Congenital Cardiac Catheterization q12–24h) dose adjusted to resolve congestion. heart disease. In: Fox PR, Sisson D, Moise r Indicated only in those cases in which the Heart rate should be maintained near NS. Textbook of Canine and Feline 𝜇 diagnosis cannot be confirmed by 150 bpm using digoxin (2–4 g/kg q12h), a Cardiology: Principles and Clinical Practice, echocardiography or if surgical correction is calcium channel blocker such as diltiazem 2nd ed. Philadelphia: Saunders, 1999, pp. r anticipated. Mitral dysplasia— (1–1.5 mg/kg q8h), or a beta-receptor 520–526. hemodynamic measurements should include blocking drug, such as atenolol Oyama MA, Sisson DD, Thomas WP, (0.5–1.5 mg/kg q12–24h). Bonagura JD. Congenital heart disease. In: left ventricular pressures, pulmonary capillary r wedge pressure or direct measurement of LA Dynamic outflow tract obstruction—titrate Ettinger SJ, Feldman EC, eds., Textbook of pressure, pulmonary artery pressures, and, in a beta-receptor blocking drug, such as Veterinary Internal Medicine, 6th ed. St. cases of dynamic obstruction, simultaneous atenolol (0.5–1.5 mg/kg q12–24h), to abolish Louis, MO: Elsevier, 2005. recording of aortic and left ventricular or diminish severity of outflow obstruction. Strickland KN. Congenital heart disease. In: pressures with medical provocation. Contrast PRECAUTIONS Tilley LP, Smith FWK, Oyama MA, Sleeper studies are best accomplished with a left Standard patient monitoring for cardiac MM, eds., Manual of Canine and Feline ventricular injection in cases of valvular medication side effects (e.g., digitalis toxicity, Cardiology, 4th ed. St. Louis, MO: insufficiency, and direct left atrial injection via azotemia). Saunders Elsevier, 2008, pp. 215–239. trans-septal catheterization in cases of valvular Author David D. Sisson r stenosis. Tricuspid dysplasia—hemodynamic Consulting Editors Larry P. Tilley and measurements should include right Francis W.K. Smith, Jr. ventricular and right atrial pressures. Contrast FOLLOW-UP studies are best accomplished with a right Client Education Handout ventricular injection in cases of valvular PATIENT MONITORING r available online insufficiency, and right atrial injection in cases Recheck yearly if no signs of heart failure. r of valvular stenosis. Recheck at a minimum of every 3 months if DIAGNOSTIC PROCEDURES signs of CHF (thoracic radiographs, ECG, and echocardiography advisable). Electrocardiographic Findings r Usually reflect pattern of chamber PREVENTION/AVOIDANCE r enlargement. Severe defects may be Do not breed affected animals. JWST589-A88-89 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:41 279mm×216mm

Canine and Feline, Sixth Edition 155 Atrioventricular Valve (Myxomatous) Disease A

r INCIDENCE/PREVALENCE Tachypnea/dyspnea/orthopnea in case of The most common cardiac disease in dogs. decompensated CHF. r BASICS The prevalence is strongly influenced by age. Respiratory crackles/rales in case of It is uncommon in young individuals but decompensated CHF. r DEFINITION common in old dogs. The prevalence reaches Pink froth, i.e., pulmonary edema may be Myxomatous mitral valve disease is > 90% in some affected dog breeds evident in the nostrils and oropharynx in > 10 years. cases with severe decompensated CHF. characterized by progressive myxomatous r Ascites if right-sided CHF. degeneration, which refers to a characteristic SIGNALMENT r pathologic weakening and disturbance in the Diagnostic imaging invariably shows left Species atrial (LA) and ventricular (LV) dilatation and organization of the connective tissue of the Mainly dogs. Extremely rare in cats. AV valve (mitral and tricuspid) apparatus. eccentric hypertrophy, sometimes bilateral Breed Predilections PATHOPHYSIOLOGY enlargement, and evidence of pulmonary r Typically small breeds (< 20 kg but may be congestion/edema. Lesions characterized by pathologic encountered in larger dogs), such as Cavalier CAUSES weakening and disorganization of valvular King Charles spaniels, Chihuahuas, Miniature Primary (inciting) factor unknown, but the connective tissue, in which the spongiosa schnauzers, Maltese, Pomeranians, Cocker disease is influenced by genetic factors in component is unusually prominent with spaniels, Pekingese, Poodles, and others. accumulation of mucopolysaccharides and affected breeds. glycosaminoglycans. Mean Age and Range RISK FACTORS r Murmur may be detected from 2 years of age r The valve leaflets become thickened and Breed elongated with disease progression. with a peak incidence at 6–8 years in affected r r Sex (males have an earlier onset) Degenerative changes in the chordae breeds, such as Cavalier King Charles tendineae lead to thickening and elongation spaniels. Onset of CHF from 8–12 years. of these structures; thereby contributing to Predominant Sex systolic atrial displacement of the valve leaflets Males develop the disease at a younger age DIAGNOSIS (valve prolapse). than females, which means a higher r With progression, the valve lesions cause prevalence at a given age in males. DIFFERENTIAL DIAGNOSIS r insufficient coaptation of the leaflets during SIGNS Dilated cardiomyopathy r systole, leading to backward regurgitation of Congenital heart disease Signs depend on the stage of disease. The r blood from the ventricle into the atrium. Bacterial endocarditis r descriptions here align with the grading r Severity and progression of AV valve Chronic airway or interstitial lung disease system described in the ACVIM consensus r regurgitation depends on severity and Pneumonia statement on myxomatous mitral valve r progression of valve lesions (leaflets and/or disease. Pulmonary embolism tendinous chords). r r Pulmonary neoplasia Compensatory mechanisms include cardiac Clinically Healthy Patients but Belonging r to a Risk Group (ACVIM Stage A) Heartworm disease dilatation and eccentric hypertrophy, CBC/BIOCHEMISTRY/URINALYSIS increased force of contraction, increased heart No abnormal findings r rate, increased pulmonary lymphatic drainage Patients Without Overt Clinical Signs CBC/Biochemistry usually unremarkable (ACVIM Stage B) unless severe disease and ongoing CHF (left-sided AV valve regurgitation), fluid r Systolic click (early stage). therapy retention, and neurohormonal modulation of r r cardiovascular function. Systolic murmur best heard over the mitral Prerenal azotemia secondary to impaired r or tricuspid areas. renal perfusion; urinary specific gravity is high With progression, the valvular regurgitation r can no longer be compensated, leading to Murmurs may range from being of soft, low unless complicated by underlying renal disease or previous diuretic administration. reduced cardiac output and increased venous intensity to loud holosystolic. With r High liver enzyme activity in many patients pressures (leading to pulmonary edema if progression, the murmur typically gets louder and radiates more widely. with right-sided CHF. left-sided congestive heart failure [CHF] and r Initially patients have no obvious OTHER LABORATORY TESTS to ascites if right-sided). With atrial tear, acute r cardiac tamponade may result. radiographic or echocardiographic changes in Natriuretic peptides—concentrations are SYSTEMS AFFECTED cardiac chamber size (ACVIM stage B1). As often unremarkable unless moderate to severe r the disease progresses, evidence of disease. Cardiovascular—both AV valves are r cardiomegaly will be seen (ACVIM stage B2), commonly affected, but semilunar valves less Serum troponin I—concentrations often before obvious clinical signs of heart unremarkable unless severe disease. commonly affected. r failure are recognized. Hepatobiliary—passive congestion. IMAGING r Renal/Urologic—prerenal azotemia. Patients with Overt Clinical Signs or Radiographic Findings r r Respiratory—if edema and/or pulmonary Stabilized by CHF Therapy (ACVIM Heart size ranges from normal to left-sided stages C and D) hypertension develops. r or generalized cardiomegaly. Usually loud heart murmur. r GENETICS r LA enlargement is usually the earliest Tachycardia and loss of respiratory sinus finding. Etiology currently unknown, but the current arrhythmia. r r Left-sided CHF—pulmonary congestion; leading scientific hypothesis is that a Arrhythmia and pulse deficit may be genetically determined dystrophic process increased interstitial pattern ± air present, most commonly supraventricular bronchograms; initially, congestion and initiates the valve degeneration. The age at premature beats or atrial fibrillation. which the disease develops is inherited as a r edema are perihilar, with all lung fields Weak femoral pulse, prolonged capillary eventually showing changes. polygenetic threshold trait (i.e., multiple refill time and pale mucous membranes in genes influence the trait and a certain Echocardiographic Findings case of low output failure. r threshold has to be reached before the disease Thickening and distortion of the AV valve develops). leaflets. JWST589-A88-89 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:41 279mm×216mm

