BLBS078-CF_A01 BLBS078-Tilley July 23, 2011 2:42

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

r r loss, discovery of fetal material, behavior Urethral obstruction Intestinal foreign r change, anorexia, vomiting, diarrhea. body, pancreatitis, peritonitis Trauma r BASICS Physical Examination Findings Impending parturition or dystocia Purulent, mucoid, watery, or sanguinous CBC/BIOCHEMISTRY/URINALYSIS DEFINITION r r r vaginal discharge; dehydration, fever, May be normal. Inflammatory leukogram Spontaneous abortion—natural expulsion abdominal straining, abdominal discomfort. or stress leukogram depending on systemic r of a fetus or fetuses prior to the point at which CAUSES disease response. Hemoconcentration and they can sustain life outside the uterus. r Infectious azotemia with dehydration. Early pregnancy loss—generalized term for r OTHER LABORATORY TESTS any loss of conceptus including early Bacterial—Salmonella spp., Chlamydia, Brucella; organisms implicated in causing Infectious Causes embryonic death and resorption. r PATHOPHYSIOLOGY abortion via ascending infection include Cytology and bacterial culture of vaginal r Escherichia coli, Staphylococcus spp., discharge, fetus, fetal membranes, or uterine Infectious causes result in pregnancy loss by Streptococcus spp., Pasteurella spp., Klebsiella contents (aerobic, anaerobic, and r directly affecting the embryo, fetus, or fetal spp., Pseudomonas spp., Salmonella spp., mycoplasma). FeLV—test for antigens in membranes, or indirectly by creating Mycoplasma spp., and Ureaplasma spp. r r queens using ELISA or IFA. FHV-1—IFA debilitating systemic disease in the queen. Protozoal—Toxoplasma gondii— r r or PCR from corneal or conjunctival swabs, Non-infectious causes of pregnancy loss uncommon. Viral—FHV-1; FIV; FIPV; viral isolation from conjunctival, nasal, or r result from any factor other than infection FeLV;FPLV—virusesarethemostreported pharyngeal swabs. FIPV—PCR for mRNA that leads to the death or premature expulsion cause of infectious abortion in the queen. of the M gene of feline coronavirus of the conceptus (e.g., inadequate maternal Non-infectious (Molecular Diagnostics, College of Veterinary nutrition, endocrine dysfunction, toxicity, r Medicine, Auburn University, genetic defects). Uterine—CEH-pyometra complex, chronic endometritis, mechanical trauma to uterus or http://www.vetmed.auburn.edu/ SYSTEMS AFFECTED r feline infectious peritonitis virus2). r r r fetus. Ovarian—hypoluteoidism; genetic r Endocrine Reproductive Other FIV—ELISA—confirm positive results with defects are more prevalent; early termination r systems—any debilitating illness can result in of corpora lutea function causes a decline in Western blot. FPLV—viral isolation from pregnancy loss. serum progesterone concentrations, resulting fetuses submitted for necropsy; document r GENETICS in early parturition (abortion). Fetal— seroconversion in the queen. Genetic defects more prevalent in highly chromosomal abnormalities resulting in Non-infectious Causes abnormal or arrested development and r inbred individuals; heritability of r Hypoluteoidism—serum progesterone susceptibility to FIPV very high. embryonic or fetal death. Systemic—taurine levels; low levels do not indicate a primary deficiency; vitamin A deficiency or toxicity; cause unless documented prior to the INCIDENCE/PREVALENCE r malnutrition; severe non-reproductive illness; abortion. To rule out anovulatory cycle, Unknown—pregnancy frequently not exogenous drug administration: estrogens, confirm progesterone rise greater than 1.5 ng/ confirmed, owners may not recognize late r glucocorticoids, prostaglandin F2α,and ml 1 week following mating. Behavioral pregnancy loss if the queen is fastidious; early dopamine agonists (cabergoline, evidence of estrus and vaginal cytology can embryonic death is difficult to document; bromocriptine) will disrupt normal corpus confirm estrus; repeatedly obtaining vaginal genetic abnormalities account for ∼15% of luteum function; fetotoxic or teratogenic cytology samples may induce ovulation. pregnancy loss in cats, including abortion. drugs: chemotherapeutic agents, anti-fungal IMAGING SIGNALMENT agents (griseofulvin), steroids, some r Abdominal ultrasound—confirm antibiotics (trimethoprim-sulfonamides, Species pregnancy; screen for evidence of resorption; quinolones, tetracyclines, gentamicin), Cats evaluate health and viability of fetus(es) and antiepileptic medications (phenytoin); Breed Predilections associated fluid and membranes; abnormal modified live vaccines. Purebred cats—higher incidence of uterine fluid accumulation and RISK FACTORS r non-infectious abortion; in-breeding increases r non-reproductive disease. Radiograph— Previous history of pregnancy loss risk of genetic disease; abortion is a r r evaluates relative size, number, and position of Concurrent systemic disease Recent consequence of certain forms of heritable r fetal skeletons; can be used to screen for fetal trauma Purebred cat with high degree of diseases (lethal genetic defect, fatal r monsters, fetal malpresentation, and COPYRIGHTEDin-breeding Very young or old MATERIAL queen chromosomal error). r r non-reproductive disease. Mean Age and Range Malnourishment Overcrowded or DIAGNOSTIC PROCEDURES unsanitary environment r Infectious abortion seen in all ages; Genetic defects—necropsy aborted non-infectious abortion seen more commonly fetus(es); submit samples from aborted and in young and aged queens. stillborn fetus to lab for karyotyping. r SIGNS Nutrition—submit sample of diet for DIAGNOSIS General Comments nutritional analysis if concerned about taurine or vitamin A levels in diet, of particular Early embryonic death and resorption DIFFERENTIAL DIAGNOSIS r importance when queen is fed a homemade frequently have no clinical symptoms; any Early pregnancy loss ◦ Failure to r r diet. Complete history and evaluation of combination of historical and physical conceive ◦ Anovulatory cycle Vulvar pedigree to calculate coefficient of examination findings may occur, with some discharge ◦ Pyometra, mucometra, uterine r in-breeding. Evaluate cattery for vaccination queens displaying no symptoms. stump pyometra ◦ Vaginitis, metritis, cystitis ◦ Impending parturition or dystocia protocols, feeding regime, general sanitation Historical Findings procedures, and quarantine procedures for ◦ Neoplasia or trauma of urinary bladder, r Failure to deliver litter at expected time, ◦ pregnant queens and new arrivals. Submit return to estrus sooner than expected, urethra, vagina, or uterus Estrus—very little discharge typically seen reproductive tract (uterus, ovaries, uterine decrease in abdominal diameter and weight r Abdominal straining or discomfort tubes) to reproductive pathologist to evaluate for anatomical and pathological changes. BLBS078-CF_A01 BLBS078-Tilley July 23, 2011 2:42

Canine and Feline, Fifth Edition 3 Abortion, Spontaneous (Early Pregnancy Loss)—Cats A

r r Send aborted, stillborn, mummified depending on bacterial culture results. determine stopping point. Serial ultrasound r fetus(es) and fetal membranes (fresh, Dinoprost tromethamine (PGF2α) 0.05– evaluation q 5–7 days to evaluate fetal viability refrigerated, on wet ice) to reproductive 0.2 mg/kg SC Q 6–12 hours for evacuation of for queens receiving tocolytics drugs if not pathologist for gross necropsy, histopathology, uterine contents; continue until uterine monitored daily with tocodynamometry. cultures, and viral isolation; serum from dam; evacuation complete based on PREVENTION/AVOIDANCE r r fetal stomach contents and fetal blood useful. ultrasonographic evaluation. Terbutaline Institute infectious disease prevention, r 0.08–1.0 mg PO as needed based on control, and surveillance plan. Replace tocodynamometry; 0.03 mg/kg PO q8h if r infertile queens with more reproductively fit r tocodynometry not available. Progesterone individuals. Avoid exposure to abortifacient, TREATMENT in oil—2.0–3.0 mg/kg IM as needed based on teratogenic, or fetotoxic drugs. tocodynamometry; q72h if tocodynometry APPROPRIATE HEALTH CARE not available. POSSIBLE COMPLICATIONS r ◦ r r Outpatient management: Typically no CONTRAINDICATIONS Depends on etiology. Metritis, medical management required for r endometritis, uterine rupture, sepsis, shock. r non-infectious stable queens; queens with PGF2α—intended pregnancy, respiratory Diabetes, CEH, masculinization of female compromise, renal compromise, severe infectious disease should be isolated and r fetuses with progesterone treatment. treated appropriately. ◦ Hypoluteoidism— uterine pathology. Terbutaline—cardiac or respiratory disease, pyometra, infectious EXPECTED COURSE AND PROGNOSIS can be managed on an outpatient basis with r r disease, hypertension. Progesterone in oil— Infectious disease—normal pregnancy, tocolytics drugs in combination with repeated abortion, or infertility possible with diabetes, pyometra, infectious disease, CEH. r tocodynamometry if value of queen outweighs viral disease. Poor prognosis for normal potential to perpetuate this possibly heritable PRECAUTIONS r pregnancy in queens with severe CEH. r r condition. Inpatient medical management: Queens tolerate PGF2α treatment well Good prognosis for successful pregnancy ◦ Required for systemic illness and treatment compared to bitches but clients should give r with treatment for hypoluteoidism; significant with prostaglandin F2α. Surgical informed consent prior to instituting therapy; monitoring required for good outcome. ◦ r management: OHE for queens with severe side effects of PGF2α treatment include Pregnancy loss due to genetic abnormalities illness due to pyometra or metritis. panting, salivation, inappetance, urination, likely to recur if queen is bred to tom with ACTIVITY diarrhea, vocalization (calling), nesting, similar pedigree. r Isolation for queens with suspected tachypnea, vomiting, restlessness, and r grooming. Side effects diminish with repeated infectious disease. No activity restrictions r for most non-infectious pregnancy losses. injections. Use of tocolytics to maintain r Restrict activity as indicated for pregnancy pregnancy requires accurate documentation of MISCELLANEOUS loss due to trauma. breeding dates to know when treatment should be discontinued; tocolytics used most AGE-RELATED FACTORS DIET r successfully in combination with Queens > 6 years old have higher incidence r Correct diets with inappropriate taurine or tocodynamometry to establish desired dosing of infertility. Pregnancy loss seen most vitamin A concentrations. interval based on increasing preterm uterine r frequently in very young and old queens. CLIENT EDUCATION activity. Terbutaline can cause hypertension ZOONOTIC POTENTIAL r leading to increased hemorrhage from the Infectious diseases—verify client is Toxoplasma gondii following good vaccination protocols and placental sites during parturition or at the SEE ALSO disease surveillance measures and is utilizing time of c-section. r quarantine facilities for pregnant queens and POSSIBLE INTERACTIONS Breeding, Timing r r new arrivals. Breeding management— Progesterone administration during ABBREVIATIONS r discuss normal reproductive behavior and pregnancy is associated with masculinization CEH = cystic endometrial hyperplasia r good breeding management; advise clients to of female fetuses; do not administer in the ELISA = enzyme-linked immunosorbent r r keep detailed records related to reproductive first half of pregnancy and use with informed assay FeLV = feline leukemia virus FHV-1 r r performance, pedigree analysis, and social consent thereafter. Use of tocolytics to = feline herpesvirus 1 FIPV = feline r behavior of queens within the cattery. maintain pregnancy is associated with infectious peritonitis virus FIV = feline r r Nutrition—discuss routine diet increased risk of dystocia, failure of normal immunodeficiency virus FPLV = feline r recommendations for breeding queens; advise placental separation at parturition, lack of panleukopenia virus IFA = indirect r homemade diets undergo nutritional analysis. mammary gland development and milk fluorescent antibody OHE = r r Genetic disease—increases in in-bred production, and poor maternal behavior for ovariohysterectomy PGF2α = prostaglandin individuals; many reproductive traits are α r the first few days post-partum. F2 heritable. Medical management—discuss ALTERNATIVE DRUG(S) INTERNET RESOURCES side effects of prostaglandin F α (PGF α); r r 2 2 Altrenogest (Regu-Mate, Hoechst-Roussel) www.theriojournal.com medical management should be attempted for r 0.088 mg/kg PO q24h—unpredictable ability www.whelpwise.com young to middle-aged queens with valuable r to maintain pregnancy in the queen. Author Milan Hess reproductive potential. Discuss risk of r Prostaglandin analogues should be avoided Consulting Editor Sara K. Lyle zoonotic disease from Toxoplasma gondii. due to their narrow margin for safety and lack of effective dosing information in the cat. Client Education Handout available online MEDICATIONS DRUG(S) OF CHOICE FOLLOW-UP r Will depend on etiology. PATIENT MONITORING r r Amoxicillin-clavulanic acid 13.75 mg/kg Serial ultrasound evaluation q 5 days for PO q12h or enrofloxacin 5 mg/kg/day PO queens treated with prostaglandin F2αα to BLBS078-CF_A02 BLBS078-Tilley July 14, 2011 8:49

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 Cystic endometrial hyperplasia and for B. canis—very sensitive; negative results r pregnancy. pyometra. Trauma—acute and chronic. reliable; prevalence of false positives as high as r r PATHOPHYSIOLOGY Neoplasia. Embryotoxic drugs. 60%; definitive diagnosis made via culture r r r Chemotherapeutic agents. Estrogens. (D-Tec CB, Synbiotics Corp., Direct causes—congenital abnormality, r r r Glucocorticoids—high dosages. 800-228-4305). Tube agglutination test for infectious disease, trauma. Indirect B. canis—gives titers; titers > 1:200 causes—infectious placentitis, abnormal Ovarian r considered positive; titers from 1:50–1:200 ovarian function, abnormal uterine Prostaglandins—lysis of corpora lutea. r r considered suspicious. Agar gel environment. Dopamine agonists—lysis of corpora lutea immunodiffusion test for B. canis—effectively SYSTEMS AFFECTED via suppression of prolactin; bromocryptine, differentiates between false positives and true r r r Reproductive. Any dysfunction of a major cabergoline. Hypoluteoidism—abnormal positives in agglutination tests; detects body system can adversely affect pregnancy. luteal function in the absence of fetal, uterine, cytoplasmic and cell surface antigens (Cornell or placental disease: progesterone GENETICS < University Diagnostic Laboratory, r concentrations 1–2 ng/ml, most often seen r No genetic basis for most causes of abortion. 607-253-3900). Baseline T4 serum r at 40–45 days gestation. Lymphocytic hypothyroidism—single-gene concentration (when no infectious agents are Hormonal Dysfunction recessive trait in borzois. r identified)—hypothyroidism is a common Hypothyroidism; new data shows this is less endocrine disease and has been suggested as a INCIDENCE/PREVALENCE common that previously thought. r r r r cause for fetal wastage; role in pregnancy loss True incidence unknown. Resorption Hyperadrenocorticism. Environmental unclear; subnormal T4 concentrations estimated between 11–13%, some estimates factors—endocrine disrupting contaminants indicate need for further testing (see up to 30% of at least one resorption. r r have been documented in human and wildlife Hypothyroidism). Serum progesterone Incidence of stillbirth reported as 2.2–4.4%; instances of fetal loss. concentration (when no infectious agents are increases with dystocia up to 22.3%. Fetal Defects identified)—hypoluteoidism may cause fetal r r SIGNALMENT Lethal chromosomal abnormality. Lethal wastage; dogs depend on ovarian progesterone Species organ defects. production throughout gestation (minimum Dogs RISK FACTORS of 2 ng/mL required to maintain pregnancy); r collect sample and determine as soon as Breed Predilections Exposure of the brood bitch to carrier r r r possible after abortion; in subsequent Familial lymphocytic hypothyroidism animals Old age Hereditary factors pregnancies, start weekly monitoring at week reported in borzois—prolonged interestrus 3, which may be before pregnancy can be interval, poor conception rates, abortion r documented with ultrasound; start biweekly midgestation, stillbirths. Many breeds sampling around the gestational age of considered at risk for familial hypothyroidism DIAGNOSIS previous loss. Pregnancy loss typically occurs (see Hypothyroidism). during the seventh week of gestation (see DIFFERENTIAL DIAGNOSIS r Mean Age and Range r Premature Labor). Vaginal culture—B. canis r Differentiate infectious from non-infectious Infectious causes, pharmacological agents with positive serologic test; Mycoplasma, causes—B. canis of immediate and zoonotic causing abortion, fetal defects—seen in all r Ureaplasma, other bacterial agents; all except r concern. Differentiate resorption from ages. Cystic endometrial hyperplasia— B. canis can be normal flora, therefore infertility—helped by early diagnosis of usually > 6 years old. r diagnosis difficult from vaginal cultures alone; pregnancy. History of drug use during Salmonella associated with systemic illness in Predominant Sex pregnancy—particularly during the first the bitch. Intact bitches trimester, or use of drugs (e.g., dexamethasone, SIGNS IMAGING prostaglandins, ketoconazole, griseofulvin, r Historical Findings doxycycline, tetracycline, dantrolene, among Radiography—identifies fetal structures r r r after 45 days of gestation; earlier, can Failure to whelp on time. Expulsion of others) known to cause fetal death. Vulvar determine uterine enlargement but cannot recognizable fetuses or placental tissues. discharges during diestrus—may mimic r assess uterine contents. Decrease in abdominal size; weight loss. abortion; evaluate discharge and origin to r r r Ultrasonography—identifies uterine size Anorexia. Vomiting, diarrhea. differentiate uterine from distal reproductive r r and contents; assesses fluid and its Behavioral changes. tract disease. Necropsy of aborted fetus, stillborn puppies, and placenta(s)—enhances consistency; assesses fetal remains or fetal Physical Examination Findings > r chances of a definitive diagnosis, refrigerate viability by noting heartbeats (normal, 200 Sanguineous or purulent vulvar discharge. but do not freeze prior to submission. bpm; stress, < 150 or > 280 bpm). r r Disappearance of vesicles or fetuses History of systemic or endocrine DIAGNOSTIC PROCEDURES previously documented by palpation, r disease—may indicate problems with the r ultrasonography, or radiography. Abdominal Vaginoscopy—identify source of vulvar r maternal environment. straining, discomfort. Depression. discharges and vaginal lesions; use a scope of r r CBC/BIOCHEMISTRY/URINALYSIS sufficient length (16–20 cm) to examine the Dehydration. Fever in some patients. r r r entire length of the vagina. Cytologic CAUSES Usually normal. Systemic disease, uterine infection, viral infection, or endocrine examination and bacterial culture—vagina Infectious may reveal an inflammatory process (e.g., r r abnormalities—may produce changes in Brucella canis. Canine herpesvirus. uterine infection); technique for culture: use a r CBC, biochemistries, or urinalysis. Toxoplasma gondii, Neospora caninum. guarded swab culture instrument to ensure an BLBS078-CF_A02 BLBS078-Tilley July 14, 2011 8:49

Canine and Feline, Fifth Edition 5 Abortion, Spontaneous (Early Pregnancy Loss)—Dogs A

anterior sample (distal reproductive tract is vaccines (e.g., some distemper, parvovirus, normally heavily contaminated with bacteria), etc., vaccines). or collection of secretions via transcervical MEDICATIONS POSSIBLE COMPLICATIONS r catheterization. Untreated pyometra—septicemia, toxemia, DRUG(S) OF CHOICE r PATHOLOGIC FINDINGS r death. Brucellosis—diskospondylitis, Histopathologic examination and culture of PGF2α (Lutalyse, dinoprost endophthalmitis, recurrent uveitis. tromethamine)—uterine evacuation after fetal and placental tissue—may reveal EXPECTED COURSE AND PROGNOSIS infectious organisms; tissue culture, abortion; 0.05–0.1 mg/kg SC q8–24h; r cloporostenol (Estrumate, cloprostenol)—1–5 Pyometra—recurrence rate during particularly of stomach contents, to identify μ subsequent cycle is high (up to 70%) unless infectious bacterial organisms. g/kg SC q24h; not approved for use in dogs, r but adequate documentation legitimizes its pregnancy is established. CEH—recovery of use; use only if all living fetuses have been fertility unlikely; pyometra common r r expelled. Antibiotics—for bacterial disease; complication. Hormonal dysfunction— often manageable; familial aspects should be initially institute broad-spectrum agent; r TREATMENT specific agent depends on culture and considered. Brucellosis—guarded; extremely APPROPRIATE HEALTH CARE sensitivity testing of vaginal tissue or necropsy difficult to successfully eliminate infection r r Most bitches should be confined and of fetus. Progesterone (Regu-Mate) at 0.088 even if combined with neutering. r isolated pending diagnosis. Hospitalization mg/kg (1 mL/25 kg PO) or progesterone in r of infectious patients preferred. B. canis— oil at 2 mg/kg IM q48–72h—for documented highly infective to dogs; shed in high numbers hypoluteodism only to maintain pregnancy, during abortion; suspected cases should be must have accurate due date to know when to MISCELLANEOUS r isolated. Outpatient medical discontinue therapy—inadvertently AGE-RELATED FACTORS prolonging gestation will result in fetal death. management—medically stable patients with Older bitches more likely to have CEH non-infectious causes of pregnancy loss, CONTRAINDICATIONS ZOONOTIC POTENTIAL endocrinopathies, or endometrial disease. Progestogen supplementation— r B. canis—can be transmitted to humans, Partial abortion—may attempt to salvage contraindicated in dogs with endometrial or especially when handling the aborting bitch the live fetuses; administer antibiotics if a mammary gland disease. bacterial component is identified. and tissues expelled; massive numbers of PRECAUTIONS organisms expelled during abortion. NURSING CARE PGF2α—metabolized in the lung; side effects Pathologists should be warned when B. canis Dehydration—use replacement fluids, are related to smooth muscle contraction, are is suspected. People that are supplemented with electrolytes if imbalances dose-related, and diminish with each immunocompromised are at greatest risk for are identified by serum biochemistries. injection; panting, salivation, vomiting, and infection. ACTIVITY defecation common; dosing critical (LD50 for SEE ALSO dinoprost—5 mg/kg). r r r Partial abortion—cage rest generally Brucellosis Hypothyroidism Infertility, r r recommended, although the positive effect on ALTERNATIVE DRUG(S) Female—Dogs Premature Labor Pyometra reducing further abortion is unknown. Oxytocin—1 U/5 kg SC q6–24h for uterine and Cystic Endometrial Hyperplasia DIET evacuation; most effective in the first 24–48 ABBREVIATIONS hours after abortion. r No special dietary considerations for CEH = cystic endometrial hyperplasia uncomplicated cases r r OHE = ovariohysterectomy PGF2α = CLIENT EDUCATION prostaglandin F α r 2 Critical for B. canis—if confirmed, FOLLOW-UP INTERNET RESOURCES euthanasia recommended due to lack of Root-Kustritz MV. Use of supplemental successful treatment and to prevent spread of PATIENT MONITORING r progesterone in management of canine infection; may try OHE and long-term Partial abortion—monitor viability of pregnancy. In: Concannon PW, England G, antibiotics; discuss surveillance program for remaining fetuses with ultrasonography; Verstegen III J, Linde-Forsberg C, eds., kennel situations: monthly serology for all monitor systemic health of the dam for r Recent Advances in Small Animal individuals, culling any positive animals, until remainder of pregnancy. Vulvar Reproduction. International Veterinary three consecutive negative tests are obtained; r discharges—daily; for decreasing amount, Information Service, Ithaca NY, www.ivis.org, discuss zoonotic potential. Primary uterine odor, and inflammatory component; for 2001; A1220.0401 disease—OHE is indicated in patients with consistency (increasing mucoid content is r Author Beverly J. Purswell no breeding value; cystic endometrial prognostically good). PGF2α—continued Consulting Editor Sara K. Lyle hyperplasia is an irreversible change. for 5 days or until most of the discharge ceases r r Infertility or pregnancy loss—may recur in (3-15 days). B. canis—monitor after subsequent estrous cycles despite successful Client Education Handout r neutering and antibiotic therapy; yearly immediate treatment. Prostaglandin serologic testing to identify recrudescence. available online treatment—discuss side effects (see Abortion, r r Hypothyroidism—treat appropriately; Termination of Pregnancy). Infectious neutering recommended (hereditary nature); diseases—establish surveillance and control see Hypothyroidism. measures. PREVENTION/AVOIDANCE r SURGICAL CONSIDERATIONS Brucellosis and other infectious agents— OHE—preferred for stable patients with no surveillance programs to prevent introduction r breeding value to kennel. OHE—for bitches with no r breeding value. Use of modified-live BLBS078-CF_A03 BLBS078-Tilley July 14, 2011 9:3

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

r Pregnancy status in early diestrus is unknown; ultrasound confirmation of BASICS DIAGNOSIS pregnancy is not possible until 4–5 weeks after breeding. r DEFINITION DIFFERENTIAL DIAGNOSIS Treatment on day 6–10 of diestrus—may r Termination of an unwanted pregnancy. May Ascertain that a breeding took place; a tie in have reduced efficacy compared to be accomplished by drugs that alter embryo the bitch and coital “after-reaction” in the midgestation but can be less distasteful to transport in the oviduct impeding queen. client (less discharge and recognizable fetuses r are not passed). establishment of a pregnancy, and/or cause Determine stage of estrous cycle: vaginal r luteal regression, terminating an established cytology, serum progesterone concentration PGF2α and bromocriptine—improves pregnancy. Due to their possible side effects (see Breeding, Timing). efficacy of either drug given alone. r (CEH, aplastic anemia and bone marrow Presence of sperm cells in vagina cytology; NURSING CARE suppression), drugs that impair embryonic absence of sperm does not rule out a previous N/A transit through the oviduct (estrogens) are not breeding. r ACTIVITY commonly used or recommended. Pregnancy diagnosis: ◦ Normal PATHOPHYSIOLOGY Abdominal palpation (bitch: 31–33 days DIET After fertilization the embryo travels the after LH surge; queen: 21–25 days after oviduct in a timely manner before entering breeding). Avoid feeding prior to each treatment and for ◦ Transabdominal ultrasound (bitch: > 25 1–2 hours after treatments (reduces nausea the uterus. Impaired embryo transport > through the oviduct leads to embryonic days after LH surge; queen: 16 days after and vomiting). degeneration and implantation abnormalities. breeding). CLIENT EDUCATION ◦ Abdominal radiographs (bitch: > 45 days r In the dog and cat, pregnancy maintenance is > Discuss patient’s reproductive future with dependent on progesterone production from after LH surge; queen: 38 days after owner. If no litters are desired, then OHE is the corpora lutea. In dogs, maintenance of the breeding). the best option. ◦ Serum relaxin concentration in the bitch r corpora lutea during the second half of > Discuss with the client the potential side gestation is also supported by prolactin. ( 28 days after LH surge) (Witness effects of the treatment options; reach a Drugs that cause luteal regression, antagonize Relaxin, Synbiotics Corp., mutual agreement on the treatment plan. http://synbiotics.com/index.html). PRL, and/or compete with progesterone SURGICAL CONSIDERATIONS receptors will terminate pregnancy. CBC/BIOCHEMISTRY/URINALYSIS r OHE is recommended for patients with no SYSTEMS AFFECTED Within normal limits during first half of reproductive value or when owners do not r pregnancy in healthy patients. Cardiovascular r desire future litters. r Digestive Decrease in PCV during second half of r pregnancy in bitches and queens is normal. Neurologic (caused by drugs used for r treatment) Recommended as screening test prior to r Reproductive treatment in patients with suspected r MEDICATIONS Respiratory underlying disease. OTHER LABORATORY TESTS DRUG(S) OF CHOICE GENETICS r r Confirmation of pregnancy before N/A Vaginal cytologic testing—determines stage of estrous cycle and presence of sperm. initiating any of the treatment protocols r INCIDENCE/PREVALENCE Serum progesterone concentration suggested below is recommended. Lengths of N/A determines if the female is in diestrus and treatment suggested may vary; treatments GEOGRAPHIC DISTRIBUTION monitors luteal regression during should be continued until abortion is treatment. complete. N/A ◦ PGF α: causes luteal regression with SIGNALMENT IMAGING 2 r subsequent decline in progesterone Species Transabdominal ultrasound (method of concentration, cervical relaxation, and Dogs and cats choice): diagnose pregnancy and monitor uterine contractions; bitches: 100 μg/kg uterine evacuation during treatment. r SC q8h for 2 days, then 200 μg/kg SC q8h Breed Predilections Abdominal radiographs. No breed predilection until pregnancy termination; queens: PATHOLOGIC FINDINGS 0.5–1 mg/kg SC q12h every other day > Mean Age and Range N/A day 40, or 2 mg/cat IM q24h for 5 days > N/A day 33. Predominant Sex ◦ Cloprostenol (prostaglandin analogue): Female bitches: 2.5 μg/kg SC q8 or q12h every SIGNS TREATMENT 48 hours until pregnancy termination r ∼ Depends on stage of gestation ( 6 days after start of treatment). APPROPRIATE HEALTH CARE ◦ ◦ None r Dexamethasone: mode of action is Physical examination before initiation of ◦ Vaginal discharge unknown; bitches: 0.2 mg/kg PO q12h for treatment. ◦ Fetal expulsion r 7 days, then decreasing from 0.16 to Monitor 30–60 minutes after treatment for CAUSES 0.02 mg/kg over the last five r side effects (vomiting, defecation, administrations; treatment failures not Impaired oviductal transport r hypersalivation, hyperpnea, micturition, uncommon. Luteal regression tachycardia). ◦ r r Cabergoline (PRL antagonist): causes Progesterone receptor antagonism Confirmation of pregnancy before initiating luteal regression; bitches: 1.65 mg/kg SC RISK FACTORS treatment is recommended; more than 60% of q24h for 5 days or 5 mg/kg PO q24h for N/A mismated bitches may not become pregnant. 5days> day 40; queens: 0.825 mg/kg SC BLBS078-CF_A03 BLBS078-Tilley July 14, 2011 9:3

Canine and Feline, Fifth Edition 7

(Continued) Abortion, Termination of Pregnancy A

q12h for 5 days > day 30 or 5–15 μg/kg ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL r PO q24h for 5 days > day 25. The following drugs are recommended for N/A ◦ Bromocriptine (PRL antagonist): causes use in bitches but not available in the United PREGNANCY/FERTILITY/BREEDING μ luteal regression; bitches: 62.5 g/kg PO States: N/A q12h for up to 6 days > day 43. ◦ Mifepristone (RU486; progestin and ◦ Cloprostenol and cabergoline glucocorticoid receptors antagonist): 2.5 SYNONYMS combination: bitches: cabergoline 5 μg/kg mg/kg PO q12h for 4.5 days > day 32 of Induced abortion PO q24h for 10 days plus cloprostenol pregnancy is recommended; no side effects SEE ALSO 2.5 μg/kg SC q24h at start of treatment, or have been reported. Breeding, Timing μ ◦ 1 g/kg SC q24h at start of treatment and Aglepristone (progestin and ABBREVIATIONS at day 5 of treatment; treatment should be glucocorticoid receptors antagonists): 10 r CEH = cystic endometrial hyperplasia initiated > 28 days post-LH surge; queen: mg/kg SC q24h for 2 days > 32 days r GnRH = gonadotropin-releasing hormone cabergoline 5 μg/kg PO q24h plus post-LH surge; pregnancy is terminated in r LH = luteinizing hormone cloprostenol 5 μg/kg SC every 48 hours 4-7 days; no side effects have been reported; r OHE = ovariohysterectomy (> 30 days after breeding) until abortion is mild vaginal discharge may be observed. r PCV = packed cell volume complete (∼9 days). ◦ GnRH antagonists (block GnRH r ◦ PGF2α = prostaglandin F2α Cloprostenol and bromocriptine receptors at the pituitary gland, causing a r = combination: bitches; bromocriptine decline in gonadotropins concentration): a PRL prolactin 30 μg/kg q8h PO of for 10 days plus single treatment with 110–330 μg/kg SC is INTERNET RESOURCES cloprostenol 2.5 μg/kg SC q24h or recommended; pregnancy is terminated Wanke MM, Romangnoli S, Verstegen J, 1 μg/kg SC at start of treatment and at day within 6–10 days after treatment; Concannon PW. Pharmacologic approaches 5 of treatment; treatment should be prepartum-like behavior has been observed; to pregnancy termination in dogs and cats initiated > 28 days post-LH surge. abortion may be followed by including the use of prostaglandins, dopamine CONTRAINDICATIONS serosanguineous vaginal discharge for 2–3 agonists, and dexamethasone. In: Concannon r days. PW, England G, Verstegen III J, PGF2α and analogues: animals with respiratory disease (bronchoconstriction); do Linde-Forsberg C, eds., Recent Advances in not administer intravenously. Small Animal Reproduction. International r Cabergoline and bromocriptine: animals Veterinary Information Service, Ithaca NY, hypersensitive to ergot alkaloids; these drugs FOLLOW-UP www.ivis.org, 2001. should be administered with caution in PATIENT MONITORING Suggested Reading patients with impaired liver function. r Transabdominal ultrasound examinations CorradaY,KlimaL,DelaSotaRL, Estrogens—may cause cystic endometrial should be performed to monitor complete Rodriquez R. Use of prostaglandins and hyperplasia, pyometra, and bone marrow evacuation of uterine contents. bromocriptine mesylate for pregnancy suppression leading to pancytopenia. PREVENTION/AVOIDANCE termination in bitches. JAVMA 2002, PRECAUTIONS r 220(7):1017–1019. r OHE for bitches and queens not intended Eilts BE Pregnancy termination in the bitch PGF2α and analogues: side effects are for breeding. r and queen. Clin Tech Small Anim Pract dose-dependent and include vomiting, Estrus suppression or confinement of defecation, dyspnea, tachycardia, salivation, 2002, 17:116–123. bitches and queens intended for breeding Fieni F, Dumon C, Tainturier D, Bruyas JF. restlessness, and anxiety; side effects subside during a later cycle to avoid mismating. within 60 minutes; the severity of effects can Clinical protocol for pregnancy termination POSSIBLE COMPLICATIONS be attenuated with premedication (> 15 in bitches using prostaglandin F2 α.JRepro minutes) with a combination of atropine Pregnancy termination may not be achieved Fert 1997, 51:245–250. (0.025 mg/kg); use extreme caution in dogs after one treatment protocol and continuation Johnston SD, Root Kustritz MV, Olson PNS. and cats with preexisting cardiopulmonary, or change in treatment protocol may be Prevention and termination of canine liver, and renal diseases. necessary. pregnancy. In: Canine and Feline r Dexamethasone: polydipsia, polyuria, and EXPECTED COURSE AND PROGNOSIS Theriogenology. Philadelphia: Saunders, r polyphagia are reported side effects. Long- The interestrous interval in bitches treated 2001, pp. 168–192. term administration has been associated with with prostaglandins and PRL inhibitors may Johnston SD, Root Kustritz MV, Olson PNS. hyperadrenocorticism. ∼ Prevention and termination of feline r be shortened ( 1 month). Queens may Cabergoline and bromocriptine: side effects resume estrous behavior 7–10 days after pregnancy. In: Canine and Feline may include vomiting and anorexia; pregnancy termination. Theriogenology. Philadelphia: Saunders, r prolonged use (> 2 weeks) may cause coat Subsequent estrus fertility is not affected. 2001, pp. 447–452. color changes. Author Jose A. Len Consulting Editor Sara K. Lyle POSSIBLE INTERACTIONS r PGF2α and analogues: effect may be reduced by concomitant administration of progestins; MISCELLANEOUS Client Education Handout use may enhance effects of oxytocin. available online r ASSOCIATED CONDITIONS Cabergoline and bromocriptine: cabergoline N/A effects may be reduced with concomitant AGE-RELATED FACTORS treatment with dopamine (D2) antagonists; avoid concomitant treatment with N/A hypotensive drugs. BLBS078-CF_A04 BLBS078-Tilley March 21, 2011 8:10

8 Blackwell’s Five-Minute Veterinary Consult A Abscessation

r A rapidly appearing painful swelling with Draining Tracts r or without discharge, if affected area is Mycobacterial disease. r BASICS visible. Mycetoma—botryomycosis, actinomycotic mycetoma, eumycotic mycetoma. Physical Examination Findings r DEFINITION r Neoplasia. Determined by the organ system or tissue r An abscess is a localized collection of purulent affected. Phaeohyphomycosis. r r exudate contained within a cavity. A discrete mass may be detectable. Sporotrichosis. r r PATHOPHYSIOLOGY Inflammation and discharge from a fistulous Systemic fungal infection—blastomycosis, r coccidioidomycosis, cryptococcosis, Bacteria are often inoculated under the skin tract may be visible if the abscess is superficial and has ruptured to an external surface. histoplasmosis, trichosporosis. via a puncture wound; the wound surface r then seals. A variably sized, painful mass of fluctuant to CBC/BIOCHEMISTRY/URINALYSIS r r When bacteria and/or foreign objects persist firm consistency attached to surrounding CBC—normal or neutrophilia with or tissues may be palpable. in the tissue, purulent exudate forms and r without regenerative left shift. Neutropenia collects. Fever if abscess is not ruptured and draining. and degenerative left shift if sepsis present. r r r Accumulation of purulent exudates—if not Sepsis occasionally, especially if abscess Urinalysis and serum chemistry ruptures internally. profile—depends on system affected. quickly resorbed or discharged to an external r surface, stimulates formation of a fibrous CAUSES Prostatic—pyuria. r r capsule; may eventually lead to abscess Foreign objects. Liver and/or pancreatic—high liver enzymes r and/or total bilirubin. rupture. Pyogenic bacteria—Staphylococcus spp.; r r Pancreatic (dogs)—high amylase/lipase. Prolonged delay of evacuation—formation Escherichia coli; β-hemolytic Streptococcus r of a fibrous abscess wall; to heal, the cavity spp.; Pseudomonas; Mycoplasma and Diabetes mellitus—persistent must be filled with granulation tissue from Mycoplasma-like organisms (l-forms); hyperglycemia and glucosuria. which the causative agent may not be totally Pasteurella multocida; Corynebacterium; OTHER LABORATORY TESTS eliminated; may lead to chronic or Actinomyces spp.; Nocardia; Bartonella. r r FeLV and FIV—for cats with recurrent or intermittent discharge of exudate from a Obligate anaerobes—Bacteroides spp.; slow-healing abscesses. r draining sinus tract. Clostridium spp.; Peptostreptococcus; CSF evaluation—increase in cellularity and SYSTEMS AFFECTED Fusobacterium. protein expected with brain abscess. r r Gastrointestinal—pancreas (dogs > cats) RISK FACTORS Adrenal function—evaluate for r r Hepatobiliary—liver parenchyma Anal sac—impaction; anal sacculitis. hyperadrenocorticism. r r Ophthalmic—periorbital tissues Brain—otitis interna sinusitis oral infection. IMAGING r > r r Reproductive—prostate gland (dogs Liver—omphalophlebitis sepsis. Radiography—soft-tissue density mass in cats); mammary gland r r Lung—foreign object aspiration bacterial affected area; may reveal foreign body. Skin/Exocrine—percutaneous (cats > pneumonia. r r Ultrasonography—determine if mass is dogs); anal sac (dogs > cats) Mammary gland—mastitis. r fluid filled or solid; determine organ system GENETICS Periorbital—dental disease; chewing of affected; reveal flocculent-appearing fluid wood or other plant material. N/A r characteristic of pus; may reveal foreign Percutaneous—fighting. INCIDENCE/PREVALENCE r object. Prostate gland—bacterial prostatitis. r r Echocardiography—helpful for diagnosis of N/A Immunosuppression—FeLV/FIV infection, pericardial abscess. r GEOGRAPHIC DISTRIBUTION immunosuppressive chemotherapy, acquired CT or MRI—helpful for diagnosis of brain N/A or inherited immune system dysfunctions, abscess. SIGNALMENT underlying predisposing disease (e.g., diabetes DIAGNOSTIC PROCEDURES mellitus, chronic renal failure, Species Aspiration hyperadrenocorticism). r Cats and dogs Reveals a red, white, yellow, or green liquid. r Protein content > 2.5–3.0 g/dL. Breed Predilections r N/A Nucleated cell count—3,000–100,000 (or more) cells/μL; primarily degenerative Mean Age and Range DIAGNOSIS neutrophils with lesser numbers of N/A DIFFERENTIAL DIAGNOSIS macrophages and lymphocytes. Predominant Sex r Mass Lesions Pyogenic bacteria—may be seen in cells and Mammary glands (female); prostate gland r Cyst—less or only transiently painful; free within the fluid. (male) r slower growing. If the causative agent is not readily r SIGNS Fibrous scar tissue—firm; non-painful. identified with a Romanowsky-type stain, r General Comments Granuloma—less painful; slower growing; specimens should be stained with an acid-fast r stain to detect mycobacteria or Nocardia and Determined by organ system and/or tissue generally firmer without fluctuant center. r PAS stain to detect fungus. affected. Hematoma/seroma—variable pain (depends r Biopsy Associated with a combination of on cause); non-encapsulated; rapid initial r inflammation (pain, swelling, redness, heat, growth but slow increase once full size is Sample should contain both normal and abnormal tissue in the same specimen. and loss of function), tissue destruction, attained; unattached to surrounding tissues; r Impression smears—stained and examined. and/or organ system dysfunction caused by fluctuant and fluid filled initially but more r accumulation of exudates. firm with organization. Tissue—submit for histopathologic r examination and culture. Historical Findings Neoplasia—variable growth; consistent; r r Contact the diagnostic laboratory for History of traumatic insult or previous painful. specific instructions. infection. BLBS078-CF_A04 BLBS078-Tilley March 21, 2011 8:10

Canine and Feline, Fifth Edition 9

(Continued) Abscessation A

r Culture SURGICAL CONSIDERATIONS Compromise of organ function. r r r Affected tissue and/or exudate—aerobic and Appropriate debridement and drainage— Delayed evacuation may lead to chronically anaerobic bacteria and fungus. may need to leave the wound open to an draining fistulous tracts. r Blood and/or urine—isolate bacterium external surface; may need to place surgical EXPECTED COURSE AND PROGNOSIS responsible for possible sepsis. drains. r r Depends on organ system involved and Bacterial sensitivity. Early drainage—to prevent further tissue amount of tissue destruction. PATHOLOGIC FINDINGS damage and formation of abscess wall. r r Pus-containing mass lesion accompanied by Remove any foreign objects(s), necrotic inflammation. tissue, or nidus of infection. r Palpable—variably firm or fluctuant mass. r MISCELLANEOUS Ruptured—may see pus draining directly ASSOCIATED CONDITIONS from the mass or an adjoining tract. r r MEDICATIONS FeLV or FIV infection Exudate—large numbers of neutrophils in r various stages of degeneration; other DRUG(S) OF CHOICE Immunosuppression inflammatory cells; necrotic tissue. r AGE-RELATED FACTORS r Antimicrobial drugs—effective against the Surrounding tissue—congested; fibrin; large infectious agent; gain access to site of N/A number of neutrophils; variable number of infection. ZOONOTIC POTENTIAL lymphocytes; plasma cells; macrophages. r r r Broad-spectrum agent—bactericidal and Minimal for pyogenic bacteria. Causative agent variably detectable. r with both aerobic and anaerobic activity; until Mycobacteria and systemic fungal infections results of culture and sensitivity are known. carry some potential. Dogs and cats: amoxicillin (11–22 mg/kg PO PREGNANCY/FERTILITY/BREEDING q8–12h); amoxicillin/clavulanic acid (12.5– TREATMENT 25 mg/kg PO q12h); clindamycin (5 mg/kg Teratogenic agents—avoid use in pregnant animals. APPROPRIATE HEALTH CARE PO q12h); and trimethoprim/sulfadiazine r (15 mg/kg PO IM q12h). Cats with SEE ALSO Depends on location of abscess and r Mycoplasma and l-forms: doxycycline Actinomycosis treatment required. r r (3–5 mg/kg PO q12h). Anaerobic Infections Outpatient—bite-induced abscesses. r r r Aggressive antimicrobial therapy—sepsis or Colibacillosis Inpatient—sepsis; extensive surgical r peritonitis. Mycoplasmosis procedures; treatment requiring extended r Nocardiosis hospitalization. CONTRAINDICATIONS r r Sepsis and Bacteremia Establish and maintain adequate drainage. N/A r ABBREVIATIONS Surgical removal of nidus of infection or PRECAUTIONS r CSF = cerebrospinal fluid foreign object(s) if necessary. N/A r r CT = computed tomography Institution of appropriate antimicrobial r POSSIBLE INTERACTIONS FeLV = feline leukemia virus therapy. r N/A FIV = feline immunodeficiency virus NURSING CARE r r ALTERNATIVE DRUG(S) MRI = magnetic resonance imaging Depends on location of abscess. r r PAS = periodic acid-Schiff Apply hot packs to inflamed area as needed. N/A r Use protective bandaging and/or Suggested Reading Elizabethan collars as needed. r Birchard SJ, Sherding RG, eds., Saunders Accumulated exudate—drain abscess; Manual of Small Animal Practice. maintain drainage by medical and/or surgical FOLLOW-UP Philadelphia: Saunders, 1994. means. r PATIENT MONITORING DeBoer DJ. Nonhealing cutaneous wounds. Sepsis or peritonitis—aggressive fluid Monitor for progressive decrease in drainage, In: August JR, ed., Consultations in Feline therapy and support. resolution of inflammation, and improvement Internal Medicine. Philadelphia: Saunders, ACTIVITY of clinical signs. 1991, pp. 101–106. McCaw D. Lumps, bumps, masses, and Restrict until the abscess has resolved and PREVENTION/AVOIDANCE adequate healing of tissues has taken place. r lymphadenopathy. In: Ettinger SJ, Feldman Percutaneous abscesses—prevent fighting. DIET r EC, eds., Textbook of Veterinary Internal r Anal sac abscesses—prevent impaction; Medicine, 4th ed. Philadelphia: Saunders, Sufficient nutritional intake to promote a consider anal saculectomy for recurrent cases. 1995, pp. 219–222. positive nitrogen balance. r r Prostatic abscesses—castration possibly Author Johnny D. Hoskins Depends on location of abscess and helpful. r Consulting Editor Stephen C. Barr treatment required. Mastitis—prevent lactation (spaying). r CLIENT EDUCATION Periorbital abscesses—do not allow chewing r Discuss need to correct or prevent risk on foreign object(s). Client Education Handout factors. POSSIBLE COMPLICATIONS available online r r Discuss need for adequate drainage and Sepsis. r continuation of antimicrobial therapy for an Peritonitis/pleuritis if intra-abdominal or adequate period of time. intrathoracic abscess ruptures. BLBS078-CF_A05 BLBS078-Tilley March 21, 2011 8:13

10 Blackwell’s Five-Minute Veterinary Consult A Acetaminophen Toxicity

SIGNALMENT one-tenth the plasma elimination rate of dogs). Species r BASICS Cats more often than dogs Blood glutathione level—low. Breed Predilections IMAGING DEFINITION N/A N/A Results from owners overdosing the patient DIAGNOSTIC PROCEDURES with over-the-counter Mean Age and Range acetaminophen-containing analgesic and N/A N/A antipyretic medications. Predominant Sex PATHOLOGIC FINDINGS r N/A Methemoglobinemia. PATHOPHYSIOLOGY r Pulmonary edema. When the normal biotransformation SIGNS r Liver and kidney congestion. mechanisms for detoxification General Comments r Dogs—centrilobular necrosis of the liver; (glucuronidation and sulfation) are Relatively common—owing to increasing use icterus in chronic cases. diminished, cytochrome P450-mediated in humans oxidation produces a toxic metabolite Historical Findings r (N-acetyl benzoquinoneimine) that is Depression. r electrophilic, conjugates with glutathione, Rapid breathing. r TREATMENT and toxicologically binds to liver proteins. Darkened mucous membranes. r Dogs Owner may recall warnings about APPROPRIATE HEALTH CARE r ≥ r Receipt of 150–200 mg/kg—sufficient acetaminophen in cats after dosing the pet. With methemoglobinemia—must evaluate electrophilic metabolite generated through Physical Examination Findings promptly. r r the cytochrome P450 pathway that RBC May develop 1–4 hours after dosing. With dark or bloody colored urine or r glutathione binding produces Progressive depression. icterus—inpatient. r methemoglobinemia and damages liver Salivation. NURSING CARE proteins. r r Vomiting. r Causes hepatotoxicity in a dose-dependent r Gentle handling—imperative for clinically Abdominal pain. affected patients. fashion r r Tachypnea and cyanosis—reflect Induced emesis and gastric lavage—useful Cats methemoglobinemia. within 4–6 hours of ingestion. r r r Lower ability to glucuronidate; more Edema—face, paws, and possibly forelimbs; Anemia, hematuria, or hemoglobinuria— limited capacity for acetaminophen after several hours. may require whole blood transfusion. elimination than dogs. r r r Chocolate-colored urine—hematuria and Fluid therapy—maintain hydration and Saturate glucuronidation and sulfation methemoglobinuria; especially in cats. electrolyte balance. r r biotransformation routes. Death. Drinking water—available at all times. r r Develop toxic cytochrome P450 metabolite CAUSES Food—offered 24 hours after initiation of at much lower doses than dogs. r Acetaminophen overdosing treatment. Poisoned by as little as 50–60 mg/kg (often RISK FACTORS ACTIVITY as little as one-half tablet); leads to rapid RBC r glutathione depletion that produces rapidly Nutritional deficiencies of glucose and/or Restricted sulfate. DIET developing methemoglobinemia, because of r the unique feline hemoglobin molecule with Simultaneous administration of other N/A eight sulfhydryl groups sensitive to oxidation. glutathione-depressing drugs. r CLIENT EDUCATION Slower-developing hepatotoxicosis may not r be fully expressed before development of fatal Warn client that treatment in clinically methemoglobinemia. affected patients may be prolonged and expensive. SYSTEMS AFFECTED DIAGNOSIS r r Inform client that patients with liver injury Hemic/Lymph/Immune—RBCs are DIFFERENTIAL DIAGNOSIS may require prolonged and costly r damaged by glutathione depletion, allowing Nitrites. management. oxidation of hemoglobin to methemoglobin. r r Phenacetin. SURGICAL CONSIDERATIONS Hepatobiliary—liver necrosis. r r Nitrobenzene. Cardiovascular (cats)—edema of the face, r N/A Phenol and cresol compounds. paws, and (to a lesser degree) forelimbs r Sulfites. through an undefined mechanism. r History of exposure—important for GENETICS differentiating from methemoglobin-forming MEDICATIONS Cats—genetic deficiency in the glucuronide drugs. conjugation pathway makes them DRUG(S) OF CHOICE CBC/BIOCHEMISTRY/URINALYSIS r vulnerable. r Activated charcoal 2 g/kg PO; immediately Methemoglobinemia and progressively after completion of emesis or gastric lavage. INCIDENCE/PREVALENCE rising serum activities of liver r r N-acetylcysteine (Mucomyst) 140 mg/kg Most common drug toxicity in cats; enzymes—characteristic. r loading dose PO, IV; then 70 mg/kg PO, IV, considerably less frequent in dogs. Heinz bodies (cats)—prominent in RBCs. r r q4h for 5–7 treatments. Over-the-counter medications—fourth Hematuria and/or hemoglobinuria. CONTRAINDICATIONS most common cause of poison exposures in OTHER LABORATORY TESTS small animals. r Drugs that contribute to methemoglobinemia Acetaminophen serum concentration— or hepatotoxicity. GEOGRAPHIC DISTRIBUTION maximally elevated 1–3 hours after ingestion; N/A decay dose-dependent in cats (approximately BLBS078-CF_A05 BLBS078-Tilley March 21, 2011 8:13

Canine and Feline, Fifth Edition 11

(Continued) Acetaminophen Toxicity A

PRECAUTIONS POSSIBLE COMPLICATIONS SEE ALSO Drugs requiring extensive liver metabolism or Liver necrosis and resulting fibrosis—may Poisoning (Intoxication) biotransformation—use with caution; expect compromise long-term liver function in ABBREVIATIONS r their half-lives to be extended. recovered patients. ALP = alkaline phosphatase r POSSIBLE INTERACTIONS EXPECTED COURSE AND PROGNOSIS ALT = alanine aminotransferase r r Drugs requiring activation or metabolism by Rapidly progressive methemoglobinemia— RBC = red blood cell the liver have reduced effectiveness. serious sign. INTERNET RESOURCES r ≥ ALTERNATIVE DRUG(S) Methemoglobin concentrations 50%— http://www.aspca.org/pet-care/ r grave prognosis. Other sulfur donor drugs—if r poison-control/. Progressively rising serum liver enzymes N-acetylcysteine not available; sodium sulfate Suggested Reading (50 mg 1.6% solution/kg IV q4h for 6 12–24 hours after ingestion—serious concern. r Hjelle JJ, Grauer GF. treatments); effective use requires Expect clinical signs to persist 12–48 hours; Acetaminophen-induced toxicosis in dogs conscientious management. death owing to methemoglobinemia possible r and cats. JAVMA 1986, 188:742–746. S-adenosyl-l-methionine (SAMe) as a at any time. r Oehme FW. Aspirin and acetaminophen. In: glutathione donor—a loading dose (40 mg/kg Dogs and cats receiving prompt treatment Kirk, R.W., ed., Current Veterinary Therapy PO) of a stable SAMe salt followed by a that reverses methemoglobinemia and IX: Small Animal Practice. Philadelphia: maintenance dose (20 mg/kg PO) q24h for 7 prevents excessive liver necrosis—may recover Saunders, 1986, pp. 188–189. days; reserved for dogs able to retain oral fully. r Rumbeiha WK, Oehme FW. Methylene blue medications and with adequate liver function Dogs—death as a result of liver necrosis may occur in a few days. can be used to treat methemoglobinemia in to metabolize SAMe. r r cats without inducing Heinz body A 1% methylene blue solution—8.8 mg/kg Cats—death as a result of hemolytic anemia. Vet Hum Toxicol 1992, IV q2–3h for 2–3 treatments; combats methemoglobinemia occurs 18–36 hours after 34:120–122. methemoglobinemia without inducing a ingestion. Savides MC, Oehme FW, Leipold HW. hemolytic crisis. r Effects of various antidotal treatments on Ascorbic acid—125 mg/kg PO q6h for 6 acetaminophen toxicosis and treatments; only slowly reduces biotransformation in cats. Am J Vet Res methemoglobinemia. MISCELLANEOUS 1985, 46:1485–1489. ASSOCIATED CONDITIONS Savides MC, Oehme FW, Nash SL, Leipold N/A HW. The toxicity and biotransformation of single doses of acetaminophen in dogs and FOLLOW-UP AGE-RELATED FACTORS Young and small dogs and cats—greater risk cats. Toxicol Appl Pharmacol 1984, PATIENT MONITORING from owner-given single-dose acetaminophen 74:26–34. r Continual clinical monitoring of medications. Wallace KP, Center SA, Hickford FH, Warner KL, Smith S. S-adenosyl- methemoglobinemia—vital for effective ZOONOTIC POTENTIAL L-methionine (SAMe) for the treatment of management; laboratory determination of None methemoglobin percentage every 2–3 hours. acetaminophen toxicity in a dog. JAAHA r Serum liver enzyme activities (ALT, ALP)— PREGNANCY/FERTILITY/BREEDING 2002, 38(3):246–254. determined every 12 hours; monitor liver Imposes additional stress and higher risk on Author Frederick W. Oehme damage. exposed animals. Consulting Editor Gary D. Osweiler r Blood glutathione level—provide evidence SYNONYMS of the effectiveness of sulfhydryl-replacement r Paracetamol Client Education Handout therapy. r Tylenol available online PREVENTION/AVOIDANCE r Never give acetaminophen to cats. r Give careful attention to the acetaminophen dose in dogs. BLBS078-CF_A06 BLBS078-Tilley March 21, 2011 8:14

12 Blackwell’s Five-Minute Veterinary Consult A Acidosis, Metabolic

decreases PCO2, which counters the effects of − low plasma HCO3 onpH.Indogs,a BASICS decrease of approximately 0.7 mm Hg in DIAGNOSIS PCO2 is expected for each 1 mEq/L decrease − DEFINITION in plasma HCO3 . Little is known about DIFFERENTIAL DIAGNOSIS − Decrease in plasma pH associated with a compensation in cats, but it appears to be Low plasma HCO3 and hyperchloremia may almost non-existent. decrease in bicarbonate concentration r also be compensatory in animals with chronic − < < Renal/Urologic—the kidneys increase net (HCO3 )(dogs, 18 mEq/L; cats, 16 respiratory alkalosis, in which PCO2 is low acid excretion, primarily by increasing and pH is high or near normal, despite mEq/L) and a compensatory decrease in + − carbon dioxide tension (PCO2). excretion of NH4 and chloride. This decreased HCO3 and increase in chloride PATHOPHYSIOLOGY compensatory mechanism is not very effective concentration. Blood gas determination is r in cats. required to differentiate. Metabolic acidosis may develop secondary to hyperphosphatemia (hyperphosphatemic SIGNALMENT LABORATORY FINDINGS acidosis), corrected hyperchloremia Any breed, age, or sex of dog and cat Drugs That May Alter Laboratory Results r (hyperchloremic acidosis), and accumulation SIGNALMENT Potassium bromide is measured as chloride of metabolically produced strong anions Historical Findings in most analyzers, so potassium bromide (strong ion gap or high anion gap acidosis). r r Chronic disease processes that lead to administration artificially decreases the anion Hyperphosphatemic acidosis: gap. ◦ metabolic acidosis (e.g., renal failure, diabetes Increase in plasma weak acids (e.g., mellitus, and hypoadrenocorticism), exposure Disorders That May Alter Laboratory inorganic phosphate) is associated with to toxins (e.g., ethylene glycol, salicylate, and Results r metabolic acidosis and increased anion gap. paraldehyde), diarrhea, administration of Too much heparin (> 10% of the sample) − At pH of 7.4, a 1 mg/dL increase in carbonic anhydrase inhibitors (e.g., decreases HCO . phosphate concentration is associated with r 3 − acetazolamide and dichlorphenamide). Blood samples stored at room temperature a 0.58 mEq/L decrease in [HCO ]anda 3 Physical Examination Findings for more than 20 minutes have low pH 0.58 mEq/L increase in AG. r r Generally relate to the underlying disease. because of increased PCO2. Hyperchloremic acidosis: r r ◦ Depression in severely acidotic patients. Hypoalbuminemia lowers AG; negative Hyperchloremic acidosis may be caused r charges of albumin are the main component by chloride retention (e.g., renal failure, Tachypnea in some patients results from compensatory increase in ventilation. of the anion gap. renal tubular acidosis), excessive loss of r sodium relative to chloride (e.g., diarrhea), Kussmaul’s respiration, typically seen in Valid if Run in Human Laboratory? or by administration of substances human beings with metabolic acidosis, is not Yes containing more chloride than sodium as commonly observed in dogs and cats. CBC/BIOCHEMISTRY/URINALYSIS r compared with normal extracellular fluid CAUSES Low total CO2—total CO2 in serum composition (e.g., administration of KCl, samples handled aerobically closely Associated with Hyperchloremia − 0.9% NaCl). (Hyperchloremic Metabolic Acidosis) approximates the serum HCO3 ◦ r Acidemia is usually not severe in patients Diarrhea. concentration; unfortunately, patients with r with hyperchloremic acidosis. Renal tubular acidosis. chronic respiratory alkalosis also have low r r High anion gap acidosis: Administration of carbonic anhydrase total CO2, and the distinction cannot be ◦ Increase in the concentration of other made without blood gas analysis. inhibitors, spironolactone, potassium r strong anions through addition (e.g., chloride, or NH Cl. Metabolic acidoses are traditionally divided r 4 ethylene glycol toxicity), excessive Fluid therapy with chloride-rich fluids (e.g., into hyperchloremic and high anion gap by production (e.g., lactate produced by 0.9% NaCl, fluids supplemented with KCl). means of the anion gap. Anion gap, the r prolonged anaerobic metabolism), or renal Total parenteral nutrition with fluids difference between the measured cations and = retention (e.g., renal failure) of strong containing cationic amino acids: lysine, the measured anions, is calculated as AG + − − + − = + anions other than chloride causes metabolic arginine, and histidine. [Na ] (HCO3 [Cl ]) or AG ([Na ] r + + − − + − acidosis without increasing chloride Rapid correction of hypocapnia (chronic [K ]) (HCO3 [Cl ]), depending on concentration (so-called normochloremic respiratory alkalosis). the preference of the clinician or laboratory. or high AG metabolic acidosis). Associated with Normochloremia (High Normal values with potassium included in the SYSTEMS AFFECTED Anion Gap Metabolic Acidosis) calculation are usually 12–24 mEq/L in dogs r r and 13–27 mEq/L in cats. The negative Cardiovascular—a fall in pH results in an Uremic acidosis. r charges of albumin are the major contributors increase in sympathetic discharge but Diabetic ketoacidosis. r to the normal anion gap; this should be taken simultaneously causes a decrease in the Lactic acidosis. r into account when evaluating anion gap in responsiveness of the cardiac myocytes and Ethylene glycol, salicylate, paraldehyde, and patients with hypoalbuminemia. At pH 7.4 in vascular smooth muscle to the effects of methanol intoxication. r dogs, a decrease of 1 g/dL in albumin is catecholamines. In mildly acidemic Hyperphosphatemia. conditions (pH greater than 7.2), the effects associated with a decrease of 4.1 mEq/L in the RISK FACTORS anion gap. of increased sympathetic stimulation r r predominate and result in a mild increase in Patients with chronic renal failure, diabetes Normal anion gap (i.e., hyperchloremic heart rate and cardiac output. More severe mellitus, and hypoadrenocorticism are at high metabolic acidosis)—most common cause is acidemia (pH below 7.1), especially if acute, risk of developing metabolic acidosis as a diarrhea; also, hypoadrenocorticism. complication of the chronic disease process. r may decrease cardiac contractility and r High anion gap (i.e., normochloremic predispose the heart to ventricular Patients with poor tissue perfusion or metabolic acidosis)—most common causes arrhythmias and ventricular fibrillation. hypoxia are at risk of developing lactic are renal failure, diabetes mellitus, lactic r + Respiratory—increased [H ] stimulates acidosis. acidosis (caused by tissue hypoperfusion), and peripheral and central chemoreceptors to hypoadrenocorticism (caused by lactic increase alveolar ventilation; hyperventilation acidosis). Hyperphosphatemia also raises the BLBS078-CF_A06 BLBS078-Tilley March 21, 2011 8:14

Canine and Feline, Fifth Edition 13

(Continued) Acidosis, Metabolic A

anion gap. At a pH of 7.4, each 1 mg/dL 1–2 mEq/kg followed by reevaluation of POSSIBLE COMPLICATIONS r increase in phosphate concentration is blood gas status is safe in most patients. Hyperkalemia in acute hyperchloremic associated with a 0.58 mEq/L increase in ◦ Potential complications of NaHCO acidosis 3 r anion gap. administration: volume overload resulting Myocardial depression and ventricular r Hyperglycemia—consider diabetes mellitus. from administered sodium, tetany from low arrhythmias r Azotemia—consider renal failure. ionized calcium concentration, increased r Hyperphosphatemia—consider renal affinity of hemoglobin for oxygen, failure, hypertonic sodium phosphate enema paradoxical CNS acidosis, overshoot toxicity, and toxicity due to urinary acidifiers metabolic alkalosis, and hypokalemia. r MISCELLANEOUS containing phosphate. Hyperchloremic acidosis: NaHCO is r 3 ASSOCIATED CONDITIONS High lactate concentration—consider lactic effective and should be considered whenever r acidosis due to poor tissue perfusion or poor pH < 7.2. Hyperkalemia r r metabolism of lactate (e.g., liver disease and Uremic acidosis: efficacy of NaHCO3 in Hyperchloremia lymphoma). acute therapy of uremic acidosis is related to AGE-RELATED FACTORS r Hyperkalemia—commonly associated with, the shift of phosphate inside the cells and None but almost never caused by, the acidosis. Only consequent amelioration of ZOONOTIC POTENTIAL acute hyperchloremic acidosis can lead to hyperphosphatemic acidosis. r None potassium translocation severe enough to Lactic acidosis: NaHCO3 increases lactate cause hyperkalemia. Otherwise, hyperkalemia production and is of little to no value in lactic PREGNANCY/FERTILITY/BREEDING results from the disease process causing the acidosis. Therapy should be directed at N/A metabolic acidosis (e.g., renal failure and augmenting oxygen delivery to the tissues and SYNONYMS r diabetes mellitus), not from the acidosis itself. reestablishing cardiac output. Small titrated Dilutional acidosis—metabolic acidosis Correction formulas to adjust potassium doses of NaHCO3 can be used as a − resulting from increased free water in plasma. r concentration based on pH changes should temporizing measure to maintain HCO3 Hyperchloremic acidosis—normal anion not be used. above 5 mEq/L, if needed. r gap acidosis. r OTHER LABORATORY TESTS Diabetic ketoacidosis: NaHCO3 adversely Hyperphosphatemic acidosis—metabolic − Blood gas analysis reveals low HCO ,low affects outcome in humans with diabetic acidosis resulting from high phosphate 3 ketoacidosis even when pH is below 7.0. PCO , and low pH. r concentration. 2 r Administration of NaHCO3 to ketoacidotic Non-respiratory acidosis. IMAGING patients cannot be recommended at any pH. r None Normochloremic acidosis—high anion gap Therapy should be direct at insulin and fluid acidosis. DIAGNOSTIC PROCEDURES r administration. Reestablishing plasma volume Organic acidosis—metabolic acidosis None and renal perfusion will allow the kidneys to resulting from accumulation of organic anions excrete ketoanions, replacing them with (e.g., ketoacidosis, uremic acidosis, and lactic chloride. acidosis). CONTRAINDICATIONS r SEE ALSO r TREATMENT Avoid NaHCO3 in patients with respiratory Diabetes Mellitus with Ketoacidosis r acidosis because it generates CO . r Acid-base disturbances are secondary r 2 Hyperchloremia Patients with respiratory acidosis cannot r phenomena; successful resolution depends on Hyperkalemia adequately excrete CO , and increased PCO diagnosis and treatment of the underlying 2 2 will further decrease the pH. ABBREVIATIONS disease process. r r = r Avoid diuretics that act in the distal AG anion gap Treat patients with blood pH ≤ 7.1 r nephron (e.g., spironolactone). CNS = central nervous system aggressively while pursuing the definitive r r + Avoid carbonic anhydrase inhibitors (e.g., H = hydrogen ion diagnosis. r − = r acetazolamide, dichlorphenamide). HCO3 bicarbonate Discontinue drugs that may cause metabolic r NaHCO3 = sodium bicarbonate acidosis. PRECAUTIONS r = r O2 oxygen Nursing care—lactated Ringer’s solution is Use NaHCO3 cautiously in patients with r PCO2 = carbon dioxide tension the fluid of choice for patients with mild congestive heart failure because the sodium metabolic acidosis and normal liver function. load may cause decompensation of the heart Suggested Reading failure. de Morais HA, Constable PD. Strong ion POSSIBLE INTERACTIONS approach to acid-base disorders. In: DiBartola SP, ed., Fluid, Electrolyte and None MEDICATIONS Acid-Base Disorders, 3rd. ed. Philadelphia: ALTERNATIVE DRUG(S) Saunders, 2006, pp. 310–321. DRUG(S) OF CHOICE None de Morais HA, Leisewitz AL. Mixed acid-base r NaHCO3 may help patients with disorders. In: DiBartola SP, ed., Fluid, hyperchloremic, hyperhosphatemic, or uremic Electrolyte and Acid-Base Disorders, 3rd. acidosis, but not patients with lactic acidosis ed. Philadelphia: Saunders, 2006, or diabetic ketoacidosis. FOLLOW-UP pp. 296–309. − ◦ × DiBartola SP. Metabolic acid-base disorders. Estimation of HCO3 dose: dogs, 0.3 PATIENT MONITORING body weight (kg) × (21 − patient In: DiBartola SP, ed., Fluid, Electrolyte and − × × Recheck acid-base status; frequency dictated HCO3 ); cats, 0.3 body weight (kg) Acid-Base Disorders, 3rd. ed. Philadelphia: − − by the underlying disease and patient response (19 patient HCO3 ). Give half of this Saunders, 2006, pp. 251–283. dose slowly IV and reevaluate blood gases to treatment. Author Helio Autran de Morais before deciding on the need for additional Consulting Editor Carl A. Osborne administration. An empirical dose of BLBS078-CF_A07 BLBS078-Tilley July 23, 2011 2:49

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 Systemic isotretinoin—use with caution, if r Inflammatory dermatitis affecting the chin and perifolliculitis with follicular pustule animal will not allow application of topical and lips formation. medications; caution: potential deleterious r r Symptoms may be recurrent or persistent Follicular rupture releases keratin, hair, and side effects in human beings (drug r Precise etiology unknown Demodex mites into the dermis; leads to interactions and teratogenicity); container SIGNALMENT furunculosis, manifested by neutrophils and should be labeled for animal use only and r numerous macrophages surrounding keratin Cats kept separate from human medications to r debris. Prevalence for sex, age, or breed not reported r avoid accidental use; currently difficult to Bacteria and Malassezia in these lesions are obtain for animal patients. SIGNS considered secondary invaders and not r Cats may have a single episode, a lifelong causative agents. r recurrent problem, or a continual disease. Demodex mites can be primary agents of r Frequency and severity of each occurrence this disease. FOLLOW-UP varies with the individual. r r Monitor for relapses. Comedones, mild erythematous papules, r serous crusts, and dark keratin debris develop Maintenance cleansing programs can be on the chin and less commonly on the lips. used to reduce relapses. r TREATMENT Swelling of the chin. r r Severe cases—nodules, hemorrhagic crusts, Initial treatment—one or a combination of pustules, cysts, fistulae, severe erythema, the drugs listed below until all lesions have alopecia, and pain. resolved. MISCELLANEOUS r r Pain often associated with bacterial Discontinue treatment by tapering medication over a 2- to 3-week period. PREGNANCY/FERTILITY/BREEDING furunculosis. r Recurrent episodes—once the recurrence Systemic isotretinoin should not be used on CAUSES & RISK FACTORS rate is determined, an appropriate breeding animals. Precise etiology unknown; may be a disorder maintenance protocol can be designed for Suggested Reading of keratinization, poor grooming, abnormal each individual. r Jazic E, Coyner KS, Loeffler DG, Lewis TP. sebum production, immunosuppression, viral Continual episodes—lifelong maintenance infection, or stress. An evaluation of the clinical, cytological, treatment necessary. infectious and histopathological features of feline acne. Vet Dermatol 2006, 17(2):134–140. Rosencrantz WS. The pathogenesis, DIAGNOSIS MEDICATIONS diagnosis, and management of feline acne. DIFFERENTIAL DIAGNOSIS DRUG(S) Vet Med 1993, 5:504–512. r r Scott DW, Miller WH, Griffin CE. Bacterial folliculitis Systemic antibiotics—amoxicillin with r Keratinization defects. In: Muller & Kirk’s Demodicosis clavulanate, a cephalosporin, or a r Small Animal Dermatology, 6th ed. Malassezia Infection fluoroquinolone. r r Philadelphia: Saunders, 2001, pp. Feline leprosy Severe cases may warrant treatment with r 1042–1043. Dermatophytosis isotretinoin (Accutane) or cyclosporine, r Werner AH, Power HT. Retinoids in Neoplasia of sebaceous or apocrine glands modified (Atopica). r r veterinary dermatology. Clin Dermatol Eosinophilic granuloma Demodicosis—oral ivermectin 400 ug/kg r 1994, 12(4):579–586. Contact hypersensitivity daily until mites are cleared. r White SD. Feline acne and results of CBC/BIOCHEMISTRY/URINALYSIS Shampoo—once or twice weekly with treatment with mupirocin in an open antiseborrheic (sulfur-salicylic acid, benzoyl N/A clinical trial: 25 cases (1994–96). Vet peroxide, or ethyl lactate). OTHER LABORATORY TESTS r Dermatol 1997, 8:157. Topical cleansing agents—benzoyl peroxide, Author David Duclos N/A salicylic acid, chlorhexidine- Consulting Editor Alexander H. Werner IMAGING phytosphingosine. r N/A Topical antibiotic ointment—mupirocin 2%. DIAGNOSTIC PROCEDURES r r Other topicals—clindamycin or Skin scrapings—demodicosis. r erythromycin solution or ointment. Fungal culture—dermatophytosis. r r Combination topicals—benzoyl Cytology—bacteria, Malassezia. r peroxide-antibiotic gels (e.g., Benzamycin). Biopsy—rarely needed; necessary in selected r Topical retinoids—Tretinoin (Retin-A cases to characterize changes such as cystic 0.01% gel). follicles, to differentiate acne from other diseases such as demodicosis, infections (bacterial, yeast, or dermatophytes), or to diagnose neoplasia. BLBS078-CF_A08 BLBS078-Tilley March 21, 2011 8:18

Canine and Feline, Fifth Edition 15 Acne—Dogs A

r Biopsy—histologic confirmation for cases in CONTRAINDICATIONS/POSSIBLE which diagnosis is in question. INTERACTIONS r Skin scrape—demodicosis. r BASICS r Benzoyl peroxide—may bleach carpets and Dermatophyte culture—dermatophytosis. fabrics; may be irritating. r OVERVIEW PATHOLOGIC FINDINGS Mupirocin ointments—greasy. r r r Chronic inflammatory disorder of the chin Clinical signs and histopathologic findings Topical retinoids—may be drying and and lips of young animals. are diagnostic. irritating. r r r Characterized by folliculitis and Initial lesions—hairless follicular papules; Topical steroids—may cause adrenal furunculosis. suppression with repeated use. r characterized histopathologically by marked r Recognized almost exclusively in follicular keratosis, plugging, dilatation, and Isotretinoin—may cause short-coated breeds. perifolliculitis. keratoconjunctivitis sicca, hyperactivity, ear r r Genetic predisposition may play a more Bacteria—not present and cannot be pruritus, erythematous mucocutaneous important role than hormonal effects. isolated from lesions in early stages. junction, lethargy with vomiting, abdominal r SIGNALMENT As disease progresses, papules enlarge and distension and erythema, anorexia with r Dogs. rupture, promoting a suppurative folliculitis lethargy, collapse, and swollen tongue; CBC r Predisposed short-coated breeds—boxer, and furunculosis. and chemistry screen abnormalities include Doberman pinscher, English bulldog, Great high platelet count, hypertriglyceridemia, Dane, Weimaraner, mastiff, rottweiler, and hypercholesterolemia, and high alanine German shorthaired pointer, pit bull terrier. transaminase. SIGNS TREATMENT r r Ventral chin and lip margins may be Depends on the severity and chronicity of minimally to markedly swollen with the disease. FOLLOW-UP numerous erythematous papules and pustules. r r Reduce behavioral trauma to the chin (e.g., Advanced stages—lesions may be exudative, PATIENT MONITORING rubbing on the carpet, chewing bones that r indicating secondary deep bacterial increase salivation). Continue until antibiotics until lesions have folliculitis-furunculosis. r healed. r Frequent cleaning with benzoyl peroxide r Lesions may be painful on palpation; most shampoo or gel. Repeat bacterial culture/sensitivity if lesions are non-painful and non-pruritic. r worsen. r Mupirocin 2% ointment to reduce the r Chronic resolved lesions may be scarred and bacterial numbers on the surface of the skin. Discontinue topical corticosteroids when r lichenified. Instruct owners to avoid expressing the possible. CAUSES & RISK FACTORS lesions, which may cause internal rupture of EXPECTED COURSE AND PROGNOSIS r Some short-coated breeds appear to be the papule and massive inflammation. Long-term topical treatment may be genetically predisposed to follicular required. r hyperkeratosis and secondary bacterial Chronic scarring may be prevented by early infection. and aggressive therapy. MEDICATIONS DRUG(S) Topical DIAGNOSIS r MISCELLANEOUS Benzoyl peroxide shampoo or gel DIFFERENTIAL DIAGNOSIS (antibacterial). PREGNANCY/FERTILITY/BREEDING r r Dermatophytosis Mupirocin 2% ointment Synthetic retinoids—teratogens; do not use in r Demodicosis (antibacterial-staphylococcus). pregnant animals, animals intended for r r Foreign body Isotretinoin (Accutane) and tretinoin reproduction, or intact female animals; should r (Retin-A)—may reduce follicular keratosis. Contact dermatitis r not be handled by women of childbearing CBC/BIOCHEMISTRY/URINALYSIS Corticosteroids—may be necessary to age. reduce inflammation; limit frequency of use N/A to avoid local and systemic effects. Suggested Reading OTHER LABORATORY TESTS Scott DW, Miller WH, Griffin CE. Bacterial Systemic N/A r skin diseases. In: Kirk’s Small Animal Antibiotics appropriate for deep bacterial Dermatology, 5th ed. Philadelphia: IMAGING infection—especially cephalosporins Saunders, 1995, pp. 304–305. N/A (cephalexin, 22 mg/kg PO q8h for 6–8 Author Karen Helton Rhodes weeks). DIAGNOSTIC PROCEDURES r Consulting Editor Alexander H. Werner r May need to perform bacterial culture and Bacterial culture and sensitivity testing—in sensitivity test. patients with suppurative folliculitis and r Oral corticosteroids: tapering dosages of furunculosis that are non-responsive to initial prednisolone (initial 0.5 mg/kg/day) to antibiotic selection. reduce significant inflammation; not for continued use. BLBS078-CF_A09 BLBS078-Tilley March 21, 2011 8:19

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

r r Bacterial culture and sensitivity—tissue Combine and/or withdraw administration should be submitted for culture and of these medications carefully. sensitivity as tissue cultures often differ from Topical BASICS r r surface culture. Food-elimination Flunixin meglumine and fluocinolone in r r OVERVIEW diet—determine food allergy. Intradermal dimethyl sulfoxide (combined). Mupirocin. allergy testing—helpful for atopic animals. r r Chronic or relapsing skin disease directly r Topical 5% benzoyl peroxide. Topical Biopsy—to rule out neoplasia, other r caused by the licking of the extremities. A r capsaicin products. Intralesional cycle of obsessive licking and secondary infections. Behavioral history. corticosteroids have been advocated but are r pruritus and infection may develop. rarely helpful. Topical medications should PATHOLOGIC FINDINGS r SYSTEMS AFFECTED be applied with gloves. Animals should be Histopathology—acanthosis, follicular kept from licking the area for 10–15 minutes. Skin/Exocrine elongation, lymphoplasmacytic dermal SIGNALMENT inflammation, folliculitis, furunculosis, CONTRAINDICATIONS/POSSIBLE r r perihidradenitis, hidradenitis, and vertical INTERACTIONS Dogs. Mostcommoninlarge r breeds—especially Doberman pinschers, streaking fibrosis. Doxepin—caution using with monoamine Labrador retrievers, Great Danes, Irish and oxidase inhibitors, clonidine, anticonvulsants, English setters, golden retrievers, Akitas, oral anticoagulants, steroid hormones, antihistamines, or aspirin. Dalmatians, shar-peis, and Weimaraners. r r r Antihistamines—caution using more than Age at onset—varies with the cause. Sex TREATMENT r predilection—some sources suggest more r one at a time. Hydroxyzine may decrease commoninmales;othersindicateno Affected animal should get plenty of seizure threshold. Avoid in epileptics. attention and exercise. r preference. r Psychotropic medications should be Counter-conditioning may be helpful. SIGNS r combined and/or withdrawn carefully. r Physical restraints—Elizabethan collars and Excessive licking and chewing of the r bandaging; short-term use. affected area. Occasionally a history of r r Ablation of the lesion with laser therapy has trauma to the affected area. Alopecic, been proposed but no publications evaluating ulcerative, thickened, and raised firm plaques, the efficacy of this modality are currently FOLLOW-UP r usually located on the dorsal aspect of the available. Monitor level of licking and chewing closely. carpus, metacarpus, tarsus, or metatarsus. r r r Diet—no modification unless food Treat underlying disease to prevent Lesions often occur singly, although they hypersensitivity is suspected. recurrence. r r may occur in more than one location. Difficult to treat, especially if no underlying If no underlying disease is detected, suspect CAUSES & RISK FACTORS cause is found; warn owner that patience and psychogenic causes (compulsive or time are necessary. self-mutilation disorder); prognosis is Associated diseases—staphylococcal r Surgery—do not consider until all other guarded. furunculosis, allergy, endocrinopathy, r demodicosis, dermatophytosis, foreign body therapies have been exhausted; will often Cardiotoxicity and hepatoxicity have been reaction, neoplasia, arthritis, trauma, and cause increased licking and attention to the reported in rare cases in animals on tricyclic psychogenic and sensory nerve dysfunction. affected area, resulting in poor wound closure; antidepressants. Select and monitor patients if underlying causes are not addressed, with caution. recurrence is likely.

DIAGNOSIS MISCELLANEOUS DIFFERENTIAL DIAGNOSIS MEDICATIONS AGE-RELATED FACTORS r r r < Neoplasia Bacterial furunculosis Focal DRUG(S) Dogs 5 years old—strongly consider allergy r demodicosis Focal dermatophytosis Antibiotics r CBC/BIOCHEMISTRY/URINALYSIS Based on bacterial culture and sensitivity. ZOONOTIC POTENTIAL r r Normal except in cases of Administer until infection is completely Transmitted to humans only if hyperadrenocorticism resolved; often at least 6 weeks. dermatophytosis is the underlying cause; exceedingly rare. OTHER LABORATORY TESTS Systemic r r Methicillin resistant staphylococcal species r Antihistamines—e.g., hydroxyzine (1–2 Low thyroid levels, elevated TSH—suggests may have zoonotic implications. hypothyroidism. mg/kg PO q12h); chlorpheniramine (4–8 r ABBREVIATIONS Abnormal ACTH-stimulation test or mg/dog PO q12h; maximum of 0.5 mg/kg r q12h). ACTH = adrenocorticotropin hormone abnormal LDDST—suggests r r = hyperadrenocorticism. SSRIs: e.g., fluoxetine (1 mg/kg PO q24h); LDDST low-dose dexamethasone- paroxetine (0.5–1 mg/kg PO q24h). suppression test IMAGING r r Dopamine antagonists: e.g., naltrexone TSH = thyroid stimulating hormone Radiology—neoplasia; some forms of trauma; (2.2 mg/kg PO q12–24h). radiopaque foreign bodies; bony proliferation r Suggested Reading Tricyclic antidepressants: e.g., amitriptyline Shumaker AK, Angus JC, et al. may be seen secondary to the chronic HCl (1.1–2.2 mg/kg PO q12h)—use at the irritation. Microbiological and histopathological lower dosage for 10 days and if no features of canine acral lick dermatitis. Vet DIAGNOSTIC PROCEDURES improvement, use at the higher dosage for r Dermatol 2008, 19(5):288–298. Skin scrapings—demodicosis. 10 days; doxepin (3–5 mg/kg PO q12h; r Author Jean S. Greek Dermatophyte culture—fungal infection. maximum 150 mg q12h); clomipramine r Consulting Editor Alexander H. Werner Epidermal cytology—bacterial infection. (1–3.5 mg/kg PO q12h). BLBS078-CF_A10 BLBS078-Tilley July 23, 2011 3:4

Canine and Feline, Fifth Edition 17 Acromegaly—Cats A

BASICS DIAGNOSIS TREATMENT OVERVIEW DIFFERENTIAL DIAGNOSIS RADIOTHERAPY r r r Uncomplicated DM or DM secondary to The only currently available means of Syndrome resulting from growth hormone r (somatotropin) hypersecretion by tumorous hyperadrenocorticism Pituitary-dependent reducing autonomous overproduction of GH or hyperplastic somatotrophs in the anterior hyperadrenocorticism and acromegaly can from the anterior pituitary. Unfortunately, r pituitary. Clinical signs are due to growth both produce insulin-resistant DM with an radiotherapy is more suited to reducing the size of the tumor than achieving clinically hormone’s direct catabolic/diabetogenic associated pituitary mass lesion. r effects and its indirect anabolic effects Differentiation may require use of a low-dose significant reductions in GH secretion. A dexamethasone suppression test to rule out total dose of between 3,500 and 5,500 cGY, mediated through insulin-like growth factor I, r which is secreted by the liver in response to PDH. Acromegaly and PDH can occur administered in variably fractionated doses is r r growth hormone stimulation. Elevated concurrently. Other disorders causing often suggested. Recent reports suggest that IGF1 activity induces excessive soft tissue weight loss with polyphagia, polyuria, and the greatest success may be achieved with a growth, visceral organomegaly, bone polydipsia such as hyperthyroidism are not total dose of 3,700 cGy administered as an usually associated with significant glucose incremental hypofractionated dosage protocol remodeling and thickening (especially in r bones formed from membranous ossification) intolerance. Insulin-resistant DM (> 2.0 U of 10 doses. Using this method, 13 of 14 resulting in arthropathy, broad facial features, of insulin/kg/12h) is to be expected in all acromegalic cats had markedly improved r and enlarged “clubbed” paws. Myocardial acromegaliccatsandthedosetendsto diabetic control. hypertrophy occurs in many cats, but heart increase over time, with doses of 12–50 HYPOPHYSECTOMY r r r failure is uncommon. The catabolic actions U/cat/12h not uncommon. Acromegaly In people with acromegaly, surgical removal of GH result from insulin antagonism leading should be suspected in any diabetic cat of small, non-invasive pituitary adenomas is eventually to pancreatic β cell exhaustion and demonstrating signs of otherwise unexplained frequently curative; most affected cats have DM. Between 25 and 33% of diabetic cats insulin resistance. large tumors, markedly decreasing the chance r may have acromegaly. Like most diabetic CBC/BIOCHEMISTRY/URINALYSIS for successful surgical removal; additionally, r cats the potential for remission remains if the Most abnormalities attributed to poorly hypophysectomy in cats has been associated excessive GH production can be normalized; with high levels of post-operative controlled DM—hyperglycemia, glucosuria, r likelihood of remission is inversely related to and elevated fructosamine levels are consistent complications. Cryohypophysectomy has the duration of DM. findings in most acromegalic cats. been described in two cats—one suffered a r r SIGNALMENT Hyperproteinemia. Traditionally hypoglycemic crisis and permanent blindness r r Cats Median age—11 years (range of associated with renal failure and hypertension, 2 months after surgery, while the other had a r 6–17 years) Approximately 80% are males. but more recent studies suggest this is not the more successful outcome. SIGNS case. r OTHER LABORATORY TESTS Initial signs relate to unregulated DM with r the vast majority of cases presenting with IGF1—diabetic cats receiving insulin can MEDICATIONS r polyuria, polydipsia, and often profound have higher IGF1 levels than normal; hence Long-acting somatostatin analogues— polyphagia accompanied with concurrent there is significant potential for overlap uniformly unsuccessful in cats. weight gain (weight loss has also been between acromegalic and non-acromegalic r r Pegvisomant, a GH-receptor antagonist, has reported). Many patients gain weight and diabetic cats; however, dramatically elevated been used effectively in people. Efficacy in IGF1 levels (e.g., > 1,000 ng/ml) are strongly r have increased body size due to increased r cats has not been assessed. As medical bone and soft tissue mass, not from increased suggestive of the acromegaly. IGF1 is well control of GH overproduction is not possible, preserved across the species, so valid assays are adipose tissue. Weight gain in an unregulated r the aim of medical therapy is the management diabetic cat strongly suggests acromegaly. commonly available. GH—elevated basal r of insulin-resistant DM to limit the level of Broadening of facial features, prognathia serum levels are diagnostic. However, as GH hyperglycemia and prevent ketoacidosis. inferior, and increased paw size reflect is not well preserved across the species, a Twice-daily dosing is essential with doses of long-standing or severe disease. validated fGH assay has limited availability. r 3–5 U/kg usual (no upper limit to the dose Organomegaly—most commonly bilateral IMAGING required). r r renomegaly and hepatomegaly. Murmur Intracranial imaging to demonstrate a and/or gallop rhythm occasionally present; r pituitary mass lesion; MRI is more sensitive signs of heart failure uncommon. Lameness r than contrast-enhanced CT, although the may develop. Neurological signs referable to FOLLOW-UP difference is modest and from a cost-benefit r intracranial disease through an expanding perspective CT is generally preferred. Clinical signs that might be attributed to r r pituitary mass lesion possible. Recent Echocardiographic abnormalities may poor diabetic control (e.g., profound reports suggest the majority of acromegalic include left atrial enlargement, asymmetric polyphagia) will not improve with improved cats are indistinguishable phenotypically from septal and left ventricular free-wall diabetic control; thus levels of glycated non-acromegalic diabetic cats. thickening, systolic anterior motion of the proteins or blood glucose levels are better CAUSES & RISK FACTORS mitral valve, and diastolic dysfunction. indicators of diabetic control than clinical r r r r GH hypersecretion. Progestins do not Radiographic changes include increased signs. Serum IGF1 levels are not suitable for monitoring therapy as they do not change cause GH secretion and acromegaly in cats as oropharyngeal soft tissue, degenerative r they do in dogs. arthropathy with periarticular osteophytosis, during or after radiotherapy. Reported spinal spondylosis deformans, and variable survival times vary enormously—from a few abdominal organomegaly. months to many years, and dying from causes unlikely to be related to acromegaly. Author David Church Consulting Editor Deborah S. Greco BLBS078-CF_A11 BLBS078-Tilley June 25, 2011 12:14