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r Elongation and rupture of the chordae ACTIVITY ◦ Mild to moderate CHF: 2–4 mg/kg r tendineae, causing mitral valve prolapse. Absolute exercise restriction for q8–24h. r Atrial dilatation (uni- or bilaterally). symptomatic patients. ◦ Severe or fulminant CHF: 4–8 mg/kg r r The LV might be distended and is Stable patients receiving medical q2–6h, preferably IV, IM, or SC. hyperdynamic if the regurgitant flow is high treatment—avoid strenuous exercise. ◦ Monitor outcome of treatment by and myocardial function intact; as the DIET respiratory rate and general clinical status. r ventricle becomes more grossly distended, it Prevent cardiac cachexia by ensuring Dosages can often be reduced when the may become normo- or, less commonly, patient has stabilized. adequate calorie intake. r hypodynamic because of myocardial failure. r Oxygen supplementation and cage rest to r Avoid food with high sodium content. Pericardial effusion (usually mild) is rarely patients with significant dyspnea. 40% inO CLIENT EDUCATION 2 seen. r cage (can go as high as 100%) up to 24 hours; r Discuss the progressive nature of the disease. Doppler studies document a jet of r nasal O2 in may be used in large-breed dogs, regurgitation into the left atrium. Mild disease severity is suggestive of a long 50–100 mL/kg/minute through humidifier. r r Doppler evaluation for the presence of period without clinical signs; moderate to Pimobendan at 0.25 mg/kg q12h PO. severe indicates a shorter period. r pulmonary hypertension should be routinely r Additional options in cases with severe performed. If the client is a breeder, inform him/her fulminant CHF: ◦ DIAGNOSTIC PROCEDURES about the genetics of the disease and impact Nitroglycerin: ointment (one-fourth r of the finding on future breeding. Systemic blood pressure should be r inch/5 kg up to 2 inches percutaneously) or Appropriate level of exercise, but at the injectable (1–5 𝜇g/kg/minute CRI). monitored in patients with severe disease or same time maintain quality of life. ◦ r Arterial vasodilator to decrease afterload receiving diuretics to check for hypotension. Common signs of CHF listed above. Hypertension is not common. r rapidly, such as hydralazine at 0.5 mg/kg r How to medicate (if indicated)—consistent Arterial/venous blood gases can be used to q12h titrated up to 2 mg/kg if necessary), dosing and that doses of diuretics should be or sodium nitroprusside at quantify hypoxemia and monitor treatment adjusted in collaboration with the 𝜇 response. 1–10 g/kg/minute. Both drugs require r veterinarian. Abdominocentesis/Pleurocentesis—a r blood pressure monitoring and should be Possible adverse side reactions of considered only in hospitalized dogs when modified transudate is characteristic of CHF. medications. r monitored by a specialist. Electrocardiographic Findings ◦ r How to monitor resting/sleeping respiratory Dobutamine (dogs, 1–10 𝜇g/kg/minute; Sinus tachycardia is common in patients rates at home, and at which rate new contact cats, 1–5 𝜇g/kg/minute). with CHF. with the clinician should be initiated. ◦ Dopamine (1–10 𝜇g/kg/minute). r r r May show evidence of LA enlargement (P Diet (if indicated)—emphasize the Antiarrhythmics—as needed. r mitrale) or LV enlargement (tall and wide R importance of avoiding cardiac cachexia by Severe ascites may require abdominal waves). r paying close attention to appetite and using paracentesis. Supraventricular, most commonly atrial an appropriate diet. Chronic CHF (Typically Treated as fibrillation, or ventricular arrhythmias may SURGICAL CONSIDERATIONS Outpatient) develop in severe disease. r Surgical valve replacement and purse-string Exact composition of medical therapy PATHOLOGIC FINDINGS depends on disease severity and clinical signs. r suture techniques to reduce the area of the Gross valvular changes range from only a mitral valve orifice have been used; experience All dogs with CHF require life-long treatment few discrete nodules at the line of closure to with these techniques and access usually with a diuretic, such as furosemide. ◦ gross distortion of the valve by gray-white limited. Mild to moderate CHF: 1 mg/kg q24h to nodules and plaques causing contraction of 3–4 mg/kg q8h PO. the cusps and rolling of the free edge; the ◦ Moderate to severe CHF: 2–3 mg/kg q12h or higher. chordae are irregularly thickened, with r regions of tapering and rupture. Pimobendan at 0.25 mg/kg q12h PO. r MEDICATIONS r Mild disease—normal cardiac size. More ACEI (i.e., enalapril, benazepril, ramipril). progressed cases—LA and LV dilation. DRUG(S) OF CHOICE Dose and dose interval dependent on ACE Degree of right-sided dilatation variable. Recommended treatment depends on the inhibitor used (enalapril [0.5 mg/kg r The degree of LV hypertrophy may be stage of the disease; these recommendations q12–24h], benazepril [0.25–0.5 mg/kg apparent only on weighing the heart. follow the guidelines set by the consensus q24h]). r r Jet lesions—irregular thickening and statement developed by the ACVIM. Spironolactone at 2 mg/kg q12–24h PO opacity of the atrial endocardium. Patients Without Overt Clinical Signs and/or hydrochlorothiazide at 2–4 mg/kg r q12h PO. Recent and healed LA splits or tears in some (ACVIM Stage B) r patients. r Digoxin at 0.22 mg/m2 q12h PO, or lower. r If no cardiac enlargement, no treatment is r Small thrombi in the LA are rarely seen. currently recommended. Adequate antiarrhythmic treatment if r significant arrhythmia is present. Administering ACE inhibitors to Stage B2 r patients is of unproven efficacy (despite two Sildenafil at 0.5–2 mg/kg in case of clinical trials). Administration of pimobendan pulmonary hypertension. TREATMENT to Stage B2 patients is of unknown value at PRECAUTIONS r APPROPRIATE HEALTH CARE this time. Use digoxin, diuretics, and ACE inhibitors with caution in patients with renal disease. Treat patients that need oxygen support as Patients Showing Overt Clinical Signs r (ACVIM stage C and D) Nitrate tolerance may develop if appropriate inpatients; if stable, patients may be managed 12-hour nitrate-free intervals are omitted at home. Signs of Acute CHF (Often Treated as Inpatient) from the dosing schedule. NURSING CARE r r Furosemide IV, SC, IM, or PO. Dose is Beta-blockers are negative inotropes and Oxygen therapy as needed for hypoxemia. dependent on severity of CHF. may have an acute adverse effect on myocardial function and clinical status. JWST589-A88-89 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:41 279mm×216mm