18 Blackwell’s Five-Minute Veterinary Consult A Actinomycosis

draining tracts and pleural or peritoneal retrospective study suggests administration for effusions must be addressed. a minimum of 3–4 months after resolution of CBC/BIOCHEMISTRY/URINALYSIS all signs; may need to be directed against other BASICS r r r Non-specific changes. Leukocytosis with a associated microbes. Penicillins—considered OVERVIEW left shift and monocytosis—reported. the drug of choice; in most cases, oral therapy r r An infectious disease caused by Nonregenerative anemia—may develop. can be initiated and parenteral is not needed; r gram-positive, branching, pleomorphic, Hypoglycemia and hyperglobulinemia— amoxicillin should be administered at 20–22 rod-shaped bacteria of the genus Actinomyces. mg/kg q8h PO. r reported. A. viscosus and A. hodeovulneris—most IMAGING CONTRAINDICATIONS/POSSIBLE commonly identified isolates (though most r INTERACTIONS isolates are not identified to the species level); Radiographs of infected bone—periosteal r new bone production, reactive osteosclerosis, Metronidazole—avoid use; actinomycosis survives in microaerophilic or anaerobic r r r and osteolysis. Thoracic radiographs— unlikely to respond. Aminoglycosides—do conditions. Rarely found as the single not use; ineffective against anaerobic alveolar and interstitial lung patterns with r bacterial agent in a lesion; more commonly, it infections. A. hordeovulneris—cell-wall is a component of a polymicrobial infection. possible lung consolidation; pleural effusion; r deficient variant (l-phase); does not usually There may be synergism between pericardial effusion; subcutaneous masses on r r respond well to penicillin; consider Actinomyces and other organisms. Organ lateral thorax. Abdominal radiographs— ◦ peritoneal effusion; mass effect in abdomen. clindamycin, erythromycin, and systems affected may include: Skin r chloramphenicol. ◦ Respiratory ◦ Cardiovascular Vertebral column radiographs—periosteal ◦ 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 FOLLOW-UP common in young male dogs of sporting in anaerobic specimen containers for culture PATIENT MONITORING breeds. (see Anaerobic Infections) can provide a definitive diagnosis; inform the lab to check SIGNS Monitor patients closely for recurrence in the r for actinomycosis; advisable to submit aerobic months after therapy discontinued. Infections—usually localized; may be r culture, as well. Fresh smears—gram PREVENTION/AVOIDANCE disseminated; cervicofacial area commonly staining, cytology, and acid-fast staining; r Avoidance of contact with grass awns and involved. Cutaneous swellings or abscesses staining does not preclude the need for prevention of bite wounds. with draining tracts—yellow granules (“sulfur culture; Actinomyces does not stain acid-fast; granules”) may be seen in associated exudates. POSSIBLE COMPLICATIONS r r Nocardia is variable. Pain, fever, and weight loss. Exudative PATHOLOGIC FINDINGS Concurrent immune-suppressive disease or pleural or peritoneal effusions; occasionally therapy may complicate management. r Histopathologic examination—sulfur pericardial effusion noted. Cough, dyspnea, EXPECTED COURSE AND PROGNOSIS decreased ventral lung sounds (empyema). granules can be difficult to find so multiple r Redevelopment of infection at the initial site Retroperitonitis—lumbar pain; rear limb tissue sections should be submitted; special r may be expected in about half of all cases. paresis or paralysis. Osteomyelitis of stains may enhance visualization of vertebrae or long bones—probably secondary organisms; granules are a useful diagnostic 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. MISCELLANEOUS r cord compression by granulomas. Pyothorax AGE-RELATED FACTORS and subcutaneous bite wounds are the most Young outdoor dogs. common presenting signs in cats. ZOONOTIC POTENTIAL CAUSES & RISK FACTORS TREATMENT r r There are no reported cases of actinomycosis Actinomyces spp. normal inhabitants of the Exudative fluid (thorax, abdomen, being transmitted from animals to man; r subcutaneous tissue) should be drained and oral cavity of dogs and cats. Loss of normal r transmission by bite wound may be possible protective barriers (mucosa, skin), lavaged. A chest tube with continuous so appropriate attention should be given to immunosuppression, or change in the suction is needed for cats with pyothorax; bite wounds. bacterial microenvironment can predispose; dogs are best served with surgical exploration thought to occur as an opportunistic of the chest prior to tube placement in order Suggested Reading r to identify and remove any grass awns. Edwards DF. Actinomycosis and mocardiosis. infection. Specific risk factors—trauma (bite r Diseased lung lobes may need to be In: Greene CE, ed., Infectious Diseases of wound), migrating foreign body (grass awn r or, in the western United States, a foxtail), removed. Dogs with solitary masses the Dog and Cat, 3rd ed. St. Louis: and periodontal disease. involving the thoracic or abdominal wall may Saunders Elsevier, 2006, pp. 451–461. experience cure with radical surgical excision. Thomovsky E, Kerl ME. Actinomycosis and nocardiosis. Compend Contin Educ Pract Vet 2008, 10:4–10. DIAGNOSIS Author Sharon Fooshee Grace MEDICATIONS Consulting Editor Stephen C. Barr DIFFERENTIAL DIAGNOSIS 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 r clinical signs. Other causes of chronic antimicrobial selection. Antibiotics—a BLBS078-CF_A12 BLBS078-Tilley July 15, 2011 1:21

Canine and Feline, Fifth Edition 19 Acute Abdomen A

r Male cats and dogs are at higher risk for Pancreas r urethral obstruction. Pain associated with inflammation, abscess, r Male Dalmatians in particular have a higher ischemia. BASICS r risk of urethral obstruction because of the Pancreatic masses or inflammation DEFINITION high incidence of urate urinary calculi. obstructing the biliary duct/papilla will cause r An emergency condition characterized by German shepherds with pancreatic atrophy jaundice. historical and physical examination findings have a higher risk of mesenteric volvulus. Hepatic and Biliary System r r of a tense, painful abdomen. May be Patients treated with corticosteroids and Rapid distention of the liver and its capsule life-threatening condition. non-steroidal anti-inflammatory drugs are at can cause pain. r PATHOPHYSIOLOGY higher risk for gastrointestinal ulceration and Gallbladder obstruction, rupture, or r perforation. A patient with an acute abdomen has pain necrosis may lead to bile leakage and SIGNS peritonitis. associated with either distention of an organ, r inflammation, traction on the mesentery or General Comments Hepatic abscess. peritoneum, or ischemia. Clinical signs vary greatly depending on the Spleen r r The abdominal viscera are sparsely type and severity of the disease leading to an Splenic torsion, splenic masses, splenic innervated, and diffuse involvement is often acute abdomen. thrombus, splenic abscess. necessary to elicit pain; nerve endings also Historical Findings Urinary Tract r r exist in the submucosa-muscularis of the Trembling, reluctance to move, Distention is the main cause of pain in the bowel wall. inappetence, vomiting, diarrhea, vocalizing, urinary tract. r r Any process that causes fluid or gaseous and abnormal postures (tucked up or praying Lower urinary tract obstruction can be due distension (i.e., intestinal obstruction, gastric position)—signs that the owner may notice. to tumors of the trigone area of the bladder or dilatation-volvulus, ileus) may produce pain. r r Question owner carefully to ascertain what urethra, urinary calculi, or granulomatous Inflammation produces abdominal pain by system is affected; for example, hematemesis urethritis. r releasing vasoactive substances that directly with a history of NSAID treatment suggests Traumatic rupture of the ureters or bladder stimulate nerve endings. r GI mucosal disruption. are associated with blunt trauma and Many nerves in the peritoneum are sensitive Physical Examination Findings increased intra-abdominal pressure. to a diffuse inflammatory response. r r Abnormalities include abdominal pain, Urethral tears can be associated with pelvic SYSTEMS AFFECTED fractures from acute trauma. r splinting of the abdominal musculature, gas- r Behavioral—trembling, inappetence, or fluid-filled abdominal organs, abdominal Free urine in the peritoneal cavity leads to a chemical peritonitis. vocalizing, lethargy, depression, and abnormal mass, ascites, pyrexia or hypothermia, r postural changes such as the praying position tachycardia, and tachypnea. Acute pyelonephritis, acute renal failure, to achieve comfort. r nephroliths, and ureteroliths are uncommon r Once abdominal pain is confirmed, attempt Cardiovascular—severe inflammation, to localize the pain to cranial, middle, or causes of acute abdomen. ischemia, and sepsis may lead to acute caudal abdomen. Genital Tract circulatory collapse (shock). r r r Perform a rectal examination to evaluate the Prostatitis and prostatic abscess, pyometra; a Gastrointestinal—vomiting, diarrhea, colon, pelvic bones, urethra, and prostate, as ruptured pyometra or prostatic abscess can inappetence, generalized functional ileus; well as the presence of melena. cause endotoxemia, sepsis, and cardiovascular r pancreatic inflammation, necrosis, and Rule out extra-abdominal causes of pain by collapse. r abscesses may lead to cranial abdominal pain, careful palpation of the kidneys and Infrequent causes include ruptures of the vomiting, and ileus. thoracolumbar vertebrae. gravid uterus after blunt abdominal trauma, r r Hepatobiliary—jaundice associated with Pain associated with intervertebral disk uterine torsion, ovarian tumor or torsion, and extrahepatic cholestasis from biliary disease often causes referred abdominal intra-abdominal testicular torsion obstruction (including pancreatitis) and bile guarding and is often mistaken for true (cryptorchid). peritonitis. r abdominal pain. Renal pain can be associated Abdominal Wall/Diaphragm Renal/Urologic—azotemia can be due to r with pyelonephritis. Umbilical, inguinal, scrotal, abdominal, or prerenal causes (dehydration, hypovolemia, CAUSES peritoneal hernias with strangulated viscera. and shock), renal causes (acute pyelonephritis r Trauma or congenital defects leading to and acute renal failure), and post-renal causes Gastrointestinal r organ displacement or entrapment in the (urethral obstruction and uroperitoneum Stomach—gastritis, ulcers, perforation, hernia will lead to abdominal pain if the from bladder rupture). foreign bodies, gastric dilatation-volvulus. r r vascular supply of the organs involved Respiratory—increased respiratory rate due Intestine—obstruction (foreign bodies, becomes impaired or ischemic. to pain or metabolic disturbances. intussusception, hernias), enteritis, ulcers, perforations. RISK FACTORS SIGNALMENT r r r Rupture after obstruction, ulceration, or Exposure to NSAIDs or corticosteroid Dogs and cats. r blunt or penetrating trauma, or due to tumor treatment—gastric, duodenal, or colonic Dogs more commonly. r growth. ulcers. Younger animals tend to have a higher r r Vascular compromise from infarction, Garbage or inappropriate food incidence of trauma-related problems, mesenteric volvulus, or torsion. ingestion—pancreatitis. intussusceptions, and acquired diet- and r Foreign body ingestion—intestinal infection-related diseases; old animals have a obstructions. greater frequency of malignancies. r Abdominal trauma—hollow viscus rupture. r Hernias—intestinal obstruction/ strangulation. BLBS078-CF_A12 BLBS078-Tilley July 15, 2011 1:21

20 Blackwell’s Five-Minute Veterinary Consult

A Acute Abdomen (Continued)

r Characterize ileus as functional (due to metabolic or infectious causes) or mechanical (due to obstruction). DIAGNOSIS r TREATMENT Foreign bodies may be radiopaque. r r DIFFERENTIAL DIAGNOSIS Upper GI barium contrast radiographs are Inpatient management with supportive care r Renal-associated pain, retroperitoneal pain, useful in evaluating the GI tract, particularly until decision about whether the problem is for determination of GI obstruction. to be treated medically or surgically. spinal or paraspinal pain, and disorders r r causing diffuse muscle pain may mimic Contrast in the area of the pancreas can be Aggressive therapy and prompt abdominal pain; careful history and physical lost with pancreatic inflammation. identification of the underlying cause is very important. examination are essential in pursuing the Abdominal Ultrasound r r Many causes of acute abdominal pain appropriate problem. A sensitive diagnostic tool for the detection r require emergency surgical intervention. Parvoviral enteritis can present similarly to of abdominal masses, abdominal fluid, intestinal obstructive disease; fecal parvoviral SUPPORTIVE CARE abscesses, cysts, lymphadenopathy, and biliary r antigen assay and CBC (leukopenia) are or urinary calculi. Keep patient NPO if vomiting, until a helpful differentiating diagnostic tests. definitive cause is determined and addressed. DIAGNOSTIC PROCEDURES r CBC/BIOCHEMISTRY/URINALYSIS Intravenous fluid therapy is usually required r Abdominocentesis/Abdominal Fluid because of the large fluid loss associated with Inflammation or infection may be Analysis associated with leukocytosis or leukopenia. r an acute abdomen; the goal is to restore the r Perform abdominocentesis on all patients normal circulating blood volume. Anemia may be seen with blood loss presenting with acute abdomen. Fluid can r associated with GI ulceration. If severe circulatory compromise (shock) r often be obtained for diagnostic evaluation exists, supplement initially with isotonic Azotemia is associated with prerenal, renal, even when only a small amount of free and post-renal causes. crystalloid fluids (90 mL/kg, dogs; 70 mL/kg, r abdominal fluid exists, well before detectable Electrolyte abnormalities can help to cats) over 1–2 hours; hypertonic fluids or radiographic sensitivity. Although colloids may also be beneficial. evaluate GI disease (i.e., hypochloremic r ultrasonography is much more sensitive than Evaluate hydration and electrolytes (with metabolic alkalosis with gastric outflow radiography for the detection of fluid, the lack obstruction) and renal disease (i.e., appropriate treatment adjustments) of such detection does not preclude frequently after commencement of treatment. hyperkalemia with acute renal failure or abdominocentesis. Abdominal fluid analysis post-renal obstruction). SURGICAL CONSIDERATIONS r with elevated WBC count, degenerate r Hyperbilirubinemia and elevated hepatic neutrophils, and intracellular bacteria is Many different causes of an acute abdomen enzymes help localize a problem to the liver or consistent with septic peritonitis and is an (with both medical and surgical treatments) biliary tract. r indication for immediate surgery. exist; make a definitive diagnosis whenever Urine specific gravity (before fluid therapy) r possible prior to surgical intervention. Diagnostic peritoneal lavage can be r is needed to differentiate prerenal, renal, and performed by introducing sterile saline This can prevent both potentially post-renal problems. r (10–20 ml/kg) and performing unnecessary and expensive surgical procedures Urine sediment may be helpful in acute abdominocentesis. and associated morbidity and mortality. r r renal failure, ethylene glycol intoxication, and Measurement of glucose concentration in It will also allow the surgeon to prepare for pyelonephritis. abdominal effusion may aid in the diagnosis the task and to educate the owner on the OTHER LABORATORY TESTS of septic abdomen. prognosis and costs involved. r r Trypsin-like immunoreactivity can be useful Pancreatitis patients may have an abdominal in evaluating feline pancreatitis. effusion characterized as a non-septic (sterile) r Canine pancreatic lipase immunoreactivity peritonitis. r is useful for canine pancreatitis. Creatinine concentration higher in MEDICATIONS IMAGING abdominal fluid than in serum indicates DRUG(S) urinary tract leakage. Abdominal Radiography r Analgesics r Similarly, higher bilirubin concentration in r May see abdominal masses or changes in abdominal fluid than in serum indicates bile Pain medication may be indicated for shape or shifting of abdominal organs. control of abdominal discomfort. r peritonitis. r Loss of abdominal detail with abdominal Opioids, such as hydromorphone at Sedation and Abdominal Palpation fluid accumulation is an indication for a r 0.05–0.1 mg/kg, are often good choices. abdominocentesis. Because of abdominal splinting associated r Histamine H2 Antagonists with pain, a thorough abdominal palpation is r Free abdominal gas is consistent with a Reduce gastric acid production. ruptured GI viscus or infection with often not possible without sedation; this is r particularly useful for detecting intestinal Famotidine 0.1–0.2 mg/kg IV, SC or IM gas-producing bacteria and is an indication q12h. for emergency surgery. foreign bodies that do not appear on survey r r Ranitidine 2 mg/kg IV q8h Use caution when interpreting radiographs radiographs. following abdominocentesis with an open Exploratory Laparotomy PPI r r needle. Free gas may be introduced with this Surgery may be useful diagnostically (as well Pantoprazole 0.5–1 mg/kg IV as a CRI over technique. as therapeutically) when ultrasonography is 24 hours. r Use caution when evaluating post-operative not available or when no definitive cause of Protectants r radiographs; free gas is a normal the acute abdomen has been established with Sucralfate 0.25–1 g PO q8h. post-operative finding. appropriate diagnostics. Antiemetics r r Ileus is a consistent finding with peritonitis. Metoclopramide 0.2–0.4 mg/kg IV q6–8h (or 24-hour continuous rate infusion). BLBS078-CF_A12 BLBS078-Tilley July 15, 2011 1:21

Canine and Feline, Fifth Edition 21

(Continued) Acute Abdomen A

r r Maropitant 1 mg/kg SC dogs, 0.5 mg/kg Pancreatitis r SC cats. Prostatitis and Prostatic Abscess r r Ondansetron 0.5–1 mg/kg IV slowly FOLLOW-UP Urinary Tract Obstruction q6–12h. ABBREVIATIONS r PATIENT MONITORING r Dolasetron 1 mg/kg IV q24h. GI = gastrointestinal Antibiotics Patients usually require intensive medical care r = r NSAID nonsteroidal anti-inflammatory Antibiotics may be indicated if signs of and frequent evaluation of vital signs and drug infection (fever, elevated white blood cell laboratory parameters. count, positive culture) are seen. Suggested Reading r Broad spectrum for gram positive, gram Beal MW. Approach to the acute abdomen. negative, and anaerobic bacteria. Vet Clin North Am Small Anim Pract 2005, r Gram stain and cultures prior to treatment MISCELLANEOUS 35:375–396. if possible. Heeren V, Edwards L, Mazzaferro EM. Acute SYNONYMS abdomen: Diagnosis. Compend Contin CONTRAINDICATIONS Colic Educ Pract Vet 2004, 26:350–363. Do not use metoclopramide if GI obstruction SEE ALSO Heeren V, Edwards L, Mazzaferro EM. Acute r is suspected. Gastric Dilation and Volvulus Syndrome abdomen: Treatment. Compend Contin r PRECAUTIONS Gastroduodenal Ulcer Disease Educ Pract Vet 2004, 26:3566–3673. r Gentamicin and most NSAIDs can be Gastrointestinal Obstruction Mazzaferro EM. Triage and approach to the r nephrotoxic and should be used with caution Intussusception acute abdomen. Clin Tech Small Anim in hypovolemic patients and those with renal Pract 2003, 18:1–6. impairment. Author Steven L. Marks Consulting Editor Albert E. Jergens BLBS078-CF_A13 BLBS078-Tilley May 31, 2011 16:59

22 Blackwell’s Five-Minute Veterinary Consult A Acute Respiratory Distress Syndrome

GENETICS CBC/BIOCHEMISTRY/URINALYSIS r Some people have been found to be more Leukocytosis or leucopenia. r BASICS prone to developing ARDS than others due to Other changes dependent on the underlying specific gene polymorphisms. This has not disease process. DEFINITION been investigated in the veterinary OTHER LABORATORY TESTS population. r Syndrome of acute onset of respiratory failure Arterial blood gases—low PaO2/FiO2 ratio typified by diffuse bilateral pulmonary INCIDENCE/PREVALENCE (where PaO2 is measured in mmHg and FiO2 infiltrates on a dorsoventral thoracic Unknown is 0.21–1.0). Normal PaO2/FiO2 ratio = 500; radiograph with no evidence of increased SIGNALMENT comparison of this ratio allows evaluation of hydrostatic pressure, cardiogenic pulmonary severity of lung disease and allows direct Species edema, or fluid overload. ARDS is due to a comparison of blood gases taken at different Dogs and cats diffuse, overwhelming inflammatory reaction FiO2.PaCO2 is often low; hypercapnia tends of the alveolocapillary membrane in response Breed Predilections to be a late (preterminal) development. r to a systemic or pulmonary inflammatory A familial form of ARDS has been reported in Total protein of airway edema fluid insult. It can be divided into two categories a group of related Dalmatian dogs; it is compared with serum total protein—ratio of based on severity. The less severe form is clinically indistinguishable from ARDS. edema fluid to serum total protein < 0.5 called acute lung injury; ALI is defined as a indicates low-protein hydrostatic pressure < Mean Age and Range PaO2/FiO2 ratio of 300; ARDS is defined Unknown pulmonary edema (e.g., heart failure); edema as a PaO2/FiO2 < 200. > Predominant Sex fluid/serum total protein ratio 0.7 indicates PATHOPHYSIOLOGY high-protein, increased permeability r Unknown ARDS is due to a diffuse inflammatory pulmonary edema such as ARDS and SIGNS insult that causes widespread damage to pneumonia. Historical Findings alveolar epithelial and endothelial cells r IMAGING resulting in impaired gas exchange. This Acute onset of respiratory distress in a Thoracic Radiographs inflammatory insult can be triggered by patient with a significant underlying disease. r r Bilateral pulmonary infiltrates. Animal is often hospitalized for its primary r primary pulmonary disease or it can be of Severity of radiographic signs may lag disease when it develops ARDS. non-pulmonary origin. Mechanisms of injury behind clinical disease by 12-24 hours. include neutrophil activation, endothelial cell Physical Examination Findings r r Can be difficult to distinguish from dysfunction, and proinflammatory Severe respiratory distress. r cardiogenic edema. Cardiac silhouette is mediator-triggered cell damage. Damage is Crackles (if present) heard bilaterally on usually normal in ARDS. thought to be exacerbated by auscultation. r Echocardiography ventilator-induced lung injury associated with Fever—depends on underlying disease. r r Attempt to rule out cardiogenic cause for alveolar over distension and cyclic opening Cyanosis in more severe cases. r r pulmonary edema. and collapse of atelectatic alveoli. Early Signs relevant to the primary disease process. r May be able to estimate degree of exudative phase—initial 12–24 hours is CAUSES typified by increased alveolar capillary pulmonary hypertension. Primary Pulmonary Causes membrane permeability; protein-rich edema r DIAGNOSTIC PROCEDURES Aspiration pneumonia fluid and white blood cells flood into the r Pulmonary artery catheter to measure Pneumonia interstitium and alveoli. Neutrophils r pulmonary artery occlusion pressure in order Pulmonary contusion exacerbate damage by further release of r to rule out cardiogenic cause for edema; by cytokines and inflammatory mediators. Near drowning r r definition, ALI and ARDS are associated with Type I alveolar epithelial cells die. Alveolar Smoke inhalation PAOP ≤ 18 mmHg. flooding and surfactant dysfunction lead to Non-pulmonary Causes r PATHOLOGIC FINDINGS collapse and consolidation of alveoli with Severe systemic inflammatory response r Gross Pathology development of severe hypoxemia. Sepsis r r Microthrombi in the pulmonary Neoplasia Lungs are dark, heavy, and ooze fluid when r vasculature, hypoxic pulmonary Pancreatitis cut. r vasoconstriction, and release of endogenous Severe trauma and shock Histopathology r r vasoconstrictors lead to pulmonary arterial Severe bee sting envenomation Acute phase—pulmonary vascular hypertension, which can lead to right-sided congestion with edema fluid and r RISK FACTORS heart failure. Hyaline membrane r inflammatory cell accumulation in the SIRS phase—hyaline membrane formation in the r interstitium and alveoli; epithelial cell Sepsis alveolar spaces 3-7 days after initial insult. r damage, hyaline membrane formation, r Severity of illness Fibroproliferative phase—if the patient r microthrombi, microatelectasis. Multiple transfusions r survives the initial 3-7 days, proliferation of r Proliferative phase—hyperplasia of type 2 Co-existing disease conditions type 2 alveolar epithelial cells and pulmonary pneumocytes, interstitial mononuclear r fibrosis occurs. An idiopathic form of infiltration, organization of hyaline ARDS associated with acute interstitial membranes, and fibroproliferation. pneumonia or idiopathic pulmonary fibrosis has been reported in people and dogs. DIAGNOSIS SYSTEMS AFFECTED DIFFERENTIAL DIAGNOSIS r r Respiratory. Left-side congestive heart failure TREATMENT r r Cardiovascular—right-side heart failure Fluid overload r APPROPRIATE HEALTH CARE secondary to pulmonary hypertension; Diffuse pneumonia r r There is no specific therapy. General aims hemodynamic compromise may be associated Pulmonary hemorrhage are to maintain tissue oxygenation and to with aggressive mechanical ventilator settings. BLBS078-CF_A13 BLBS078-Tilley May 31, 2011 16:59

Canine and Feline, Fifth Edition 23

(Continued) Acute Respiratory Distress Syndrome A

minimize iatrogenic lung injury while treating r the underlying disease. Oxygen therapy—no > more than is required to maintain PaO2 MEDICATIONS MISCELLANEOUS 60–80 mmHg to minimize oxygen toxicity. r Positive-pressure ventilation is essential in DRUG(S) OF CHOICE ASSOCIATED CONDITIONS r r the management of ARDS patients. It is No specific drug therapy. Antibiotics for Systemic inflammatory response syndrome, indicated in patients that are hypoxemic the underlying disease, if necessary. multiple organ dysfunction syndrome, r despite oxygen therapy, patients requiring Vasoactive drugs to maintain blood sepsis. r high levels of inspired oxygen for prolonged pressure. Anesthetic drugs to allow SYNONYMS r r periods, or patients working so hard to positive-pressure ventilation. Analgesia as Acute hypoxemic respiratory failure r r breathe that they are at risk of exhaustion. appropriate. Low-dose corticosteroid—use Acute interstitial pneumonia r Lung-protective strategies of positive-pressure remains controversial with conflicting reports Adult respiratory distress syndrome r ventilation with moderate to high PEEP, low of efficacy for low-dose steroids in early or late High-protein pulmonary edema r tidal volumes, and permissive hypercapnia are ARDS. Shock lung recommended to minimize ventilator-induced ALTERNATIVE DRUG(S) SEE ALSO lung injury. Tidal volumes of 6 ml/kg have r Furosemide may produce pulmonary venous Dyspnea and Respiratory Distress been found to increase survival significantly in r dilation and improve lung function, as an Panting and Tachypnea human ARDS patients compared to tidal r r intermittent bolus of 1 mg/kg IV q6–12h or Pulmonary Edema, Non-cardiogenic volumes of 12 ml/kg. Recruitment as a CRI of 0.2 mg/kg/h IV. r maneuvers and high levels of PEEP can both Sepsis and Bacteremia cause significant hemodynamic compromise ABBREVIATIONS r and patients should have constant direct ALI = acute lung injury arterial blood pressure monitoring. r = r FOLLOW-UP ARDS acute respiratory distress Intensive supportive care of the syndrome r cardiovascular system and other organ systems PATIENT MONITORING CRI = constant rate infusion r is vital, as these patients are at high risk for Arterial blood gases, pulse oximetry, end-tidal DIC = disseminated intravascular development of multiple organ dysfunction. carbon dioxide, thoracic radiographs, arterial coagulation r NURSING CARE blood pressure, ECG, temperature, urine PAOP = pulmonary artery occlusion r Monitor temperature closely, especially if output, CBC, coagulation profiles, serum pressure (formerly pulmonary capillary wedge using an oxygen cage, as animals with chemistry, blood cultures, monitoring for pressure [PCWP]) r = excessive work of breathing can easily become other organ dysfunction. PEEP positive end-expiratory pressure r r = hyperthermic. Ventilator patients require PREVENTION/AVOIDANCE PPV positive-pressure ventilation r r = frequent position changes and physiotherapy; Aggressive therapy of primary disease SIRS systemic inflammatory response regular oral care with a dilute chlorhexidine processes to reduce the inflammatory insult to syndrome r solution is very important to reduce oral the lung. Intensive cardiovascular INTERNET RESOURCES colonization as a source of sepsis, and monitoring and support of critically ill http://www.ardsnet.org. frequent endotracheal tube suctioning is animals to ensure adequate tissue perfusion. r needed to prevent occlusion. Inflate cuff Careful management of recumbent animals Suggested Reading carefully and change endotracheal cuff to reduce the chance of aspiration, especially Marino PL. Acute respiratory distress position regularly to prevent tracheal damage. syndrome. In: The ICU Book, 2nd ed. r if patient has neurologic disease or upper Blood pressure monitoring, as septic Baltimore: Williams & Wilkins, 1998, r airway disorders that reduce the ability to patients are prone to hypotension. Fluid protect the airway. pp. 371–387. Parent C, King LG, Van Winkle TJ, Walker therapy is important to support the POSSIBLE COMPLICATIONS cardiovascular system and to maintain r LM. Respiratory function and treatment in Multiorgan dysfunction syndrome—acute normovolemia while avoiding fluid overload. dogs with acute respiratory distress renal failure, DIC, and gastrointestinal disease syndrome: 19 cases (1985–1993). JAVMA ACTIVITY are the more common organ dysfunctions r 1996, 208:1428–1433. If not anesthetized for ventilation, strict cage seen. Barotrauma—can result in Syrja P, Saari S, Rajamaki M, Saario E, confinement. pneumothorax. Incidence is thought to be less Jarvinen A-K. Pulmonary histopathology in DIET with lower tidal volume ventilation strategies. r Dalmatians with familial acute respiratory Nutritional support is important but Ventilator-associated pneumonia—patients distress syndrome (ARDS). J Comp Pathol challenging. Enteral feeding is desired over on PPV have increased risk of pneumonia 2009, 141(4):254–259. parenteral nutrition, but must consider high that may be difficult to differentiate from Ware LB, Bernard GR. Acute lung injury and risk of regurgitation and aspiration in a worsening of the initial lung injury. Airway acute respiratory distress syndrome. In: cultures should be considered in deteriorating recumbent patient. r Textbook of Critical Care, 5th ed. CLIENT EDUCATION patients. Oxygen toxicity may be Philadelphia: Elsevier Saunders, 2005, unavoidable due to severity of hypoxemia in pp. 571–579. Clients need to be aware of the guarded spite of PPV. Oxygen toxicity is Ware LB, Matthay MA. The acute respiratory prognosis and high costs of therapy. indistinguishable from ARDS on distress syndrome. N Engl J Med 2000, SURGICAL CONSIDERATIONS histopathology making the incidence of this 342:1334–1349. The underlying disease may require surgery. problem impossible to determine. Author Kate Hopper EXPECTED COURSE AND PROGNOSIS Consulting Editor Lynelle R. Johnson r Mortality in human patients remains at 40–60%. r Mortality in veterinary patients likely approaches 100%. BLBS078-CF_A14 BLBS078-Tilley June 25, 2011 14:46

24 Blackwell’s Five-Minute Veterinary Consult A Adenocarcinoma, Anal Sac

DIAGNOSTIC PROCEDURES EXPECTED COURSE AND PROGNOSIS r r Fine-needle aspiration of anal sac mass to Guarded prognosis with both local r BASICS rule out conditions other than progression and metastasis occurring. Cures adenocarcinoma; differentiation of benign may occur if tumor is found early and treated r OVERVIEW versus malignant neoplasm of perianal masses aggressively. Growth of the tumor may be r r Uncommon malignant neoplasm derived is difficult. Fine-needle aspiration of slow and debulking lymph node metastatic r from apocrine glands of the anal sac. Locally enlarged lymph nodes, liver, or splenic disease may significantly prolong survival. r r r invasive. High metastatic rate, often to nodules to confirm metastasis. Incisional Hypercalcemia is variably associated with a r r sublumbar lymph nodes. Frequently biopsy for histopathology required for poor prognosis. Four papers (involving 200 associated with hypercalcemia, secondary to definitive diagnosis, although excisional dogs) showed median survival times of 6 to parathyroid hormone—related peptide biopsy may be appropriate if location of mass 20 months, depending on stage and r r secretion by tumor cells. Prognosis guarded and cytology are supportive of anal gland treatment. A recent report on 16 dogs to fair. neoplasia. without metastasis showed a median survival SIGNALMENT time not met with a follow-up of 33 months. r ◦ Dogs with lymph node metastasis lived Older dogs; extremely rare in cats. r significantly longer if the nodes were Females overrepresented in a few small r r extirpated. Ultimately, dogs that cannot studies, not in larger studies. May have TREATMENT r r have their tumors excised completely increased risk with neutering (particularly Surgical resection—treatment of choice. If r r succumb to hypercalcemia-related males). English cocker spaniels significantly caught early, cure is possible. Resection of complications or mass effect from primary overrepresented, springer and Cavalier King primary tumor and enlarged lymph nodes r tumor or sublumbar nodal metastases. Charles spaniels also overrepresented. may prolong survival. If mass is large and regionally invasive at diagnosis, surgery often SIGNS r palliative, not curative. Debulking all disease Historical Findings present may control hypercalcemia until r MISCELLANEOUS Signs may be due to primary tumor (rectal tumor recurrence. Saline diuresis (200–300 mass, tenesmus), local lymph node metastasis mL/kg/day) preoperatively if hypercalcemia is ASSOCIATED CONDITIONS (tenesmus, constipation, stranguria), or r severe. Radiation may help delay local Hypercalcemia as a paraneoplastic syndrome hypercalcemia (anorexia, polyuria/polydipsia, recurrence and control growth of sublumbar lethargy). ABBREVIATIONS metastases—acute and chronic radiation side = Physical Examination Findings PTHrP parathyroid hormone-related r effects can be moderate to severe. Mass associated with anal sac; may be quite peptide small despite massive metastatic disease. r Suggested Reading Sublumbar lymphadenopathy—on rectal or Anderson CR, McNeil EA, Gillette EL, et al. abdominal palpation. MEDICATIONS Late complications of pelvic irradiation in CAUSES & RISK FACTORS 16 dogs. Vet Radiol Ultrasound 2002, DRUG(S) Hormonal role hypothesized r 43:187–192. Limited reports of partial responses to Emms SG. Anal sac tumours of the dog and platinum compounds in dogs—cisplatin their response to cytoreductive surgery and (70 mg/m2 IV with 6-hour saline chemotherapy. Australian Vet J 2005, diuresis—18.3 mL/kg/hour), carboplatin 83:340–343. DIAGNOSIS (300 mg/m2 IV as a slow bolus) every 3 r Polton GA, Brearley MJ. Clinical stage, DIFFERENTIAL DIAGNOSIS weeks. Mitoxantrone (5 mg/m2 IV every 3 therapy, and prognosis in canine anal sac r r Anal sac abscess Perianal adenoma/ weeks for five treatments) in combination gland carcinoma. J Vet Intern Med 2007, r adenocarcinoma Mast cell tumor with radiation therapy used in one small case 21:274–280. r r r Lymphoma Squamous cell carcinoma series. Possible role for melphalan after Turek MM, Forrest LJ, Adams WM, et al. r 2 Perineal hernias debulking surgery (7 mg/m PO daily for 5 Postoperative radiotherapy and days every 3 weeks). CBC/BIOCHEMISTRY/URINALYSIS mitoxantrone for anal sac adenocarcinoma r CONTRAINDICATIONS/POSSIBLE in the dog: 15 cases (1991-2001). Vet Hypercalcemia—25–50% of cases r INTERACTIONS Comp Onc 2003, 1:94–104. Secondary renal failure may develop r Avoid platinum chemotherapeutic agents in Williams LE, Gliatto JM, Dodge RK, et al. OTHER LABORATORY TESTS r dogs with renal insufficiency. Do not use Carcinoma of the apocrine glands of the Parathyroid hormone and PTHrP cisplatinincats. anal sac in dogs: 113 cases (1985–1995). levels—high PTHrP will help to support JAVMA 2003, 223:825–831. neoplasia as the cause of hypercalcemia. Author Laura D. Garrett IMAGING Consulting Editor Timothy M. Fan r Abdominal radiography—to evaluate FOLLOW-UP sublumbar lymph nodes and lumbar and r PATIENT MONITORING Client Education Handout pelvic bones. Thoracic radiography—to r available online evaluate for pulmonary metastasis. Complete resection—physical examination, r Abdominal ultrasonography—may identify thoracic radiography, abdominal mildly enlarged sublumbar lymph nodes not ultrasonography, and serum biochemistry at 1, 3, 6, 9, and 12 months post-operatively. visible radiographically, also nodules in r liver/spleen. Incomplete resection—monitor tumor size and blood calcium and renal values. BLBS078-CF_A15 BLBS078-Tilley March 21, 2011 9:42

Canine and Feline, Fifth Edition 25 Adenocarcinoma, Lung A

IMAGING CONTRAINDICATIONS/POSSIBLE r Thoracic radiography—usually INTERACTIONS r BASICS demonstrates a focal, solitary, Doxorubicin—monitor patients with well-circumscribed mass; must be performed underlying cardiac disease carefully; consider OVERVIEW in cats presenting with multiple digit tumors pretreatment with diphenhydramine and r Comprises 75% of primary pulmonary to screen for primary lung tumor (lung-digit serial echocardiograms and ECGs. r r r tumors in dogs and cats. Primary syndrome). Ultrasonography—may help Cisplatin—do not give to cats (fatal); do pulmonary tumors are rare in dogs and cats. with obtaining an aspirate or biopsy specimen, not use in dogs with preexisting renal disease; r r Strongest predictors of outcome are tumor or to evaluate abdomen. CT—most accurate never use without appropriate and concurrent grade, node involvement, and clinical signs. assessment for determining surgical feasibility, diuresis. r r May metastasize. May be associated with and identification of lymphadenopathy (93% hypertrophic osteopathy. accuracy) and metastatic disease. SIGNALMENT DIAGNOSTIC PROCEDURES r FOLLOW-UP Dogs Thoracocentesis with cytologic examination r r 1% of all tumors. Mean age of affected (for pleural effusion). PATIENT MONITORING r r r animals 10 years, most dogs are older. No Cytology—transthoracic fine-needle Serial thoracic radiographs—consider every sex predilection, though more females in aspiration (83% agreement with 3 months; administer a minimum of two r some reports. Boxers or brachycephalic histopathology); this may be guided by cycles of chemotherapy before evaluating r r breeds may be predisposed. Medium to imaging such as CT scan or fluoroscopy, or if response to treatment. Perform CBC (with large breeds overrepresented. the tumor is peripherally located against the any chemotherapy) and renal panel (cisplatin) thoracic wall, then ultrasound may be used. Cats r before each chemotherapy treatment. r r Percutaneous tissue biopsy—use Tru-Cut More rare than in dogs. Mean age of r POSSIBLE COMPLICATIONS r instrument. Open lung biopsy—specimen affected animals 11 years. No breed Pneumothorax or hemothorax r via thoracotomy, or minimally invasive predilection. Some studies suggest females EXPECTED COURSE AND PROGNOSIS thoracoscopy. are overrepresented. r PATHOLOGIC FINDINGS Metastasis to the tracheobronchial lymph SIGNS r nodes—single best prognostic indicator; Adenocarcinoma—classified according to Historical Findings median survival without metastasis location (bronchial, bronchiolar, Related to Presence of a Lung Mass approaches 1 year and with metastasis, r bronchiolar-alveolar, or alveolar) and degree r ∼ Non-productive cough (> 50% of dogs). r 60 days. Post-operative survival in dogs ( 1 r of differentiation. Thyroid transcription ∼ Dyspnea (may be related to pneumothorax). yr)isbetterthanincats( 4 months), but r r r factor-1 positivity may distinguish primary around 2 years in either species if positive Tachypnea. Weight loss. Hemoptysis. r r r from metastatic carcinoma. Undifferentiated prognostic factors are present. Other Pain—pleural involvement. tumors—more invasive and more likely to Paraneoplastic Signs patient, tumor, and treatment factors r metastasize than well-differentiated tumors; Lameness—bone metastasis or hypertrophic influencing prognosis—complete surgical sites of metastasis include lymph nodes, < osteopathy (dogs or cats), weight-bearing lytic excision; size of the primary tumor ( 5cm r bones, pleura, eyes (choroid), and CNS. digit metastasis (cats). Polyuria or r better); metastasis (better if none); degree of Cats tend to have less differentiated tumors, cell differentiation (histologic score, better if polydipsia—hypercalcemia or corresponding to more aggressive behavior. hyperadrenocorticism from ectopic well differentiated), lack of clinical signs prior r production of ACTH. Weakness or muscle to surgery. wasting—polyneuropathy; polymyopathy. Physical Examination Findings r r TREATMENT May be asymptomatic. Tachypnea and r r r r MISCELLANEOUS dyspnea. Fever. Limb swelling. Pleural Surgery—mainstay of treatment; partial or r effusion. Caval syndrome. complete lobectomy with tracheobronchial PREGNANCY/FERTILITY/BREEDING lymph node biopsy or removal. Chemotherapy is not advised in pregnant CAUSES & RISK FACTORS r r Radiotherapy—reports are anecdotal, but animals Potential urban environment risk r r certain patients may benefit. Chemotherapy ABBREVIATIONS Potential exposure to passive cigarette smoke r should be considered following surgery for ACTH = adrenocorticotropic hormone r r tumors that are high grade, undifferentiated, CNS = central nervous system CT = r and/or have nodal involvement. Select centers computed tomography ECG = DIAGNOSIS may offer inhalant chemotherapy for higher electrocardiogram local concentrations with less systemic side DIFFERENTIAL DIAGNOSIS r Suggested Reading r effects. Intracavitary chemotherapy can be Paoloni MC, Adams WM, Dubielzig RR, et Granulomatous lesion (fungal, foreign body, r used to treat pleural effusion. al. Comparison of results of computed parasitic) Lymphomatoid or eosinophilic r r tomography and radiography with granulomatosis Pulmonary abscess Other r histopathologic findings in tracheobronchial primary lung tumor Metastatic lung tumor r r r lymph nodes in dogs with primary lung Pneumonia Asthma Pulmonary r r MEDICATIONS tumors: 14 cases (1999–2002). JAVMA thromboembolism Congenital cyst Lung 2006, 228(11):1718–1722. torsion or hematoma DRUG(S) r Rissetto KC, Lucas P, Fan TM. An update on CBC/BIOCHEMISTRY/URINALYSIS Vinorelbine concentrates in lungs and r diagnosing and treating primary lung No specific abnormalities responses have been seen. Doxorubicin, cisplatin, carboplatin, mitoxantrone, tumors. Vet Med 2008, 103(3):154. OTHER LABORATORY TESTS Author KimA.Selting r r vinorelbine, and/or vindesine—rational Arterial blood gas. Clotting times should choices for palliation. Consulting Editor Timothy M. Fan be performed prior to aspirate or biopsy. Acknowledgement Renee Al-Saraff BLBS078-CF_A16 BLBS078-Tilley March 21, 2011 9:45

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

CBC/BIOCHEMISTRY/URINALYSIS r r Usually normal Occasional blood loss BASICS anemia FOLLOW-UP OTHER LABORATORY TESTS OVERVIEW r PATIENT MONITORING r Cytologic examination: occasionally helpful Represents less than 5% of all tumors in (e.g., aspirates of the subcutaneous mass if Survey skull radiography or preferably r r dogs and cats. Progressive local and regional facial deformity). Coagulation profile. CT/MRI when clinical signs recur or periodically. invasion of the nasal cavity, paranasal sinuses, IMAGING and surrounding tissues by neoplastic r EXPECTED COURSE AND PROGNOSIS epithelial and glandular epithelial cells. Survey skull radiography—may show r r Untreated—median survival around 3–4 Often has progressed to bilateral asymmetrical destruction of turbinates r r months. Radiation therapy—median involvement by the time of diagnosis. Many accompanied by a soft tissue mass effect; may r see fluid density in the frontal sinuses survival times around 12–18 months in dogs arise from the frontal sinuses. In dogs, r secondary to outflow obstruction. Thoracic and 10–18 months in cats; 1-year survival rate adenocarcinoma is more common than 20–57% (dogs and cats); 2-year survival rate squamous cell carcinoma, chondrosarcoma, radiography—evaluate for lung metastasis r r r 20–48% (dogs and cats). Presence of brain and other histologies. In cats, most common (uncommon). CT or MRI best imaging method for local staging and observing involvement or metastatic disease (advanced sinonasal tumor is lymphoma, followed by stage) are poor prognostic indicators. adenocarcinoma and other histologies. integrity of cribriform plate or orbital r invasion, and also used for therapeutic Ophthalmic complications of radiation SIGNALMENT therapy—more likely in dogs than cats. r r planning. r Dogs and cats. Median age in dogs is 10 Chronic rhinitis is common following r DIAGNOSTIC PROCEDURES years, versus 13 years in cats. In dogs, r radiation therapy for sinonasal tumors and Blood pressure, thorough oral exam under medium to large breeds affected more r may require symptomatic therapy. commonly with a possible overrepresentation anesthesia. Rhinoscopy may permit visual of mesocephalic and dolichocephalic breeds. observation of the mass; avoid progressing caudally into the cribriform plate. Procedure SIGNS may not be necessary if mass confirmed via MISCELLANEOUS Historical Findings advanced imaging or when facial deformity is r r Intermittent and progressive history of identified. Tissue biopsy necessary for ABBREVIATIONS r r unilateral to bilateral epistaxis and/or definitive diagnosis. Biopsies may be CT = computed tomography MRI = mucopurulent discharge (median duration, 3 performed blind, following advanced magnetic resonance imaging r r months). Epiphora. Sneezing and imaging, using pinch biopsy instrument, increased upper respiratory noises. cannula (closed suction), or hydropulsion Suggested Reading r r r Adams WA, Bjorling DE, McAnulty JF, et al. Open-mouth breathing. Halitosis. techniques. Cytologic evaluation of regional r r Outcome of accelerated radiotherapy alone Anorexia (more frequent in cats). Seizures lymph nodes to detect metastatic disease. or accelerated radiotherapy followed by (secondary to invasion of cranial vault). exenteration of the nasal cavity in dogs with Physical Examination Findings r intranasal neoplasia: 53 cases (1990–2002). Nasal discharge (blood, mucopurulent). r JAVMA 2005, 227:936–941. Facial deformity, exophthalmia. TREATMENT r Hahn KA, Knapp DW, Richardson RC, Space-occupying orbital mass (eye cannot r r Surgery alone ineffective due to extent and Matlock CL. Clinical response of nasal r be retropulsed). Pain upon nasal or invasiveness. Turbinectomy may be done adenocarcinoma to cisplatin chemotherapy paranasal sinus palpation or upon opening the r r before or after irradiation. Radiation in 11 dogs. JAVMA 1992, 200:355–357. mouth. Decreased or absent airflow in the therapy is standard therapy and provides best Henry CJ, Brewer WG, Tyler JW, et al. nasal passages (unilateral or bilateral). r r clinical results in dogs and cats. Survival in dogs with nasal adenocarcinoma: Regional lymphadenomegaly. Abnormal 64 cases (1981–1995). J Vet Intern Med mentation or other neurological findings. 1998, 12:436–439. CAUSES & RISK FACTORS LaDueTA,DodgeR,PageRL,etal.Factors Dolichocephalic morphology, urban MEDICATIONS influencing survival after radiotherapy of environment, and second-hand smoke may all nasal tumors in 130 dogs. Vet Radiol DRUG(S) Ultrasound 1999, 40:312–317. play a role. r Chemotherapy may benefit some patients. Langova V, Mutsaers AJ, Phillips B, Straw R. Various drugs have been described including Treatment of eight dogs with nasal tumours cisplatin (dogs only), carboplatin, with alternating doses of carboplatin and doxorubicin, and piroxicam. Consult with an doxorubicin in conjunction with oral DIAGNOSIS r oncologist for more details. Adequate piroxicam. Australian Vet J 2004, DIFFERENTIAL DIAGNOSIS analgesic therapy should be employed as 82:676–680. r Other sinonasal tumors (e.g., squamous cell needed in patients suffering from invasive Rassnick KM, Goldkamp CE, Erb HN, et al. r carcinoma, lymphoma, sarcomas). Viral disease with bone destruction, signs of pain, Evaluation of factors associated with survival r and painful radiation therapy side effects. in dogs with untreated nasal carcinomas: infection—cats. Fungal infections including r aspergillosis (dogs) and cryptococcosis (cats). Novel therapies may be considered with 139 cases (1993–2003). JAVMA 2006, r r r Foreign body. Trauma. Tooth root cases that are unresponsive to standard 229:401–406. r abscess and oronasal fistula. Coagulopathies. therapy. Author Louis-Philippe de Lorimier r r Parasites (e.g., nasal mites). Ehrlichiosis, Consulting Editor Timothy M. Fan r CONTRAINDICATIONS/POSSIBLE leishmaniasis. Systemic hypertension. r INTERACTIONS Bacterial sinusitis—rare. Cisplatin—never use in cats BLBS078-CF_A17 BLBS078-Tilley March 21, 2011 9:47