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POSSIBLE INTERACTIONS ◦ Thereafter once every 3-6 months if the SEE ALSO r r Furosemide potentiates the effects of an patient is stable on the medication. More Atrial Wall Tear r ACE-inhibitor, spironolactone, or a thiazide. severe cases may require more frequent Congestive Heart Failure, Left-Sided r r Nonsteroidal anti-inflammatory drugs monitoring. Congestive Heart Failure, Right-Sided r should be used with caution in patients Monitor BUN and creatinine when ABBREVIATIONS r receiving furosemide and ACEI. diuretics and ACE inhibitors are used in ACE = angiotensin converting enzyme r ALTERNATIVE DRUG(S) combination. Monitor potassium levels, AV = atrioventricular r r Diuretics—add thiazide and/or potassium especially when combinations of CHF = congestive heart failure r sparing diuretic (e.g., spironolactone) in spironolactone, ACE inhibitors and digoxin LA = left atrium r refractory animals. are used. LV = left ventricle r r Torsemide and bumetanide are alternatives POSSIBLE COMPLICATIONS MAVD = myxomatous mitral valve disease r to furosemide. Asymptomatic patients may develop CHF r r Suggested Reading Vasodilators—isosorbide dinitrate can be Recurrent CHF in patients stabilized by Atkins C, Bonagura JD, Ettinger SJ, et al. used in place of nitroglycerin ointment in medical therapy r Guidelines for the diagnosis and treatment patients requiring long-term nitrate Pulmonary hypertension r of canine chronic valvular heart disease. administration. Biventricular CHF in patients with initial J Vet Intern Med 2009, 23:1142–1150. left-sided CHF r Hoijer-Olsen¨ L, Haggstr¨ om¨ J, Pedersen HD. Mild pleural and/or pericardial effusion r Acquired valvular heart disease. In: Ettinger Arrhythmia, most commonly atrial SJ, Feldman E, (eds). Textbook of fibrillation FOLLOW-UP r Veterinary Internal Medicine: Diseases of Rupture of first-order tendinous chord(s), Dogs and Cats. 7th ed. Philadelphia: WB PATIENT MONITORING leading to a flail valve leaflet r r Saunders, 2010, pp 1209–1319. Frequency of reexaminations depends on Atrial tear leading to acquired atrial septal Borgarelli M, Haggstr¨ om¨ J. Canine severity of myxomatous valve disease and defect or cardiac tamponade r degenerative myxomatous mitral valve severity of CHF (if present). Formation of intracardiac thrombus and/or r disease: natural history, clinical presentation Dogs without signs of CHF. myocardial infarction. ◦ and therapy. Vet Clin North Am Small Slight to moderate disease severity: EXPECTED COURSE AND PROGNOSIS Perform echocardiography when a murmur Anim Pract 2010, 40:651–663. The lesions on the AV valves are progressive in is first detected and every 6-12 months Authors Ingrid Ljungvall and Jens Haggstr¨ om¨ nature and myocardial function may worsen, thereafter to document progressive Consulting Editors Larry P. Tilley and necessitating increasing drug dosages; cardiomegaly. A baseline radiograph may be Francis W.K. Smith, Jr. long-term prognosis depends on response to useful. ◦ treatment and stage of heart failure. Moderate to severe disease severity may Client Education Handout require more frequent monitoring. r available online Dogs with signs of CHF: ◦ Once acute CHF has been successfully treated, dogs can be treated at home. MISCELLANEOUS ◦ Reexamination after 1 to 2 weeks of SYNONYMS r therapy (check for signs of decompensated Chronic valvular disease (CVD) r CHF, dehydration, electrolyte imbalance, Chronic mitral valve disease r renal dysfunction, and presence of a Degenerative valvular disease r complication). Moderate to severe disease Degenerative mitral valve disease (DMVD) r severity may require more frequent Myxomatous mitral valve disease (MMVD) r monitoring. Endocardiosis JWST589-A90 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:44 279mm×216mm