Canine and Feline, Fifth Edition 27 Adenocarcinoma, Pancreas A

r IMAGING Peritonitis r r Abdominal radiographs may reveal a mass Metastasis BASICS or loss of serosal detail associated with EXPECTED COURSE AND PROGNOSIS concurrent pancreatitis. r Progression to death is often rapid given that OVERVIEW Ultrasonography may reveal a mass or r there is no successful curative treatment Malignant tumor of ductal or acinar origin concurrent pancreatitis (mixed echogenicity, available. arising from the exocrine pancreas. large pancreas, hyperechoic peripancreatic r Usually metastatic by the time of diagnosis. fat). Pancreatic thickening, abdominal SIGNALMENT effusion, and single to multiple nodules of r varying size may be identified. Sonographic Rare in dogs—0.5–1.8% of all tumors MISCELLANEOUS r findings may be impossible to distinguish Rare in cats—2.8% of all tumors r from pancreatic nodular hyperplasia. Rarely ASSOCIATED CONDITIONS Older female dogs and Airedale terriers at the ultrasound of the pancreas may appear higher risk than others Gastrin-secreting pancreatic carcinoma r normal except for dilation of the pancreatic Median age (dogs)—9.2 years (gastrinoma) has been reported in dogs and duct. cats. Clinical signs are associated with SIGNS r DIAGNOSTIC PROCEDURES hypergastrinemia, which results in r Non-specific—fever; vomiting; weakness; Surgical biopsy—definitive diagnosis inappropriate hydrochloric acid secretion by anorexia; icterus; maldigestion; weight loss. r r Fine-needle aspirate cytology—supportive the stomach, leading to gastroduodenitis. Abdominal pain—variable. r diagnosis Metastasis to bone and soft tissue common. Suggested Reading r Pathologic fractures secondary to metastasis Cave T, Evans H, Hargreavest J, et al. reported. Metabolic epidermal necrosis in a dog r Abdominal mass. associated with pancreatic adenocarcinoma, r Paraneoplastic syndromes of epidermal TREATMENT hyperglucagonaemia, hyperinsulinaemia, r necrosis, hyperinsulinemia, and None reported curative. and hypoaminoacidaemia. J Small Anim r hyperglucagonemia may be present. Palliation of pain and intestinal and biliary Pract 2007, 48:522–526. CAUSES & RISK FACTORS obstruction—surgery, if necessary. Hecht S, Penninck DG, Keating JH. Imaging r Partial or total pancreatectomy. findings in pancreatic neoplasia and nodular Unknown r Treat concurrent pancreatitis. hyperplasia in 19 cats. Vet Radiol r Antiemetics and supportive care (hydration Ultrasound 2006, 48:45–50. and caloric requirements). Lurcye JC, Behrend EN. Endocrine tumors. Vet Clin North Am Small Anim Pract 2001, DIAGNOSIS 31:1083–1110. DIFFERENTIAL DIAGNOSIS Morrison WB. Primary cancers and r cancer-like lesions of the liver, biliary Primary pancreatitis; may be concurrent MEDICATIONS epithelium, and exocrine pancreas. In: and complicate or delay early diagnosis. r DRUG(S) Morrison WB, ed., Cancer in Dogs and Pancreatic pseudocyst. r r Cats: Medical and Surgical Management. Pancreatic nodular hyperplasia. Gemcitabine is used in humans for the r Jackson, WY: Teton NewMedia, 2002, Hepatic neoplasia. treatment of pancreatic carcinoma, and while r pp. 535–544. Other causes of vomiting and icterus. used in dogs with cancer, it has not been established as the standard of care for dogs Newman SJ, Steiner JM, Woosley K, et al. CBC/BIOCHEMISTRY/URINALYSIS with pancreatic adenocarcinoma. Correlation of age and incidence of r r Usually non-specific changes (e.g., mild Always consult a veterinary oncologist for pancreatic exocrine nodular hyperplasia in anemia and neutrophilia). the dog. Vet Pathol 2005, 42:510–513. r updates in treating this rare neoplasm. Hyperamylasemia less reliable than CONTRAINDICATIONS/POSSIBLE Quigley KA, Jackson ML, Haines DM. hyperlipasemia. Hyperlipasemia in 6 dogs with pancreatic or r Lipase concentrations are often markedly INTERACTIONS hepatic neoplasia: Evidence for tumor lipase elevated and may be of tumor origin and N/A production. Vet Clin Pathol 2001, therefore can serve as a non-invasive 30:114–120. biochemical marker of neoplasia of the Author Wallace B. Morrison pancreas and liver in dogs. Consulting Editor Timothy M. Fan OTHER LABORATORY TESTS FOLLOW-UP Rarely there may be significant metabolic POSSIBLE COMPLICATIONS alterations that affect glucagon, insulin, and Intestinal Obstruction amino acid concentrations. r Biliary obstruction r Pancreatic abscess BLBS078-CF_A18 BLBS078-Tilley March 21, 2011 9:53

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

r r Post-renal azotemia may be present if Pain relief with NSAIDs, morphine-derived urethral obstruction exists. drugs. r r BASICS It is prudent to evaluate urine samples via Stool softeners to relieve tenesmus. cystocentesis and free-catch techniques, as CONTRAINDICATIONS/POSSIBLE OVERVIEW hematuria, pyuria, and malignant epithelial INTERACTIONS r cells may be observed in free-catch samples Prostatic adenocarcinoma is a malignant N/A tumor that occurs in both neutered and intact but are unusual in samples obtained by male dogs. cystocentesis. r Although this neoplasm represents < 1% of OTHER LABORATORY TESTS all canine malignancies, it is the most Serum and seminal plasma markers such as FOLLOW-UP common prostatic disorder in neutered male acid phosphatase, prostate specific antigen, dogs. PATIENT MONITORING r and canine prostate specific esterase are not Metastases to regional lymph nodes, lungs, elevated in dogs with PAC. Ability to urinate and defecate, pain secondary and the lumbosacral skeleton are common. IMAGING to skeletal metastases, quality of life. SIGNALMENT r PREVENTION/AVOIDANCE r Thoracic radiography—metastases may Dogs and rarely cats r appear as pulmonary nodules or increased Keeping dogs sexually intact may decrease Medium- to large-breed intact or neutered interstitial markings. risk male dogs r r Abdominal radiography—sublumbar POSSIBLE COMPLICATIONS Median age of 9–10 years r lymphadenomegaly, mineralization of the Urethral obstruction SIGNS r prostate, lytic lesions to the lumbar vertebrae Metastasis to regional lymph nodes, or pelvis may be seen. Historical Findings r skeleton, and lungs r Abdominal ultrasonography—focal to Tenesmus (with the production of EXPECTED COURSE AND PROGNOSIS ribbon-like stool) multifocal hyperechogenicity with asymmetry r ± Guarded to poor, survival of 2–6 months Weight loss and irregular prostatic outline, prostatic r depending upon presenting clinical Stranguria and dysuria mineralization. r r symptoms. Rear limb lameness Contrast cystography may help differentiate r Lethargy prostatic from urinary bladder disease. r Exercise intolerance DIAGNOSTIC PROCEDURES r Physical Examination Findings Prostatic aspirate (percutaneous or r transrectal). MISCELLANEOUS A firm, asymmetrical, and immobile r prostate gland. Prostatic wash. ASSOCIATED CONDITIONS r r Prostatomegaly is common, but is not Prostatic biopsy performed percutaneously None or surgically. always present. r AGE-RELATED FACTORS r Percutaneous biopsy has been associated Pain may be elicited in response to None abdominal or rectal palpation. with tumor seeding along the biopsy tract. r ZOONOTIC POTENTIAL Caudal abdominal mass, cachexia, pyrexia, and dyspnea may also be identified. None CAUSES & RISK FACTORS PREGNANCY/FERTILITY/BREEDING Neutered males are at increased risk for TREATMENT N/A r prostatic neoplasia Prostatectomy if local disease (success of this ABBREVIATIONS r procedure depends on the skill of the surgeon NSAID = nonsteroidal anti-inflammatory and extent of disease). drug r r Radiation therapy may palliate signs and PAC = prostatic adenocarcinoma prolong survival. DIAGNOSIS r Neutering—however, most tumors are not Suggested Reading DIFFERENTIAL DIAGNOSIS Bryan JN, et al. A population study of r androgen responsive. Other primary neoplasia (i.e., squamous cell neutering status as a risk factor for canine carcinoma, transitional cell carcinoma). prostate cancer. Prostate 2007, r Metastatic or locally invasive neoplasia (i.e., 67:1174–1181. transitional cell carcinoma). Author Ruthanne Chun r MEDICATIONS Acute or chronic prostatitis, benign Consulting Editor Timothy M. Fan DRUG(S) prostatic hypertrophy, and prostatic cysts are r possible differentials in intact male dogs but Chemotherapy—carboplatin, cisplatin, or are highly unlikely in neutered dogs. doxorubicin; may offer short-term benefit. CBC/BIOCHEMISTRY/URINALYSIS r Inflammatory leukogram possible. r Alkaline phosphatase may be high. BLBS078-CF_A19 BLBS078-Tilley March 21, 2011 9:54

Canine and Feline, Fifth Edition 29 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 locally invasive, and often bilateral. r r reported in up to 16% of patients. Adenocarcinoma—median reported survival Renal cystadenocarcinoma, a rare heritable r Abdominal radiographs—mass visualized in of 49 dogs was 16 months (range 0–59). syndrome with a less aggressive behavior and r 81% of patients. Cystadenocarcinoma—few large studies of better long-term prognosis than renal r Abdominal ultrasonography, CT, or this rare disease, reported median survival of adenocarcinoma, has been described in + German shepherd dogs. contrast radiography—useful in identifying 12 months with no definitive therapy. and staging the disease. SIGNALMENT r DIAGNOSTIC PROCEDURES Adenocarcinoma—older (8–9 years) dogs, Renal biopsy (ultrasound-guided or surgical) 1.6:1 male-to-female ratio, no breed MISCELLANEOUS predilection. for definitive diagnosis. r Cystadenocarcinoma—German shepherd ASSOCIATED CONDITIONS r dogs, often female. The paraneoplastic syndromes of SIGNS hypertrophic osteopathy, polycythemia, and a r TREATMENT Adenocarcinoma—insidious, non-specific neutrophilic leukocytosis have been reported r in isolated cases. signs such as weight loss, inappetance, Aggressive surgical excision is the treatment r of choice for unilateral disease. Renal failure. lethargy, hematuria, and pale mucous r r membranes. Successful chemotherapeutic management Nodular dermatofibrosis and uterine r of either disease has not been described. leiomyomas are commonly associated with Cystadenocarcinoma—may present for r nodular dermatofibrosis, a syndrome of Supportive management for patients in cystadenocarcinoma. painless, firm, fibrous lesions of the skin and renal failure may be necessary. ABBREVIATIONS r subcutaneous tissues. CT = computed tomography CAUSES & RISK FACTORS r Suggested Reading Adenocarcinoma—unknown. r Bryan JN, et al. Primary renal neoplasia of Cystadenocarcinoma—heritable in German MEDICATIONS dogs. J Vet Intern Med 2006, shepherd dogs. DRUG(S) 20:1155–1160. None Knapp DW. Tumors of the urinary system. CONTRAINDICATIONS/POSSIBLE In:WithrowSJ,VailDM,eds.,Small Animal Clinical Oncology, 4th ed. DIAGNOSIS INTERACTIONS Philadelphia: Saunders, 2007, pp. 649–658. N/A Author Ruthanne Chun DIFFERENTIAL DIAGNOSIS r Consulting Editor Timothy M. Fan Other primary neoplasia (i.e., lymphoma, nephroblastoma). r Metastatic neoplasia (i.e., FOLLOW-UP hemangiosarcoma). r Renal adenoma or cyst. PATIENT MONITORING r r Pyelonephritis. Renal failure—measure serum urea nitrogen and creatinine; urinalysis. CBC/BIOCHEMISTRY/URINALYSIS r r Quality of life if bilateral or otherwise CBC may show paraneoplastic non-surgical disease. polycythemia or leukocytosis, or anemia. BLBS078-CF_A20 BLBS078-Tilley March 21, 2011 9:55

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

CAUSES & RISK FACTORS Unknown BASICS MEDICATIONS OVERVIEW DRUG(S) r Tumor arising from major (e.g., parotid, DIAGNOSIS Chemotherapy efficacy is largely unreported; mandibular, sublingual, or zygomatic) or however, may be indicated for DIFFERENTIAL DIAGNOSIS minor salivary glands. r treatment/palliation of metastatic disease. r Squamous cell carcinoma. Mandibular or parotid glands constitute r CONTRAINDICATIONS/POSSIBLE 80% of cases. Mucocele. r r INTERACTIONS Mandibular gland most frequently affected Abscess. r N/A in dogs. Soft tissue sarcoma, e.g., malignant fibrous r histiocytoma or fibrosarcoma. Parotid gland most frequently affected in r cats. Lymphoma. r Locally invasive. CBC/BIOCHEMISTRY/URINALYSIS r FOLLOW-UP Cats typically have more advanced disease Results often normal than dogs at time of diagnosis. r OTHER LABORATORY TESTS PATIENT MONITORING Metastasis—regional lymph node in 39% of Evaluations—physical examination and cats and 17% of dogs at diagnosis; distant N/A IMAGING thoracic radiographs every 3 months metastasis reported in 16% of cats and 8% of r reasonable if aggressive surgery and/or dogs at diagnosis but may be slow to develop. Regional radiographs usually are normal; r radiation therapy employed. Other salivary gland neoplasms— may see periosteal reaction on adjacent POSSIBLE COMPLICATIONS carcinoma; squamous cell carcinoma; mixed bones or displacement of surrounding neoplasia. structures. Temporary acute side effects (e.g., moist r r Epithelial malignancies—constitute roughly MRI or CT imaging allows superior dermatitis and alopecia) expected with 85% of salivary gland tumors. discrimination of tumor for surgery and/or radiation therapy. r Fibrosarcomas, lipomas, mast cell tumors, radiation treatment planning. EXPECTED COURSE AND PROGNOSIS r r and lymphomas have involved the salivary Thoracic radiographs indicated to check for Improved survival time in dogs without glands by direct extension and invasion. A lung metastases. evidence of nodal or distant metastasis at concurrent malignant fibrous histiocytoma DIAGNOSTIC PROCEDURES diagnosis; clinical stage not prognostic for (giant cell type) and malignant mixed tumor r cats. Cytologic examination of aspirate may r (likely of ductal origin) within the salivary differentiate salivary adenocarcinoma from Median survival 550 days for dogs and 516 gland has also been described. mucocele and abscess. days for cats in retrospective study. r r r Adenomas comprise only 5% of salivary Needle core or wedge biopsy for Local control through radiation or multiple tumors. histopathology—definitive diagnosis. surgeries remains critical. SIGNALMENT r Dogs and cats r Mean age, 10–12 years r Siamese cats—may be at relatively higher TREATMENT MISCELLANEOUS risk r r ABBREVIATIONS Male cats affected twice as often as female Aggressive surgical resection—when r CT = computed tomography cats possible; most are invasive and difficult to r r excise completely. MRI = magnetic resonance imaging No other breed or sex predilection has been r determined Radiotherapy—good local control and Suggested Reading prolonged survival in three reported cases. SIGNS r Hammer A, Getzy D, Ogilvie G, et al. r Aggressive local resection (usually Unilateral, firm, painless swelling of the Salivary gland neoplasia in the dog and cat: histologically incomplete) followed by Survival times and prognostic factors. upper neck (mandibular and sublingual), ear adjuvant radiation can achieve local control base (parotid), upper lip or maxilla JAAHA 2001, 37:478–482. and long-term survival, but further studies are Author Anthony J. Mutsaers (zygomatic), or mucous membrane of lip needed to determine the most effective (accessory or minor salivary tissue). Consulting Editor Timothy M. Fan r treatment, including the possible role for Other signs may include halitosis, weight chemotherapy. loss, anorexia, dysphagia, exophthalmus, Horner’s syndrome, sneezing, and dysphonia. BLBS078-CF_A21 BLBS078-Tilley March 21, 2011 10:0

Canine and Feline, Fifth Edition 31 Adenocarcinoma, Skin (Sweat Gland, Sebaceous) A

DIAGNOSTIC PROCEDURES r Biopsy for histopathology and definitive diagnosis BASICS r FOLLOW-UP Cytologic examination or biopsy of regional r OVERVIEW lymph nodes Sebaceous gland adenocarcinoma—little Malignant growth originating from sebaceous PATHOLOGIC FINDINGS known about the metastatic potential of this r malignancy, but may be rapidly metastatic to or apocrine sweat glands of the skin. Apocrine sweat gland carcinomas are regional lymph nodes in some patients; SIGNALMENT typically invasive into the underlying stroma long-term prognosis is anecdotally good with r and blood vessels, and often show poorly Apocrine sweat gland—rare in dogs, multimodal therapy combining aggressive demarcated borders and a high mitotic index. uncommon in cats. r surgery, chemotherapy, and radiation therapy. r 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 a negative Female dogs overrepresented for apocrine prognostic factor systemic metastases; adenocarcinoma in one study. aggressive surgical resection (local and SIGNS TREATMENT regional tumor control) followed by adjuvant r r May appear as solid, firm, raised, superficial Aggressive en bloc surgical excision, chemotherapy is recommended to improve skin lesions. survival. A study reported a post-excisional r including resection of draining lymph node, May be ulcerated and bleeding and recommended for both types. median survival time of 30 months in dogs. accompanied by inflammation of the Histopathologic analysis of lymph nodes 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 MISCELLANEOUS underlying tissue; may occur anywhere on the evaluated histologically to assess completeness body, frequently affecting the trunk in dogs. of resection. Suggested Reading r r Sebaceous gland—often ulcerated and Radiation therapy may be recommended for Carpenter JL, Andrews LK, Holzworth J. inflamed, moderate risk of lymph node treatment of draining lymph nodes site after Tumors and tumor like lesions. In: involvement. resection to prevent recurrence and Holzworth J, ed., Diseases of the Cat: CAUSES & RISK FACTORS development of regional metastasis; treatment Medicine and Surgery. Philadelphia: Saunders, 1987, pp. 406–596. Unknown of primary tumor site recommended when wide and complete resection not possible. Pakhrin B, Kang MS, Bae IH, et al. Retrospective study of canine cutaneous tumors in Korea. J Vet Sci 2007, 8:229–236. Simko E, Wilcock BP, Yager JA. A DIAGNOSIS MEDICATIONS retrospective study of 44 canine apocrine DIFFERENTIAL DIAGNOSIS sweat gland adenocarcinomas. Can Vet J r DRUG(S) 2003, 44(1):38–42. Other more frequent skin tumors r r Thomas RC, Fox LE. Tumors of the skin and Cutaneous histiocytic diseases Multiple chemotherapy drugs have been r subcutis. In: Morrison WB, ed., Cancer in Immune-mediated skin diseases used for the treatment of both tumor types, in r Dogs and Cats: Medical and Surgical Bacterial/fungal infections both species, with anecdotal benefit (including cisplatin, carboplatin, Management. Jackson, WY: Teton CBC/BIOCHEMISTRY/URINALYSIS mitoxantrone, and gemcitabine). NewMedia, 2002, pp. 469–488. r Normal Contact a veterinary oncologist for any Author Louis-Philippe de Lorimier OTHER LABORATORY TESTS updated treatments that may be available. Consulting Editor Timothy M. Fan r N/A Nonsteroidal anti-inflammatory drugs and Acknowledgement The author and editors acknowledge the prior contribution of Phyllis IMAGING other analgesics are recommended, as indicated, for pain control. Glawe. Thoracic radiographs recommended at the time of diagnosis to assess for distant CONTRAINDICATIONS/POSSIBLE metastases. INTERACTIONS None BLBS078-CF_A22 BLBS078-Tilley July 15, 2011 17:53

32 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 Uncommon tumor arising from the r and abdominal ultrasound—at 1, 3, 6, 9, and Ultrasound—may reveal a thickened 12 months post-surgery. epithelial lining of the gastrointestinal tract. stomach or bowel wall; may see mass in the r EXPECTED COURSE AND PROGNOSIS Prognosis guarded to poor. gastrointestinal tract, enlarged lymph nodes. r SIGNALMENT Positive contrast radiography—filling defect Dogs r r Dogs more commonly affected than cats. (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—10 intestine and rectum; polypoid or annular months. SIGNS r space-occupying masses. Mean survival large intestinal—annular Historical Findings r DIAGNOSTIC PROCEDURES 1.6 months versus pedunculated 32 months. Signs related to gastrointestinal tract. r r Cats Stomach—vomiting, anorexia, weight loss, Ultrasound-guided fine-needle aspirate of r Guarded. hematemesis, and melena. bowel mass or enlarged lymph node may r r Few reported cases, but may have prolonged Small intestine—vomiting, weight loss, reveal carcinoma cells on cytology, which can survival (> 1 year). borborygmus, flatulence, and melena. be useful to rule out lymphoma. r r Large intestine and rectum—mucous and Endoscopic biopsy may be non-diagnostic blood-tinged feces and tenesmus. because tumors are frequently deep to the mucosal surface; thus surgical biopsy Physical Examination Findings r frequently required. MISCELLANEOUS Stomach—non-specific. r Small intestine—may feel midabdominal Suggested Reading mass; distended, painful loops of small bowel; Crawshaw J, Berg J, Sardinas JC, et al. melena on rectal exam. Prognosis for dogs with nonlymphomatous r TREATMENT Large intestine and rectum—palpable mass r small intestinal tumors treated by surgical per rectum, may form annular ring, or Surgical resection—treatment of choice; excision. JAAHA 1998, 34:451–456. seldom curative. multiple nodular lesions protruding into the r Lubbes D, Mandigers PJ, Heuven HC, et al. Gastric—usually non-resectable. colon; bright red blood on feces. r [Incidence of gastric carcinoma in Dutch CAUSES & RISK FACTORS Small intestine—remove by resection and Tervueren shepherd dogs born between r anastomosis; metastasis to regional lymph Unknown. 1991 and 2002]. Tijdschr Diergeneeskd r nodes and the liver common. Nitrosamines—reported as causative agent r 2009, 134:606–610. Large intestine and rectal—may in experimental literature. Morrison WB. Nonlymphomatous cancers of r occasionally be resected by a pull-through Possible genetic cause—gastric the esophagus, stomach, and intestines. In: surgical procedure; metastasis common; adenocarcinomas in related Belgian shepherds Morrison WB, ed., Cancer in Dogs and transcolonic debulking may provide palliation and in Dutch Tervueren shepherds. Cats: Medical and Surgical. Jackson, WY: of obstruction. Teton NewMedia, 2002, pp. 527–534. Swann HM, Holt DE. Canine gastric adenocarcinoma and leiomyosarcoma: A retrospective study of 21 cases (1986–1999) DIAGNOSIS MEDICATIONS and literature review. JAAHA 2002, DIFFERENTIAL DIAGNOSIS 38:157–164. r DRUG(S) Foreign body r Takiguchi M, Yasuda J, Hashimoto A, et al. r Chemotherapy—only anecdotal reports, Inflammatory bowel disease Esophageal/gastric adenocarcinoma in a r usually unsuccessful. Lymphoma r dog. JAAHA 1997, 33:42–44. r Piroxicam 0.3 mg/kg PO q24h can provide Parasites Author Laura D. Garrett r palliation for large intestinal and rectal Leiomyoma Consulting Editor Timothy M. Fan r tumors. Leiomyosarcoma r Pancreatitis CONTRAINDICATIONS/POSSIBLE CBC/BIOCHEMISTRY/URINALYSIS INTERACTIONS r Stomach and small intestine—may see Seek advice before initiating treatment with microcytic, hypochromic anemia cytotoxic drugs. (iron-deficiency anemia). r Large intestine and rectum—no characteristic changes. BLBS078-CF_A23 BLBS078-Tilley June 16, 2011 10:8

Canine and Feline, Fifth Edition 33 Adenocarcinoma, Thyroid—Dogs A

r r If functional thyroid tumor—may see Specimen almost always heavily polyuria, polydypsia, polyphagia, weight loss, contaminated with blood owing to highly restless behavior, diarrhea. vascular nature of tumor. BASICS r r If hypothyroid—may see poor hair coat, Homogeneous population of epithelial cells, DEFINITION weight gain, lethargy. sometimes with colloid and/or A malignant tumor arising from the follicular Physical Examination Findings tyrosine-containing granules. r r or parafollicular cells (medullary/C-cells) of Freely movable or fixed cervical mass, Unable to differentiate malignant from the thyroid gland. unilateral or bilateral. benign thyroid cells; but almost all thyroid r PATHOPHYSIOLOGY Rarely may see Horner’s syndrome, or neoplasms in dogs are malignant. r cranial vena cava syndrome. PATHOLOGIC FINDINGS About 60% of patients are euthyroid, 30% r hypothyroid, and 10% hyperthyroid. If hyperthyroid—cardiac arrhythmias or Gross r r Typically very invasive tumors with high rate murmurs. Characterized by high vascularity with areas of metastasis (lungs, retropharyngeal lymph CAUSES of hemorrhage and necrosis. r nodes, liver), with up to 35–40% of dogs Unknown Usually poorly encapsulated; often invade having metastasis at the time of diagnosis. adjacent tissues (e.g., trachea and esophagus, r RISK FACTORS Animals with bilateral tumors have a sixteen r and surrounding vasculature); may adhere to Untreated hypothyroidism has been shown times greater risk of developing metastatic the jugular vein, carotid artery, and to be a risk factor in a colony of beagles. disease than animal with unilateral tumors. r vagosympathetic trunk. Breed predilection. SYSTEMS AFFECTED r Histopathology r Iodine deficiency. r Cardiovascular—hyperthyroid dogs are Three main types—follicular, papillary, and usually tachycardic and may have systemic compact (solid); mixed follicular and solid tumors most common in dogs. hypertension; may see anemia and DIC in r advanced disease. C-cell (e.g., parafollicular, medullary) r DIAGNOSIS Endocrine/Metabolic—affected dogs may carcinomas less common. be hypothyroid, euthyroid, or hyperthyroid; DIFFERENTIAL DIAGNOSIS r hypercalcemia may be seen as a paraneoplastic Other primary neoplasms—lymphoma; soft syndrome or secondary to concurrent tissue sarcoma; salivary gland parathyroid hyperplasia or parathyroid adenocarcinoma; parathyroid carcinoma; TREATMENT adenocarcinoma. carotid body tumor. r r APPROPRIATE HEALTH CARE Respiratory—dogs may be dyspneic owing Secondary tumors—metastatic oral r to a space-occupying mass adjacent to the squamous cell carcinoma; oral melanoma. Definitive treatment is dependent on tumor r trachea; metastasis to the lungs common. Inflammatory—abscess or granuloma. stage (tumor size, mobility and evidence of r metastatic disease). GENETICS Salivary mucocele. r Complete surgical excision recommended Unknown CBC/BIOCHEMISTRY/URINALYSIS r for freely movable thyroid tumors. Usually normal. r INCIDENCE/PREVALENCE r Full course external beam radiation therapy Accounts for 1.2–3.8% of all canine tumors May see non-regenerative normocytic recommended preoperatively for large and represents 10–15% of all primary head normochromic anemia of chronic disease, tumors, as a sole therapy for non-resectable leukocytosis. and neck tumors. r tumors, or post-operatively for incompletely Rare—hypercalcemia; isosthenuria; DIC. surgically removed tumors. GEOGRAPHIC DISTRIBUTION r OTHER LABORATORY TESTS Palliative radiation and/or chemotherapy May be more common in iodine-deficient recommended for tumors that are metastatic areas Thyroid hormone (T4 and/or free T4 levels) and endogenous TSH levels. at presentation. SIGNALMENT r IMAGING Also can use iodine-131 but doses are very Species r large (60–100 mCi) and therefore there are Thoracic radiography (3 view)—evaluation limited facilities that offer this therapy. Dogs of lungs and other thoracic structures for Breed Predilections metastasis. NURSING CARE r Boxers, golden retrievers, and beagles at Cervical ultrasonography and computed Varies with signs on examination increased risk but seen in any breed. tomography—evaluation of tissue of origin, ACTIVITY Mean Age and Range vascularity, invasion, and cervical lymph Restrict activity if dyspneic nodes. Older dogs (median 9–11 years; range 4–18 r DIET years) Technetium-99m scintigraphy to evaluate for ectopic thyroid tissue or metastatic lesions. N/A Predominant Sex r Radioiodine studies—may provide CLIENT EDUCATION No gender predilection r information about the tumor’s ability to Warn owners of the importance of SIGNS produce thyroid hormone. controlling heart rate and rhythm in General Comments r DIAGNOSTIC PROCEDURES hyperthyroid patients and of the possibility of Usually not diagnosed until a large mass is episodes of collapse. Biopsy r palpable Warn owners of possible post-operative r Tru-Cut not recommended owing to high risk Approximately 65% are unilateral, 35% are laryngeal paralysis and intraoperative of severe hemorrhage; open biopsy usually bilateral hemorrhage. required. r Historical Findings Warn owners of acute radiation therapy r Cytology Palpable mass/swelling in cervical neck, r toxicities—moist desquamation, laryngitis, Examination of fine-needle aspirate from coughing, dyspnea, dysphagia, dysphonia, tracheitis, esophagitis. tumor and palpable regional lymph nodes. facial edema, neck pain. BLBS078-CF_A23 BLBS078-Tilley June 16, 2011 10:8

34 Blackwell’s Five-Minute Veterinary Consult

A Adenocarcinoma, Thyroid—Dogs (Continued)

r SURGICAL CONSIDERATIONS POSSIBLE INTERACTIONS Palliative radiation therapy in 13 See “Appropriate Health Care” Verapamil—may potentiate dogs—MST 24 months. r 131 Risks doxorubicin-induced cardiotoxicity I therapy in combination with r 131 Marked hemorrhage—tumors highly ALTERNATIVE DRUG(S) surgery—MST 34 months, or Ialone MST 30 months. vascular and invasive into surrounding N/A r structures including vasculature; may need Animals treated with cisplatin alone (13 blood transfusion and intensive post-operative dogs)—overall response rate was 53%, median care. progression free interval for responders was r Laryngeal paralysis—owing to trauma to FOLLOW-UP 202 days and overall MST was 98 days. recurrent laryngeal nerve. r PATIENT MONITORING Damaged parathyroid glands—may occur r during surgery. Serum calcium concentration—if bilateral thyroidectomy was performed; signs of MISCELLANEOUS hypocalcemia (agitation, panting, muscle ASSOCIATED CONDITIONS tremors, tetany, and seizures) may be r Non-thyroidal malignancies common MEDICATIONS observed. r ◦ Treat with 10% calcium gluconate (1–1.5 Multiple endocrine neoplasia reported DRUG(S) OF CHOICE mL/kg IV over 10–20 minutes). AGE-RELATED FACTORS r Chemotherapeutic agents: ◦ Maintain serum calcium with None ◦ Chemotherapy is recommended as a sole dihydrotachysterol (vitamin D) orally. r ZOONOTIC POTENTIAL therapy, or in combination with surgery Thyroid hormone—supplementation with N/A and/or radiation therapy. thyroxine may be necessary after bilateral ◦ Cisplatin (60 mg/m2 every 3 weeks) or thyroidectomy. PREGNANCY/FERTILITY/BREEDING r doxorubicin (30 mg/m2 every 3 TSH concentration—a goal of thyroxin It is not recommended to breed animals with weeks)—reported to effect partial supplementation is to downregulate the cancer. Chemotherapy is teratogenic—do not remission in approximately 50% of cases. body’s secretion of TSH. give to pregnant animals. r ◦ Cisplatin—nephrotoxic; must use with Site of primary tumor—physical SYNONYMS saline diuresis (18.3 mL/kg/hour IV over examination and cervical ultrasound; thoracic Thyroid carcinoma 6 hours; give cisplatin after 4 hours). radiographs every 3 months to detect r ABBREVIATIONS Antiemetics for cisplatin therapy: pulmonary metastasis. r = ◦ Maropitant 1 mg/kg SC before cisplatin, DIC disseminated intravascular PREVENTION/AVOIDANCE coagulation or r Unknown MST = median survival time ◦ Dolasetron 0.6–1 mg/kg IV or PO q24h, r POSSIBLE COMPLICATIONS TSH = thyroid stimulating hormone or r ◦ Butorphanol 0.4 mg/kg IM before and Tumor—anemia; thrombocytopenia; Suggested Reading after cisplatin. hypercalcemia; DIC; respiratory distress. r r Bailey DB, Page RL. Tumors of the endocrine Thyroid management: Chemotherapy—dilated cardiomyopathy; system. In: Withrow SJ, Vail DM, eds., ◦ Thyroxine—maintenance doses to renal failure; pancreatitis; sepsis; Small Animal Clinical Oncology, 4th ed. gastrointestinal upset. decrease TSH production have been r Philadelphia: Saunders, 2007, pp. 591–596. recommended; some tumors contain TSH Surgery—hemorrhage; hypothyroidism; KleinMK,PowersBE,WithrowSJ,etal. receptors; value of hormone-replacement hypoparathyroidism leading to hypocalcemia; Treatment of thyroid carcinoma in dogs by laryngeal paralysis. therapy in affected dogs not determined. r surgical resection alone: 20 cases ◦ Methimazole 5 mg PO q8h for medium Radiotherapy—acute side effects—moist (1981–1989). JAVMA 1995, to large dogs; may be beneficial for desquamation, pharyngeal mucositis; 206:1007–1009. hyperthyroid patients. esophagitis; tracheitis; late side Liptak JM. Canine thyroid carcinoma. Clin ◦ β-blockers—may be indicated for effects—alopecia, and skin or coat color Tech Small Anim Pract 2007, 22(2):75–81. tachycardia or hypertension in change (at radiation site). Pack L, Roberts RE, Davson SD, Dookwah hyperthyroid patients. EXPECTED COURSE AND PROGNOSIS HD. Definitive radiation therapy for r CONTRAINDICATIONS Prognosis—related to stage of disease infiltrative thyroid carcinoma in dogs. Vet r Doxorubicin is cumulatively toxic to cardiac (tumor size, mobility and evidence of Radiol Ultrasound 2001, 42:471–474. myocytes causing decreased myocardial metastatic disease) with small, non-attached Walers CB, Scott-Moncrieff JCR. Cancer of function. Do not give to animals with poor unilateral, non-metastatic tumors having best endocrine origin. In: Morrison WB, ed., cardiac function or dilated cardiomyopathy. prognosis. Cancer in Dogs and Cats: Medical and r r Cisplatin is nephrotoxic; do not give to MST after surgical removal of freely Surgical Management, 2nd ed. Jackson, movable thyroid tumor is > 36 months. WY: Teton NewMedia, 2002, pp. 573–580. animals with renal disease. r Author Rebecca G. Newman PRECAUTIONS For animals treated with full course external beam radiation therapy—progression free Consulting Editor Timothy M. Fan Chemotherapy can cause gastrointestinal, survival at 1 year—80%, and 72% at 3 years Acknowledgement The author and editors bone marrow, cardiac, and other in one study and in another study MST acknowledge the prior contribution of Linda toxicities—seek advice from a medical 24.5 months. S. Fineman. oncologist if unfamiliar with cytotoxic drugs. BLBS078-CF_A25 BLBS078-Tilley July 23, 2011 4:15

Canine and Feline, Fifth Edition 35 Aggression, Fear—Cats A

Behavior Modification Exercises with monoamine oxidase inhibitors. Avoid Desensitization and Counter-Conditioning use in the aggressor cat; may increase any r r BASICS Desensitization: exposing cat to the “bully” behavior. Neither SSRIs nor TCAs fear-inducing stimulus (scary person) at a low should be given with each other, nor in r OVERVIEW level so the cat does NOT react fearfully or combination with MAOIs. SSRIs: side Fear-motivated human-directed feline aggressively. Over time, the intensity of the effects include mild sedation and decreased aggression. stimulus is increased (i.e., the distance appetite, constipation, and urinary retention. SYSTEMS AFFECTED between the cat and stimulus is decreased) Competitive inhibition of cytochrome P450 r r without causing fearful responses. liver enzymes; when administered Behavioral Gastrointestinal—decreased r r Counter-conditioning: rewarding the cat concurrently with medication utilizing the appetite Hemic/Lymphatic/Immune— with a special treat, toy, grooming, petting, P450 enzymes, elevated plasma levels of the chronic stress effects on immune function r etc., for relaxation. medications may increase, causing toxic levels. Ophthalmic—dilated pupils in response to r CLASSICAL CONDITIONING TCAs: side effects include sedation, autonomic nervous system stimulation r r Classical conditioning: pairing the stimulus constipation, diarrhea, urinary retention, Skin/Exocrine—may show secondary appetite changes, ataxia, decreased tear problem behavior such as overgrooming (person threatening to the cat) with a tasty treat, toy, petting. Example: scary person = production, mydriasis, cardiac arrhythmias, SIGNALMENT tachycardia, and changes in blood pressure. tuna fish. As cat relaxes in the presence of the r Cats of any age, gender, or neuter status person, relaxation is rewarded. Benzodiazepines: side effects include SIGNS sedation, ataxia, muscle relaxation, increased Ears back, body and tail lowered, piloerection, appetite, paradoxical excitation, and increased friendliness. Idiopathic hepatic necrosis has pupil dilation; may hiss and growl. Avoidance r of person(s) who elicit the aggression. Attacks MEDICATIONS been reported in cats. Specific recommendations for the use of diazepam: possible if approached and/or cornered. Medication may be necessary to decrease baseline physical exam, CBC, and blood Extreme cases: expression of anal glands, overall levels of anxiety and reactivity. chemistries to confirm good health. Repeat urination, and/or defecation. Hiding DRUG(S) behavior. the blood chemistries at 3–5 days. Elevated Azapirones ALT or AST, discontinue the medication. CAUSES & RISK FACTORS r Buspirone 0.5–1.0 mg/kg q12h. Most Poor socialization with humans and/or feral useful for fearful and withdrawn cats. living, an aversive event associated with a Decreases anxiety and may increase person, or people in general. “self-confidence.” Anecdotal reports of FOLLOW-UP “increase in affection” and possible increase in PATIENT MONITORING aggression when given to the aggressor. Weekly follow-up is recommended, especially Response noted in 1–2 weeks. DIAGNOSIS when on medication(s). For cats on Selective Serotonin Reuptake Inhibitors medication, follow-up blood work r DIFFERENTIAL DIAGNOSIS Fluoxetine, paroxetine, sertraline 0.5–1.5 recommended every 6–12 months. r r Pain-motivated aggression Play-motivated mg/kg q24h PREVENTION/AVOIDANCE r r aggression Petting intolerance Redirected Tricyclic Antidepressants Avoidance of the fear-inciting stimuli if at all r aggression Amitriptyline 0.5–2.0 mg/kg q12–24h possible. Early socialization to people and r CBC/BIOCHEMISTRY/URINALYSIS Clomipramine 0.25–1.3 mg/kg q24h events may help prevent some occurrences of r Use to rule out contributing medical SSRIs and TCAs must be given daily. May fear-related responses to people. conditions. Urinalysis if inappropriate take 4–8 weeks to reach peak effects. POSSIBLE COMPLICATIONS elimination and/or urine marking. Benzodiazepines r Potential human injury—especially if the cat OTHER LABORATORY TESTS Alprazolam 0.125–0.25 mg/cat q8–24h r is approached or cornered. Senior cats: a complete thyroid panel Diazepam 0.1–1.0 mg/kg q12–24h (rarely EXPECTED COURSE AND PROGNOSIS used due to potential hepatopathies) IMAGING r Progress occurs slowly. Relearning is a process Benzodiazepines can be given “as needed” and each case is individual. If medications are Based on clinical examination and/or for specific encounters with people inducing indicated, begin at a low dose and work up as suspected pain component the fear response and during the DS&CC and necessary. To discontinue taking medication, DIAGNOSTIC PROCEDURES classical conditioning sessions. The wait until the new behavior is stable (8–12 benzodiazepines can be used in conjunction Thorough behavioral history including a weeks) and wean off slowly, usually over with the azapirones, SSRIs, and TCAs. description of the cat’s postures during weeks. If fearful behavior recurs, return to the aggression and injuries inflicted, litter box use, Pheromones r last dose that controlled the anxiety and food consumption, and hiding behaviors. Feliway—available in diffuser and spray r continue treatment. Used to help calm the cat during stressful situations. CONTRAINDICATIONS/POSSIBLE TREATMENT MISCELLANEOUS INTERACTIONS r CLIENT EDUCATION None of the medications listed are approved ZOONOTIC POTENTIAL r Avoidance of Fear-Inducing Situations for use in cats. All of the medications are to People injured during a fear-motivated attack r Ongoing exposure to the fear-inducing be administered orally, as they have not been should seek prompt medical attention. situations may worsen signs, cause severe shown to be effective through transdermal Infection by Bartonella henselae can result r stress, and compromise animal welfare. dosing. Azapirones: side effects are from a cat scratch or bite. r Exposure to the stimuli only under uncommon but occasional excitement is Author Terry Marie Curtis controlled exercises described below. noted. Should not be given in combination Consulting Editor Debra F. Horwitz BLBS078-CF_A26 BLBS078-Tilley May 31, 2011 17:32

36 Blackwell’s Five-Minute Veterinary Consult A Aggression, Fear/Defensive—Dogs

r DIAGNOSTIC PROCEDURES Gradually expose the dog to a greatly N/A reduced stimulus so no fearful reaction is elicited. BASICS r The non-fearful behavior is rewarded. r OVERVIEW Gradually increase the level of stimulation Occurs when the dog perceives a situation as TREATMENT staying below the threshold that would result in fear and/or aggression. threatening. May be within the range of CLIENT EDUCATION r normal behavior but excessive fearfulness or r Progress is slow, and careful monitoring of phobic behavior is also possible. Treatment is aimed at controlling the responses is essential. problem, not at achieving a “cure.” Successful r SYSTEMS AFFECTED Relapses are common, and owners must r treatment, as measured by a decrease in always be vigilant and in control of the dog’s Behavioral. r aggressive incidents, depends upon owner behavior. Signs of sympathetic stimulation (e.g., understanding of basic canine social behavior, tachypnea, tachycardia). risks involved in living with an aggressive dog, SIGNALMENT how to follow safety and management r Dogs. recommendations, and correct identification MEDICATIONS r of the fear-eliciting stimuli. No gender predilection; not affected by r Owners must be aware the only way to DRUG(S) neutering. r r prevent all future injuries is euthanasia. There are no medications licensed for the Can occur at any age. Signs often develop as r puppies leave the peak period for socialization If owners elect not to euthanize, they must treatment of canine aggression. Owners must (approximately 12–16 weeks of age) and again be aware that their primary responsibility is be aware the use of medication is off-label. at 6–9 months. preventing human injury by conscientiously Because of liability concerns, note in the SIGNS avoiding situations that may evoke an patient’s record that the owners were r aggressive reaction, including situations that informed of potential risks and side effects. A Aggression (growling, lip-lifting, barking, have resulted in the dog’s being fearful even if signed informed consent form is advisable. r snarling, snapping, lunging, biting) not aggressive. NEVER use medications without behavior r accompanied by fearful or submissive body Owners may be more compliant with modification. r postures/facial expression (head down, avoidance recommendations if they Before prescribing medication, be sure that crouching, backing away, ears back, tail understand that in many jurisdictions dog owners understand the risks in owning an tucked, looking away, lip licking). r owners are liable for bites and can face aggressive dog, will follow safety procedures, History may include the dog having been civil/criminal prosecutions should a person be and will not rely on medication to keep others hurt or startled in a similar situation. r injured. safe. Often directed toward unfamiliar people. r r r Treatment is more likely to be successful if a Medication may not be appropriate in some May occur when the dog is cornered or period of preventing exposure to family situations, (e.g., those with small cannot escape. r fear-provoking stimuli is instituted prior to children, family members with disabilities, or May be more severe on- than off-leash. behavior modification. immunocompromised individuals). CAUSES & RISK FACTORS r Safety Recommendations Research has confirmed there is a strong r r May be a normal canine behavior Confine the dog away from potential placebo effect when using medications to treat depending on the circumstances. r victims or have the dog be under the direct canine aggression. Studies have not shown a Strongly influenced by previous experience physical control of a responsible adult robust effect of drug treatment on aggression. (e.g., inadequate early socialization, painful whenever an aggression-provoking situation Selective Serotonin Reuptake Inhibitors r conditions, rough handling, inappropriate could arise (e.g., in any public location, on Fluoxetine 0.5–2 mg/kg PO q24h (canine) r punishment). walks, when visitors arrive at the house). Paroxetine 0.5–1 mg/kg PO q24h (canine) r r r Underlying medical conditions, especially Teach the dog to be comfortable wearing a Sertraline 1–3 mg/kg PO q24h (canine) r pain, may increase the level of aggression. head halter (e.g., Gentle Leader) and basket Side effects: sedation, irritability, GIT muzzle for easier and safer control. effects; anorexia is common and usually r Due to the current resurgence in popularity transient. of punishment-/dominance-based training Tricyclic Antidepressants r DIAGNOSIS techniques, owners must be educated about Clomipramine 2–4 mg/kg PO q24h or DIFFERENTIAL DIAGNOSIS the etiology (i.e., fear) for their dog’s divided q12h (label-restricted for aggression) r aggression. Use of these techniques may result Dominance/social status aggression (canine) r in increased aggression, fear, agitation, and/or r Conflict aggression Side effects: sedation, GIT effects, r injuries. Others depending on circumstances anticholinergic, possible cardiac conduction Behavior Therapy disturbances if predisposed. CBC/BIOCHEMISTRY/URINALYSIS r Affection control: used to increase Benzodiazepines Usually unremarkable. Abnormalities suggest predictability of dog’s life and decrease r an underlying or contributing medical Alprazolam 0.05–0.1 mg/kg PO q12h or occurrence of fear-provoking situations (see PRN condition. Aggression Toward Familiar People—Dogs). r PRECAUTIONS OTHER LABORATORY TESTS Behavior modification: systematic r Usually unremarkable. desensitization and counter-conditioning Any psychotropic medication may increase rather than decrease aggression. IMAGING to specific fear- and aggression-provoking r stimuli (see Aggression Toward Familiar Use caution when prescribing MRI if CNS disease suspected. Other People—Dogs). benzodiazepines as disinhibition of aggression imaging as needed to rule out underlying r Teach the dog to sit and relax on a verbal may result due to a reduction in fear-based medical conditions. command in neutral locations using food inhibition to biting. rewards. BLBS078-CF_A26 BLBS078-Tilley May 31, 2011 17:32