158 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Valvular Stenosis

INCIDENCE/PREVALENCE RISK FACTORS Rare Breed predispositions (see above); see “Risk BASICS GEOGRAPHIC DISTRIBUTION Factors” for Endocarditis, Infective; Worldwide permanent transvenous pacing. DEFINITION SIGNALMENT Atrioventricular valvular stenosis is a pathologic narrowing of the mitral or Species tricuspid valve orifice due to valvular dysplasia Dog and cat DIAGNOSIS or an obstructive, supravalvular ring. Breed Predilections r DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY MS is overrepresented in bull terriers and r Newfoundlands, and in Siamese cats. Atrioventricular valvular stenosis must be Atrioventricular stenosis increases the r differentiated from the more common causes resistance to ventricular filling. TS has been reported most often in Old r English sheepdogs and Labrador retrievers. of mitral and tricuspid regurgitation in the Ventricular filling in clinically significant absence of stenosis. These include both disease requires a persistent diastolic pressure Mean Age and Range congenital and acquired lesions of the gradient between atrium and ventricle. Most patients are presented at a young age, r atrioventricular valves and support apparatus. Concomitant valvular regurgitation is although exceptions occur, especially in cats. Acquired lesions that obstruct the inflow common. r Predominant Sex tracts (see “Causes”). Cor triatriatum dexter The increased atrial pressure leads to atrial N/A and cor triatriatum sinister can mimic some dilation, venous congestion, and often to SIGNS of the clinical findings of pure tricuspid and CHF. Pulmonary edema occurs with mitral mitral valve stenosis, respectively. Historical Findings stenosis; whereas ascites, pleural effusion and r Exercise intolerance CBC/BIOCHEMISTRY/URINALYSIS chylothorax can develop in cases of severe r Syncope May be normal or reflect changes related to tricuspid stenosis. r r Exertional dyspnea or tachypnea CHF or drug therapy for CHF. The foramen ovale can remain patent (PFO) r Cough—MS IMAGING in patients with tricuspid stenosis, allowing r Cyanosis right-to-left shunting with signs of cyanotic r Thoracic Radiography heart disease. Abdominal distention—TS r r r Atrial enlargement is the most consistent Partial atrioventricular septal defect Acute posterior paresis—cats with MS and and outstanding feature; may see generalized arterial thromboembolism (primum ASD and abnormal atrioventricular r cardiomegaly, especially with atrioventricular Stunted growth valve) is observed in some cats with r valve regurgitation. supravalvular mitral (ring) stenosis. Hemoptysis from rupture of r r MS—may see pulmonary venous Cardiac output and therefore exercise intrapulmonary vessels—MS congestion and pulmonary edema; capacity are limited with atrioventricular Physical Examination Findings intrapulmonary hemorrhage can be valvular stenosis. r r Soft diastolic murmur with point of misinterpreted as pneumonia or another The atrial pressure increases maximal intensity over the left apex (MS) or parenchymal disease. disproportionally with faster heart rates, right hemithorax (TS). r r TS—may see hepatomegaly; increased thereby creating the risk for “flash” pulmonary Holosystolic murmur of mitral or tricuspid diameter of caudal vena cava. edema in dogs or cats with mitral stenosis. regurgitation is more often detected. r r Echocardiography Development of atrial tachyarrhythmias, r Tachypnea, dyspnea from pulmonary Diagnostic test of choice. especially atrial fibrillation, is associated with edema or pleural effusion. r cardiac decompensation. r Two-dimensional echocardiography reveals r Crackles from pulmonary edema. Pulmonary hypertension can develop r a markedly dilated atrium and attenuated Jugular distention, jugular pulses, ascites, valve excursion during diastole, often with consequent to MS, leading to exercise hepatomegaly with TS or biventricular CHF intolerance and right ventricular hypertrophy. thickened, irregular AV valve leaflets; valve associated with pulmonary hypertension and leaflets may appear to “dome” during diastole. This can be severe, especially in cats with atrial fibrillation in chronic MS. mitral stenosis. r A supravalvular obstructing ring also may be Cyanosis from right to left shunting with evident as well as other lesions (see “Causes” SYSTEMS AFFECTED TS or from venous admixture and pulmonary above). r r Respiratory—with MS—bronchial edema with MS. M-mode studies show an enlarged atrium compression from enlarged left atrium, CAUSES and concordant motion of the AV valve r pulmonary edema from left heart failure; Usually due to congenital dysplasia of the leaflets indicating commissural fusion; the potential for hemoptysis due to rupture of mitral or tricuspid valve. E-to-F slope is decreased. r r pulmonary venous–bronchial venous Supravalvular obstructing rings of tissue Color-flow imaging reveals a turbulent connections; pleural effusion with atelectasis have been associated with atrioventricular diastolic jet that originates proximal to the in tricuspid stenosis or in long-standing MS stenosis; this is especially important in cats. stenotic valve and projects toward the apex of r complicated by pulmonary hypertension or Infective endocarditis, intracardiac the ventricle; AV valve regurgitation is often atrial fibrillation. neoplasia, and hypertrophic cardiomyopathy present. r r Hepatobiliary—with TS—hepatic with scarring are rare causes of acquired AV Spectral Doppler studies show increased congestion, ascites. valve stenosis. diastolic transvalvular flow velocities; r GENETICS Acquired tricuspid stenosis has been prolonged calculated pressure half-time is a r Uncertain in most cases. observed due to fibrous scarring of the hallmark feature; E-wave/A-wave amplitude r Tricuspid valve dysplasia in Labrador tricuspid valve in dogs with transvenous reversal is often evident in cases still in normal pacing leads. sinus rhythm. retrievers has been localized to a defect in dog r chromosome 9 inherited as an autosomal Right-sided chamber enlargements in MS dominant trait with reduced penetrance. with pulmonary hypertension or with chronic atrial fibrillation. 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(Continued) Atrioventricular Valvular Stenosis A

r Concurrent defects such as patent foramen disturbances, especially AF, is also important. Atrial Tachyarrhythmias r ovale, ASD, or bridging septal leaflet. These patients are typically complicated and Digoxin—dogs, 3–5 𝜇g/kg PO q12h; cats, Angiography consultation with a cardiologist is highly one-fourth of a 0.125-mg tablet PO q24–48h; r recommended. Electrocardioversion of atrial adjust dosage based on serum concentrations. Right atrium: injection demonstrates a r markedly dilated atrium in TS; with fibrillation should be considered but advanced Beta-blockers such as atenolol or the concurrent PFO or ASD, opacification of the atrial disease can render the procedure less calcium channel blocker diltiazem for left atrium is also observed following right effective or limit the duration of sinus rhythm. suppression of frequent atrial premature atrial injection. NURSING CARE complexes and for heart rate control in atrial r Might visualize thickened, irregular valve Sedation with butorphanol is appropriate for tachyarrhythmias such as atrial leaflets or a stenotic valve funnel. dyspneic patients. Oxygen therapy should be tachycardia/flutter/fibrillation. Beware: using r these drugs in uncontrolled CHF. Ventricular injection often reveal valvular administered to the patient with dyspnea or r regurgitation. Typical atenolol dosages: dogs, r hypoxemia from left-sided congestive heart There can be delayed opacification ofthe failure. Fluid therapy is typically 0.25–1.0 mg/kg q12h; cats, 6.25–12.5 mg/cat q12–24h; start low and titrate to effect. ventricles and great vessels. contraindicated in the patient with overt r Diltiazem dosages: dogs, 2–6 mg/kg daily in Cardiac Catheterization CHF except in cases of moderate to severe r azotemia, renal compromise, or severe two (long-acting diltiazem) or three divided A diastolic pressure gradient is identified dosages; start low and titrate to effect); cats, between the atrium and ventricle. A large “A” dehydration. Therapeutic paracentesis may be considered in the patient with pleural 7.5 mg diltiazem HCl PO q8h.. Higher wave is common if atrial function is preserved. dosages are sometimes needed. r effusions or tympanic ascites. r High left atrial, pulmonary capillary wedge, Sotalol for intractable/recurrent and pulmonary artery pressures occur in MS. ACTIVITY r arrhythmias—dogs, 1–2 mg/kg PO q12h; High right atrial and central venous Exercise restriction is important cats, 10–20 mg/cat q12h. pressures are present in TS. r r recommended for any animal with this Dogs can be referred for Ventricular pressure may be normal in the condition because tachycardia increases the electrocardioversion to convert AF to sinus absence of concurrent defects. mean gradient across the stenotic valve rhythm (with follow-up therapy with sotalol DIAGNOSTIC PROCEDURES predisposing to pulmonary edema or venous or amiodarone); however, reversion back to Electrocardiography congestion. Cage rest for patients with CHF. AF is common owing to marked atrial r Variable enlargement and ventricular DIET dilatation. conduction patterns are observed. Widened Feed a sodium-restricted diet to patients in Pulmonary Hypertension or tall P-waves are commonly observed. CHF. r r Sildenafil—dogs, 0.5–3 mg/kg PO q8–12 Splintered R-waves are present in some dogs CLIENT EDUCATION hours. with tricuspid dysplasia. r The client must be advised of symptoms PRECAUTIONS Axis deviation due to hypertrophy or r associated with CHF and the urgency of As a general rule pimobendan is relatively ventricular conduction disturbances is treatment, particularly with left-sided CHF. contraindicated in pure valvular stenosis; relatively common in cats with mitral valve The likelihood of recurrent bouts of CHF however, many dogs and cats with advanced malformation. r should also be discussed. Development of CHF have been treated with this drug with Ectopic rhythms, especially of atrial origin, atrial fibrillation can lead to marked apparent success, especially when there is are often observed. Atrial fibrillation is the dcompensation. combined stenosis/regurgitation of the valve. most important rhythm disturbance as atrial r Use ACE inhibitors or other vasodilators contribution to filling is lost and the R toR SURGICAL CONSIDERATIONS r judiciously in patients with CHF; cardiac intervals vary with short cycles increasing the Surgical valve replacement or repair requires output is limited and vasodilation may induce mean diastolic gradient. cardiopulmonary bypass or hypothermia; hypotension. Monitor arterial blood pressure PATHOLOGIC FINDINGS cost, availability, and high complication and r mortality rates are greatly limiting factors. and renal function. r The atrioventricular valve is abnormal, with Balloon valvuloplasty is an alternative POSSIBLE INTERACTIONS thickened leaflets and fused commissures. r referral treatment and has been used Furosemide and ACE inhibitors can affect Other lesions may be identified such as a successfully for managing some cases of AV kidney function, alter blood electrolytes, and supra-mitral ring (see “Causes”). r stenosis. reduce blood pressure; these parameters Many cases also have abnormal chordae should be monitored. tendineae and papillary muscles. r r Sildenafil can also reduce systemic blood Atrial dilation and hypertrophy are pressure and should not be used with common. r nitroglycerin paste or other nitrates. Patent foramen ovale with TS or partial MEDICATIONS atrioventricular septal defect (primum ASD DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) and bridging septal leaflet) with supravalvular Spironolactone (2 mg/kg PO q12–24h) CHF mitral (ring) stenosis. r should be considered as an ancillary diuretic Furosemide—dogs, 2–6 mg/kg IV, IM, SC, and for its antifibrotic benefit (as an PO q8–24h; cats, 1–4 mg/kg IV, IM, SC, PO aldosterone antagonist). q8–24h. r ACE inhibitor—enalapril—dogs, TREATMENT 0.25–0.5 mg/kg PO q12h; cats, APPROPRIATE HEALTH CARE 0.25–0.5 mg/kg PO q12–24h; see below under “Follow-Up” for patient monitoring. FOLLOW-UP Patients in overt CHF should be treated with r Nitroglycerin paste (1/4 to 1 inch topically PATIENT MONITORING inpatient medical management. Surgical or r catheter-based interventions can be q12h) to reduce pulmonary venous pressures, Thoracic radiographs for pulmonary edema considered once heart failure has been but this has not been evaluated critically. or pleural effusion. stabilized. Control of heart rhythm JWST589-A90 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:44 279mm×216mm