Canine and Feline, Fifth Edition 37

(Continued) Aggression, Fear/Defensive—Dogs A

r Do not combine SSRIs, TCAs, MAO POSSIBLE COMPLICATIONS ABBREVIATIONS r inhibitors (e.g., amitraz, selegiline), or Human injuries; euthanasia or relinquishment CNS = central nervous system r tramadol—can result in potentially fatal of patient GIT = gastrointestinal tract r serotonin syndrome. MAO = monoamine oxidase EXPECTED COURSE AND PROGNOSIS r MRI = magnetic resonance imaging There is no cure. Prognosis for improvement r = is better if aggression is at a low intensity and SSRI selective serotonin reuptake inhibitor occurs only in a few predictable situations. r = FOLLOW-UP Prognosis is highly dependent on owner TCA tricyclic antidepressant PATIENT MONITORING compliance. Suggested Reading r Clients often need ongoing assistance and Herron ME, Shofer SS, Reisner IR. Survey of should receive at least one follow-up call the use and outcome of confrontational and within the first 1–3 weeks after consultation. non-confrontational training methods in Provisions for further follow-up should be MISCELLANEOUS client-owned dogs showing undesired made at that time. Ongoing communication ASSOCIATED CONDITIONS behaviors. Appl Anim Behav Sci 2009, improves client compliance. 177:47–54. May see other fear- or anxiety-based Moffat K. Addressing canine and feline PREVENTION/AVOIDANCE conditions (e.g., noise phobias, separation r aggression in the veterinary clinic. Vet Clin Treatment recommendations are anxiety). North Am Small Anim Pract 2008, lifelong—aggression may recur with ZOONOTIC POTENTIAL 38(5):983–1003. treatment lapses and continued exposure to Human injury and bite wounds Virga V, Houpt KA, Scarlett JA. Efficacy of the fear-producing stimuli. Owners must PREGNANCY/FERTILITY/BREEDING amitriptyline as a pharmacological adjunct always be vigilant and in control of the dog’s to behavioral modification in the behavior. Do not breed dogs with extremely fearful r behavior or fear/aggression. management of aggressive behaviors in dogs. Appropriate early socialization and JAAHA 2001, 37:325–330. SEE ALSO habituation may help avoid fear-based Author Laurie Bergman and Meredith Stepita behaviors later in life. This includes attending Aggression Toward Familiar People—Dogs Consulting Editor Debra F. Horwitz well-structured, positive reinforcement puppy classes starting during the peak period for socialization. BLBS078-CF_A27 BLBS078-Tilley July 15, 2011 17:33

38 Blackwell’s Five-Minute Veterinary Consult A Aggression, Food, Possessive, and Territorial—Dogs

IMAGING aggression-provoking stimuli. Use pea-sized MRI if CNS disease suspected. Other pieces of food to reduce the likelihood of a BASICS imaging as needed to rule out underlying food-aggressive dog becoming aggressive medical conditions. during behavior modification (see Aggression OVERVIEW DIAGNOSTIC PROCEDURES Toward Familiar People—Dogs). r r Aggressively guarding food (e.g., in food N/A Teach the dog to perform alternate bowl, rawhides, bones, stolen/found items) or behaviors (e.g., a “Quiet” command, objects (e.g., toys, stolen objects). relinquishing objects to “Drop,” or get off r Territorial aggression—aggressively furniture with “Off”) on command for defending a territory. Territory may be a fixed TREATMENT rewards. Often referred to as counter location (e.g., home, yard, car, bed, or resting commanding or response substitution. area) and not be evident in other locations. In CLIENT EDUCATION other cases, the territory is mobile and is an Safety Recommendation r area around the dog; aggressive responses may Always confine the dog away from potential occur at any time. Territorial aggression may victims or the dog must be under the direct MEDICATIONS be exacerbated if the dog is restrained. r physical control of a responsible adult DRUG(S) Usually within the range of normal r whenever an aggression-provoking situation There are no medications licensed for the behavior; learning may contribute to excessive could arise. expression of aggression. r treatment of canine aggression. Owners must Feed dogs confined away from people; be aware that the use of medications is SYSTEMS AFFECTED prevent access to items that may evoke off-label. Because of liability concerns, note in aggression. Behavioral r the patient’s record that the owners were SIGNALMENT Confine territorial dogs in locations where informed of potential risks and side effects. A they cannot see/hear people approaching No breed or gender predilections exist for signed informed consent form is advisable. territory before they become aggressively NEVER use medications without behavior food/possessive aggression. Territorial aroused. r modification. Before prescribing medication, aggression is more common in intact males Teach the dog to be comfortable wearing a and initial signs are usually present by age 1. be sure that owners understand the risks in head halter (e.g., Gentle Leader) and basket owning an aggressive dog, will follow safety muzzle for easier control of potentially procedures, and will not rely on medication to SIGNS dangerous situations. r r keep others safe. Medication may not be Food/possessive—aggression (growling, The goal of treatment is control of the appropriate in some family situations (e.g., lip-lifting, barking, snarling, snapping, problem, not a cure. r those with small children, family members lunging, biting) toward people or other Success is measured by a decrease in with disabilities, or immunocompromised animals in the presence of valued food items aggressive incidents. r individuals). or objects. r r Success depends on owner understanding of Research has confirmed there is a strong Territorial—aggression in defense of a basic canine social behavior, risks involved in placebo effect when using medications to treat location or space. living with an aggressive dog, and ability to canine aggression. Studies have not shown a CAUSES & RISK FACTORS follow safety and management robust effect of drug treatment on aggression. r recommendations. May be part of normal canine behavior. r Selective Serotonin Reuptake Inhibitors The only way to absolutely prevent future r Strongly influenced by previous experiences of Fluoxetine 0.5–2 mg/kg PO q24h (canine) injuries is euthanasia. r successfully defending food, objects, or r Paroxetine 0.5–1 mg/kg PO q24h (canine) If the dog remains in the home, the primary r territory through aggression. Sertraline 1–3 mg/kg PO q24h (canine) r responsibility is preventing human injury by r Underlying medical conditions and Side effects: sedation, irritability, GIT medications, especially those causing conscientiously avoiding situations that may evoke an aggressive reaction. effects; anorexia is common and usually polyphagia, or calorie-restricted diets may r transient. increase level of food aggression. To aid in compliance, help owners understand that dog owners are often liable Tricyclic Antidepressants r for bites and can face civil/criminal Clomipramine 2–4 mg/kg PO q24h or prosecutions should a person be injured. divided q12h (label restriction for aggression) r A period of preventing exposure to (canine) r DIAGNOSIS aggression-provoking stimuli prior to Side effects: sedation, GIT effects, DIFFERENTIAL DIAGNOSIS behavior modification may aid in success. anticholinergic effects, and cardiac r r Fear aggression Due to the current resurgence in popularity conduction disturbances if predisposed. r Social status/dominance or conflict of punishment/dominance-based training CONTRAINDICATIONS/POSSIBLE aggression techniques, owners must be educated about r INTERACTIONS Others depending on circumstances the etiology (i.e., fear) of their dog’s r aggression. Use of these techniques may result Any psychotropic medication may increase CBC/BIOCHEMISTRY/URINALYSIS rather than decrease aggression. in increased aggression, fear, agitation and/or r Usually unremarkable. Abnormalities suggest injuries. Use caution when prescribing an underlying or contributing medical benzodiazepines, as disinhibition of Behavior Modification condition. r aggression may result due to a reduction in Affection control: used to help increase fear-based inhibition to biting. OTHER LABORATORY TESTS r owners’ leadership over dogs (see Aggression Do not combine SSRIs, TCAs, or MAO Usually unremarkable. Toward Familiar People—Dogs). r inhibitors (e.g., amitraz, selegiline) and Systematic desensitization and tramadol—can result in potentially fatal counter-conditioning to specific serotonin syndrome. BLBS078-CF_A27 BLBS078-Tilley July 15, 2011 17:33

Canine and Feline, Fifth Edition 39 Aggression, Food, Possessive, and Territorial—Dogs A

Suggested Reading deKeuster T, Jung H. Aggression toward FOLLOW-UP MISCELLANEOUS familiar people and animals. In: Horwitz DF, Mills D, eds., BSAVA Manual of PATIENT MONITORING ASSOCIATED CONDITIONS Canine and Feline Behavioural Medicine, Clients often need ongoing assistance. Should Fear and dominance/conflict aggression 2nd ed. Gloucestershire, UK: BSAVA, 2009, receive at least one follow-up call within the ZOONOTIC POTENTIAL pp. 182–210. first 1–3 weeks after the consultation. Human injury and bite wounds Herron ME, Shofer SS, Reisner IR. Survey of Provisions for further follow-up are made at the use and outcome of confrontational and PREGNANCY/FERTILITY/BREEDING that time. non-confrontational training methods in PREVENTION/AVOIDANCE Do not breed dogs with extreme client-owned dogs showing undesired aggression. Treatment recommendations are behaviors. Appl Anim Behav Sci 2009, SEE ALSO 177:47–54. lifelong—may see recurrence of aggression r Aggression, Fear/Defensive—Dogs Landsberg G, Hunthausen W, Ackerman L. with treatment lapses and continued exposure r to aggressive triggers. Aggression Toward Familiar People—Dogs Handbook of Behavior Problems of the Dog POSSIBLE COMPLICATIONS ABBREVIATIONS and Cat. Oxford: Butterworth-Heinemann, r 1997. CNS = central nervous system Human injuries; euthanasia or relinquishment r Mertens PA. Canine aggression. In: Horwitz GIT = gastrointestinal tract of patient r D, Mills D, Heath S, eds., BSAVA Manual MAO = monoamine oxidase EXPECTED COURSE AND PROGNOSIS r of Canine and Feline Behavioural Medicine. MRI = magnetic resonance imaging There is no cure. Prognosis for improvement r Gloucestershire, UK: BSAVA, 2002, SSRI = selective serotonin reuptake is better if aggression is at a low intensity and pp. 195–215. inhibitor occurs in only a few predictable situations. r Authors Laurie Bergman and Meredith TCA = tricyclic antidepressant Prognosis is highly dependent on owner Stepita compliance. Consulting Editor Debra F. Horwitz BLBS078-CF_A28 BLBS078-Tilley July 15, 2011 17:59

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

or both cats, one or multiple cats reaching DIAGNOSTIC PROCEDURES r social maturity, moving, changing furniture or Obtain a detailed oral or written history. r r BASICS other resting areas, etc. Exposure to agitating Identify: the number, location, and types of stimuli (interloping cats in the yard, visitors, litter boxes, where each of the cats spends OVERVIEW noises, scents, etc.) can cause redirected most of his/her time. r r aggressive behaviors that can develop into If there are multiple cats within the Staring, displacing, vocalizing (growling, r yowling, shrieking), spitting, hissing, persistent aggressive interactions. Lack of household, attempt to determine which cats appropriate socialization to other cats as a spend time together and which cats avoid swatting, lunging, chasing/stalking, and/or r biting other cats. Multiple motivations exist. kitten. Genetically unrelated cats and cats each other, the locations of feeding, play, and SYSTEMS AFFECTED that have only recently moved in together are resting areas, and locations of any house r more likely to show aggressive behaviors soiling or marking. Behavioral r r r toward each other. Medical problems If a house call is not possible, have the Hemic/Lymphatic/Immune r r causing pain or increased irritability. Some clients draw a floor plan with the above Nervous aggression between cats is normal in cat social details. r r SIGNALMENT systems. Resident cats commonly take Video and still photographs of cats r No age, sex, or breed distribution noted. prolonged exposure to new cats before being interacting can be informative. r r Can occur at any age as a chronic willing to accept them into a group without Note any other changes in demeanor, manifestation of redirected aggression or displaying defensive or offensive behaviors. routine, and eating and grooming habits of all when the social environment changes (for participants. instance, addition of a new cat, return of a cat from the veterinarian, etc.). r Previously stable cat relationships can DIAGNOSIS disintegrate as cats reach social maturity. TREATMENT DIFFERENTIAL DIAGNOSIS SIGNS r Behavioral Differentials For chronic, severe cases or for aggression Aggressor r that does not respond to treatment, clients r Fear-related aggression, status-related Covert signs: staring, displacing other cats, may elect permanent separation either by aggression, territorial aggression, redirected stiff body language/movements while rehoming one of the cats or by splitting up aggression, failure of recognition (most likely approaching the other cat. the residence. Be prepared to provide r due to change in smell of victim), maternal Overt signs: Growling, yowling, spitting, recommendations about this process. aggression, intermale aggression, sexual r hissing, swatting, lunging, chasing/stalking, Neuter intact males. aggression, predatory behavior and/or biting other cats, dilated pupils, may FOR CASES THAT HAVE A LOW Medical Differentials be accompanied by body language of fear r FREQUENCY OF INTENSE, (such as the classic Halloween cat Any illness causing malaise, pain, or increased irritability (hypertension, arthritis, INJURIOUS AGGRESSIVE stance—piloerection, back arched, tail up) or r more offensive body language (stiff muscles, abscess, dental disease) Endocrine: OUTBURSTS r r tail head elevated but rest of tail down, back hyperthyroidism Neurologic: Separate the cats when they cannot be straight or slightly slanted toward the head, space-occupying lesions (meningioma, directly supervised (create “safe zones”). r ears forward or to the side), excessive facial lymphoma), encephalitis, seizures, feline Either keep the spaces the same each day in ischemic encephalopathy, trauma, sensory or marking, and perhaps urine marking. r an effort to form a separate core territory for Victim cognitive decline Infectious: rabies, each cat, or “time share” the spaces between r Covert: avoidance of aggressor, hiding, toxoplasmosis, aberrant parasitic migrations cats in order to avoid each cat exploiting only (such as cuterebriasis), FIV, FeLV change in grooming and eating habits, r a small area over the long term. Iatrogenic: administration of medications r hypervigilance, dilated pupils. If you elect to keep the safe zones the same r that can increase irritability or disinhibit Overt: hissing, swatting, running, vocalizing for each cat, give the aggressor the smaller area aggression (such as mirtazapine, (including growling), Halloween cat stance, r (keep the aggressor’s core area small). benzodiazepines, buspirone) Toxins: lead, r may escalate to defensive attack if cornered. For multiple cats, separate by stability of illicit substance ingestion relationship between cats. Any despotic/bully Elimination Outside of the Litter Box r CBC/BIOCHEMISTRY/URINALYSIS cats should be confined alone. Aggressors may block access to the litter box r r Obtain at initial consultation or before Reward the cats with food, play, and/or area, forcing victims to choose alternative attention for being in the same room together elimination locations; secondary substrate specialty referral to rule out any contributory medical problems. without having aggressive events. Cats should and/or location preferences and aversions can r stay at a distance that allows for calm develop. If patient placed on psychotropic r participation. medication: repeat every 6 months to 1 year r Both victims and aggressors may urine mark Engage the cats in daily sessions of either horizontally or vertically. depending on age and general health of pet. r pleasurable activities (play, training, eating Extremely fearful cats may urinate or OTHER LABORATORY TESTS r > delectable food treats, etc.) at distances that defecate in the midst of aggressive events. Cats 6 years should have T4/free T4 have a very low likelihood of creating Causes & Risk Factors measured. r r aggressive events. Gradually move the fun Resource limitation (not enough vertical Urine culture and sensitivity should be sessions closer to each other. r and/or horizontal space, lack of appropriate obtained from cats that are urinating outside The goal of management and safety hiding areas, and limited access to food, of the box unless there is a clear diagnosis of r is to prevent aggressive events from occurring. water, and litter boxes, etc.). Social and urine marking for all urinations out of the In an emergency, judicious use of interrupters environmental instability such as the addition box. (such as water gun sprays, blankets of a new cat, loss of a resident cat, change in IMAGING tossed on the cats, etc.) can stop events smell (return of a cat from the veterinarian or Housesoiling cats should have abdominal in progress but should not be considered giving one cat a bath), aging or illness of one radiographs and/or ultrasounds. mainstays of treatment. These should be used BLBS078-CF_A28 BLBS078-Tilley July 15, 2011 17:59

Canine and Feline, Fifth Edition 41

(Continued) Aggression, Intercat Aggression A

r as the aggressive behavior is just beginning to Side effects include: may increase intercat be most effective. If it can be safely done, the aggression as victim may now “fight back.” aggressor should be placed or lured into his/her Benzodiazepines FOLLOW-UP r safe zone at the first sign of any threatening Lorazepam 0.125 mg–0.25 mg/cat PO up r Clinicians should be updated q2 weeks after behavior. Use of interrupters and punishers to q12–24h r treatment initiation either by phone or in can increase aggressive behavior in some Oxazepam 0.2 mg–0.5 mg/kg PO q12–24h person. A recheck should be performed no cats and increase negative associations with (feline dose) r later than 8 weeks into treatment. other cats, and so must be used cautiously. For fearfully aggressive cats. r r r Recheck laboratory work every 6 months to Distracters such as laser pointers, tossed Side effects include increased sociability, 1 year depending on the health and age of the toys, and remote activated toys can be used to decreased hiding, increased appetite, and patients for cats on long-term medication. redirect aggressors at the beginning of the disinhibition of aggression, ataxia. r aggression sequence (staring, tail twitching, May see clinical effects within 1 hour. PREVENTION/AVOIDANCE r and pupil dilation) and do not risk creating Note: controlled substance, dependence can Proper socialization can help decrease the negative associations between the cats. develop. likelihood of intercat aggression in some cats. r r Bell the aggressor (using a quick release or Need client update no more than 48 hours Gradual introduction more closely resembles safety collar) so both the owner and the victim after starting medication. the natural process through which new cats can quickly identify his/her location. r Selective Serotonin Reuptake Inhibitors are admitted to an existing group, therefore Increase the number of resources this method is preferred when introducing throughout the residence. Fluoxetine 0.5–1 mg/kg PO q24h (feline r dose) new cats. Genetically related cats may be less Increase litter box number to the number of likely to have intense intercat aggression. In cats plus one (three boxes for two cats). Paroxetine 0.5–1 mg/kg PO q24h (feline r dose) stable households avoid adding additional Add litter boxes to different locations so cats. that one cat cannot keep others from For aggression, anxiety, and/or urine marking, may decrease impulsivity. EXPECTED COURSE AND PROGNOSIS accessing the boxes; locations with more than r one exit/entry are ideal. Need client update q2 weeks. Plan to use for Recent and mild (low-intensity, r Increase the number and locations of food at least 4–6 weeks after resolution of signs. low-frequency, rare/mild injuries) cases seem Side effects of SSRIs include sedation, urinary to have better long-term outcomes. and water areas. r r Increase the number of hiding places and retention, gastrointestinal upset (including The prognosis is complicated by prolonged comfortable resting areas; especially diarrhea, constipation, vomiting, anorexia), duration, high severity, underlying medical concentrate on increasing vertical space (i.e., increased agitation/irritability. conditions, and incomplete owner resting areas on shelves, window sills, etc.). Tricyclic Antidepressants compliance. r r Increase play and add food-dispensing toys. Amitriptyline 0.5–1 mg/kg PO q12–24h ABBREVIATIONS r r No new cats should be added to the house. (feline dose): for anxious cats with co-morbid FeLV = feline leukemia virus recurrent, severe FIC/FLUTD symptoms r = FOR CASES WHERE THE CATS r FIC/FLUTD feline idiopathic cystitis/ Clomipramine 0.3–0.5 mg/kg PO q24h feline lower urinary tract disease CANNOT BE IN THE SAME ROOM r (feline dose): for anxious and/or aggressive FIV = feline immunodeficiency virus r WITHOUT IMMEDIATELY BECOMING cats, with or without urine marking SSRI = selective serotonin reuptake AGITATED components inhibitor r r r Separate cats completely when Need client update q2 weeks. Plan to use for T4 = thyroxine at least 4–6 weeks after resolution of signs. r = unsupervised. r TCA tricyclic antidepressant r Side effects of TCAs include sedation, Meet each cat’s needs for play, litter boxes, Suggested Reading food, water, and attention. increased thirst, urinary retention, r Amat M, et al. Evaluation of inciting causes, Set up systematized desensitization and constipation, and lowered seizure threshold. alternative targets, and risk factors counter-conditioning sessions daily; initially Do not use in patients with arrhythmias or associated with redirected aggression in cats. utilize physical and visual barriers. cardiopathies. r JAVMA 2008, 233(4):586–589. Teach both cats to tolerate harnesses and Pheromones Curtis TM, Knowles RJ, Crowell-Davis SL. leashes so that they can be used during r Feliway and Felifriend (two different feline Influence of familiarity and relatedness on training sessions. This is especially valuable facial pheromone fractions) may be helpful in proximity and allogrooming in domestic for the aggressor. r cases of intercat aggression when used with a cats (Felis catus). Am J Vet Res 2003, When ready to allow the cats more freedom multimodal plan 64:1151–1154. with each other, follow the instructions for CONTRAINDICATIONS/POSSIBLE Heath S. Feline aggression. In: Horwitz DF, less severe interact aggression (above). INTERACTIONS Mills D, Heath, S, eds., BSAVA Manual of r SSRIs and TCAs should be used with Canine and Feline Behavioral Medicine. caution in patients with histories of cardiac Gloucestershire, UK: BSAVA, 2002, pp. 216–228. MEDICATIONS abnormalities, seizure histories, and/or liver disease and should not be used together. Landsberg G, Hunthausen W, Ackerman L. r DRUG(S) Benzodiazepines should be used with Feline aggression. In: Handbook of Behavior Problems of the Dog and Cat, 2nd Azapirone caution in cats due to the potential to cause r hepatopathies. ed. Philadelphia: Elsevier Saunders, 2003, Buspirone 0.5–1 mg/kg PO q8–24h (feline r pp. 427–453. dose) Medications that alter serotonin levels can r Author E’Lise Christensen Bell Reserved for victims due to potential to have important interactions with other medications (such as selegiline and amitraz). Consulting Editor Debra F. Horwitz increase social confidence, can potentially r help stop the run-chase cycle, may also In the United States, all medications for improve urine marking. behavior problems in cats are off-label at this r Need client update q2 weeks. Plan to use for time. at least 4–6 weeks after resolution of signs. BLBS078-CF_A29 BLBS078-Tilley May 31, 2011 18:3

42 Blackwell’s Five-Minute Veterinary Consult A Aggression, Interdog Aggression

r behavior and result in escalation of the Treatment is more likely to be successful if a interdog aggression. For example, an owner period of preventing exposure to BASICS calling dog “A” into a room when the other aggression-provoking stimuli is instituted dog “B” has blocked its access even though prior to behavior modification. r OVERVIEW “A” was willing to remain outside of the room The dog must be confined away from r Two basic forms: aggression toward other or the owner punishing dog “B” for blocking potential victims or under the direct physical dog(s) within a household and aggression dog “A’s” access. Both of these situations control of a responsible adult whenever an toward unfamiliar dogs. A variety of different undermine dog “B” in its hierarchal position aggression-provoking situation could arise motivations exist, including fear, territoriality, while it was subtly asserting control that dog (e.g., in any public location, on walks, around “A” was willing to respect. food/other valued resources). and social status. Usually within the range of r r normal behavior, but excessive aggression due Underlying medical conditions, especially Teaching the dog to be comfortable wearing to learning or genetics (dogs bred for fighting) pain, may increase the level of aggression. a head halter (e.g., Gentle Leader) and basket is also possible. muzzle makes controlling potentially dangerous situations easier and safer. SYSTEMS AFFECTED r For aggression within a household, Behavioral DIAGNOSIS determine which dog is the more appropriate SIGNALMENT controlling/dominant individual and r Dog. DIFFERENTIAL DIAGNOSIS reinforce that dog by providing him with r r More common in intact males. Play behavior/excited non-aggressive arousal priority access to valued resources (e.g., food, r r Breed predilection in “fighting breeds” (e.g., Others depending on circumstances toys, resting areas, human attention). r pit bull terriers) and terriers. Be aware of “bullies” and that access to r CBC/BIOCHEMISTRY/URINALYSIS Signs usually develop at sexual Usually unremarkable. Abnormalities suggest resources between household dogs can be (approximately 6–9 months of age) or social an underlying or contributing medical context dependent. maturity (approximately 18–36 months of condition. Behavior Therapy age). r OTHER LABORATORY TESTS Systematic desensitization and SIGNS counter-conditioning to specific r Usually unremarkable. Aggression (growling, lip-lifting, barking, aggression-provoking stimuli. IMAGING r snarling, snapping, lunging, biting) toward NEVER allow dogs to “fight it out” (see MRI if CNS disease suspected; as needed to Aggression Toward Familiar People—Dogs). other dogs. This may be accompanied by r fearful or submissive body postures/facial rule out underlying medical conditions. Affection control: especially for aggression expressions (crouching, backing away, ears DIAGNOSTIC PROCEDURES between dogs within a household. To increase back, tail tucked, looking away, lip licking) or N/A owners’ leadership over dogs and confident/dominant body postures (standing predictability of dogs’ lives (see Aggression straight up, approaching/direct contact with Toward Familiar People—Dogs). the other dog, tail up, ears forward). r History may include the dog having been TREATMENT the victim of aggression from other dogs (especially if aggression is toward unfamiliar CLIENT EDUCATION r MEDICATIONS dogs). Treatment is aimed at controlling the r DRUG(S) When fighting occurs within a household, problem, not at achieving a “cure.” Successful r history prior to the onset of fights may include treatment, as measured by a decrease in There are no medications licensed for the subtle signs of social control/dominance (e.g., aggressive incidents, depends upon owner treatment of canine aggression. Owners must staring, lying across doorways to block the understanding of basic canine social behavior, be aware that the use of medication is other dog’s access to a room) and submission risks involved in living with an aggressive off-label. Because of liability concerns, note in (e.g., turning away from the staring dog or dog(s), and how to follow safety and the patient’s record that the owners were not entering the same room as the other dog). management recommendations. informed of potential risks and side effects. r r r Dogs fighting in a household may get along Owners must be aware that the only way to A signed informed consent form is advisable. well except in specific situations. absolutely prevent future injuries is rehoming r CAUSES & RISK FACTORS (if household dog aggression) or euthanasia. NEVER use medications without behavior r modification. r If owners elect not to euthanize, they must r May be a normal canine behavior; strongly Before prescribing medication, be sure that influenced by previous experience (e.g., be aware that their primary responsibility is preventing human injury by conscientiously owners understand the risks in owning an inadequate early socialization, aggressive aggressive dog, will follow safety procedures, encounters with other dogs, inappropriate avoiding situations that may evoke an aggressive reaction, including situations that and will not rely on medication to keep others punishment in the presence of other dogs). safe. r have resulted in the dog’s being fearful even if r Breed predilections due to selective breeding Medication may not be appropriate in some for interdog aggression. not aggressive. Dogs within a household may r family situations (e.g., those with small Aggression is likely to be more severe toward need to be kept separated to prevent contact and fighting. children, family members with disabilities, or dogs of the same sex. r r immunocompromised individuals). In cases of aggression within a household, If needed, owners must be instructed in r methods of safely breaking up dog fights. Research has confirmed there is a strong there may be history of owners interfering in r placebo effect when using medications to treat normal canine communication methods, Owners may be more compliant with avoidance recommendations if they canine aggression. Studies have not shown a especially when one dog appears to be robust effect of drug treatment on aggression. understand that in many jurisdictions dog r denying another dog access to something that Medications are most likely to be helpful in the owners think they should “share.” This owners are liable for bites and can face civil/criminal prosecutions should a person be situations where there is a strong fear/anxiety shift may actually support one dog in what component, as opposed to situations where would be considered inappropriate “canine” injured. BLBS078-CF_A29 BLBS078-Tilley May 31, 2011 18:3

Canine and Feline, Fifth Edition 43

(Continued) Aggression, Interdog Aggression A

closely ranked dogs use aggression to establish within the first 1–3 weeks after the ABBREVIATIONS r dominance. consultation. Provisions for further follow-up CNS = central nervous system r = Selective Serotonin Reuptake Inhibitors should be made at that time. GIT gastrointestinal tract r r = Fluoxetine 0.5–2 mg/kg PO q24h (canine) PREVENTION/AVOIDANCE MAO monoamine oxidase r r = Paroxetine 0.5–1 mg/kg PO q24h (canine) MRI magnetic resonance imaging r Treatment recommendations are r = Sertraline 1–3 mg/kg PO q24h (canine) SSRI selective serotonin reuptake r lifelong—aggression may recur with Side effects: sedation, irritability, GIT inhibitor treatment lapses and continued exposure to r = effects; anorexia is common and usually aggressive triggers. TCA tricyclic antidepressant transient. POSSIBLE COMPLICATIONS Suggested Reading Tricyclic Antidepressants deKeuster T, Jung H. Aggression toward r Injuries to dogs and humans involved; Clomipramine 2–4 mg/kg PO q24h or euthanasia or relinquishment of patient. familiar people and animals. In: Horwitz DF, Mills D, eds., BSAVA Manual of divided q12h (label restriction for aggression) EXPECTED COURSE AND PROGNOSIS (canine) Canine and Feline Behavioural Medicine, r Side effects: sedation, GIT effects, There is no cure. Prognosis for improvement 2nd ed. Gloucestershire, UK: BSAVA, 2009, anticholinergic effects, and cardiac is better if aggression is at a fairly low intensity pp. 182–210. conduction disturbances if predisposed. and occurs in only a few predictable Herron ME, Shofer SS, Reisner IR. Survey of situations. Prognosis is highly dependent on Benzodiazepines the use and outcome of confrontational and r owner compliance. Alprazolam 0.05–0.1 mg/kg PO q12h or non-confrontational training methods in PRN client-owned dogs showing undesired behaviors. Appl Anim Behav Sci 2009, CONTRAINDICATIONS/POSSIBLE 177:47–54. INTERACTIONS MISCELLANEOUS Mertens PA. Canine aggression. In: Horwitz r Any psychotropic medication may increase ASSOCIATED CONDITIONS D, Mills D, Heath S, eds., BSAVA Manual rather than decrease aggression. of Canine and Feline Behavioural Medicine. r May see other fear- or anxiety-based Use caution when prescribing conditions (e.g., noise phobias, separation Gloucestershire, UK: BSAVA, 2002, benzodiazepines as disinhibition of aggression anxiety); territorial aggression. pp. 195–215. may result due to a reduction in fear-based Authors Laurie Bergman and Meredith inhibition to biting. ZOONOTIC POTENTIAL Stepita r Do not combine SSRIs, TCAs, MAO Human injury and bite wounds when Consulting Editor Debra F. Horwitz inhibitors (e.g., amitraz, selegiline) or separating fighting dogs. tramadol—can result in potentially fatal PREGNANCY/FERTILITY/BREEDING serotonin syndrome. Do not breed dogs with extreme interdog aggression. SEE ALSO r Aggression, Fear/Defensive—Dogs FOLLOW-UP r Aggression Toward Familiar People—Dogs PATIENT MONITORING Clients often need ongoing assistance and should receive at least one follow-up call BLBS078-CF_A30 BLBS078-Tilley July 29, 2011 19:24

44 Blackwell’s Five-Minute Veterinary Consult A Aggression, Overview—Cats

Redirected Aggression (Toward People Pain Aggression (Toward People and or Other Animals) Animals) r BASICS Cats who see, hear, or smell a trigger and Cats who are in pain may show aggression direct aggressive behavior toward the closest (hiss, growl, scratch, bite) when they are DEFINITION innocent bystander. physically handled or prior to or after r Aggression In some cases, one person or animal in the movements such as jumping onto or off of a r A behavioral strategy used to manage home becomes the designated victim, and the piece of furniture. aversive situations. cat may bypass a nearby individual and look Maternal Aggression r for the preferred victim. May be normal and appropriate in certain r A female cat may show aggressive behaviors contexts. Some cats may stay aroused for 24–72 hours toward individuals approaching her r after a triggered event. May be abnormal with serious deleterious r kittens. A common trigger inciting redirected effects on the cat’s physical and emotional Impulse Control Aggression well-being. aggression is the cat seeing another cat or r wildlife outside. Cats who show intense aggressive responses to Aggressivity: describes both mood and mild stimuli without much or any warning temperamental traits relating to the Fear/Defensive Aggression (Toward may have a deficiency in serotonin often People or Other Animals) propensity to show aggression when r called an impulse control disorder. environmental circumstances dictate it might The cat will show body postures indicative Frustration-Induced Aggression (To be used. of fear/anxiety and may use aggression as a People and Other Animals) strategy to manage that aversive situation. OVERVIEW OF TYPES r Typical behaviors shown include a Some cats have very outgoing, social Play Aggression (Toward People) personalities and exhibit aggression if the r combination of any of the following: hissing, Typically refers to a cat who scratches and spitting, piloerection, arched back, turning captive life indoors does not meet their bites the owners during play. behavioral needs. r away, running away, cowering, rolling on its Not true aggression but overzealous play back and pawing (defensive position, not Contact-Induced/Petting Aggression without proper impulse control due to lack of (Toward People) submissive position) if cornered. r training or proper intraspecific social Cats will show early signs of aversion when feedback. Territorial Aggression (Toward People or r people stroke their cats, with their ears going The cat’s intent is not to harm the person. Other Animals) r r back and tail swishing. Behavior encouraged and rewarded by Some cats, particularly male cats, show r territorial behaviors in domestic home If physical contact continues, they typically owners through rough play with a kitten; bite. settings due to size and the presence of more r when larger and stronger, becomes perceived Owners often miss the early warning signs. as aggression rather than overzealous play. resources (e.g., people, food, resting areas, r feeding areas, elimination sites, etc.) to defend When cats groom one another, they Predatory Aggression (Toward People or in a smaller area. typically limit the grooming to the head Other Animals) r region. r Territorial behaviors include marking with r Cats have an innate drive to “hunt” or show urine, feces, or bunting (the rubbing of the To some cats it may be abnormal and predation behavior, which includes stalk, cheeks on surfaces to deposit pheromones) unwanted to be stroked along the dorsum, the hide, and pounce. common method used by owners. r and scratching (also deposits pheromones and Predation is not a direct function of hunger. Intercat Aggression within a Home r leaves visual marker) and may be associated r Typically stimulated by fast movements and with aggression. Fifty percent of cat owners report fighting r can progress to the cat hiding and waiting for In severe cases, the aggressor may seek out (scratching and biting) after introducing a an animal or person to walk by. the other individuals and attack. new cat to the home. r r r Play is a common way for young cats to Body posture with territorial aggression is The number of cats, gender, and age are not perfect predation skills; play aggression and assertive and confident. significant factors in predicting which cats predatory aggression may overlap. will show aggression.

Learning

Communication

Social interactions

Environment Genetics AGGRESSION

physiology

Learning

Figure 1. BLBS078-CF_A30 BLBS078-Tilley July 29, 2011 19:24

Canine and Feline, Fifth Edition 45

(Continued) Aggression, Overview—Cats A

r r r Any of the above categories of aggression are Males were more likely to show aggression Implement safety measures (soft claws, all possibilities for fights between or among to cats than females. wearing long pants/long sleeves, keep r cats. Abyssinian, Russian blue, Somali, Siamese, flattened cardboard boxes around home to r Fear/anxiety is the most common cause of and chinchilla breeds showed more aggression. place between yourself and your cat, redirect r intraspecific aggression. Maine coon, ragdoll, and Scottish folds the behavior in early arousal phase). r CONTRIBUTING FACTORS TO THE showed the least aggressiveness. Behavior modifications to redirect the cat PATHOPHYSIOLOGY SIGNS and reduce arousal (specific plans are r dependent upon the specifics of each case). Behavior problems are typically multifactorial May appear at social maturity (2–4 years of r age) except for play-related and should occur Train your cat to commands such as “sit,” in cause, and below is a diagram illustrating “go to place,” etc. in specific social contexts/interactions. If age r some of the more common components that Implement environmental enrichment. need to be evaluated to accurately diagnose of onset occurs in an older cat, medical causes r should be ruled out first. Teach owners to identify early signs of and treat aggression cases. r General comments: most owners are able to arousal so the cat can be redirected or so they SYSTEMS AFFECTED can avoid the cat. r detect overt signs of aggression (biting, r Behavioral—vary with type of aggression, hissing, growling) but may miss more subtle After a very aggressive outburst, keep occur alone or in combination: tail signs of aggression that typically occur aggressor isolated in a room for at least 24 swishing/twitching, ears turned sideways or between cats (staring) and the resulting hours (if this is a cat who remains aroused flattened, stiffening of shoulders/legs, after an attack). anxious behaviors that can result in aggression r crouching, dilation of pupils, hissing, spitting, Pheromones. (meatloaf position, averting gaze, etc.). r growling, piloerection, staring, chasing, Videotapes of intercat interactions allow the Medications. stalking, pawing, lunging. r clinician to assess the behavior. Cardiovascular—signs associated with sympathetic activation and HPA activation. CAUSES r r Endocrine and Metabolic—long-term Underlying medical issues can cause MEDICATIONS aggression. aggression associated with fear/stress/anxiety, r r symptoms associated with long-term Temperament/behavior is influenced by SSRIs: fluoxetine and paroxetine 0.5 mg/kg PO q24h activation of the HPA system. genetics, rearing, socialization, environment r r TCAs: clomipramine 0.5 mg/kg PO q24h Gastrointestinal—with chronic HPA in which the cat lives, and types of r Amitryptiline 0.5–1.0 mg/kg PO q12–24h stimulation may see a cat more prone to GI interactions the cat has with people. r Buspirone 0.5–1.0 mg/kg PO q8–24h ulcers. With acute fear aggression: evacuation r of the bowel and possible diarrhea. IBD Benzodiazepenes: oxazepam 0.2–0.5 mg/kg possible in chronic stress. q12–24h r r Hemic/Lymphatic/Immune—decreased DIAGNOSIS SAMe: 90 mg PO q24h immune response with chronic HPA CONTRAINDICATIONS DIFFERENTIAL DIAGNOSIS r stimulation; stress leukogram. Cats with renal or hepatic disease. r r r Musckuloskeletal—an outcome of the CNS diseases (infections, toxins, tumors, Caution with TCAs and SSRIs in diabetics. etc.) r aggression may result in damage to the skin, r TCAs in patients with cardiac abnormalities. muscles from damage by the nails and teeth. Hyperthyroid r r POSSIBLE INTERACTIONS Hepatic encephalopathy r Both the victim and the aggressor may r TCAs and SSRIs should not be used suffer injuries. With chronic activation of the Any condition causing pain (arthritis, pancreatitis, dental disease, anal sacculitis, etc.) together. HPA, may see muscle wasting. r r r Lead poisoning Certain flea collars. Nervous—increased reactivity for up to r r Rabies Certain herbals. 72 hours following an aggressive outburst. r r Diabetic neuropathy (pain-induced Mirtazapine should not be used in May see an increase in aggression with combination with a TCA or SSRI. aggression when paws touched) r decreased provocation as the synapases in the Any other medication the cat is on, the CBC/CHEMISTRY/URINALYSIS amygdala become sensitized. Some animals practitioner should look up which liver may have decreased serotonin, causing All of the above should be done. enzyme system is utilized in metabolism to aggressive outbursts. Depending on the type OTHER LABORATORY TESTS maximize safety in combining medications. of aggression, may see ritualized motor r Any cat that bites or scratches people should patterns, shaking, or trembling. r have a Bartonella test. Ophthalmic—dilated pupils with r Thyroid levels. sympathetic stimulation. r r Urinalysis = /– culture if housesoiling is FOLLOW-UP Renal/Urologic—may see associated part of the aggression issue. spraying or small amounts of urine on r PATIENT MONITORING Feline serology (FCV, FeLV, FIV). r horizontal surfaces. May exhibit signs Call owners once every 1–2 weeks for the consistent with FLUTD with aggression that first 2 months after a treatment plan has been is due to stress/anxiety/fear. r recommended. Determine implementation of Respiratory—tachypnea in acute cases or safety recommendations and the behavioral when stressed. TREATMENT plan. r r r Skin/Exocrine—damage due to fights. Never use physical correction/punishment; If medications are involved, the medication Damage due to excessive grooming associated may escalate the aggression. dose should be reevaluated every 3–4 weeks. r r with fear-based aggression/anxiety/distress. Never try to physically handle or Frequency of follow-up will be dictated SIGNALMENT manipulate a cat in an aggressive state. by the severity of the case and owner r r Avoid known triggers. compliance. There is preliminary evidence that r r behavioral traits in cats vary by breed and Identify triggers and desensitize and CBC, chemistry, T4 prior to medication. gender. counter-condition the cat to the triggers. Recheck liver and kidney values 2–3 weeks BLBS078-CF_A30 BLBS078-Tilley July 29, 2011 19:24

46 Blackwell’s Five-Minute Veterinary Consult

A Aggression, Overview—Cats (Continued)

r after starting medication. Recheck bloodwork Age 2–4—social maturity, when cats may Levine ED. Feline fear and anxiety. Vet Clin annually in young healthy patients, start to show certain kinds of aggression. North Am Small Anim Pract 2008, semiannually in older patients. ABBREVIATIONS 38:1065–1079. r r Repeat physical exams in older patients CNS = central nervous system Levine ED, Perry P, Scarlett J, et al. Intercat r semiannually, as painful conditions may start FCV = feline calicivirus aggression in households following the r to contribute to/exacerbate the pain. FeLV = feline leukemia virus introduction of a new cat. Appl Anim Behav r EXPECTED COURSE AND PROGNOSIS FIV = feline immunodeficiency virus Sci 2004, 90:325–336. r r Ultimately depends on the specific kind of FLUTD = feline lower urinary tract disease Author Emily D. Levine r aggression and the compliance of clients with GI = gastrointestinal Consulting Editor Debra F. Horwitz r the suggested treatment plan. HPA = hypothalamic-pituitary-adrenal Acknowledgement Karen L. Overall r r Most cases of aggression need a IBD = inflammatory bowel disease r = combination of behavioral modification, SAMe S-adenosyl-L-methionine-tosylate Client Education Handout environmental modification, training, and, disulfate r available online when necessary, medication to maximize SSRI = selective serotonin reuptake chances of improvement. inhibitor r r Some types of aggression can resolve or TCA = tricyclic antidepressant improve within a few weeks, whereas others Suggested Reading may take several months or longer. r Crowell-Davis SL, Murray T. Veterinary Some forms of aggression have a poor Psychopharmacology. Ames, IA: Blackwell, prognosis. 2006.