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r Echocardiography with Doppler studies—to ABBREVIATIONS r estimate pulmonary pressures and subjectively ACE = angiotensin converting enzyme r assess right heart function if on sildenafil. AF = atrial fibrillation r MISCELLANEOUS r Digoxin level—check 7–10 days following AV = atrioventricular r institution of therapy; 8- to 12-hour trough ASSOCIATED CONDITIONS CHF = congestive heart failure r should be 0.8–1.5 ng/mL. ECG = electrocardiogram r Concurrent congenital defects are common r Renal function, electrolyte status, and MS = mitral stenosis (e.g., subaortic stenosis in MS, PFO in TS; r arterial blood pressure when on diuretic PFO = patent foramen ovale primum ASD in cats with supravalvular r and/or ACE inhibitor. TS = tricuspid stenosis r mitral (ring) stenosis). Standard rhythm ECG or Holter PREGNANCY/FERTILITY/BREEDING Suggested Reading (ambulatory ECG) if arrhythmias are present. The possibility that this may be a heritable Arndt JW, Oyama MA. Balloon valvuloplasty POSSIBLE COMPLICATIONS r defect must be considered in assessing of congenital mitral stenosis. J Vet Cardiol CHF r suitability of the animal for breeding, 2013, 15:147–151. Atrial fibrillation r particularly in breeds with a predilection for Boon JA. Veterinary Echocardiography. 2nd Syncope r this defect. The additional hemodynamic ed. Wiley-Blackwell, 2011, pp.507–515. Arterial thromboembolism—cats with MS r burden of gestation may be poorly tolerated Brown WA, Thomas WP. Balloon Pulmonary hemorrhage with MS by an already compromised heart. In general valvuloplasty of tricuspid stenosis in a EXPECTED COURSE AND PROGNOSIS breeding is strongly discouraged. Labrador Retriever. J Vet Intern Med 1995, r Morbidity is high; except for mild cases, SYNONYMS 9:419–424. Campbell FE, Thomas WP. Congenital prognosis is generally poor once an animal Atrioventricular valve dysplasia with stenosis; supravalvular mitral stenosis in 14 cats. J Vet becomes symptomatic. However, some supravalvular mitral ring. Cardiology 2012, 14:281–292. animals will live for many years even with SEE ALSO relatively severe stenosis of the mitral or r Lehmkuhl LB, Ware WA, Bonagura JD. Atrioventricular Valve Dysplasia tricuspid valve. r Mitral stenosis in 15 dogs. J Vet Intern Med r Surgical intervention or balloon Endocarditis, Infective 1994, 8:2–17. valvuloplasty might alter course of disease, Stamoulis ME, Fox PR. Mitral valve stenosis but data are limited. in three cats. J Small Anim Pract 1993, 34:452–456. Authors Lora S. Hitchcock and John D. Bonagura Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr. JWST589-A91 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:48 279mm×216mm