MISCELLANEOUS AGE-RELATED FACTORS r Older cats—cognitive decline, CNS disease, arthritis, meningioma, other medical conditions. BLBS078-CF_A31 BLBS078-Tilley July 15, 2011 2:16

Canine and Feline, Fifth Edition 47 Aggression, Overview—Dogs A

r INCIDENCE/PREVALENCE Triggers (human directed): reaching for pet, r Canine aggression is the most common patting on head, approaching or displacing BASICS diagnostic category seen by board-certified when on elevated resting sites, approaching veterinary behaviorists in the United States. food, toys, or stolen objects. r DEFINITION According to the Centers for Disease Defensive r r Action by one dog directed against another Control and Prevention (2009), about Often directed toward unfamiliar humans organism with the result of harming, limiting, 4.7 million people are bitten by dogs each or dogs that approach, stand over, or reach or depriving that organism. year in the United States. for. Certain familiar people may be exempt. r r r Numerous functional types have been Almost one in five of those who are bitten May be location-specific, as when strangers (a total of 885,000) require medical attention approach home, yard, or car. posited. Here, aggression is classified on the r basis of two categories, offensive or defensive. for dog bite–related injuries. May be exacerbated if restrained. r r r Offensive aggression is an unprovoked Among adults and children, males are more As distance from stimulus decreases, likely than females to be bitten. response may escalate to agitation, barking, response directed toward an individual in r The rate of dog bite–related injuries is lunging, baring teeth. order to control access to some resource at the r highest for children ages 5–9 years. Approach/avoidance behavior is common. expense of that individual; includes social r status/dominance aggression, possessive GEOGRAPHIC DISTRIBUTION Maternal aggression is directed toward aggression, intermale aggression, interfemale Worldwide individuals approaching the whelping area or puppies. aggression, and predatory aggression. SIGNALMENT Common targets are familiar individuals. Physical Examination Findings r r Defensive aggression is directed toward an Species Usually unremarkable; no specific signs individual perceived as an instigator or threat; Dogs universally associated with this condition. r includes fear-motivated, territorial, protective, Breed Predispositions Offensive and defensive aggression may be r irritable (pain-associated or Any breed. observed during the course of the r frustration-related), and maternal aggression. Pit bull types and rottweilers are the most examination. Common targets are unfamiliar individuals. r r common breed types implicated in fatal dog Use extreme care when handling aggressive Probability of overt aggression may be bites in the United States, although dogs; use muzzles and other restraints to influenced by motivation, arousal, and comparative rates of aggression based on prevent injury. r anxiety. Specific incidents may involve both breed occurrence are not available. Abnormalities on the neurologic offensive and defensive components. r r Selective breeding for behavioral traits may examination may suggest an organic disease In all cases, medical explanations (including predispose dogs to specific types of aggression; process (e.g., rabies). pain) must be ruled out. for example, dogs of breeds bred for dog CAUSES PATHOPHYSIOLOGY fighting may be aggressive toward other dogs. r r r Part of the normal range of behavior; Aggression is a normal form of English springer spaniels appear at risk for strongly influenced by breed, sex, early communication in dogs. impulsive (“rage”) aggression. r socialization, handling, individual Some pathologic conditions are associated Mean Age and Range r temperament, and other variables. with an increase in aggression because of CNS Any age. r r Manifestation of an organic effects. Aggression commonly becomes more condition—possible but rare. r r Rage syndrome–impulsive aggression, problematic at social maturity, 1–2 years of In all cases, rule out medical causes of usually directed toward familiar individuals; age. aggression. abnormalities in the CNS serotonin Predominant Sex RISK FACTORS neurotransmitter system have been r Males—intact or castrated are most Male, unneutered. implicated. r r commonly implicated in dog bites. Inadequate socialization during critical Aggression may have a learned component, Signs period (3–14 weeks). leading to an increase in aggression over time. r r Traumatic/negative experience(s). Except when in actual self-defense, General Comments r r Predisposing environmental confrontational techniques should not be Behavioral warning signs—include conditions—associating with other dogs in a used to manage aggression. Although widely immobility, growls, snarls, or air snaps. pack; barrier frustration or tethering; cruel promoted, confrontational management ◦ Offensive—head up, tail up with stiff handling and abuse; and dog baiting and techniques increase the probability of wag, direct stare, face-on immobility. fighting. fear-motivated defensive aggression, leading ◦ Defensive—head lowered, tail down, r Previous aggression/bite history (number of to an increase in the frequency of aggression body withdrawn, forepaw lifted. r incidents, target, severity of aggression); legal over time. History—basis for risk analysis and details citation for biting. SYSTEMS AFFECTED of treatment program. Important questions: r What are the circumstances in which Unpredictability of aggressive incidents Behavior without warning signals. aggression occurs? Who is the target? How r GENETICS severe were the resulting injuries? Inability of owner to safely confine or r manage the dog in order to prevent future Some breed-specific aggressive tendencies Historical Findings and bite styles have been selected for in incidents. Methods include a barrier fence, a Vary according to the situation and the muzzle, a collar or head halter, a leash. breeding programs, although this cannot functional type of aggression. r predict the behavior of individual dogs. Presence of children, elderly people, or r Offensive One study linked aggressive English r other humans or animals at high risk living in Often directed toward familiar household or visiting this household. springer spaniels to one breeding sire, members. implicating a heritable component. BLBS078-CF_A31 BLBS078-Tilley July 15, 2011 2:16

48 Blackwell’s Five-Minute Veterinary Consult

A Aggression, Overview—Dogs (Continued)

r control, behavior modification, and The dog should calmly be removed from pharmacotherapy. aggression-provoking situations. r r DIAGNOSIS A veterinarian with experience and training Euthanasia should be considered if safe in aggression management should be management cannot be employed, or when DIFFERENTIAL DIAGNOSIS consulted. the risk of injury is high. r r Identify pathologic conditions associated Euthanasia should be recommended when SURGICAL CONSIDERATIONS with aggression before a purely behavioral the risk of injury is high. Note Castration of males diagnosis. recommendation in medical record. r A thorough medical evaluation should be NURSING CARE conducted on all cases of aggression. r A boarding facility able to safely manage the Rule out developmental abnormalities dog may be used until a safe management MEDICATIONS (hydrocephaly, lissencephaly, hepatic shunts), plan can be implemented, or until an metabolic disorders (hypoglycemia, hepatic outcome decision made. DRUG(S) OF CHOICE encephalopathy, diabetes), r ACTIVITY None approved by the FDA for the neuroendocrinopathies (hypothyroidism, treatment of aggression. r hyperadrenocorticism), dermatopathy, Since frustration and arousal may increase the No drug will eliminate the probability of neurologic conditions (intracranial neoplasm, incidence of aggression, an appropriate and aggression. r seizures), toxins, inflammatory diseases safe exercise regime should be incorporated Use drugs only when a safe management (encephalitis, rabies), cognitive dysfunction, into the treatment program. plan has been implemented. r acute or chronic pain, and iatrogenic causes, DIET Inform the client of the experimental nature such as glucocorticoid administration. There is modest evidence that a low-protein of medication and risk involved; document in CBC/BIOCHEMISTRY/URINALYSIS diet may reduce territorial aggression in dogs, the medical record, obtain signed informed r Usually normal. an effect that may be enhanced by tryptophan consent. r r Abnormalities may suggest underlying supplementation. Drugs that increase serotonin may be metabolic, endocrine causes, or other medical CLIENT EDUCATION helpful to reduce anxiety, arousal, and r impulsivity. conditions. Safe practices should dictate all decisions. r OTHER LABORATORY TESTS These practices include safe confinement, Treatment duration: minimum 4 months, maximum: lifetime. physical barriers, head halters, leash control, r As indicated (e.g., thyroid panel, See Table 1 for drugs used to facilitate ACTH-stimulation test, other appropriate muzzle use, and supervision by a competent adult. management of aggression in combination tests). r The client should be advised to consider with a safe management plan. IMAGING personal and legal liability risks of keeping the CONTRAINDICATIONS r r May be indicated to identify sources of pain dog. Human injury, bite-related lawsuits, and Fluoxetine is contraindicated in cases of or disease. loss of homeowners insurance can result from liver disease, seizures. r r MRI or CT—particularly if cerebral canine aggression. Such risk assessment may Clomipramine is contraindicated in cases of neoplasia suspected. help the client objectively evaluate the cardiac conduction disturbances or seizures; DIAGNOSTIC PROCEDURES situation. in one study, no more effective than control in r Situations that have led to aggression in the cases of owner-directed aggression. Postmortem fluorescent antibody test is r indicated for any aggressive dog for which past should be listed and a specific plan Amitriptyline is contraindicated in patients rabies is a differential diagnosis, including any developed to avoid these situations and with cardiac conduction disturbances, associated locations in the future. glaucoma, or liver disease. dog not quarantined for 10 days after a bite r injury to a human or other animal. Punishment should be avoided, as it has PRECAUTIONS Pathologic Findings been shown to increase arousal, fear, and Avoid the use of benzodiazepines (e.g., defensive behavior. None, unless an underlying medical etiology r diazepam) in aggressive dogs because of the is suspected. Confrontational techniques, such as risk of behavioral disinhibition. Aggression roll-overs, increase the probability of a may increase when dogs lose their fear of the defensive aggressive response, may lead to repercussions of biting. human injury, and should be strictly avoided. r POSSIBLE INTERACTIONS TREATMENT Non-confrontational techniques that manage resources and teach the dog Do not use SSRIs or TCAs with monoamine APPROPRIATE HEALTH CARE oxidase inhibitors, including amitraz and r appropriate responses should be employed. Management success—combination of L-deprenyl, or with each other because of the multiple modalities: environmental risk of serotonin syndrome.

Table 1 Drugs and dosages used to manage canine aggression.

Drug Drug Class Oral Dosage in Dog (mg/kg) Dosing Frequency

Fluoxetine SSRI 1–2 mg/kg q24h Paroxetine SSRI 1–2 mg/kg q24h Sertraline SSRI 2–4 mg/kg q24h Clomipramine TCA 1–2 mg/kg q12h Amitriptyline TCA 1–2 mg/kg q12h BLBS078-CF_A31 BLBS078-Tilley July 15, 2011 2:16

Canine and Feline, Fifth Edition 49

(Continued) Aggression, Overview—Dogs A

r r ALTERNATIVE DRUG(S) Prognosis is case-dependent due to risk ASPCA Aggression in Dogs: http://www. r L-Tryptophan 10 mg/kg PO q12h factors and management features of each aspcabehavior.org/articles/49/Aggression-in- r Megestrol acetate 1 mg/kg PO q24h for situation. Dogs.aspx. r 2 weeks; then taper to lowest effective dosage; Centers for Disease Control and Prevention drug of last resort in cases of Dog Bite Prevention: http://www.cdc.gov/ dominance-related and intermale aggression; homeandrecreationalsafety/dog-bites/ side effects include obesity, blood dyscrasias, biteprevention.html. MISCELLANEOUS r pyometra, polyuria/polydipsia, diabetes University of California–Davis, Companion ASSOCIATED CONDITIONS mellitus, mammary hyperplasia, and Animal Behavior Program, Dog Aggression: mammary carcinoma N/A http://www.vetmed.ucdavis.edu/CCAB/ AGE-RELATED FACTORS aggression.html. Adult-onset aggression suggests a medical Suggested Reading cause; carefully evaluate sensory acuity, Bain M. Aggression toward unfamiliar people FOLLOW-UP sources of pain, cognitive function. and animals. In: Horwitz DF, Mills D, eds., PATIENT MONITORING ZOONOTIC POTENTIAL BSAVA Manual of Canine and Feline r r Dog bites are significant public health risk. Behavioural Medicine, 2nd ed. Weekly to biweekly contact recommended r in the initial phases. Rabies is a potential cause of aggression. Gloucestershire, UK: BSAVA, 2009, pp. r Clients need feedback and assistance with PREGNANCY/FERTILITY/BREEDING 211–222. behavior modification plans and medication Tricyclic antidepressants are contraindicated deKeuster T, Jung H. Aggression toward management. in breeding males and pregnant females. familiar people and animals. In: Horwitz DF, Mills D, eds. BSAVA Manual of PREVENTION/AVOIDANCE SEE ALSO r r Canine and Feline Behavioural Medicine, To prevent aggressive incidents, avoid all Aggression, Fear/Defensive—Dogs r 2nd ed. Gloucestershire, UK: BSAVA, 2009, situations that have led to aggression in the Aggression, Food, Possessive, and 182–210. past, using safe confinement, gates, halters, Territorial—Dogs r Herron ME, Shofer FS, Reisner IR. Survey of collars, leashes, muzzles. Aggression, Interdog Aggression r r the use and outcome of confrontational and Reduce the risk of aggression in young dogs Aggression Toward Familiar People—Dogs non-confrontational training methods in with a positive socialization program ABBREVIATIONS client-owned dogs showing undesired (3–14 weeks); avoid intimidation techniques r ACTH = adrenocorticotropic hormone behaviors. Appl Anim Behav Sci 2009, and negative, fear-inducing situations. r CNS = central nervous system 117(1–2):47–54. POSSIBLE COMPLICATIONS r = Luescher AU, Reisner IR. Canine aggression r CT computed tomography Injury to humans or animals. r = toward familiar people: A new look at an old r FDA U.S. Food and Drug In cases of interdog aggression, although not Administration problem. Vet Clin North Am Small Anim r the intended target, humans who interfere are MRI = magnetic resonance imaging Pract 2008, 38:1107–1130. r often seriously injured either by accident or by SSRI = selective serotonin reuptake Reisner, IR. Differential diagnosis and redirected aggression; owners should not reach inhibitor management of human-directed aggression for fighting dogs; pull apart with leashes. r = in dogs. Vet Clin North Am Small Anim r TCA tricyclic antidepressant Liability to client, veterinarian. INTERNET RESOURCES Pract 2003, 33:303–320. EXPECTED COURSE AND PROGNOSIS r Author Barbara L. Sherman r American Veterinary Medical Association Consulting Editor Debra F. Horwitz Aggressive dogs weighing over 18.5 kg are at Dog Bite Prevention: http://www.avma.org/ risk for behavioral euthanasia. r public health/dogbite/default.asp. Overtly aggressive dogs are never cured; Client Education Handout depending on the situation, they may be available online managed successfully. BLBS078-CF_A31a BLBS078-Tilley July 23, 2011 4:26

50 Blackwell’s Five-Minute Veterinary Consult A Aggression toward Familiar People—Dogs

members or persons that have an established relationship with the dog. Aggressive BASICS behaviors may be seen in other contexts, DIAGNOSIS including but not limited to defense of DEFINITION territory, when dogs are reprimanded or DIFFERENTIAL DIAGNOSIS r r denied access to items or activities, and Fear-based aggression Anxiety conditions Aggression (growling, lip-lifting, barking, r snarling, snapping, lunging, biting), usually toward unfamiliar people. History-taking Pathological disease conditions associated directed toward household members or people should attempt to establish aggression triggers with aggression (e.g., painful conditions, and frequency/severity of aggressive episodes. with an established relationship with the dog r endocrinopathies) in situations involving access to valued Aggression may not occur every time the CBC/BIOCHEMISTRY/URINALYSIS dog is in a certain situation and may not be resources. Also referred to as dominance Usually unremarkable. Abnormalities may directed uniformly toward each person within aggression, status-related aggression, conflict r indicate an underlying or contributing the household. Stiff body posture, staring, or competitive aggression. medical condition. PATHOPHYSIOLOGY head up, ears up and forward, or tail up usually accompanies aggressive behavior. OTHER LABORATORY TESTS Has been thought of as normal canine social Owners may report a combination of these As indicated to rule out underlying diseases. behavior directed toward people. However, postures with more submissive postures (e.g., IMAGING these dogs may show anxiety or be impulsive tail is up but ears are tucked, eyes averted), and unpredictable. MRI if CNS disease is suspected; as needed to which may represent an element of conflict, rule out underlying medical conditions; may SYSTEMS AFFECTED anxiety, or fear in the dog’s motivation. r be useful to rule out sources of pain. Behavioral Owners often describe these dogs as GENETICS “moody” and may be able to judge when the Breed predilections exist. Pedigree analyses dog is likely to be aggressive. In early episodes have shown increased occurrence in related the dog may show fear through eye aversion, TREATMENT dogs. Mode of inheritance is unknown. tail tucking, and avoidance that may diminish as the dog becomes more confident that APPROPRIATE HEALTH CARE INCIDENCE/PREVALENCE r aggression will change the outcome. Anxiety Outpatient behavior modification; medical 20–40% of behavioral referral case loads. may be noted in pet-owner interactions and management as needed. GEOGRAPHIC DISTRIBUTION other situations such as owner departure or ACTIVITY novel situations. Some dogs control their Regional breed differences exist. Appropriate physical activity may help SIGNALMENT environment using aggression only because it is effective, but they are anxious about every decrease incidences of aggression. Species encounter, while other dogs appear confident DIET Dogs and secure. Low-protein/high-tryptophan diets may help Breed Predilections Physical Examination Findings reduce aggression but are unlikely to make a r r Spaniels (English springer and cocker), Usually unremarkable. Medical significant difference without behavior terriers, Lhasa apsos, and rottweilers, but may conditions, especially pain, may contribute to modification. be exhibited by any breed. the expression of aggression. These dogs may CLIENT EDUCATION Mean Age and Range not show aggression toward a confident but General Comments r Usually manifested at the onset of social non-threatening examiner. However, extreme Successful treatment, resulting in a decrease maturity (12–36 months of age). May be seen caution should be taken when examining in aggressive incidents, depends upon owner in young dogs. dogs that show aggression, including the use understanding of basic canine social behavior, Predominant Sex of muzzles or other humane restraint devices. risks involved in living with an aggressive dog, Males (castrated and intact) more commonly CAUSES and how to implement safety and r r presented than females. May be part of a normal canine social management recommendations. Treatment is aimed at controlling the problem, not at SIGNS behavioral repertoire, but its expression is r influenced by environment, learning, and achieving a “cure.” Owners must be aware General Comments r that the only way to prevent future injuries is genetics. The manifestation of aggression r Careful history-taking is needed to make a may be influenced by underlying medical euthanasia. It is very important that owners diagnosis, assess the risks to the owners and conditions, early experiences (learning that are educated about the risks of using physical public, and formulate a safe and realistic aggression works to control situations), and punishment and training techniques that rely treatment plan. Owners may not recognize or inconsistent or lack of clear rules and routines on owners learning to “dominate” their dogs. give credence to more mild signs of aggression within the household and within human-pet In recent years, there has been a resurgence of r such as staring, growling, baring teeth, or interactions. Aggression is rarely a symptom these training techniques. The improper and snapping, which are often present before bites of medical conditions; however, concurrent inappropriate use of physical punishments/ occur. Details of early aggressive episodes are disease must be ruled out, since illness and/or dominance techniques ranging from vital for establishing the diagnosis and pain may influence the tendency for corrections with choke chains to so-called prognosis. Clinicians should be aware that not aggressive behaviors. alpha rolls to setting up situations to provoke all owner-directed aggression is motivated by RISK FACTORS and then correct aggression can lead to the desire to control but often is anxiety- or human injury, increased aggression, an Inconsistent or inappropriate physical fear-based. increase in anxiety, and a disruption of the punishment and inconsistent owner Historical Findings human-animal bond. r interactions may contribute to the Aggression around resting areas, food, toys, development of conflicted and/or aggressive Safety Recommendations handling (e.g., petting and reaching toward), r behavior. If owners elect not to euthanize, they must and favored possessions, including people. be aware that their primary responsibility is Aggression is directed toward household preventing human injury by conscientiously BLBS078-CF_A31a BLBS078-Tilley July 23, 2011 4:26

Canine and Feline, Fifth Edition 51

(Continued) Aggression toward Familiar People—Dogs A

avoiding situations that may evoke an threshold that would result in fear and/or tramadol—can result in potentially fatal aggressive reaction, including situations that aggression. Progress is slow and careful. serotonin syndrome. have resulted in the dog’s being fearful even if Monitoring of responses is essential. not aggressive. Use information from the SURGICAL CONSIDERATIONS r r patient’s history to help owners identify Neuter intact males. Females that start to specific situations to avoid. Do not allow the show dominance aggression at less than 6 FOLLOW-UP dog on furniture. Do not give valuable treats months of age may be less aggressive when PATIENT MONITORING or toys (e.g., rawhides). Pick up toys and have mature if not spayed. owners control playtime and activity. Limit Clients often need ongoing assistance with physical contact with the dog, including behavior cases, especially aggression. At least petting. Do not physically punish or one follow-up call within the first 1–3 weeks r reprimand the dog. Treatment is more likely after consultation is advisable. Provisions for to be successful if a period of preventing MEDICATIONS further follow-up either by phone or in exposure to aggression-provoking stimuli is DRUG(S) OF CHOICE person should be made at that time. instituted prior to behavior modification. r PREVENTION/AVOIDANCE r There are no medications licensed for the Teaching the dog to be comfortable wearing treatment of canine aggression. Owners must Treatment recommendations are a head halter (e.g., Gentle Leader) with a be aware that the use of medications is lifelong—may see recurrence of aggression lightweight 8- to 10-foot leash attached and off-label. Due to liability concerns, note in with treatment lapses. Continued avoidance basket muzzle whenever in contact with the patient’s record that owners were of aggression triggers may be necessary. people makes controlling potentially r informed of potential risks and side effects. A POSSIBLE COMPLICATIONS dangerous situations easier and safer. Use signed informed consent form is advisable. Human injuries; euthanasia or relinquishment the long leash to safely remove the dog from NEVER use medications without behavior of patient. situations that may elicit aggression; do not modification. Before prescribing medication, EXPECTED COURSE AND PROGNOSIS reach for the dog directly. be sure that owners understand the risks in Behavioral Therapy owning an aggressive dog, will follow safety There is no cure. Prognosis for improvement r Behavior modification—use procedures, and will not rely on medication to is better if aggression is at a low intensity and non-confrontational methods to teach the dog keep others safe. Medication may not be occurs in relatively few predictable situations. to view people as leaders and reward-based appropriate in some family situations (e.g., Prognosis is highly dependent on owner training techniques to teach the dog to obey those with small children, family members compliance. commands from people without experiencing with disabilities, or immunocompromised r r conflict or becoming aggressive. Affection individuals). Medication studies, including control—require the dog to follow a a double-blind placebo-controlled study of command before receiving anything it desires medication for dominance aggression, have MISCELLANEOUS from people (also known as “Nothing in life is shown a strong placebo effect and no ASSOCIATED CONDITIONS free” or “Learn to earn”). For example, the dog difference between placebo and medication in Other forms of aggression, especially must sit or lie down before feeding, petting, reducing aggressive behaviors. territorial and interdog aggression. Aggressive play, or going for a walk. For the initial 2- to Selective Serotonin Reuptake Inhibitors r dogs often have underlying anxiety. 3-week period, owners should give the dog Fluoxetine 0.5–2 mg/kg PO q24h (canine) r AGE-RELATED FACTORS attention only during brief, structured (e.g., Paroxetine 0.5–1 mg/kg PO q24h (canine) r Bitches showing dominance aggression when command-response-reward) periods. At other Sertraline 1–3 mg/kg PO q24h (canine) r less than 6 months old may show a reduction times, they must ignore the dog, especially if Side effects: sedation, irritability, GIT in the level of aggression if not spayed. it is soliciting attention. The owner initiates effects; anorexia is common and usually interaction by giving a command and ZOONOTIC POTENTIAL r transient. terminates interaction. Use positive Tricyclic Antidepressants Human injury from bite wounds. reinforcement (e.g., food, toys, play, petting) r Clomipramine 2–4 mg/kg PO q24h or PREGNANCY/FERTILITY/BREEDING to teach behaviors that are incompatible to divided q12h (label restriction for aggression) Do not breed aggressive dogs. those that have resulted in aggression. For r (canine) Side effects: sedation, GIT effects, example, teach an “Off” command to move SYNONYMS anticholinergic effects, and cardiac r r off furniture or “Drop it” command to release Competitive aggression Conflict conduction disturbances if predisposed. r toys. Also referred to as counter commanding aggression Dominance-related aggression r r r or response substitution. Desensitization CONTRAINDICATIONS Rage syndrome Status-related aggression and counter-conditioning—technique Use caution when prescribing ABBREVIATIONS r r used to decrease reactivity to situations that benzodiazepines, as disinhibition of CNS = central nervous system GIT = r have resulted in aggression in the past. A aggression may result due to a reduction in gastrointestinal tract MAO = monoamine r muzzle may be needed for safety. Do not fear-based inhibition to biting. oxidase MRI = magnetic resonance imaging r begin until the owner has assumed a greater PRECAUTIONS SSRI = selective serotonin reuptake r level of control over the dog through affection Any psychotropic medication may increase inhibitor TCA = tricyclic antidepressant control and reward-based training. The dog is rather than decrease aggression. Author Laurie Bergman and Meredith Stepita first taught to sit and relax on a verbal Corticosteroids are contraindicated in Consulting Editor Debra F. Horwitz command in neutral locations using food food-aggressive dogs; polyphagia can lead to rewards. Gradual exposure of the dog to a increased frequency/intensity of greatly reduced stimulus is attempted so no aggression. Client Education Handout fearful and/or aggressive reaction is elicited. POSSIBLE INTERACTIONS available online The non-fearful and non-aggressive behavior is rewarded. The level of stimulation is Do not combine SSRIs, TCAs, or MAO increased gradually, staying below the inhibitors (e.g., amitraz, selegiline) and BLBS078-CF_A32 BLBS078-Tilley March 21, 2011 20:15

52 Blackwell’s Five-Minute Veterinary Consult A Alkalosis, Metabolic

with mineralocorticoid excess have excessive chloride loss and chloride administration does BASICS not lead to hyperchloremia and correction of DIAGNOSIS metabolic alkalosis (so-called DEFINITION chloride-resistant metabolic alkalosis). DIFFERENTIAL DIAGNOSIS r + − Increase in pH associated with an increase in Respiratory—low [H ] reduces alveolar High plasma HCO3 and hypochloremia in − plasma bicarbonate concentration (HCO3 ) ventilation. Hypoventilation increases PCO2 animals can also be compensating for chronic (dogs, > 24 mEq/L; cats, > 22 mEq/L) and a and helps offset the effects of high plasma respiratory acidosis, in which PCO2 is high − − compensatory increase in carbon dioxide HCO3 onpH.Indogs,anincreaseof and pH is low despite high HCO3 and low tension (PCO2). approximately 0.7 mm Hg in PCO2 can be chloride concentration; blood gas expected for each 1 mEq/L increase in plasma PATHOPHYSIOLOGY − determination required to differentiate. r HCO3 . Limited data is available for cats, LABORATORY FINDINGS Metabolic alkalosis may develop secondary but the degree of respiratory compensation to corrected hypochloremia (hypochloremic appears to be similar. Drugs That May Alter Laboratory Results alkalosis) or hypoalbuminemia None (hypoalbuminemic alkalosis). SIGNALMENT r Any breed, age, or sex of dog and cat Disorders That May Alter Laboratory Hypochloremic alkalosis: Results ◦ Loss of chloride—fluid rich in chloride SIGNS r Too much heparin (> 10% of the sample) and hydrogen ion may be lost via the − Historical Findings decreases HCO . alimentary tract or kidneys. Loss of r r 3 + Administration of loop diuretics (e.g., Blood samples stored at room temperature chloride and H is associated with an − furosemide) or thiazides. for more than 20 minutes have low pH increase in plasma HCO concentration. r 3 Vomiting. because of increased PCO . With chloride loss and volume depletion, 2 − Physical Examination Findings Valid if Run in Human Laboratory? the kidneys reabsorb sodium with HCO3 r instead of chloride, perpetuating the Signs related to the underlying disease or Yes metabolic alkalosis. accompanying potassium depletion (e.g., CBC/BIOCHEMISTRY/URINALYSIS ◦ weakness, cardiac arrhythmias, and ileus). r Chronic administration of alkali (fluids r High total CO (total CO in samples Muscle twitching caused by low ionized 2 2 with high sodium and poor chloride handled aerobically closely approximates calcium concentration. − concentration)—also may result in r HCO ). Dehydration in volume-depleted patients. r 3 transient metabolic alkalosis. Renal r Low blood ionized calcium concentration. Muscle twitching and seizures in patients r excretion of exogenously administered Serum electrolyte abnormalities vary with with neurologic involvement (rare). alkali is effective, and it is difficult to create underlying cause. − r metabolic alkalosis by increasing HCO3 CAUSES r Hypochloremia—consider hypochloremic intake unless the patient has renal Chloride-responsive—diuretic metabolic alkalosis, the most common reason dysfunction. r administration, vomiting of stomach for metabolic alkalosis in dogs and cats, which Hypoalbuminemic alkalosis: contents, and rapid correction of chronic usually results from diuretic administration or ◦ Decrease in plasma weak acids—loss of hypercapnia (respiratory acidosis). vomiting of stomach contents. r r albumin, a weak acid, is associated with Chloride-resistant—hyperadrenocorticism High sodium but normal chloride metabolic alkalosis. and primary hyperaldosteronism. r concentration—consider chloride-resistant SYSTEMS AFFECTED Oral administration of metabolic alkalosis (e.g., r Nervous—muscle twitching and seizures alkali—administration of sodium bicarbonate hyperadrenocorticism or primary occur rarely in dogs. Metabolic alkalosis and or other organic anions with sodium (e.g., hyperaldosteronism) or administration of lactate, acetate, gluconate); administration of alkali. associated hypokalemia may precipitate r hepatic encephalopathy in patients with liver cation-exchange resin with non-absorbable Hypoalbuminemia—consider failure. alkali (e.g., phosphorus binders). hypoalbuminemic metabolic alkalosis (e.g., r r Renal/Urologic—the kidneys rapidly and Hypoalbuminemia. liver failure, protein-losing enteropathy, and effectively excrete excessive alkali. In patients RISK FACTORS protein-losing nephropathy). In vitro, a 1 r with chloride deficiency (and less importantly, Administration of loop or thiazide diuretics. g/dL decrease in albumin concentration is r volume depletion), the kidneys cannot excrete Vomiting. associated with an increase in pH of 0.093 in r the excessive alkali and metabolic alkalosis is Stomach drainage. cats and 0.047 in dogs. r r maintained. In these patients, chloride Diseases associated with hypoalbuminemia Hypokalemia—hypokalemia likely results administration is required for renal (e.g., nephritic syndrome, liver failure). from metabolic alkalosis or the underlying compensation to occur, whereas volume problem (e.g., vomiting of stomach contents expansion will hasten compensation. Patients or loop diuretic administration); hypokalemia-induced metabolic alkalosis does not occur in dogs and cats. BLBS078-CF_A32 BLBS078-Tilley March 21, 2011 20:15

Canine and Feline, Fifth Edition 53

(Continued) Alkalosis, Metabolic A

r OTHER LABORATORY TESTS If the metabolic alkalosis is associated with SYNONYMS − r Blood gas analysis reveals high HCO , high hypokalemia and total body potassium Non-respiratory alkalosis. 3 r PCO2, and high pH. deficits, correcting the deficit with KCl is a Chloride-responsive metabolic IMAGING particularly effective way to reverse the alkalosis—metabolic alkalosis that responds alkalosis. to chloride administration. None r Chloride-resistant alkalosis—metabolic DIAGNOSTIC PROCEDURES Hypoalbuminemic Alkalosis Treatment for hypoalbuminemic alkalosis alkalosis secondary to increased None should be directed at the underlying cause and mineralocorticoid activity that does not respond to chloride administration. the decreased colloid oncotic pressure. r Hypochloremic alkalosis—metabolic CONTRAINDICATIONS r alkalosis caused by low chloride Avoid chloride-free fluids—they may concentration. TREATMENT r r correct volume depletion but will not correct Hypoalbuminemic alkalosis—metabolic Acid-base disturbances are secondary hypochloremic alkalosis. alkalosis caused by low albumin phenomena. Diagnosis and treatment of the r Avoid using salts of potassium without concentration. underlying disease process is integral to the r chloride (e.g., potassium Concentration alkalosis—metabolic successful resolution of acid-base disorders. r phosphate)—potassium will be excreted in alkalosis resulting from decreased free water in Severe alkalemia is uncommon, but may be the urine and will correct neither the alkalosis plasma. life-threatening. Patients with chronic r nor the potassium deficit. Contraction alkalosis—metabolic alkalosis respiratory disease and respiratory alkalosis are PRECAUTIONS formerly attributed to volume contraction, at risk of developing severe alkalemia if they but now known to be caused by chloride start vomiting or receive diuretics. Do not use distal blocking agents (e.g., r depletion. Volume depletion is a common but Discontinue drugs that may cause metabolic spironolactone) in volume-depleted patients. not essential feature. alkalosis. POSSIBLE INTERACTIONS SEE ALSO NURSING CARE r Hypochloremia The fluids of choice contain chloride; give None r Hypokalemia patients with volume depletion an intravenous ALTERNATIVE DRUG(S) infusion of 0.9% NaCl supplemented with None ABBREVIATIONS r + KCl; patients with hypokalemia may require H = hydrogen ion r − HCO = bicarbonate large doses of KCl (see Hypokalemia). r 3 PCO2 = carbon dioxide tension FOLLOW-UP Suggested Reading de Morais HA. Chloride ion in small animal MEDICATIONS PATIENT MONITORING Acid-base status—frequency dictated by the practice: The forgotten ion. J Vet Emerg DRUG(S) OF CHOICE underlying disease and patient response to Crit Care 1992, 2:11–24. de Morais HA, Constable PD. Strong ion Hypochloremic Alkalosis treatment. r approach to acid-base disorders. In: If there is evidence of volume depletion, the POSSIBLE COMPLICATIONS r DiBartola SP, ed., Fluid, Electrolyte and deficit should be repaired with a Hypokalemia Acid-Base Disorders, 3rd. ed. Philadelphia: chloride-containing fluid (e.g., 0.9% NaCl). r r Neurologic signs Saunders, 2006, pp. 310–321. If the underlying cause cannot be corrected de Morais HA, Leisewitz AL. Mixed acid-base (e.g., chronic heart failure patients receiving disorders. In: DiBartola SP, ed., Fluid, diuretics), oral compounds containing Electrolyte and Acid-Base Disorders, 3rd. chloride without sodium (e.g., KCl, NH4Cl) MISCELLANEOUS ed. Philadelphia: Saunders, 2006, pp. can be tried; also consider simultaneous use of 296–309. distal tubule blocking agents (e.g., ASSOCIATED CONDITIONS r DiBartola SP. Metabolic acid-base disorders. spironolactone). Hypokalemia r r In: DiBartola SP, ed., Fluid, Electrolyte and H2-blocking agents such as ranitidine or Hypochloremia Acid-Base Disorders, 3rd. ed. Philadelphia: famotidine reduce gastric acid secretion and AGE-RELATED FACTORS Saunders, 2006, pp. 251–283. may be considered as adjunctive therapy if None Robinson EP, Hardy RM. Clinical signs, gastric losses are ongoing. r diagnosis, and treatment of alkalemia in Chloride-resistant metabolic alkalosis can ZOONOTIC POTENTIAL None dogs: 20 cases (1982–1984). JAVMA 1988, only be corrected by resolution of the 192:943–949. underlying disease; metabolic alkalosis is PREGNANCY/FERTILITY/BREEDING Author Helio Autran de Morais and Stephen usually mild in these patients. N/A P. D i B a r t o l a Consulting Editor Carl A. Osborne BLBS078-CF_A33 BLBS078-Tilley July 15, 2011 2:40

54 Blackwell’s Five-Minute Veterinary Consult A Alopecia—Cats

r r Often misdiagnosed in cases of allergic Sebaceous glands are selectively destroyed dermatitis. by toxic intermediate metabolites or r Often misdiagnosed as endocrine alopecia. immunologic mechanisms. BASICS r r The pattern of alopecia is frequently Possible dramatic pigment accumulation DEFINITION symmetrical without associated inflammation. along the eyelid margins. r r Common problem Allergic Dermatitis Questionable association with systemic r Pattern of hair loss—varied or symmetrical r disease (e.g., inflammatory bowel disease, r Varies from mild partial alopecia with little Causes—multifactorial inflammation to severe excoriation and lupus-like syndromes, upper respiratory tract PATHOPHYSIOLOGY ulceration. infections). r Barbering of the hair coat often occurs Squamous Cell Carcinoma In Situ Specific and unique for each cause r SYSTEMS AFFECTED clandestinely leading to a misdiagnosis of Multicentric premalignant dermatosis in old r endocrine alopecia. cats. Endocrine/Metabolic r r r Distribution—varied; often the head and Associated with papilloma virus; Bowenoid Hemic/Lymphatic/Immune neck region are most severely affected. in situ carcinoma. r r r Skin/Exocrine Food allergy, atopy/contact atopy, and Slightly elevated, often pigmented, SIGNALMENT ectoparasite hypersensitivity. plaque-like or papillated lesions with scaling r No specific age, breed, or sex predilection. Hyperthyroidism and partially alopecic surfaces. r r r Neoplastic and paraneoplastic associated Partial to complete alopecia from Often misdiagnosed as seborrhea before alopecias—generally recognized in older cats. self-barbering. distinct lesions develop. r r SIGNS Varied pattern. About 25% may convert to squamous cell r carcinoma with in situ lesions along the Depends on specific diagnosis Middle-aged to old cats. r borders (histologically). CAUSES Often misdiagnosed in cases of allergic r dermatoses, compulsive disorder, or other Epitheliotropic Lymphoma r Neurologic/behavioral—compulsive endocrine alopecia. Early stages—varying degrees of alopecia disorder. r associated with scaling and erythema. Diabetes Mellitus r Endocrine—sex hormone alopecia, r Later stages—plaques and nodules. hyperthyroidism, hyperadrenocorticism, Partial alopecia with an unkempt hair coat r and excessive scaling. Old cats. diabetes mellitus. r r Poor wound healing. Alopecia Immunologic—allergic dermatitis, alopecia r Increased susceptibility to infections. Areata/Pseudopelade/Lymphocytic areata, alopecia mucinosa, lymphocytic mural r folliculitis, pseudopelade. Cutaneous xanthomatosis secondary to Mural Folliculitis r r Parasitic—demodicosis, cheyletiellosis. hyperlipidemia (nodular to linear, yellow-pink This group of differentials is often r Infections—dermatophytosis. alopecic plaques that tend to ulcerate). considered preneoplastic with an r Physiologic/metabolic—sebaceous adenitis. Hyperadrenocorticism immunologic inciting cause. r r r Neoplastic—paraneoplastic dermatitis, Rare; characterized by alopecia and fragility Alopecia areata—rare; complete alopecia in squamous cell carcinoma in situ, of the skin. a patchy distribution with no inflammation; r epitheliotropic lymphoma, thymoma with Truncal alopecia, with or without a rattail head, neck, ears; histologic lymphocytic exfoliative dermatitis. and a curling of the pinnal tips. accumulation around the hair bulb. r r r Idiopathic/inherited—alopecia universalis, Extreme skin fragility noted in Lymphocytic mural folliculitis—diffuse hypotrichosis, spontaneous pinnal alopecia, approximately 70%. alopecia of the face, eyelids, muzzle; skin has a r anagen and telogen defluxion. Occurs secondary to pituitary or adrenal thick waxy feel; histologic lymphocytic r Injection site reaction. tumors. invasion of the follicular outer root sheath r r Medication effect—corticosteroids. Iatrogenic form less common in cats than in and epidermis. r r Viral—FeLV- and FIV-associated disease dogs. Pseudopelade—well-circumscribed non-pruritic alopecia that often starts on the (giant cell dermatosis). Paraneoplastic Alopecia r face; nails may slough. RISK FACTORS Most cases associated with pancreatic Alopecia Universalis (Sphynx Cat) FeLV/FIV—for demodicosis exocrine adenocarcinomas, bile duct r Hereditary. carcinomas, exfoliative dermatitis with r thymoma. Complete absence of primary hairs; r decreased secondary hairs. Middle-aged to old cats (9–16 years). r r Thickened epidermis; normal dermis. DIAGNOSIS Pancreatic carcinoma/bile duct carcinoma: r acute onset, progress rapidly, bilaterally Sebaceous and apocrine ducts open directly onto the skin surface; oily feel to skin. DIFFERENTIAL DIAGNOSIS symmetrical, ventrally distributed (also r Endocrine Alopecia/Sex Hormone located along the bridge of the nose and Wrinkled foreheads; gold eyes; no whiskers; r downy fur on paws, tip of tail, and scrotum. Rarely a hormonal abnormality. periocular), hair epilates easily, rare pruritus, r r Comedones with or without secondary Hormonal causes—primarily castrated erythema with dry fissuring footpads, folliculitis. males; alopecia along the caudal aspect of the glistening appearance to alopecic skin, skin is often thin and hypotonic, rapid weight loss. Feline Hypotrichosis hind limbs, which may extend along the r r perineum. Thymoma with exfoliative dermatitis: Siamese and Devon Rex cats (autosomal r Excessive corticosteroid administration. non-pruritic scaling dermatitis that starts at recessive alopecia). r r Megestrol acetate—may produce lesions the head and neck. Poorly developed primary telogen hair similar to/associated with diabetes mellitus or Sebaceous Adenitis follicles. r r hyperadrenocorticism. Slowly progressive partial alopecia associated Born with a normal coat; becomes thin and Compulsive Disorder with scaling along the dorsum of the body sparse as young adult. r and the extremities. Spontaneous Pinnal Alopecia Uncommon as sole source of symptoms. r Siamese cats predisposed. BLBS078-CF_A33 BLBS078-Tilley July 15, 2011 2:40

Canine and Feline, Fifth Edition 55

(Continued) Alopecia—Cats A

r r May represent a form of alopecia areata or Removal of an offending dietary item may POSSIBLE COMPLICATIONS pattern baldness. alleviate the symptoms of food allergy. Determined by specific diagnosis r Anagen and Telogen Defluxion If the pet is compliant, shampoo and topical EXPECTED COURSE AND PROGNOSIS r Acute loss of hair due to interference with therapy may relieve secondary problems, such Determined by specific diagnosis the growth cycle. as hyperkeratosis in sebaceous adenitis, r Causes—stress, infection, endocrine crusting in demodicosis, secondary bacterial disorder, metabolic disorder, fever, surgery, infection, and malodor for greasy dermatoses. anesthesia, pregnancy, drug therapy. MISCELLANEOUS Demodicosis r ZOONOTIC POTENTIAL Rare. r Dermatophytosis—can cause skin lesions in Partial to complete multifocal alopecia of MEDICATIONS humans. the eyelids, periocular region, head, and neck. DRUG(S) r r Cheyletiellosis—can cause irritation in Variable pruritus with erythema, scale, and r Compulsive disorder—amitriptyline (10 humans. crust, and ceruminous otitis externa. mg/cat/day) as well as other r PREGNANCY/FERTILITY/BREEDING Demodex cati (elongated shape) often behavior-modifying medications. r associated with metabolic disease (e.g., FIV, Endocrine alopecia (males)—testosterone Retinoids and griseofulvin should not be systemic lupus erythematosus, diabetes supplementation. administered to pregnant animals. r mellitus). Allergic dermatitis—antihistamines, SEE ALSO r r Short/blunted D. gatoi mite is rarely a restricted-ingredient diet, corticosteroids, Cheyletiellosis r marker for metabolic disease; this form may allergen-specific immunotherapy, ectoparasite Demodicosis r be transferable from cat to cat and has been control. Dermatophytosis r r associated with pruritus. Hyperthyroidism—oral medications such as Diabetes Mellitus without Complication, Cheyletiellosis methimazole (tapazole) or radioactive iodine Cats r r Variable pruritus with scaling. therapy. Feline Paraneoplastic Alopecia r r r Not all animals in the household may be Diabetes mellitus—regulation of glucose Hyperthyroidism levels (insulin). r affected. r Sebaceous Adenitis, Granulomatous Dermatophytosis Hyperadrenocorticism—surgery; no known ABBREVIATIONS r effective medical therapy. r Numerous clinical manifestations; always r ACTH = adrenocorticotropic hormone Paraneoplastic alopecia—no therapy; often r associated with alopecia. ANA = antinuclear antibody fatal. r CBC/BIOCHEMISTRY/URINALYSIS r CT = computed tomagraphy Epitheliotropic lymphoma—retinoids r FeLV = feline leukemia virus Abnormalities may be noted with diabetes (isotretinoin), corticosteroids, interferon, r FIV = feline immunodeficiency virus mellitus, hyperadrenocorticism, and cyclosporine, lomustine. r r HDDST = high-dose hyperthyroidism. Sebaceous adenitis—retinoids, dexamethasone-suppression test OTHER LABORATORY TESTS corticosteroids, cyclosporine. r r r LDDST = low-dose FeLV and FIV—risk factors for demodicosis. Squamous cell carcinoma in situ—surgical r dexamethasone-suppression test Thyroid hormones—document excision, retinoids (topical and oral), topical hyperthyroidism. imiquimod cream. Suggested Reading r r ANA titer—look for systemic lupus Alopecia areata—no therapy; possibly Baer KE, Helton KA. Multicentric squamous erythematosus. counterirritants. cell carcinoma in situ resembling Bowens’ r r ACTH-response test, LDDST, and Demodicosis—lime sulfur dips at weekly disease in cats. Vet Pathol 1993, intervals for four to six dips. 30:535–543. HDDST—diagnose hyperadrenocorticism. r IMAGING Cheyletiellosis—topical antiparasiticides Helton Rhodes KA, Wallace M, Baer KE. r and environmental control. Cutaneous manifestations of feline r Abdominal ultrasound—assess adrenals in Dermatophytosis—griseofulvin (caution: hyperadrenocorticism. In: Ihrke PJ, Mason hyperadrenocorticism and look for cancer in idiosyncratic toxicity), itraconazole, IS, White SD. Advances in Veterinary animals with paraneoplastic syndrome. r terbinafine. Dermatology. New York: Pergamon, 1993. CT scan—look for pituitary tumors in Scott DW, Griffin CE, Miller BH. Acquired animals with hyperadrenocorticism. PRECAUTIONS Toxicity with griseofulvin and itraconazole alopecia. In: Muller & Kirk’s Small Animal DIAGNOSTIC PROCEDURES Dermatology, 5th ed. Philadelphia: r (see Dermatophytosis) Skin biopsy Saunders, 1995, pp. 720–735. r Skin scrapes POSSIBLE INTERACTIONS Scott DW, Griffin CE, Miller BH. Congenital r Dermatophyte culture N/A and hereditary defects. In: Muller & Kirk’s r Shirts/collar to prove self-trauma ALTERNATIVE DRUG(S) Small Animal Dermatology, 5th ed. r Food elimination trials Philadelphia: Saunders, 1995, pp. 736–805. r N/A Intradermal allergy test Scott DW, Griffin CE, Miller BH. Endocrine and metabolic diseases. In: Muller & Kirk’s Small Animal Dermatology, 5th ed. FOLLOW-UP Philadelphia: Saunders, 1995, pp. 627–719. TREATMENT Author Karen Helton Rhodes r PATIENT MONITORING Consulting Editor Alexander H. Werner Therapy is limited for many of these Determined by specific diagnosis disorders. r PREVENTION/AVOIDANCE Behavioral modification or protecting hair Client Education Handout Determined by specific diagnosis coat with a shirt may prevent self-barbering. available online BLBS078-CF_A34 BLBS078-Tilley June 16, 2011 10:41