Canine and Feline, Sixth Edition 161 Azotemia and Uremia A

coma, impaired thermoregulation Post-renal Azotemia (hypothermia). Urinary obstruction; rupture of the excretory r BASICS Ophthalmic—scleral and conjunctival pathway. injection, retinopathy, acute-onset blindness. r RISK FACTORS DEFINITION Respiratory—dyspnea. r r r Medical conditions—kidney disease, Azotemia is an excess of urea, creatinine, or Skin/Exocrine—pallor, bruising, increased hypoadrenocorticism, low cardiac output, other non-protein nitrogenous substances in shedding, unkempt appearance, loss of hypotension, fever, sepsis, polyuria, liver blood, plasma, or serum. normal sheen to coat. r disease, pyometra, hypoalbuminemia, Uremia is the polysystemic toxic syndrome SIGNALMENT dehydration, acidosis, exposure to that results from marked loss in kidney Dog and cat nephrotoxic chemicals, gastrointestinal functions. Uremia occurs simultaneously in SIGNS hemorrhage, urolithiasis, urethral plugs in animals with increased quantities of urine cats, urethral trauma, and neoplasia. r constituents in blood (azotemia), but General Comments Advanced age may be a risk factor. r azotemia may occur in the absence of uremia. Azotemia may not be associated with Drugs—potentially nephrotoxic drugs, PATHOPHYSIOLOGY historical or physical abnormalities. Unless nonsteroidal anti-inflammatory drugs, r patient has uremia, clinical findings are Azotemia can be caused by (1) increased diuretics, antihypertensive medications; limited to the disease responsible for azotemia. failure to adjust dosage of drugs primarily production of non-protein nitrogenous Findings described here are those of uremia. substances, (2) decreased glomerular filtration eliminated by the kidneys to correspond with Historical Findings rate, or (3) reabsorption of urine that has r decline in renal function. Weight loss r escaped from the urinary tract into the r Toxins—ethylene glycol, grapes (dogs), lilies Declining appetite or anorexia bloodstream. High production of non-protein r (cats). Reduced activity nitrogenous waste substances may result from r Depression high intake of protein (diet or gastrointestinal r Fatigue bleeding) or accelerated catabolism of r Weakness endogenous proteins. Glomerular filtration r DIAGNOSIS Vomiting rate may decline because of reduced renal r Diarrhea DIFFERENTIAL DIAGNOSIS perfusion (prerenal azotemia), acute or r r Halitosis Dehydration, poor peripheral perfusion, chronic kidney disease (renal azotemia), or r Constipation low cardiac output, history of recent fluid urinary obstruction (post-renal azotemia). r Polyuria loss, high protein diet, or black, tarry Reabsorption of urine into the systemic r Changes in urine volume (increase or stools—rule out prerenal azotemia. circulation may also result from leakage of r decrease) Recent onset of altered urine output (high urine from the excretory pathways (also a r form of post-renal azotemia). Poor haircoat or unkempt appearance or low), clinical signs consistent with uremia, r Pathophysiology of uremia—incompletely Physical Examination Findings exposure to possible nephrotoxicants or r understood; may be related to (1) metabolic Muscle wasting: sarcopenia/cachexia ischemic renal injury, or kidney size normal or r and toxic systemic effects of waste products Mental depression enlarged—rule out acute renal failure. r r retained because of renal excretory failure, Dehydration Progressive weight loss, polyuria, polydipsia, r (2) deranged renal regulation of fluids, Weakness small kidneys, disparate kidney size (cats—big r electrolytes, and acid-base balance, and Pallor kidney and little kidney), pallor, and signs of r (3) impaired renal production and Petechiae and ecchymoses uremia that have developed over several weeks r degradation of hormones and other Dull and unkempt haircoat to months—rule out chronic renal failure. r r substances (e.g., erythropoietin and Uremic breath Abrupt decline in urine output and onset of r 1,25-dihydroxycholecalciferol). Uremic stomatitis (including oral ulcers, signs of uremia; disparate kidney size infarctions of the tongue) (cats—big kidney and little kidney), SYSTEMS AFFECTED r r Scleral and conjunctival injection occasionally dysuria, stranguria, and Uremia affects virtually every body system. r r Relative hypothermia hematuria; large urinary bladder or fluid-filled Cardiovascular—arterial hypertension, left abdomen—rule out post-renal azotemia. ventricular hypertrophy, heart murmur, CAUSES CBC/BIOCHEMISTRY/URINALYSIS cardiomegaly, cardiac rhythm disturbances. Prerenal Azotemia r r CBC Endocrine/Metabolic—renal secondary Reduced renal perfusion due to low blood r hyperparathyroidism, inadequate production volume or low blood pressure. Nonregenerative anemia (normocytic, r of 1,25-dihydroxycholecalciferol (calcitriol) Accelerated production of nitrogenous waste normochromic)—often present with chronic renal failure. and erythropoietin, hypergastrinemia, weight products because of enhanced catabolism of r loss. Hemoconcentration—often present with r tissues in association with infection, fever, Gastrointestinal—anorexia, nausea, trauma, corticosteroid excess, or burns. prerenal azotemia; can also be seen with acute r vomiting, diarrhea, uremic stomatitis, Increased gastrointestinal digestion and renal failure and post-renal azotemia. xerostomia, uremic breath, constipation. absorption of protein sources (diet or Biochemistry r r Hemic/Lymph/Immune—anemia and gastrointestinal hemorrhage). Serial determinations of serum urea immunodeficiency. r Renal Azotemia nitrogen and creatinine concentrations may Neuromuscular—dullness, drowsiness, Acute or chronic kidney diseases (primary help differentiate the cause of azotemia. lethargy, fatigue, irritability, tremors, gait kidney disease affecting glomeruli, renal Appropriate therapy to restore renal perfusion imbalance, flaccid muscle weakness, tubules, renal interstitium, and/or renal typically yields a dramatic reduction in myoclonus, behavioral changes, dementia, vasculature) that impair at least 75% of azotemia in patients with prerenal azotemia isolated cranial nerve deficits, seizures, stupor, kidney function (glomerular filtration rate). (typically within 24–48 hours). Correcting JWST589-A91 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:48 279mm×216mm

162 Blackwell’s Five-Minute Veterinary Consult

A Azotemia and Uremia (Continued)