56 Blackwell’s Five-Minute Veterinary Consult A Alopecia—Dogs

r r Rabies vaccine vasculitis—well-demarcated Color mutant/ dilution alopecia—thinning patch of alopecia observed 2–3 months of the hair coat with secondary folliculitis. r post-vaccination. Follicular dysplasia—slowly progressive BASICS r Localized scleroderma—well-demarcated, alopecia. r DEFINITION shiny, smooth, alopecic, thickened plaque. Anagen defluxion and telogen r r Alopecia areata—non-inflammatory areas of defluxion—acute onset of alopecia. Common disorder. r r complete alopecia. Hypothyroidism—diffuse thinning of the Characterized by a complete or partial lack r of hair in areas where it is normally present. Sebaceous adenitis (short-coated hair coat. r r May be associated with multiple causes, be breeds)—annular to polycyclic areas of Hyperadrenocorticism—truncal alopecia alopecia and scaling. with thin skin and formation of comedones. the primary problem, or be secondary to an r underlying cause. Symmetrical Epitheliotropic lymphoma—diffuse, r PATHOPHYSIOLOGY Hyperadrenocorticism—truncal alopecia generalized truncal alopecia with scaling and r erythema, later nodule and plaque formation. Multiple causes. associated with atrophic skin, comedones, and r r pyoderma. Pemphigus foliaceus—hair loss associated Represents a disruption in the growth of the r with scale and crust formation. hair from infection, trauma, immunologic Hypothyroidism—alopecia is an r uncommon presentation. Keratinization disorders—alopecia attack, mechanical “plugging,” endocrine r Non-inflammatory alopecia (alopecia associated with excessive scale and greasy abnormalities, neoplasia, and/or blockage of surface texture. the receptor sites for stimulation of the hair X)—symmetrical truncal alopecia associated with hyperpigmentation; alopecia often starts Specific Locations growth cycle. r SYSTEMS AFFECTED along the collar area of the neck; Pomeranian, Pinnal alopecia/pattern r chow chow, Akita, Samoyed, Keeshonden, baldness—miniaturization of hairs and Endocrine/Metabolic r Alaskan malamute, and Siberian husky. progressive alopecia; dachshund, greyhound, Hemic/Lymphatic/Immune r r Hyperestrogenism (females)—symmetrical American water spaniel, Portuguese water Skin/Exocrine alopecia of the flanks and perineal and spaniel, Boston terrier, Manchester terrier, SIGNALMENT inguinal regions with enlarged vulva and whippet, Italian greyhound, Chihuahua. r mammary glands. Traction alopecia—hair loss on the top and Breed predilection listed below r SIGNS Hypogonadism in intact females—perineal, lateral aspect of the cranium secondary to r flank, and truncal alopecia. having barrettes or rubber bands applied to May be acute in onset or slowly progressive. r r Testosterone-responsive dermatosis in the hair. Multifocal patches of circular r castrated males—slowly progressive truncal Post-clipping alopecia—failure to regrow alopecia—most frequently associated with alopecia. after clipping; may be associated with hair folliculitis from bacterial infection and r Male feminization from Sertoli cell growth cycle disruption. demodicosis. r r tumor—alopecia of the perineum and genital Melanoderma (alopecia of Yorkshire Large, more diffuse areas of alopecia—may region with gynecomastia. terriers)—symmetrical alopecia of the pinnae, indicate a follicular dysplasia or metabolic r Castration-responsive dermatosis—hair loss bridge of the nose, tail, and feet. component. r r in the collar area, rump, perineum, and flanks. Seasonal flank alopecia/cyclic flank The pattern and degree of hair loss are r Estrogen-responsive dermatosis in spayed alopecia—serpiginous flank alopecia with important for establishing a differential female dogs—alopecia of the perineum and hyperpigmentation; boxer, English bulldog, diagnosis. genital regions. Airedale terrier. r r CAUSES Seasonal flank alopecia/cyclic flank Black hair follicular dysplasia—alopecia of Multifocal alopecia—serpiginous flank alopecia with the black-haired areas only. r r Localized demodicosis—partial to complete hyperpigmentation; boxer, English bulldog, Dermatomyositis—alopecia of the face, tip alopecia with erythema and mild scaling; Airedale terrier. of ears, tail, and digits; associated with scale lesions may become inflamed and crusted. Patchy to Diffuse crusting and scarring. r r Dermatophytosis—partial to complete Demodicosis—often associated with Breed-Related Alopecia r alopecia with scaling; with or without erythema, folliculitis, and hyperpigmentation. Alopecic breeds: Chinese crested, Mexican erythema; not always ring-like. r r Bacterial folliculitis—multifocal area of hairless, Inca hairless, Peruvian Inca Orchid, Staphylococcal folliculitis—circular patterns circular alopecia to coalescing large areas of American hairless terrier (often associated of alopecia with epidermal collarettes, hair loss; epidermal collarettes. with comedones, folliculitis, and r erythema, crusting, and hyperpigmented Dermatophytosis—often accompanied by furunculosis). r macules. scale. Congenital hypotrichosis: cocker spaniel, r r Injection reactions—inflammation with Sebaceous adenitis—alopecia with a thick Belgian shepherd, poodle, whippet, beagle, alopecia and/or cutaneous atrophy from adherent scale; predominantly on the dorsum French bulldog, Yorkshire terrier, Labrador scarring. of the body, including the head and retriever, bichon frise, Lhasa apso, basset extremities. hound. BLBS078-CF_A34 BLBS078-Tilley June 16, 2011 10:41

Canine and Feline, Fifth Edition 57

(Continued) Alopecia—Dogs A

r Color dilution alopecia: blue or fawn ZOONOTIC POTENTIAL Doberman pinscher, silver Labrador, cream Dermatophytosis can cause skin lesions in chow chow, blond Irish setter, blue pit bull TREATMENT people. terrier, other breeds with dilute coat colors. r PREGNANCY/FERTILITY/BREEDING r Demodicosis—amitraz, ivermectin, Melanoderma with alopecia in Yorkshire Avoid retinoids and griseofulvin in pregnant terrier. milbemycin. r r animals. Seasonal flank alopecia/cyclic flank Dermatophytosis—griseofulvin, SEE ALSO alopecia—serpiginous flank alopecia with ketoconazole, itraconazole, lime sulfur dips, r Alopecia, Non-inflammatory—Dogs hyperpigmentation; boxer, English bulldog, terbinafine. r r Demodicosis Airedale terrier. Staphylococcal folliculitis—shampoo and r r Dermatomyositis Pinnal alopecia/pattern antibiotic therapy. r r Dermatophytosis baldness—miniaturization of hairs and Sebaceous adenitis—keratolytic shampoo, r progressive alopecia; dachshund, greyhound, essential fatty acid supplementation, Hyperadrenocorticism (Cushing’s Syndrome)—Dogs American water spaniel, Portuguese water retinoids, cyclosporine. r r Hypothyroidism spaniel, Boston terrier, Manchester terrier, Keratinization disorders—shampoos, r Pemphigus whippet, Italian greyhound, Chihuahua. retinoids, vitamin D, cyclosporine. r r r Sebaceous Adenitis, Granulomatous Non-inflammatory alopecia (alopecia Endocrine—ovariohysterectomy, castration, r X)—symmetrical truncal alopecia associated Lysodren, trilostane, adrenalectomy. SertoliCellTumor with hyperpigmentation; alopecia often starts ABBREVIATIONS r along the collar area of the neck; Pomeranian, ACTH = adrenocorticotropic hormone r chow chow, Akita, Samoyed, Keeshonden, HDDST = high-dose Alaskan malamute, and Siberian husky. MEDICATIONS dexamethasone-suppression test r = RISK FACTORS DRUG(S) OF CHOICE LDDST low-dose dexamethasone-suppression test N/A Varies with specific cause; see “Treatment” CONTRAINDICATIONS Suggested Reading N/A Helton-Rhodes KA. Cutaneous manifestations of canine and feline DIAGNOSIS PRECAUTIONS endocrinopathies. Probl Vet Med 1990, Toxicity with griseofulvin, retinoids, DIFFERENTIAL DIAGNOSIS 12:617–627. r ivermectin, trilostane, lysodren, cyclosporine. Schmeitzel LP. Growth hormone responsive Pattern and degree—important features for alopecia and sex hormone associated formulating a differential diagnosis. r POSSIBLE INTERACTIONS dermatoses. In: Birchard SJ, Sherding RG, Inflammation, scale, crust, and epidermal eds., Saunders Manual of Small Animal collarettes—important for determining None ALTERNATIVE DRUG(S) Practice. Philadelphia: Saunders, 1994, diagnosis. pp. 326–330. CBC/BIOCHEMISTRY/URINALYSIS None Scott DW, Griffin CE, Miller BH. Acquired Rule out metabolic causes such as alopecia. In: Muller & Kirk’s Small Animal hyperadrenocorticism Dermatology, 5th ed. Philadelphia: OTHER LABORATORY TESTS Saunders, 1995, pp. 720–735. r FOLLOW-UP Thyroid testing—diagnose hypothyroidism. Scott DW, Griffin CE, Miller BH. Endocrine r ACTH-response test, LDDST, and PATIENT MONITORING and metabolic diseases. In: Muller & Kirk’s HDDST—evaluate for hyperadrenocorticism. Determined by cause Small Animal Dermatology, 5th ed. r Philadelphia: Saunders, 1995, pp. 627–719. Sex hormone profiles (questionable POSSIBLE COMPLICATIONS validity). Scott DW, Griffin CE, Miller BH. N/A Keratinization defects. In: Muller & Kirk’s IMAGING Small Animal Dermatology, 5th ed. Ultrasonography—evaluate adrenal glands for Philadelphia: Saunders, 1995, pp. 736–805. evidence of hyperadrenocorticism. Author Karen Helton Rhodes DIAGNOSTIC PROCEDURES MISCELLANEOUS Consulting Editor Alexander H. Werner r Response to therapy as a trial ASSOCIATED CONDITIONS r Fungal culture r N/A Skin scraping Client Education Handout r AGE-RELATED FACTORS Cytology available online r Skin biopsy N/A BLBS078-CF_A34a BLBS078-Tilley June 16, 2011 10:43

58 Blackwell’s Five-Minute Veterinary Consult A Alopecia, Non-inflammatory—Dogs

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 Hypothyroidism and out the more common endocrine alopecias. hyperadrenocorticism—critical to rule out as r and distal extremities. Uncommon with Alopecia X has also been called growth hyperandrogenism. these diseases may cause a very similar pattern r hormone-responsive alopecia, Hair coat—may be dry or bleached. of diffuse alopecia associated with lack of hair r follicle cycling. castration-responsive alopecia, adrenal Secondary seborrhea, pruritus, pyoderma, r hyperplasia-like syndrome, among others. comedones, ceruminous otitis externa, and Follicular dysplasias including color-dilution PATHOPHYSIOLOGY hyperpigmentation—variable. alopecia and black hair follicular r r dysplasia—alopecia should be color-restricted. There are many factors that affect the hair Enlargement of nipples, mammary glands, r Patterned alopecia of various breeds cycle, both hormonal and non-hormonal. vulva, prepuce—may be associated with r (dachshund, Boston terrier, greyhound, water Increased sex hormones can affect the hair hyperestrogenism. r spaniel, and others)—breed-specific alopecias cycle. Estrogen is a known inhibitor of Macular melanosis and linear preputial of unknown cause. anagen, the growth phase of the hair follicle. dermatitis—may be associated with r r Cyclic flank alopecia—alopecia of the flank The mechanism by which alopecia X hyperestrogenism. r and dorsum, often bizarre patterns with influences the hair cycle is not known. Abnormal-sized testicles—may be associated with hyperestrogenism or hyperandrogenism. hyperpigmentation, more often in SYSTEMS AFFECTED r r Testicles may also appear normal in size. short-coated breeds (boxer, English bulldog, Behavioral r r Tail gland hyperplasia and perianal gland Airedale) and may recur seasonally. Endocrine/Metabolic r r hyperplasia—usually associated with Post-clipping alopecia—hair fails to regrow Hemic/Lymphatic/Immune r hyperandrogenism. following clipping; however, hair regrowth Skin/Exocrine r occurs within a year. Systemic signs (PU/PD/polyphagia) are r GENETICS usually NOT present. Telogen defluxion—alopecia occurs 1–2 months following an illness or severe stressful Breed predispositions exist for alopecia X; CAUSES however, the mode of inheritance is episode and is usually more sudden in onset Hyperestrogenism—Females with relative ease of epilation. unknown. r INCIDENCE/PREVALENCE Estrogen excess associated with cystic CBC/BIOCHEMISTRY/URINALYSIS r r ovaries, ovarian tumors (rare), or exogenous Usually unremarkable. Hyperestrogenism and hyperandrogenism estrogen supplementation. r are uncommon to rare causes of alopecia. r Anemia and/or bone marrow hypoplasia or r Animals with normal serum estrogen Alopecia X is relatively common in aplasia can be associated with concentrations may have increased numbers hyperestrogenism. predisposed breeds. of estrogen receptors in the skin GEOGRAPHIC DISTRIBUTION OTHER LABORATORY TESTS (undocumented). r Serum sex hormone concentrations—often None Hyperestrogenism—Males r normal, treat according to suspected diagnosis SIGNALMENT Estrogen excess due to Sertoli cell tumor based on clinical signs and ruling out other (most common), seminoma, or interstitial cell Species disorders. tumor (rare). r Dogs r Serum estradiol concentrations—sometimes Associated with male elevated in male dogs with testicular tumors Breed Predilections pseudohermaphrodism in miniature r or female dogs with cystic ovaries; however, Hyperestrogenism and schnauzers. hyperandrogenism—no breed predilections. normal fluctuation of estradiol occurs r Alopecia X—miniature poodle and Hyperandrogenism—Males throughout the day, making interpretation of plush-coated breeds such as Pomeranian, Androgen-producing testicular tumors estradiol concentrations difficult. chow chow, Akita, Samoyed, Keeshonden, (especially interstitial cell tumors). IMAGING Alaskan malamute, and Siberian husky. Alopecia X Radiography, ultrasonography, and Mean Age and Range Hairs fail to cycle but an underlying laparoscopy—identify cystic ovaries, ovarian r Hyperestrogenism and endocrine cause has not been identified. tumors, testicular tumors (scrotal or hyperandrogenism—middle-aged to old RISK FACTORS abdominal), sublumbar lymphadenopathy, r intact dogs. Intact male and female dogs are at increased and possible thoracic metastases of malignant r Alopecia X—1–5 years of age; however, risk for developing testicular tumors and tumors. older dogs may develop the condition. ovarian cysts/tumors, respectively. DIAGNOSTIC PROCEDURES r r Predominant Sex Cryptorchid males are at increased risk for Preputial cytology—may demonstrate r Hyperandrogenism, primarily intact males. developing testicular tumors. cornification of cells in males with r r Hyperestrogenism, primarily intact females Exogenous estrogen supplementation. hyperestrogenism (similar to a bitch in estrus). r r or males There are no known risk factors for alopecia Skin biopsy. r Alopecia X, neutered or intact dogs of either X other than breed predisposition. sex. BLBS078-CF_A34a BLBS078-Tilley June 16, 2011 10:43

Canine and Feline, Fifth Edition 59

(Continued) Alopecia, Non-inflammatory—Dogs A

PATHOLOGIC FINDINGS Alopecia X POSSIBLE COMPLICATIONS Histologic changes associated with endocrine Melatonin—3 mg q12h for small breeds and None dermatoses (telogen hairs, follicular keratoses, 6–12 mg q12h for large breeds; hair regrowth EXPECTED COURSE AND PROGNOSIS r hyperkeratosis, excess trichilemmal can take up to 3 months to become evident. Female hyperestrogenism—improvement keratinization [flame follicles], thin epidermis This treatment works in approximately 40% should occur within 3–6 months after and thin dermis) may also be seen with of cases. Because this treatment is the most ovariohysterectomy. r non-inflammatory alopecias including benign, it is considered the treatment of Estrogen- and androgen-secreting hyperestrogenism and alopecia X. choice following neutering. Once hair tumors—resolution of signs should occur Histopathology will help rule out regrowth has occurred, discontinue treatment. within 3–6 months after castration. r inflammatory causes of alopecia and some of Alopecia X—hair regrowth will only occur the other differentials listed above. CONTRAINDICATIONS in a portion of dogs regardless of treatment None chosen and hair loss may recur in spite of PRECAUTIONS continued treatment. Therefore, if hair regrowth occurs, discontinue treatment to TREATMENT Melatonin at high doses can cause insulin resistance; therefore, use caution in treating preserve treatment for future recurrence of the APPROPRIATE HEALTH CARE dogs with diabetes mellitus. alopecia. Risk of treatment should be weighed withthefactthatthisisacosmeticdisease. N/A POSSIBLE INTERACTIONS NURSING CARE None N/A ALTERNATIVE DRUG(S) r ACTIVITY Mitotane—15–25 mg/kg—one daily as MISCELLANEOUS None induction for 5–7 days, followed by twice ASSOCIATED CONDITIONS weekly maintenance; hair regrowth occurs in r DIET Pyoderma, seborrhea, comedones may be a portion of dogs treated and can take up to None associated with the alopecia. 3 months to become evident. Use of this drug r Behavioral—changes associated with Client Education can result in an Addisonian crisis and other hyperestrogenism or hyperandrogenism. Alopecia X is a cosmetic condition resulting side effects as for treatment of Cushing’s in coat loss only and there is not a definitive syndrome. Electrolytes and cortisol with AGE-RELATED FACTORS cure for the hair loss. The risk of treatment ACTH stimulation testing should be None should be weighed with these facts. Hair monitored regularly. ZOONOTIC POTENTIAL regrowth will only occur in a portion of dogs r Trilostane—dosages as described for None regardless of treatment chosen and hair loss treatment of Cushing’s syndrome; hair PREGNANCY/FERTILITY/BREEDING may recur months to years later in spite of regrowth occurs in a portion of dogs treated continued treatment. and can take up to 3 months to become N/A—neutering is usually recommended for SURGICAL CONSIDERATIONS evident. Use of this drug can result in an managing these conditions. Hyperestrogenism/Hyperandrogenism Addisonian crisis and other side effects as for SYNONYMS r Castration—scrotal testicular tumors. treatment of Cushing’s syndrome. Electrolytes Alopecia X—growth hormone-responsive r Exploratory laparotomy—diagnosis and and cortisol with ACTH stimulation testing alopecia, castration-responsive alopecia, should be monitored regularly. surgical removal (ovariohysterectomy and r adrenal hyperplasia-like syndrome, among castration) for ovarian cysts and tumors and Growth hormone administration and others. abdominal testicular tumors. methyltestosterone may result in hair ABBREVIATIONS regrowth. Growth hormone can cause r Alopecia X ACTH = adrenocorticotropic hormone diabetes mellitus. Methyltestosterone can r PU/PD = polyuria/polydipsia Neuter intact animals—a certain number will result in increased aggression, regrow hair following neutering. Hair cholangiohepatitis, and seborrhea oleosa. INTERNET RESOURCES regrowth can take up to 3 months to become Therefore, these drugs are not recommended. http://www.vet.utk.edu/hairloss/. evident. Suggested Reading Frank LA. Sex hormone and endocrine look-alike dermatoses. In: Birchard SJ, FOLLOW-UP MEDICATIONS Sherding RG, eds., Saunders Manual of PATIENT MONITORING Small Animal Practice, 3rd ed. Philadelphia: DRUG(S) OF CHOICE r Mitotane—electrolytes and cortisol with Saunders, 2006, p. 517. General Treatments ACTH stimulation testing regularly. Author Linda A. Frank r r Topical antiseborrheic shampoos—for Trilostane—electrolytes and cortisol with Consulting Editor Alexander H. Werner comedones and seborrhea associated with ACTH stimulation testing regularly. alopecia. r PREVENTION/AVOIDANCE Antibiotics—for secondary skin infections Client Education Handout None associated with alopecia. available online BLBS078-CF_A35 BLBS078-Tilley July 15, 2011 20:0

60 Blackwell’s Five-Minute Veterinary Consult A Amebiasis

contaminated water or colonization of the IMAGING skin or cornea; hematogenous spread or direct MRI—shows brain granulomas. BASICS spread from the nasal cavity through the DIAGNOSTIC PROCEDURES cribiform plate to the central nervous system Brain biopsy—required to definitively OVERVIEW may occur, resulting in a granulomatous r diagnose neurologic forms antemortem. Facultative parasitic amoeba that infects amoebic meningoencephalitis. people and non-human primates, including dogs and cats. r Found primarily in tropical areas TREATMENT throughout the world, including North DIAGNOSIS r America. Colitis (caused by E. histolytica)—responds DIFFERENTIAL DIAGNOSIS SIGNALMENT to metronidazole, although dogs continue to r Dogs shed organisms. Dogs and cats. r r r Causes of bloody diarrhea or tenesmus, Systemic forms (particularly neurologic Mainly young and/or immunosuppressed disease)—invariably fatal despite treatment. animals are infected. including constipation; food intolerance/ 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 asymptomatic. (parvovirus, clostridial enteritis, bacterial r DRUG(S) Severe infections—result in ulcerative colitis overgrowth and other bacterial causes, fungal r to cause dysentery (may be fatal). such as histoplasmosis or blastomycosis); Tinidazole (44 mg/kg PO q24h for 6 days) r Hematogenous spread—results in failure neoplasia; ulcerative colitis; endocrinopathy in dogs—found to be more effective than states of the organs (invariably fatal). (Addison’s disease); toxic (lead, fungal, or metronidazole in treating amebiasis in people. r r Granulomatous amoebic plant); occasionally major organ disease Metronidazole (20 mg/kg PO q12h for 7 meningoencephalitis (caused by causing colonic ulceration such as renal days). failure. CONTRAINDICATIONS/POSSIBLE Acanthamoeba spp.)—causes signs similar to r distemper (anorexia, fever, lethargy, Other causes of diffuse neurologic disease in INTERACTIONS oculonasal discharge, respiratory distress, and young animals, including infectious High doses of metronidazole (usually diffuse neurologic abnormalities). (distemper, fungal such as Cryptococcus, > r 30 mg/kg) for extended periods may cause Syndrome of inappropriate secretion of Blastomyces, Histoplasma, bacteria, protozoa neurologic signs in dogs. antidiuretic hormone has been reported in a such as Toxoplasma and Neospora); toxic young dog with acanthamoebisis causing (lead, organophosphate); trauma; GME; granulomatous meningoencephalitis with extracranial (hypoglycemia; hepatic invasion of the hypothalamus. encephalopathy); inherited epilepsy; FOLLOW-UP Cats neoplasia. r Pets usually acquire infections from the same Colitis—causing chronic intractable Cats r source as their owners; veterinarians must diarrhea (as per dogs). Other causes of diarrhea, including food r warn owners of possible risk. Systemic amebiasis or Acanthamoeba—not intolerance/allergy; inflammatory bowel reported in cats. disease; parasitism (giardiasis, parasites such as CAUSES & RISK FACTORS hookworms, roundworms, tritrichomonas); r infectious (panleukopenia, FIV, FeLV Entamoeba histolytic—infection occurs by producing panleukopenia-like syndrome, MISCELLANEOUS ingesting cysts from human feces. r bacterial including Salmonella,rarely Encystment of trophozoites seldom occurs ABBREVIATIONS Campylobacter); drug (acetaminophen); r in dogs or cats so they are not a source of CSF = cerebrospinal fluid r neoplasia; pancreatitis; and major organ r infection. Oneofthefeworganisms FeLV = feline leukemia virus dysfunction. r transmitted from man to pets but rarely from FIV = feline immunodeficiency virus r r pets to man. Trophozoites (the pathogenic CBC/BIOCHEMISTRY/URINALYSIS GME = granulomatous meningoencephalopathy stage)—inhabit the colonic lumen as Normal; can reflect severe diarrhea. r H&E = hematoxylin and eosin commensals or invade the colonic wall but OTHER LABORATORY TESTS r r HGE = hemorrhagic gastroenteritis can disseminate to other organs (rare) Microscopic examination—colonic biopsies r MRI = magnetic resonance imaging including lungs, liver, brain, and skin. (H&E) obtained via endoscopy is the most r r WBC = white blood cell Trophozoites damage intestinal epithelial reliable method. cells by secreting enzymes that lyse cells and r r Trophozoites in feces—very difficult to Suggested Reading disrupt intercellular connections. Certain detect; methylene blue staining improves Brofman PJ, Knostman KAB, Dibartola SP. bacteria and a diet deficient in protein chances. Granulomatous amebic r r increase the virulence of the amoeba. The Trichrome and iron-hematoxyline—the meningoenchephalitis causing the syndrome host’s immune response to invasion r ideal fecal stains but require a reference of inappropriate secretion of antidiuretic exacerbates pathology. Colonic ulceration laboratory to perform. hormone in a dog. J Vet Intern Med 2003, r results when trophozoites in the submucosa Fecal concentration techniques—no help. 17:230–234. r r undermine the mucosa. Acanthamoeba CSF—elevated WBC count (70% Fung HB, Doan TL. Tinidazole: A castellani and A. culbertsoni— mononuclear cells), protein and nitroimidazole antiprotozoal agent. Clin free-living species found in freshwater, xanthochromia in dogs with granulomatous Ther 2005, 27:1859–1884. saltwater, soil, and sewage; can infect dogs. r amebic meningoencephalitis due to Author Stephen C. Barr Acanthamoeba spp.—infection thought to Acanthamoeba. Consulting Editor Stephen C. Barr be by inhalation of organisms from BLBS078-CF_A36 BLBS078-Tilley July 15, 2011 20:13

Canine and Feline, Fifth Edition 61 Ameloblastoma A

r Other tumors related to the odontogenic CONTRAINDICATIONS/POSSIBLE apparatus INTERACTIONS BASICS CBC/BIOCHEMISTRY/URINALYSIS N/A Unaffected OVERVIEW r OTHER LABORATORY TESTS Common oral tumor of odontogenic (tooth structure) ectoderm origin. N/A r FOLLOW-UP Biologically these tumors are benign IMAGING r Careful oral examination at 1, 3, 6, 9, and 12 histologically but possess locally invasive Radiographs of skull often show bone lysis months after definitive treatment is properties. deep to the superficial mass. r r recommended to monitor treatment A rare malignant (highly invasive) form has Regional and distant metastasis has not outcomes. been described. been described. r r Tumors may arise anywhere within the Computed tomography may be helpful for dental arcade. planning surgery or radiation therapy. r Several histologic subtypes exist and all have DIAGNOSTIC PROCEDURES MISCELLANEOUS similar invasive behavior. Deep tissue biopsies are necessary and SIGNALMENT recommended for definitive diagnosis. Suggested Reading r Middle-aged and old dogs Gelberg HB. Alimentary system. In: McGavin r Rare in cats MD, Carlton WW, Zachary JF, eds., SIGNS Thompson’s Special Veterinary Pathology. Dogs may present with a smooth, firm, TREATMENT St. Louis: Mosby, 2001, pp. 1–79. gingival mass that is usually non-ulcerated. r Morrison WB. Cancers of the head and neck. Radical surgical excision such as In: Morrison WB, ed., Cancer in Dogs and CAUSES & RISK FACTORS mandibulectomy or maxillectomy with at Cats: Medical and Surgical Management. N/A least 1–2-cm margins is recommended to Jackson, WY: Teton NewMedia, 2002, ensure complete excision. r pp. 489–496. Radiation therapy may be curative without Walsh KM, Denholm LJ, Cooper BJ. disfigurement associated with surgery. Epithelial odontogenic tumors in domestic DIAGNOSIS animals. J Comp Pathol 1987, 97:503–521. Author Wallace B. Morrison DIFFERENTIAL DIAGNOSIS r Consulting Editor Timothy M. Fan Epulis r MEDICATIONS Malignant oral tumor r DRUG(S) Gingival hyperplasia N/A BLBS078-CF_A37 BLBS078-Tilley July 23, 2011 4:31

62 Blackwell’s Five-Minute Veterinary Consult A Amitraz Toxicosis

CAUSES & RISK FACTORS r Ingestion of impregnated collar or pieces of collar. BASICS r TREATMENT Inappropriate direct dermal application. r r OVERVIEW Ingestion of undiluted product. Inpatient—severely affected patients. r r r Amitraz—formamidine acaricide; applied After application of properly diluted and Mild sedation after correctly applied topically to control ticks, mites, and lice. applied solutions—less common. sponge-on solutions—often transient; may r r require no treatment. Amitraz-containing products (for Elderly, sick, toy breed, or debilitated r dogs)—formulated as a 19.9% emulsifiable animals—may be predisposed. Mild signs after topical concentrate in 10.6-mL bottles for dilution application—wearing gloves, scrub with a and sponge-on; as a 9% impregnated 25-inch hand dishwashing detergent; rinse with 27.5-g collar and an 18-inch 18.5-g collar; as copious amounts of warm water; institute a 14.34% component of a 0.023 fl. oz., 0.045 DIAGNOSIS non-specific supportive therapy (e.g., fl. oz., 0.113 fl. oz., 0.180 fl. oz., or 0.225 fl. intravenous fluids, maintenance of normal DIFFERENTIAL DIAGNOSIS body temperature, and nutritional support); oz. spot-on. r r monitor 1–2 days until improvement is noted. Systems affected—nervous; endocrine/ Recreational and prescription r metabolic (β cells of the pancreas); drugs—marijuana; opioids; barbiturates; Ingestion of collar possible—endoscopic gastrointestinal. benzodiazepines; phenothiazines; retrieval of the collar—removal of large r Clinical signs—most associated with antihypertensive medications; skeletal muscle segments from the stomach may be beneficial; relaxants; antidepressants (tricyclic, SSRIs), usually numerous small pieces are located α2-adrenoreceptor agonist. r and other depressant drugs or chemicals. throughout the gastrointestinal tract, making After high-dose oral administration r (dogs)—peak plasma concentration reached Ivermectins, avermectins, milbemycins— removal unrealistic. at approximately 6 hours; elimination half-life generally very high dose or exceptionally sensitive breed. as long as 24 hours; metabolites excreted in r the urine. Alcohols—ethanol; ethylene glycol r Ingestion of sustained-release- impregnated (antifreeze); methanol (windshield washer MEDICATIONS fluid); isopropyl alcohol (rubbing alcohol). collars—constant release and continued r DRUG(S) systemic exposure until collar segments have Tick paralysis, botulism, cranial trauma, Collar Ingestion, Asymptomatic Patient passed in the stool. diabetes, hyperadrenocorticism, r r Emetic—3% USP hydrogen peroxide Toxicosis—generally occurs when hypothyroidism, severe anemia, cardiac (2.2 mL/kg PO; maximum 45 mL after impregnated collars are ingested, when failure, and anaphylactic shock—marked feeding a moist meal); apomorphine and improperly diluted solutions are applied depression or weakness. r especially xylazine not recommended. topically, or when solutions are taken orally or Depends on clinical signs, history of r Activated charcoal has not been shown to be applied to the wrong size animal. exposure, or evidence of exposure and r effective. Idiosyncratic reactions may occur. elimination of other causes. r CBC/BIOCHEMISTRY/URINALYSIS Bulk diet (whole wheat bread, lactulose, SIGNALMENT pumpkin). r r r Thorough history—usually identifies use Hyperglycemia—common, related to Warm tap water enema (5–10 ml/kg); will topically or as a collar. insulin inhibition r r stimulate GI motility and help pass pieces of Dogs—common, owing to more common Elevated liver enzymes— uncommon collar through the GI tract. use. IMAGING r Marked Depression r Cats—more sensitive than dogs although Abdominal radiography—may reveal a collar May require pharmacologic reversal of the cats are less likely involved. r buckle in the gastrointestinal tract. α -adrenergic effects. r 2 Predilection for old and toy breed animals. DIAGNOSTIC PROCEDURES Yohimbine (Yobine) 0.11 mg/kg IV, SIGNS Identify amitraz on hair or in gastrointestinal administered slowly; reverses depression and Historical Findings contents—analytical methods described; bradycardia within minutes; improves GI Develop acutely after exposure (topical or useful only to prove exposure; no data motility; objective is to keep the patient in a oral) available correlating concentration with state of low-level depression with normal Physical Examination Findings clinical signs. heart rate, blood pressure, body temperature, r and blood glucose concentrations. Minor to severe depression PATHOLOGIC FINDINGS r r Collar ingestion—monitor for recurrence of Ataxia High-dose, prolonged exposure—increased r symptoms; may need additional yohimbine Bradycardia liver weight; slight enlargement of r until collar segments appear in the stool. Vomiting hepatocytes; thinning of the zonae fasciculata r r Atipamezole (Antisedan) 0.05 mg/kg IM; Hyperthermia/hypothermia and reticularis; slight hyperplasia of the zona r reported to reverse clinical signs within Hyperglycemia glomerulosa of the adrenal glands. r minutes; repeat as needed; an alternative Hypotension r when yohimbine is unavailable. Polyuria r Gastrointestinal stasis r Mydriasis r Death (prognosis is typically good with treatment) BLBS078-CF_A37 BLBS078-Tilley July 23, 2011 4:31

Canine and Feline, Fifth Edition 63

(Continued) Amitraz Toxicosis A

r Yohimbine and atipamezole—may require ABBREVIATIONS r repeated administration (as needed) possibly CNS = central nervous system r every 4–8 hours, because half-life in dogs is GI = gastrointestinal FOLLOW-UP r = short and elimination half-life of amitraz is r SSRI selective serotonin reuptake longer. Body temperature, blood pressure, serum inhibitor r Do not use atropine to reverse bradycardia; glucose, and heart rate—important INTERNET RESOURCES parameters. use is contraindicated because of potentiation r http://www.aspcapro.org/animal-poison of GI stasis. Close observation for recurrence of clinical signs—required for 24–72 hours. -control-center-articles.php. CONTRAINDICATIONS/POSSIBLE r Yohimbine and atipamezole—requires INTERACTIONS Suggested Reading readministration in severe cases, because Grossman MR. Amitraz toxicosis associated Yohimbine and atipamezole—excessive reversal effects subside before collar segments with ingestion of an acaricide collar in a administration may result in apprehension, have passed or before amitraz has been dog. JAVMA 1993, 203:55–57. CNS stimulation, and rarely seizures. eliminated from the body. r Hugnet C, Buronfosse F, Pineau X, et al. No long-term adverse effects expected. Toxicity and kinetics of amitraz in dogs. Am AGE-RELATED FACTORS J Vet Res 1996, 57:1506–1510. Elderly, sick, or debilitated animals may take Author Steven R. Hansen longer to fully recover. Consulting Editor Gary D. Osweiler BLBS078-CF_A37a BLBS078-Tilley June 16, 2011 10:46

64 Blackwell’s Five-Minute Veterinary Consult A Amphetamine Toxicosis

r SIGNALMENT Chemistry— ◦ Species Azotemia: prerenal—secondary to BASICS Dogs and cats, although more prevalent in dehydration; renal—secondary to dogs; other species rhabdomylosis and myoglobinuria (rare). DEFINITION ◦ Breed Predilections High liver enzymes—secondary to seizures and/or hyperthermia (rare). Acute gastrointestinal, neurological, N/A ◦ Hypoglycemia. neuromuscular, and cardiac toxicosis as the r result of excessive consumption of Mean Age and Range Urinalysis—evidence of myoglobinuria, amphetamine or a derivative. N/A urine specific gravity (high—prerenal PATHOPHYSIOLOGY Predominant Sex azotemia; isosthenuria—renal failure). r N/A OTHER LABORATORY TESTS Amphetamine and its derivatives belong to r the CNS stimulant class phenylethylamines. SIGNS Electrolytes—imbalances secondary to gastrointestinal signs. Various substitutions of the basic Historical Findings r r Acid-base status—acidosis may occur. phenylethylamine structure account for many Abnormal behavior—usually hyperactivity, r pharmaceutical and illicit compounds found anxiety or pacing, anorexia, fast heart rate, Over-the-counter urine drug today. screens—watch for false positives or negatives. r panting; observed or evidence of exposure by Amphetamine is a sympathomimetic that is owner/caretaker. Check the user handbook for further r information. structurally related to norepinephrine. Onset of signs typically begins within 30 r ◦ Centrally—stimulates cortical centers minutes to 6 hours post-ingestion. Amphetamines are present in blood, urine, and saliva; check with local veterinary including cerebral cortex, medullary Physical Examination Findings r diagnostic lab or human hospital for respiratory center, and reticular activating Nervous—hyperactivity, agitation, systems. availability and proper sample submission. ◦ restlessness, head bobbing, pacing, circling, Peripherally—directly stimulates alpha vocalization, disorientation, hyperesthesia, IMAGING and beta receptors and stimulates the ataxia, lethargy or depression (less common). N/A r release of norepinephrine from stores in Cardiovascular—tachycardia or bradycardia DIAGNOSTIC PROCEDURES adrenergic nerve terminals. r ◦ (less common, may be reflexive), Electrocardiogram for presence of any Amphetamine may slow down hypertension. r tachyarrhythmia or less commonly catecholamine metabolism by inhibition of Neuromuscular—muscle fasciculation or monoamine oxidase. bradyarrhythmia. r tremors, seizures. r r Blood pressure—identification of Amphetamines are well absorbed orally and Gastrointestinal—vomiting, diarrhea, reach peak plasma levels in 1–3 hours. hypertension. r anorexia, excessive salivation. r PATHOLOGIC FINDINGS The half-life, which varies from 7–34 hours, Respiratory—tachypnea. r and rate of excretion of unchanged Ophthalmic—mydriasis with possibly poor On necropsy presence of amphetamines may amphetamine in the urine are both dependent to unresponsive pupillary light response. be found in the gastric contents, urine, r upon urine pH, with shorter half-lives being Other—hyperthermia. plasma, liver, kidney, or muscle. associated with more acidic urine. r CAUSES Oral LD50 of amphetamine sulfate in dogs is 20–27 mg/kg, and for methamphetamine Accidental ingestion or administration, sulfate it is 9–11 mg/kg. malicious poisoning. r TREATMENT Clinical signs may be seen at doses below 1 RISK FACTORS mg/kg. APPROPRIATE HEALTH CARE r Households with children or adults currently Amphetamine and its derivatives are used in taking prescription or illicit amphetamine or Majority of cases require emergency inpatient humans to treat ADD/ADHD, narcolepsy, derivative. intensive care management. and obesity. NURSING CARE r r Illicit use of amphetamines in humans is Intravenous fluid therapy to correct also prevalent. dehydration and electrolyte imbalances as well SYSTEMS AFFECTED as help support renal function and promote r DIAGNOSIS Cardiovascular—stimulation most excretion of amphetamines. Use blood DIFFERENTIAL DIAGNOSIS common: tachycardia and hypertension. r pressure to help guide fluid rate. r Strychnine r Gastrointestinal—anorexia, vomiting, r Cool intravenous fluids, fans, cool water Organochlorine insecticides diarrhea. r baths for hyperthermia. r Methylxanthine Nervous—stimulation most common, r ACTIVITY 4 aminopyridine depression uncommon. r Minimize activity and stimuli r Metaldehyde Neuromuscular—stimulation: muscle r Phenylpropanolamine DIET tremors and seizures. r r Albuterol Withhold food if moderately to severely Ophthalmic—mydriasis. r r Nicotine affected. Bland diet for a few days Respiratory—stimulation: tachypnea. r Tremorgenic mycotoxins post-exposure if significant gastrointestinal GENETICS r Hypernatremia signs were noted. r N/A Pseudoephredrine, phenylephrine r CLIENT EDUCATION INCIDENCE/PREVALENCE 5 fluorouracil r In case of an exposure, owner should contact N/A Ma huang, guarana, or ephedra local veterinarian or veterinary poison center GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS immediately. r N/A CBC—disseminated intravascular SURGICAL CONSIDERATIONS coagulopathy secondary to severe N/A hyperthermia (rare). BLBS078-CF_A37a BLBS078-Tilley June 16, 2011 10:46

Canine and Feline, Fifth Edition 65

(Continued) Amphetamine Toxicosis A

r Amphetamines potentiate the metabolism SYNONYMS r of coumarin anticoagulants, monoamine Common brand names of prescription MEDICATIONS oxidase inhibitors, opioid analgesics, and amphetamine drugs and their active tricyclic antidepressants. ingredient: Adderall (amphetamine and DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) dextroamphetamine); Ritalin, Metadate, Decontamination Concerta (methylphenidate); Daytrana r Phenobarbital, pentobarbital, and propofol Induce emesis—if a recent exposure and pet for CNS stimulatory signs. (methylphenidate transdermal patch); Focalin is not already symptomatic. (dexmethylphenidate); Vyvanse ◦ Apomorphine—0.04 mg/kg IV, (lisdexamfetamine), Cylert (pemoline), subconjuctival. Adipex-P (phentermine), Dexedrine ◦ (Dextroamphetamine). Hydrogen peroxide 3%—2.2 ml/kg, FOLLOW-UP r maximum dose 45 mls. Illicit drug street names: ice, glass, crank, r PATIENT MONITORING speed, uppers, ecstasy, meth, and many others. Gastric lavage if extremely large ingestion or r patient is already symptomatic. Monitor in hospital until resolution of SEE ALSO r r Activated charcoal with a cathartic. clinical signs. Antidepressants—SSRI Toxicosis r r CNS Signs of Stimulation If severely affected, monitor liver and Antidepressants—Tricyclic Toxicosis r kidney values every 24 hours for 72 hours or r Acepromazine 0.05–1.0 mg/kg IV or IM Pseudoephredrine Toxicosis r until resolution. r Chlorpromazine 10–18 mg/kg IV Strychnine Poisoning r Cyproheptadine (serotonin antagonist): PREVENTION/AVOIDANCE ABBREVIATIONS r dogs, 1.1 mg/kg orally or rectally; cats, 2–4 All medications and illicit drugs should be ADD = attention deficit disorder r mg/cat kept out of pets’ reach at all times. ADHD = attention deficit hyperactivity Cardiovascular Signs POSSIBLE COMPLICATIONS disorder r r CNS = central nervous system Tachyarrhythmia—beta blockers such as Acute renal failure secondary to r propranolol 0.02–0.04 mg/kg IV or myoglobinuria or DIC (rare). DIC = disseminated intravascular metoprolol. coagulation r EXPECTED COURSE AND PROGNOSIS r Ventricular premature Expected course of clinical signs is 12–72 INTERNET RESOURCES contractions—lidocaine: dogs at 2–4 mg/kg hours, depending on dose, effectiveness of http://www.aspcapro.org/animal-poison- IV (to maximum of 8 mg/kg over a decontamination and treatment, and rate of control-center-articles.php. 10-minute period). Cats—start with 0.1–0.4 elimination. mg/kg and increase cautiously to 0.25–0.75 r Suggested Reading Prognosis—most patients do well with Cudia SP, Poppenga RH, Birdsall WJ. mg/kg IV slowly if no response. Cats are prompt and appropriate veterinary care. reportedly very sensitive to lidocaine, so Pemoline toxicosis in a dog. JAVMA 1998, Seizures or severe hyperthermia may be a poor 212(1):74–76. monitor carefully if used. prognostic indicator. Promote Elimination Mckinney PE, Palmer RB. Amphetamines and derivatives. In: Brent J, et al., eds., Ascorbic acid or ammonium chloride—for Critical Care Toxicology. Philadelphia: urinary acidification to promote elimination; Elsevier, 2005, pp. 761–775. however, only use if can measure acid-base MISCELLANEOUS Teitler JB. Evaluation of a human on-site status. ASSOCIATED CONDITIONS urine multi drug test for emergency use with CONTRAINDICATIONS r N/A dogs. JAAHA 2009, 45(2):59–66. While diazepam has been successfully used Volmer PA. “Recreational” drugs. In: Peterson AGE-RELATED FACTORS to treat amphetamine exposures, there is ME, Talcott PA, eds., Small Animal evidence that benzodiazepines may intensify N/A Toxicology. St. Louis: Elsevier, 2006, neurological signs. ZOONOTIC POTENTIAL r pp. 276–280. Urinary acidification if unable to monitor Pets exposed to human waste products from Volmer PA. Human drugs of abuse. In: acid-base status or if myoglobinuria is present. r those taking amphetamines or derivatives Bonagua JD, Twedt DC, eds., Current Inducing emesis in a symptomatic patient. could become symptomatic. Veterinary Therapy XIV. St. Louis: Elsevier, PRECAUTIONS PREGNANCY/FERTILITY/BREEDING 2009, pp. 144–145. N/A Amphetamines are a known teratogen in Author Kirsten E. Waratuke POSSIBLE INTERACTIONS humans. They have been found to cross the r Consulting Editor Gary D. Osweiler Amphetamines inhibit the metabolism of placenta in animals and may also be found in adrenergic blockers (doxazosin, milk. phenoxybenzamine, prazosin, terazosin), Phenobarbital, and phenytoin. BLBS078-CF_A38 BLBS078-Tilley July 23, 2011 4:35