obstruction to urine flow or a rent in the urinary obstruction or rupture of the excretory pathway typically is followed by a excretory pathway. rapid reduction in the magnitude of azotemia. r DIAGNOSTIC PROCEDURES MEDICATIONS Concurrent hyperkalemia may be consistent Renal biopsy can be used to confirm the with post-renal azotemia, primary renal DRUG(S) OF CHOICE diagnosis of primary kidney disease, to r azotemia due to oliguric renal failure, or differentiate acute from chronic kidney Symptomatic therapy may be indicated for prerenal azotemia associated with disease, and to attempt to establish the uremia in patients with kidney disease. hypoadrenocorticism. r r underlying disease process responsible for Famotidine (0.5–1.0 mg/kg PO, SC, IM, Increased serum albumin and globulin primary kidney disease. IV q12–24h) or other H2-receptor concentration suggest prerenal azotemia or a antagonists may be used to reduce gastric prerenal component.s hyperacidity and nausea (dogs). r Urinalysis Antiemetics such as maropitant (1 mg/kg r A urine specific gravity value ≥ 1.030 in q24h PO or SC for 5 days) are indicated for ≥ TREATMENT dogs and 1.035 in cats supports a diagnosis r vomiting. of prerenal azotemia. Administration of fluid Prerenal azotemia caused by impaired renal CONTRAINDICATIONS therapy before urine collection may interfere perfusion—correct the underlying cause of Administration of nephrotoxic drugs renal hypoperfusion; aggressiveness of with interpretation of low specific gravity PRECAUTIONS values. treatment depends on the severity of the r r Azotemic patients that have not been underlying condition and the probability that Use caution when administering drugs treated with fluids and have urine specific persistent renal hypoperfusion will lead to requiring renal excretion. Consult appropriate < < primary renal injury or failure. references concerning dose-reduction gravity 1.030 in dogs and 1.035 in cats r typically have primary renal azotemia. A Primary renal azotemia and associated schedules or adjustments of maintenance intervals. notable exception to this rule is dogs and cats uremia—(1) specific therapy directed at r with glomerular disease. Glomerulopathy is halting or reversing the primary disease Use caution in administering fluids to sometimes characterized by glomerulotubular process affecting the kidneys, and (2) patients that are oliguric or anuric. Monitor imbalance in which adequate urine- symptomatic, supportive, and palliative urine production rates and body weight concentrating ability may persist despite therapies that ameliorate clinical signs of during fluid therapy to minimize the likelihood of inducing overhydration. sufficient renal glomerular damage to cause uremia; minimize the clinical impact of r primary renal azotemia; these patients are deficits and excesses in fluid, electrolyte, Stop fluid therapy in overhydrated recognized by moderate to marked proteinuria acid-base balances; minimize the effects of oliguric/anuric patients. Use caution in in the absence of hematuria and pyuria. inadequate renal biosynthesis of hormones administering drugs that may promote r Urine specific gravity is not useful in and other substances, and maintain adequate hypovolemia or hypotension (e.g., diuretics); identifying post-renal azotemia. nutrition. carefully monitor the response to such drugs r by assessing hydration status, peripheral OTHER LABORATORY TESTS Post-renal azotemia—eliminate urinary obstruction or repair rents in the excretory perfusion, and blood pressure, with serial Endogenous or exogenous creatinine, iohexol, evaluation of renal function tests. pathway; supplemental fluid administration is r or inulin clearance tests or other specific tests often required to prevent dehydration that Corticosteroids may worsen azotemia by of glomerular filtration rate may be used to may develop during the solute diuresis that increasing catabolism of endogenous proteins. confirm that azotemia is caused by reduced follows correction of post-renal azotemia. ALTERNATIVE DRUG(S) glomerular filtration rate. r Fluid therapy—indicated for most azotemic N/A IMAGING patients; preferred fluids include 0.9% saline r Abdominal radiographs—used to determine or lactated Ringer’s solution. Determine fluid kidney size (small kidneys consistent with volume to administer on the basis of severity chronic kidney disease; mild-to-moderate of dehydration or volume depletion. If no FOLLOW-UP enlargement of kidneys may be consistent clinical dehydration is evident, cautiously with acute renal failure or urinary assume that the patient is less than 5% PATIENT MONITORING obstruction) and to rule out urinary dehydrated and administer a corresponding Serum urea nitrogen and creatinine obstruction (marked dilation of the urinary volume of fluid. Generally provide 25% of concentrations 24 hours after initiating fluid bladder or mineral densities within the calculated fluid deficit in the first hour. administration; also urine production, body excretory pathway). Thereafter, serially monitor perfusion r weight, and hydration status. Ultrasonography—may detect changes in (capillary refill time, pulse pressure, heart rate, POSSIBLE COMPLICATIONS echogenicity of the renal parenchyma and size and temperature of feet), blood pressure and r and shape of kidneys that support a diagnosis urine output to assess adequacy of fluid Failure to correct prerenal azotemia caused of primary renal azotemia; useful to rule out therapy. If perfusion has not improved, by renal hypoperfusion rapidly could result in ischemic primary kidney disease. post-renal azotemia characterized by additional fluid should be administered. r distension of the excretory pathway and Provide the remaining fluid deficit over the Primary renal azotemia can progress to uremia. uroliths or masses within or impinging on the next 12–24 hours. Fluid therapy should be r excretory pathway and intra-abdominal fluid cautiously administered to patients with overt Failure to restore normal urine flow in accumulation (with rupture of the excretory or suspected cardiac failure and patients that patients with post-renal azotemia can result in pathway). are oliguric or anuric. progressive renal damage or death due to r r Excretory urography, pyelography, or Treat patients in shock appropriately. hyperkalemia and uremia. r cystourethrography—may help establish the Consider feeding diets formulated for diagnosis of post-renal azotemia due to kidney disease to reduce the magnitude of azotemia, hyperphosphatemia, and acidosis. JWST589-A91 JWST589-Tilley Printer: Yet to Come August 3, 2015 10:48 279mm×216mm

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(Continued) Azotemia and Uremia A

patients are also at higher risk for prerenal and INTERNET RESOURCES post-renal causes for azotemia. International Renal Interest Society (IRIS): MISCELLANEOUS ZOONOTIC POTENTIAL www.iris-kidney.com. Leptospirosis ASSOCIATED CONDITIONS Suggested Reading PREGNANCY/FERTILITY/BREEDING Polzin D. Chronic kidney disease. In: Ettinger An association may exist between r Data on azotemia and pregnancy in dogs SJ, Feldman EC, eds., Textbook of hypokalemia and azotemia in cats. Veterinary Internal Medicine, 7th ed. Preliminary findings suggest that hypokalemia and cats are very limited. Humans may tolerate minimal renal disease well during Philadelphia: Saunders, 2010, pp. may be associated with functional or 2036–2067. structural renal changes leading to azotemia. pregnancy; however, ability to sustain a viable pregnancy declines as renal function declines. Ross L. Acute renal failure. In: Bonagura JD, AGE-RELATED FACTORS r Pregnant azotemic animals—pharmacologic Twedt DC, Kirk’s Veterinary Therapy XIV. Primary renal failure may occur in animals of agents excreted by non-renal pathways are Philadelphia: Saunders, 2009, pp. 879–882. any age, but geriatric dogs and cats appear to preferred. Author David J. Polzin be at substantially higher risk for both acute Consulting Editor Carl A. Osborne SEE ALSO and chronic kidney disease. However, do not r assume that azotemia in geriatric dogs and Chapters on acute and chronic kidney disease cats indicates primary kidney disease; these r Urinary Tract Obstruction