66 Blackwell’s Five-Minute Veterinary Consult A Amyloidosis

Breed Predilections hepatic disease (e.g., jaundice, cachexia, and r Dogs—Chinese shar-pei, beagle, collie, spontaneous hepatic rupture with BASICS pointer, English foxhound, and walker intraperitoneal bleeding). hound; German shepherd dog and mixed CAUSES DEFINITION r r breeds are at lower risk. Cats: Abyssinian, Neoplasia and chronic infectious and A group of conditions of diverse cause in Oriental shorthair, and Siamese. non-infectious inflammatory conditions can which extracellular deposition of insoluble Mean Age and Range r be found in 30–50% of dogs with reactive fibrillar proteins (amyloid) in various organs Most affected dogs and cats are more than r r amyloidosis. Chronic inflammation— and tissues compromises their normal function. 5 years old. Dogs—mean age at diagnosis is r systemic mycoses (e.g., blastomycosis, PATHOPHYSIOLOGY 9 years; range, 1–15 years. Cats—mean age coccidioidomycosis), chronic bacterial at diagnosis 7 years; range, 1–17 years. r r r infections (e.g., osteomyelitis, Patients usually affected by systemic reactive Prevalence increases with age. Abyssinian r bronchopneumonia, pleuritis, steatitis, amyloidosis; tissue deposits contain AA, cats—range < 1–17 years. Chinese shar-pei pyometra, pyelonephritis, chronic suppurative which is a fragment of an acute-phase reactant r dogs—usually < 6 years of age when signs of dermatitis, chronic suppurative arthritis, protein called SAA. Phases of amyloid renal failure develop; range, 1.5–6 years. ◦ r chronic peritonitis, nocardiosis, chronic deposition: Predeposition phase: SAA Siamese cats with familial amyloidosis of the stomatitis), parasitic infections (e.g., concentration is high but without amyloid liver and thyroid gland usually develop signs dirofilariasis, leishmaniasis, hepatozoonosis), deposits; colchicine administration during of liver disease when 1–4 years old. and immune-mediated diseases (e.g., systemic r this phase may prevent development of the lupus erythematosus). Neoplasia (e.g., disease. ◦ Deposition phase (rapid portion): Predominant Sex Dogs and Abyssinian cats—females appear to lymphoma, plasmacytoma, multiple amyloid deposits increase rapidly; colchicine < myeloma, mammary tumors, testicular be at a slightly higher risk ( 2:1). r administration delays but does not prevent tumors). Familial (e.g., Chinese shar-pei, tissue deposition of amyloid; DMSO may Female-to-male ratio is higher in Chinese shar-pei dogs (∼2.5 : 1). English foxhound, and beagle dogs; promote resolution of amyloid deposits and a Abyssinian, Siamese, and Oriental shorthair persistent decrease in SAA concentration. SIGNS r ◦ cats). Others—cyclic hematopoiesis in gray Deposition phase (plateau portion): net General Comments collies; juvenile polyarteritis in beagles. deposition of amyloid changes little; neither r r Depend on the organs affected, the amount RISK FACTORS DMSO or colchicine is beneficial. Clinical of amyloid, and the reaction of the affected r r Chronic inflammation or neoplasia signs in dogs and cats usually are associated organs to amyloid deposits. Usually caused r with amyloid deposition in the kidneys. Family history in certain breeds r by renal involvement; occasionally, hepatic Dogs—amyloid deposits usually found in involvement may cause signs in Chinese the glomeruli leading to proteinuria and r shar-pei dogs and Oriental shorthair and nephrotic syndrome. Cats—amyloid Siamese cats. deposits usually found in the medullary Historical Findings DIAGNOSIS interstitium but may occur in glomeruli. r r No clear history of a predisposing disorder DIFFERENTIAL DIAGNOSIS Some Chinese shar-pei dogs with familial r in most (∼75%) cases. Anorexia, lethargy, r amyloidosis have medullary amyloidosis Dogs—glomerulonephritis; proteinuria r polyuria and polydipsia, weight loss, without glomerular involvement. Siamese tends to be more severe in dogs with vomiting, and diarrhea (uncommon). and Oriental shorthair cats with familial r glomerular amyloidosis than those with r Ascites and peripheral edema in animals amyloidosis have hepatic amyloidosis. A r glomerulonephritis but there is great overlap. with nephrotic syndrome. Chinese shar-pei r different type amyloid, pancreatic islet Cats and Chinese shar-pei dogs with dogs may have a history of previous episodic amyloid polypeptide, or amylin, deposits in medullary amyloidosis—consider other causes joint swelling and high fever that resolves the pancreas of old cats. Amylin is a hormone r of medullary renal disease (e.g., spontaneously within a few days. Beagle secreted along with insulin by the pancreatic pyelonephritis, chronic interstitial disease). dogs with juvenile polyarteritis may have a beta cells. Chronic increased stimulus for CBC/BIOCHEMISTRY/URINALYSIS history of fever and neck pain that persist for secretion of amylin by beta cells (e.g., states of r r 3–7 days. Oriental shorthair and Siamese Nonregenerative anemia is found in some insulin resistance) lead to pancreatic islet cell cats may present with spontaneous hepatic dogs and cats with amyloid-induced renal amyloidosis. r hemorrhage leading to acute collapse and failure. Dogs—may see SYSTEMS AFFECTED hypercholesterolemia (> 85%), azotemia hemoabdomen. > Renal/Urologic—predilection for renal AA ( 70%), hypoalbuminemia (70%), Physical Examination Findings > deposition; liver, spleen, adrenal glands, r hyperphosphatemia ( 60%), hypocalcemia Related to renal failure—oral ulceration, (50%), and metabolic acidosis. pancreas, tracheobronchial tree, and emaciation, vomiting, and dehydration; r gastrointestinal tract also may be affected. Hypercholesterolemia—common finding in kidneys usually small, firm, and irregular in cats with renal disorders (> 70% of cats with GENETICS affected cats; they may be small, normal-sized, r renal disease in one study) but does not No genetic involvement is clearly established; or slightly enlarged in affected dogs. Signs reliably predict glomerular disease. familial amyloidosis occurs in Chinese of nephrotic syndrome (e.g., ascites, r r Hypoproteinemia—more common than shar-pei, English foxhound, and beagle dogs, subcutaneous edema). Related to the hyperproteinemia (24 vs. 8.5%) in dogs with and in Abyssinian, Oriental shorthair, and primary inflammatory or neoplastic disease amyloidosis; hyperglobulinemia common in r r Siamese cats. process. Thromboembolic phenomena cats. Proteinuria—with an inactive INCIDENCE/PREVALENCE —may occur in up to 40% of affected dogs; sediment common in dogs; mild or absent in Uncommon occurs mostly in dogs; rare in signs vary with the location of the thrombus; animals with medullary amyloidosis without cats, except Abyssinians. patients may develop pulmonary glomerular involvement (most mixed-breed thromboembolism (e.g., dyspnea) or iliac or SIGNALMENT cats, at least 25% of Abyssinian cats, and at femoral artery thromboembolism (e.g., caudal least 33% of Chinese shar-pei dogs). r r Species paresis). Chinese shar-pei dogs and Oriental Isosthenuria, and hyaline, granular, and Dogs and cats shorthair and Siamese cats may have signs of waxy casts in some patients. BLBS078-CF_A38 BLBS078-Tilley July 23, 2011 4:35

Canine and Feline, Fifth Edition 67

(Continued) Amyloidosis A

OTHER LABORATORY TESTS CLIENT EDUCATION drugs cautiously in patients with medullary r r Proteinuria—urinary protein:creatinine ratio Discuss progression of the disease. Discuss amyloidosis; they can decrease renal blood to estimate severity. familial predisposition in susceptible breeds. flow in dehydrated patients. r IMAGING Discuss potential complications (e.g., hypertension, thromboembolism). Abdominal Radiographic Findings r Kidneys usually small in affected cats. r FOLLOW-UP Kidneys small, normal-sized, or large in affected dogs. PATIENT MONITORING MEDICATIONS r Abdominal Ultrasonographic Findings Appetite and activity level daily by the r r Kidneys usually hyperechoic and small in DRUG(S) OF CHOICE owner; body weight weekly. Serum r albumin, creatinine, and BUN concentrations affected cats; may be small, normal-sized, or Identify underlying inflammatory and r large in affected dogs. neoplastic processes and treat if possible. every 2–6 months in stable patients. Can r assess degree of proteinuria serially by urine DIAGNOSTIC PROCEDURES Manage renal failure according to the principles of conservative medical treatment protein:creatinine ratios. Renal biopsy needed to differentiate (see Renal Failure, Acute, and Renal Failure, PREVENTION/AVOIDANCE amyloidosis from glomerulonephritis. In dogs r Chronic). Normalize blood pressure in other than Chinese shar-pei, amyloidosis is Do not breed affected animals patients with hypertension (see Hypertension, primarily a glomerular disease; diagnose by r POSSIBLE COMPLICATIONS Systemic). Patients with thromboembolic r r renal cortical biopsy. In most domestic cats, Renal failure Nephrotic syndrome syndrome and nephrotic syndrome caused by r r some Abyssinian cats, and some Chinese Systemic hypertension Hepatic rupture glomerular amyloidosis usually have a low shar-pei dogs, medullary amyloidosis can causing intraperitoneal hemorrhage plasma concentration of antithrombin; thus r occur without glomerular involvement; Thromboembolic disease heparin is relatively ineffective. Aspirin (0.5 diagnose by renal medullary biopsy. mg/kg PO q12h) has been suggested for dogs EXPECTED COURSE AND PROGNOSIS PATHOLOGIC FINDINGS Disease is progressive and usually advanced at r with glomerular disease; this low dosage is as Small kidneys in cats; small, normal, or effective in preventing platelet aggregation as the time of diagnosis. Prognosis improves if r r large kidneys in dogs. Amyloid deposits is 10 mg/kg PO q24h. DMSO—may help an underlying immune, inflammatory, or appear homogeneous and eosinophilic when patients by solubilizing amyloid fibrils, neoplastic disease is detected and successfully stained by hematoxylin and eosin and viewed reducing serum concentration of SAA, and treated. Survival for dogs with glomerular by conventional light microscopy. They reducing interstitial inflammation and fibrosis amyloidosis varied from 3 to 20 months in 1 demonstrate green birefringence after Congo in the affected kidneys; may cause lens study; some dogs may occasionally live longer. red staining when viewed under polarized opacification in dogs. Perivascular Cats with renal failure because of amyloidosis light. Evaluation of Congo red—stained inflammation and local thrombosis may occur usually survive < 1 year. Mildly affected cats sections before and after permanganate if undiluted DMSO is administered may not develop renal failure and have an oxidation permits presumptive diagnosis of intravenously. Subcutaneous administration almost normal life expectancy. AA amyloidosis (vs. other types) because AA of undiluted DMSO may be painful. The amyloidosis loses its Congo red affinity after r authors have used 90% DMSO diluted 1 : 4 permanganate oxidation. The liver is very with sterile water subcutaneously at a dosage friable and usually contains extensive amyloid of 90 mg/kg three times per week in dogs. MISCELLANEOUS deposits in cats presented with acute hepatic Whether or not DMSO treatment benefits ASSOCIATED CONDITIONS hemorrhage. renal amyloidosis in dogs remains r r r Urinary tract infection Polyarthritis in r controversial. Methylsulfonylmethane is an Chinese shar-pei dogs Polyarteritis in beagle active metabolite of DMSO that can be given dogs orally and lacks the smell of DMSO. It has TREATMENT been used empirically in dogs with PREGNANCY/FERTILITY/BREEDING amyloidosis, but there is no evidence that it High risk in affected animals APPROPRIATE HEALTH CARE r benefits dogs with renal amyloidosis. SEE ALSO Hospitalize patients with chronic renal r r r Colchicine—impairs release of SAA from Glomerulonephritis Nephrotic Syndrome failure and dehydration for initial medical r r r r hepatocytes; prevents development of Proteinuria Renal Failure, Acute Renal management. Can manage stable patients amyloidosis in humans with familial Failure, Chronic and those with asymptomatic proteinuria as Mediterranean fever (a familial amyloidosis) ABBREVIATIONS outpatients. and stabilizes renal function in patients with r r AA = amyloid A protein DMSO = NURSING CARE nephrotic syndrome but without overt renal r dimethylsulfoxide SAA = serum amyloid A Correct dehydration with 0.9% NaCl failure; no evidence of benefit once the patient protein solution or lactated Ringer’s solution; patients develops renal failure; may cause vomiting, with severe metabolic acidosis may benefit diarrhea, and idiosyncratic neutropenia in Suggested Reading from bicarbonate supplementation (see dogs. Colchicine (0.01–0.04 mg/kg PO DiBartola SP. Renal amyloidosis. In: Osborne Acidosis, Metabolic). q24h) is used particularly in shar-pei dogs CA, Low D, Finco DR, eds., Canine and ACTIVITY with episodic fever or polyarthritis before Feline Urology, 2nd ed. Philadelphia: development of renal failure. Normal Saunders, 1995, pp. 400–415. CONTRAINDICATIONS Authors Helio Autran de Morais and Stephen DIET r Avoid use of nephrotoxic drugs P. D i B a r t o l a Patients with chronic renal failure—restrict Consulting Editor Carl A. Osborne phosphorus and moderately restrict protein. PRECAUTIONS r r Patients with hypertension—restrict Dosage of drugs excreted by the kidneys may need adjustment in patients with renal Client Education Handout sodium. r failure. Use nonsteroidal anti-inflammatory available online BLBS078-CF_A39 BLBS078-Tilley March 21, 2011 21:12

68 Blackwell’s Five-Minute Veterinary Consult A Anaerobic Infections

r CBC/BIOCHEMISTRY/URINALYSIS Cefoxitin—a cephalosporin with reliable r Neutrophilic leukocytosis and monocytosis activity against anaerobes. r r BASICS common. Biochemical abnormalities Clindamycin—may be especially useful for depend on specific organ involvement. respiratory tract infections; concentrated r r OVERVIEW Systemic spread of infection suggested by within leukocytes. Chloramphenicol—good r Anaerobic bacteria (i.e., bacteria requiring leukocytosis, hypoglycemia, increased ALP, tissue penetration but bacteriostatic and low oxygen tension) comprise a large portion and hypoalbuminemia. associated with adverse effects, especially in cats; concern for human exposure also limits of the normal flora, especially on mucosal OTHER LABORATORY TESTS r r r surfaces. May be gram-positive or Culture of anaerobic bacteria is often use. Metronidazole—useful against all r clinically significant anaerobes (except gram-negative cocci or rods. Most common unrewarding because of their fastidious nature r Actinomyces). Aminoglycosides—uniformly genera—Bacteroides, Fusobacterium, and errors in sample handling and r r Actinomyces, Propionibacterium, submission. Appropriate media and ineffective. Trimethoprim-sulfa Peptostreptococcus (enteric Streptococcus), combinations—ineffective; poor penetration r containers should be on-hand prior to sample r Porphyromonas,andClostridium. Most collection; diagnostic laboratories can provide into exudates. Quinolones—routinely r anaerobic infections are polymicrobial and guidance. Samples should not be ineffective, although newer r contain at least two different anaerobe species refrigerated prior to submission. Suitable expanded-spectrum quinolones do have admixed with facultative anaerobes or aerobic activity against anaerobes (e.g., r samples for culture may include fluid (e.g., bacteria (especially E. coli). Individual pleural, peritoneal, etc.) or tissue. pradofloxacin). organisms vary in potential to withstand r IMAGING oxygen exposure. Injurious toxins and enzymes may be elaborated by the organisms, As required for the circumstances of the leading to extension of the infection into individual patient (e.g., suspected bone FOLLOW-UP r infection, peritonitis, etc.). adjacent, healthy tissue. All body systems PATIENT MONITORING are at potential risk for anaerobic infection. DIAGNOSTIC PROCEDURES r Monitoring parameters will vary with the SIGNALMENT Cytologic inspection reveals abundant circumstances of each patient. Dogs and cats degenerate neutrophils with morphologically diverse forms of intracellular and extracellular POSSIBLE COMPLICATIONS SIGNS bacteria; presence of large filamentous Localized infection may progress to systemic r General Comments bacteria is suggestive. If not performed r infection if not appropriately identified and Determined by the body system involved. in-house, gram staining should be requested r treated. Certain areas more commonly associated when the sample is submitted. EXPECTED COURSE AND PROGNOSIS with anaerobic infection (mucous membrane r Dependent upon identification and resolution It is possible to overlook proximity). of the underlying cause; long-term antibiotic anaerobes in an infectious process, leading to therapy may be required. confusion in interpreting culture results and MEDICATIONS selection of antimicrobials. r Thoracic drainage—important with Physical Examination Findings r r pyothorax (see specific chapter). Hyperbaric A foul odor associated with a wound or r oxygen—some potential use; limited in MISCELLANEOUS exudative discharge. Gas in the tissue or r availability. associated exudates. Discolored tissue, ASSOCIATED CONDITIONS r SURGERY especially when black. Peritonitis, r See “Causes & Risk Factors” r Should not be delayed when anaerobes are pyothorax, or pyometra. Severe dental r ABBREVIATIONS r suspected. Combined with systemic r r disease. Wounds or deep abscesses that do ALP = alkaline phosphtase FeLV = feline antimicrobial therapy—the best chance of a r not heal as anticipated. r leukemia virus FIV = feline positive outcome. Usually indicated when CAUSES & RISK FACTORS immunodeficiency virus r anaerobic organisms complicate pyometra, r Usually caused by normal flora of the body; osteomyelitis, and peritonitis. Cleanse the Suggested Reading a break in protective barriers allows bacterial r wound of toxins and devitalized tissue. Hirsh DC, Jang SS. Anaerobic infections. In: invasion. Infection in the proximity of a r r Enhance drainage of pus. Improve local Greene CE, ed., Infectious Diseases of the mucous membrane should raise one’s index of r blood flow. Increase oxygen tension. Dog and Cat, 3rd ed. St. Louis: Saunders suspicion for anaerobe involvement. r Elsevier, 2006, pp. 381–388. Predisposing factors—immunosuppression, DRUG(S) r Author Sharon Fooshee Grace bite wounds, dental disease, open fractures, Antimicrobial therapy alone—unlikely to be successful; poor drug penetration into Consulting Editor Stephen C. Barr abdominal surgery, and foreign bodies. r exudates. Antibiotic selection—largely empiric, owing to the difficulty of isolating anaerobes and the delay in return of culture r DIAGNOSIS results. Because most anaerobic infections are polymicrobial, therapy targeted against DIFFERENTIAL DIAGNOSIS both anaerobes and any aerobic components r offers the greatest chance of success. Wounds that fail to respond to appropriate r medical therapy—if aerobic cultures are Amoxicillin with clavulanate—in many r negative, suspect anaerobic organisms. Cats cases, considered the antibiotic of choice; with non-healing wounds—test for FeLV and convenient and accessible; clavulanate r improves activity against Bacteroides. FIV. Middle-aged and old animals—tumor r invasion (e.g., in the gastrointestinal tract). Imipenem—beta lactam with significant activity against serious, resistant infections. BLBS078-CF_A40 BLBS078-Tilley July 15, 2011 5:20

Canine and Feline, Fifth Edition 69 Anal Sac Disorders A

r r Colitis or other intestinal disorder. Anal sac excision with chronic disease. r r Keratinization disorder. Surgical excision and staging of anal sac r Anal sac neoplasia (including neoplasia; combine with chemotherapy. BASICS r adenocarcinoma, squamous cell carcinoma). Identification of underlying causes of r OVERVIEW Perianal adenoma. predisposing disease. r r r Perianal adenocarcinoma. Feeding high-fiber diets may help natural Anal sacs are reservoirs for secretions r normally evacuated during fecal excretion. Perianal fistulae. expression of anal sacs. r Disorders include impaction, infection CBC/BIOCHEMISTRY/URINALYSIS r (sacculitis), and neoplasia. Usually normal r r Treatment options include manual Hypercalcemia—anal sac adenocarcinoma expression, flushing, antibiotics, and surgical OTHER LABORATORY TESTS MEDICATIONS excision. None unless indicated by an underlying DRUG(S) SIGNALMENT r r cause Infection—use of appropriate antibiotics: Dogs and cats (rarely). r IMAGING cephalexin (22 mg/kg q12h), amoxicillin Breeds predisposed: trihydrate-clavulanate potassium (10–15 ◦ Impaction—miniature and toy poodle, None unless indicated by an underlying cause mg/kg q12h), clindamycin (11 mg/kg American cocker and English springer q12–24h), trimethoprim-sulfamethoxasole DIAGNOSTIC PROCEDURES spaniel, Chihuahua. (15 mg/kg q12h); metronidazole (15 mg/kg ◦ r Neoplasia (adenocarcinoma)—German Digital palpation of the anal sacs—normal q12h); enrofloxacin(10–20 mg/kg q12h dogs; shepherd dog, golden retriever, American anal sacs are not palpable externally. r cats 5 mg/kg/day), and orbifloxacin (5 mg/kg cocker and English springer spaniel. Normal anal sac contents vary widely in q24h). r r No age or sex predispositions. gross appearance and microscopic Chronic disease associated with perianal SIGNS characteristics; usually thin or watery, with fistulae; cyclosporine (5 mg/kg q24h) and/or r Anal pruritus—often manifested by minimal cellularity and primarily extracellular topical tacrolimus. “scooting” organisms. CONTRAINDICATIONS/POSSIBLE r r Perianal pruritus Impaction—generally more thick, pasty r INTERACTIONS Hesitancy to defecate brown secretion; higher numbers of r N/A Tenesmus Malassezia and intracellular bacteria. r r Tail chasing Anal sacculitis and abscessation—purulent, r often blood-tinged, foul-smelling discharge. Foul-smelling, non-fecal matter anal r discharge Cytology of anal sac secretions—increased r FOLLOW-UP Refusal to sit and/or lift tail number of neutrophils, Malassezia,and intracellular bacteria indicate infection; r CAUSES & RISK FACTORS Reassess patients weekly initially; then as r reports vary but gram-positive cocci more necessary to monitor healing. Possible predisposing factors—soft feces or common in normal secretions. r r Manually express anal sac contents and/or diarrhea, excessive glandular secretions, and Bacterial culture and sensitivity—normal dermatologic disorders that alter the flush contents until sacs empty without secretions may contain Proteus mirabilis, intervention. characteristics (cellularity and organism Streptococcus spp., Escherichia coli, Bacillus colonization) of anal sac secretions. r spp., Clostridium perfringens,andPseudomonas Retained secretions may lead to infection aeruginosa. and abscess formation. MISCELLANEOUS SEE ALSO r Adenocarcinoma, Anal Sac TREATMENT r DIAGNOSIS r Perianal Fistula Gentle manual expression of contents for DIFFERENTIAL DIAGNOSIS impaction and sacculitis. Suggested Reading r r Adverse food reaction or food Sedation may be necessary to flush severely Muse R. Diseases of the anal sac. In: hypersensitivity. impacted or painful anal sacs. Bonagura JD, Twedt DC, eds., Kirk’s r r Flea bite hypersensitivity. Infusion of antibiotic and/or corticosteroid Current Veterinary Therapy, 14th ed. St. r Atopic dermatitis. medications directly into the anal sacs. Louis: Saunders, 2009, pp. 465–468. r r Tapeworm infestation. Drainage of abscesses. Zoran DL. Rectoanal disease. In: Ettinger SJ, r r Tail fold bacterial folliculitis. Use of appropriate oral antibiotics and/or ed., Textbook of Veterinary Internal r Malassezia dermatitis. antiyeast medication. Medicine, 6th ed. Philadelphia: Saunders, r Compulsive disorder (anal licking). 2005, pp. 1408–1420. Author Alexander H. Werner Consulting Editor Alexander H. Werner BLBS078-CF_A41 BLBS078-Tilley March 21, 2011 21:23

70 Blackwell’s Five-Minute Veterinary Consult A Anaphylaxis

SIGNALMENT can be made largely on the basis of history Species and clinical signs. BASICS Dogs and cats CBC/BIOCHEMISTRY/URINALYSIS Breed Predilections Because of the acute onset of disease, no tests DEFINITION r r Dogs—numerous breeds documented as available that reliably predict individual Acute manifestation of a Type I having a predilection for developing atopy. susceptibility. r hypersensitivity reaction mediated through Cats—no breeds documented as having OTHER LABORATORY TESTS the rapid introduction of an antigen into a predilection for atopy. r host having antigen-specific antibodies of the Intradermal skin testing to identify IgE subclass. Mean Age and Range allergens. r r r The binding of antigen to mast cells Dogs—age of clinical onset ranges from 3 Radioallergosorbent test to quantify the sensitized with IgE results in the release of months to several years of age; most affected concentration of serum IgE specific for a animals 1–3 years old. particular antigen. preformed and newly synthesized chemical r mediators. Cats—age of clinical onset ranges from 6 IMAGING r Anaphylactic reactions may be localized months to 2 years. N/A Predominant Sex (atopy) or systemic (anaphylactic shock). r DIAGNOSTIC PROCEDURES r Dogs—atopy more common in females. Anaphylaxis not mediated by IgE is r Limited because a severely allergic animal can Cats—no reported sex predilection. designated an anaphylactoid reaction and will develop an anaphylactic reaction when not be discussed. SIGNS exposed to even small quantities of antigen. PATHOPHYSIOLOGY General Comments PATHOLOGIC FINDINGS r r r First exposure of the patient to a particular Initial clinical signs vary depending on the Lesions vary, depending on severity of antigen (allergen) causes a humoral response route of exposure to the inciting antigen reaction, from localized cutaneous edema to and results in production of IgE, which binds (allergen). r severe pulmonary edema (in cats) and visceral to the surface of mast cells; the patient is then Shock—end result of a severe anaphylactic pooling of blood (in dogs). considered to be sensitized to that antigen. reaction. r r r Other non-specific findings vary and are Second exposure to the antigen results in Shock organ—dogs, liver; cats, respiratory characteristic of shock. cross-linking of two or more IgE molecules on and gastrointestinal systems. r r Non-specific characteristics of localized the cell surface, resulting in mast cell Maybelocalizedtothesiteofexposurebut reactions include edema, vasculitis, and degranulation and activation; release of mast may progress to a systemic reaction. thromboembolism. cell granules initiates an anaphylactic reaction. r Historical Findings r Major mast cell-derived mediators include Onset of signs immediate (usually within histamine, eosinophilic chemotactic factor, minutes). r arachidonic acid, metabolites (e.g., Dogs—pruritus, urticaria, vomiting, TREATMENT prostaglandins, leukotrienes, and defecation, and urination. r APPROPRIATE HEALTH CARE thromboxanes), platelet-activating factor, and Cats—intense pruritus about the head, proteases, which cause an inflammatory dyspnea, salivation, and vomiting. In an acutely affected animal, the reaction is response of increased vascular permeability, considered a medical emergency requiring Physical Examination Findings smooth muscle contraction, inflammatory cell r hospitalization. influx, and tissue damage. Localized cutaneous edema at the site of r exposure. NURSING CARE Clinical manifestations depend on the route r Hepatomegaly in some dogs. Elimination of inciting antigen, if possible. of antigen exposure, the dose of antigen, and r Hyperexcitability possible in early stages. Systemic Anaphylaxis the level of the IgE response. r r SYSTEMS AFFECTED Depression and collapse terminally. Goal—emergency life support through the r CAUSES maintenance of an open airway, preventing Gastrointestinal—salivation, vomiting, and circulatory collapse, and reestablishing diarrhea Virtually any agent; those commonly reported r physiologic parameters. Hepatobiliary (dogs)—because of portal include venoms, blood-based products, r Administer fluids intravenously at shock hypertension and vasoconstriction vaccines, foods, and drugs. r dosages to counteract hypotension. Respiratory (cats)—dyspnea and cyanosis RISK FACTORS r Skin/Exocrine—pruritus, urticaria, and Previous exposure (sensitization) increases Localized Anaphylaxis edema the chance of the animal developing a Goal—limit the reaction and prevent GENETICS reaction. progression to a systemic reaction. ACTIVITY Familial basis reported for Type I hypersensitivity reaction in dogs. N/A INCIDENCE/PREVALENCE DIET r Localized Type I hypersensitivity reactions DIAGNOSIS If a food-based allergen is suspected not uncommon. DIFFERENTIAL DIAGNOSIS (uncommon), avoid foods associated with r r hypersensitivity reaction. Systemic Type I hypersensitivity reactions Other types of shock. r rare. Trauma. CLIENT EDUCATION r r GEOGRAPHIC DISTRIBUTION Depends on the major organ system Discuss the unpredictable nature of the None involved or if reaction is localized; diagnosis disease. BLBS078-CF_A41 BLBS078-Tilley March 21, 2011 21:23

Canine and Feline, Fifth Edition 71

(Continued) Anaphylaxis A

r Discuss the need to recognize that the CONTRAINDICATIONS animal has an allergic condition that may None require immediate medical care. PRECAUTIONS MISCELLANEOUS SURGICAL CONSIDERATIONS Localized reaction can develop into systemic ASSOCIATED CONDITIONS None reaction. None POSSIBLE INTERACTIONS AGE-RELATED FACTORS N/A None ALTERNATIVE DRUG(S) MEDICATIONS ZOONOTIC POTENTIAL N/A DRUG(S) OF CHOICE None Systemic Anaphylaxis PREGNANCY/FERTILITY/BREEDING r Epinephrine hydrochloride parenterally N/A (1 : 1,000; 0.01 mL/kg) for shock. FOLLOW-UP SEE ALSO r r Corticosteroids for shock—prednisolone PATIENT MONITORING Shock, Cardiogenic sodium succinate (2 mg/kg IV q8h) or INTERNET RESOURCES dexamethasone sodium phosphate (0.25 Closely monitor hospitalized patients for mg/kg IV q12h). 24–48 hours. Merck Veterinary Manual: r Atropine sulfate (0.04 mg/kg IM) to PREVENTION/AVOIDANCE www.merckvetmanual.com. counteract bradycardia and hypotension. If inciting antigen (allergen) can be identified, r Suggested Reading Aminophylline (10 mg/kg IM or slowly IV) eliminate or reduce exposure. Mueller DL, Noxon JO. Anaphylaxis: in severely dyspneic patients. POSSIBLE COMPLICATIONS Pathophysiology and treatment. Compend Localized Anaphylaxis Contin Educ Pract Vet 1990, 12:157–170. r None Diphenhydramine hydrochloride (1-2 EXPECTED COURSE AND PROGNOSIS Author Paul W. Snyder mg/kg IV or IM). r Consulting Editor A.H. Rebar r If localized reaction is treated early, Prednisolone (2 mg/kg PO). r prognosis is good. Epinephrine hydrochloride (0.15 ml SC at r If the animal is in shock on examination, site of initiation). Client Education Handout r prognosis is guarded to poor. If shock develops, initiate treatment for a available online systemic anaphylaxis. BLBS078-CF_A42 BLBS078-Tilley March 21, 2011 21:25

72 Blackwell’s Five-Minute Veterinary Consult A Anemia of Chronic Kidney Disease

high calcium; variably low bicarbonate and antibody induction; should be used potassium. preferentially to epoetin alfa. r r High BUN:creatinine ratio may predict Target PCV—dogs, 37–45%; cats, 30–40%. BASICS r concurrent gastrointestinal blood loss. Initial dosage: darbepoetin alfa—0.45–0.6 r DEFINITION Impaired urine-concentrating ability, mild mcg/kg (for cats and small dogs 2.5–5 mcg) Progressive decreases in PCV, RBC count, to moderate proteinuria, and variably active SC once weekly until PCV reaches low end of and hemoglobin and hypoplasia of erythroid sediment. target, then decrease to q2 weeks. Epoetin elements of the bone marrow are predictable OTHER LABORATORY TESTS alfa—50–100 U/kg SC thrice weekly until r features of progressive CKD. Anemia is Serum iron—normal or variably low. low end of target, then decrease to twice r normocytic, normochromic, nonregenerative, Transferrin saturation—normal or variably weekly. If converting from epoetin alfa to and proportional to the stage of CKD. low (< 20%). darbepoetin—divide weekly units by 400 to r establish mcg to give once weekly. Principal cause is bone marrow failure FeLV and FIV or haemobartonella testing r secondary to inadequate production of (cats) or rickettsial titers or PCR (dogs) to Maintenance dosage: darbepoetin erythropoietin by the kidneys. Shortened exclude agent-induced myelodyscrasia. alfa—2.5–5 mcg q2–3 weeks. Epoetin r RBC lifespan, uremic inhibitors of Serum erythropoietin—normal alfa—50–100 U/kg SC once or twice weekly erythropoiesis, blood loss, nutritional (inappropriately) or low. to maintain target PCV. Individualize to each patient; life-long treatment required. If giving deficiencies, and marrow fibrosis may IMAGING contribute. r epoetin alfa once weekly, give darbepoetin Small, irregular kidneys with loss or every 2 weeks with conversion. SIGNALMENT r disruption of renal architecture detected by If PCV exceeds target, discontinue until Middle-aged to old dogs and cats mostly radiography or ultrasonography. r upper target range is achieved, then decrease affected; seen in young animals with heritable, Enlarged, polycystic, hydronephrotic, previous dosage by 25–50% or increase congenital, or acquired CKD. infiltrative. dosage interval. r SIGNS DIAGNOSTIC PROCEDURES Serum iron and transferrin saturation r Anemia contributes to development of Cytologic examination of bone should be normalized before initiating and anorexia, weight loss, fatigue, lethargy, marrow—erythroid hypoplasia; during treatment. Injectable iron (50 mg/kg depression, weakness, apathy, cold myeloid:erythroid ratio normal or high; IM q4–8 weeks) is preferable and better intolerance, and behavior and personality tolerated than oral preparations. stainable iron normal or variably low. r changes characterizing CKD. Species-specific erythropoietins for dogs and r Pallor of the mucous membranes. cats and alternative erythropoietin stimulating r Tachypnea. treatments are under development as r Tachycardia. alternatives for erythropoiesis stimulating r TREATMENT Systolic murmur. proteins. r r Syncope and seizures (rare). Increase RBC mass if patient is Blood Transfusion ≤ r CAUSES & RISK FACTORS symptomatic for anemia (dogs, PCV 25%; Short-term or rapid correction (PCV ≤ r cats, PCV ≤ 23). All inherited, congenital, and acquired r 20%)—give compatible whole blood or forms of CKD (e.g., pyelonephritis, Stabilize azotemia in patients in uremic packed RBCs. crisis. r glomerulonephritis, amyloidosis, polycystic r Target PCV is 25–30%. Establish appropriate nitrogen, caloric, r kidney disease, and lymphoma). May be given intermittently for prolonged r Exacerbated by iron deficiency, phosphate, vitamin, and iron intake to reduce management. inflammatory or neoplastic disease, uremic inhibitors and bleeding tendency and lengthen life span of RBCs. Anabolic Steroids gastrointestinal blood loss, hemolysis, and r r Ensure that iron is not deficient. Little or no efficacy or indication for use. myeloproliferative disorders. r Correct gastrointestinal ulceration and blood loss by administrating famotidine, ranitidine, omeprazole, or sucralfate. r Correct systemic hypertension. FOLLOW-UP DIAGNOSIS PATIENT MONITORING DIFFERENTIAL DIAGNOSIS r r PCV—weekly to semimonthly for 3 Anemia of chronic infectious, inflammatory, months, then monthly to bimonthly. r or neoplastic disease; myeloproliferative MEDICATIONS Blood pressure—semimonthly to monthly. r disease; chronic blood loss; aplastic anemia; DRUG(S) AND FLUIDS Iron and transferrin saturation—at 1, 3, and endocrine disease; drug reaction; and chronic 6 months, then semiannually. Erythropoietin Replacement r immune-mediated, toxic, viral, rickettsial, or r Discontinue erythropoietin if patient Epoetin alfa (r-HuEPO)—original synthetic parasitic anemia; hemodilution. develops evidence of erythrocythemia, local or r erythropoiesis stimulating protein, replica of Regenerative anemia excludes diagnosis of systemic sensitivity, anti-r-HuEPO antibody human erythropoietin (Epogen and Procrit); anemia of CKD. formation, pure red cell aplasia, or refractory r provides consistent, rapid, and long-term Generally masked until advanced CKD. hypertension. correction of anemia in dogs and cats with CBC/BIOCHEMISTRY/URINALYSIS POSSIBLE COMPLICATIONS r CKD; potential for anti-r-HuEPO antibody Normocytic, normochromic, production and pure red cell aplasia. Erythropoietin-Related r r hypoproliferative anemia (progressive; anemia Darbepoetin alfa (Aranesp), a new Development of erythrocythemia, seizures, maybemaskedbydehydration). r hyperglycolylated analogue of r-HuEPO with hypertension, iron depletion, injection pain, Reticulocytes—low corrected indices and prolonged half-life and sustained effects; and mucocutaneous reactions. absolute counts (≤ 10,000/ul). r r appears to be equipotent to r-HuEPO and, Development of a pure red cell aplasia Moderate to advanced CKD—elevated with current experience, little tendency for during the course of epoetin alfa treatment BUN, creatinine, and phosphorus; variably suggests formation of anti-r-HuEPO BLBS078-CF_A42 BLBS078-Tilley March 21, 2011 21:25

Canine and Feline, Fifth Edition 73

(Continued) Anemia of Chronic Kidney Disease A

antibodies, which neutralize r-HuEPO and Transfusion-Related r native erythropoietin, causing severe anemia Incompatibility reaction r in 20–30% of animals; often reversible with Circulatory or iron overload r MISCELLANEOUS cessation of treatment. Systemic hypertension r r Signs associated with production of Transmissible infection ABBREVIATIONS r anti-r-HuEPO antibodies while the patient is CKD = chronic kidney disease EXPECTED COURSE AND PROGNOSIS r receiving epoetin alfa include decreasing PCV, r FeLV = feline leukemia virus Correction of anemia increases appetite, r erythroid hypoplasia, absolute reticulocyte FIV = feline immunodeficiency virus activity, grooming, affection and playfulness, r counts approaching zero, and PCR = polymerase chain reaction ≥ weight gain, and cold tolerance, and decreases r = myeloid:erythroid ratio 8. These signs also sleeping. PCV packed cell volume r r = should be monitored with darbepoetin alfa Use of erythropoietin replacement in dogs RBC red blood cell treatment. r = r and cats requires careful assessment of the r-HuEPO recombinant human Erythropoietin replacements should be used risks and benefits for individual patients. erythropoietin r cautiously or withheld if hypertension or iron Short-term prognosis depends on the deficiency develop; treatment can be Suggested Reading severity of the renal failure. Long-term Cowgill LD, et al. Use of recombinant human reinstituted once hypertension and iron prognosis is guarded to poor because of the deficiency are corrected. erythropoietin for management of anemia underlying chronic renal failure. in dogs and cats with renal failure. JAVMA 1998, 212:521–528. Author Larry D. Cowgill Consulting Editor Carl A. Osborne BLBS078-CF_A43 BLBS078-Tilley May 31, 2011 18:56

74 Blackwell’s Five-Minute Veterinary Consult A Anemia, Aplastic

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 DIFFERENTIAL DIAGNOSIS decreased production of granulocytes, FOLLOW-UP Causes of pancytopenia with normal to erythrocytes, and platelets, resulting in PATIENT MONITORING pancytopenia in the peripheral blood. The increased bone marrow cellularity (e.g., r Daily physical examination. disease is sometimes also referred to as aplastic myelodysplastic disorders, leukemia, r CBC every 3-5 days to weekly. pancytopenia. myelofibrosis). r r Repeat bone marrow evaluation if necessary. In the acute form, neutropenia and CBC/BIOCHEMISTRY/URINALYSIS r PREVENTION/AVOIDANCE thrombocytopenia predominate because of Leukopenia characterized by neutropenia r Castration of cryptorchid males. the shorter life spans of these cells; in the with or without lymphopenia. r r Vaccination for infectious diseases. chronic form, nonregenerative anemia also Normocytic, normochromic, r occurs. In both forms, the bone marrow nonregenerative anemia. Frequent monitoring of CBC in cancer exhibits variable degrees of panhypoplasia. r patients receiving chemotherapy or radiation. r Thrombocytopenia. There are many precipitating causes of OTHER LABORATORY TESTS POSSIBLE COMPLICATIONS r deficient hematopoiesis, including infectious r Sepsis diseases, drug administration, starvation and Immunologic tests for infectious diseases r (e.g., serologic titers, ELISA, IFA). Hemorrhage toxin exposure; immune-mediated r PCR for infectious agents. EXPECTED COURSE AND PROGNOSIS mechanisms are often suspected. r r r Hemic/lymphatic/immune systems affected. Serologic test for antierythrocyte antibodies Guarded to poor. (Coombs’ test). r SIGNALMENT Recovery of hematopoiesis may take weeks IMAGING to months, if it occurs at all. r Dogs and cats, no apparent breed or sex Spontaneous recovery occasionally occurs, predilection. In one study, the mean age of N/A DIAGNOSTIC PROCEDURES especially in young animals. nine affected dogs was 3 years. r SIGNS Bone marrow aspiration—frequently an r Acute form: fever, petechial hemorrhages, inadequate or fatty sample is obtained because epistaxis, hematuria, melena; i.e., signs due to of decreased hemopoietic tissue and MISCELLANEOUS replacement by lipocytes. neutropenia and thrombocytopenia. r r SEE ALSO Chronic form: pale mucous membranes, Bone marrow core biopsy—allows an weakness, lethargy; i.e., signs due to anemia, evaluation of architecture and reveals Pancytopenia in addition to signs observed in acute forms. hypoplasia of cell lines and replacement by ABBREVIATIONS adipose tissue. r CAUSES & RISK FACTORS ELISA = enzyme-linked immunosorbent assay Often not identified r FeLV = feline leukemia virus Infectious Agents r r FIV = feline immunodeficiency virus FeLV, FIV TREATMENT r r IFA = immunofluorescent antibody (test) Canine and feline parvovirus r r Supportive treatment, antibiotics, blood NSAID = nonsteroidal anti-inflammatory Rickettsial organisms (e.g., Ehrlichia spp.) drug component therapy, as dictated by clinical r Drugs and Chemicals PCR = polymerase chain reaction r condition. r Estrogen (exogenous administration, Sertoli rhG-CSF = recombinant human and interstitial cell tumors). r granulocyte colony-stimulating factor Methimazole (cats). r Suggested Reading Chemotherapeutic drugs, including MEDICATIONS azathioprine, cyclophosphamide, cytosine Brazzell JL, Weiss DJ. A retrospective study of arabinoside, doxorubicin, vinblastine, and DRUG(S) OF CHOICE aplastic pancytopenia in the dog: 9 cases r hydroxyurea. Cyclosporine A—10–25 mg/kg PO q12h (1996–2003). Vet Clin Path 2006, r Antibiotics, including (dogs), 4-5 mg/kg PO q12h (cats). 35:413–417. r trimethoprim-sulfadiazine, cephalosporins, Recombinant hematopoietic growth factors Weiss DJ. Aplastic anemia. In: Weiss DJ, and chloramphenicol. (e.g., rhG-CSF: 5 μg/kg/day SC). Wardrop KJ, eds., Schalm’s Veterinary r r Griseofulvin. Androgen and corticosteroid administration Hematology, 6th ed. Ames, IA: Blackwell r NSAIDs, including phenylbutazone and have been largely unsuccessful. Publishing Ltd., 2010, pp. 256–260. meclofenamic acid. Author Darren Wood r CONTRAINDICATIONS/POSSIBLE Fenbendazole, albendazole. Consulting Editor A.H. Rebar r INTERACTIONS Captopril. r Quinidine. N/A BLBS078-CF_A44 BLBS078-Tilley May 31, 2011 19:0

Canine and Feline, Fifth Edition 75 Anemia, Heinz Body A

naphthalene (moth ball ingestion in dogs), skunk musk exposure (dogs). BASICS MEDICATIONS OVERVIEW DRUG(S) OF CHOICE r r Heinz bodies cause hemolytic anemia and Severe methemoglobinemia—single slow IV r DIAGNOSIS indicate oxidative damage to RBCs. Heinz injection of methylene blue (0.2 mg/kg). DIFFERENTIAL DIAGNOSIS r bodies form when oxidants overwhelm r Acetaminophen toxicity in cats—N- protective reductive pathways in RBCs and Other causes of regenerative, hemolytic acetylcysteine (140 mg/kg PO or IV, followed anemia (e.g., immune mediated, cause irreversible denaturation of hemoglobin r by seven additional treatments of 70 mg/kg (sulfhydryl groups and/or hemichromes), hemoparasites). Heinz bodies may be found every 8 hours). precipitation and attachment of altered in healthy or ill cats without anemia. CONTRAINDICATIONS/POSSIBLE Diagnosis of a Heinz body anemia requires hemoglobin to the cell membrane, clustering INTERACTIONS of band 3, and alteration of surface antigens. documentation of a regenerative anemia, r Methylene blue may aggravate The RBCS are less deformable, targeted for supporting evidence of a hemolytic process oxidant-induced hemolysis. removal by macrophages in the spleen, and (e.g. hyperbilirubinemia), identification of r may undergo intravascular lysis. The pitting Heinz bodies on a smear, and elimination of ALTERNATIVE DRUG(S) function of the spleen may remove Heinz other causes of hemolysis or blood loss. The use of dietary antioxidants (vitamin C, r bodies, resulting in spherocytes. Heinz CBC/BIOCHEMISTRY/URINALYSIS vitamin E, bioflavonoids) is controversial but bodies are usually caused by exposure to r may help prevent further formation of Heinz r Regenerative anemia (decreased HCT, chemical or dietary oxidants. Cats are polychromasia, nucleated RBCs) is expected if bodies. particularly susceptible to Heinz body there has been sufficient time for a bone formation because their hemoglobin is rich in marrow response; the severity of anemia sulfhydryl groups and the feline spleen is depends on dose of oxidant and duration of non-sinusoidal with limited pitting function. r FOLLOW-UP r exposure. Hemoglobin concentration and Healthy cats may have Heinz bodies with no MCHC may be falsely increased due to Heinz r r PATIENT MONITORING anemia. Heinz bodies are frequently found body interference. Heinz bodies are visible Serial CBCs and review of blood smears are in cats with hyperthyroidism, lymphoma, and on a routine blood smear as small, pale red, recommended to assess RBC regeneration and diabetes mellitus (particularly if ketoacidotic), round inclusions that may protrude from disappearance of Heinz bodies. possibly due to increased endogenous RBC surface. They may be difficult to identify oxidants (e.g., β-hydroxybutyrate). Anemia r PREVENTION/AVOIDANCE r if there is marked poikilocytosis. Single, may or may not be present. Heinz bodies small (< 0.5 μm) Heinz bodies may be found Counsel clients about preventing exposure to may be accompanied by methemoglobinemia r oxidants. + in RBCs of cats without anemia. Large (hemoglobin containing Fe3 ) and/or and/or multiple Heinz bodies in an anemic POSSIBLE COMPLICATIONS eccentrocytes (oxidative damage to RBC cat suggest a Heinz body hemolytic anemia. r N/A membranes with hemoglobin displaced to one Dogs may have concurrent eccentrocytes on r EXPECTED COURSE AND PROGNOSIS side). The factors that control which type(s) a blood smear. Hyperbilirubinemia and r of oxidative damage occurs are not clear. bilirubinuria are possible. Hemoglobinemia Prognosis is good with removal of oxidant and SIGNALMENT and hemoglobinuria are uncommon but supportive care once the hemolytic crisis is r r occur with severe intravascular hemolysis. over. Dogs and cats. No sex, breed, or age r disposition. Neutrophilia and monocytosis may occur. SIGNS OTHER LABORATORY TESTS r Historical Findings New methylene blue stains Heinz bodies MISCELLANEOUS r r blue, making them easy to identify and Exposure to oxidant. Sudden onset of r quantify, even with marked poikilocytosis. SEE ALSO weakness, lethargy, or anorexia. Reddish- r r r Methemoglobin test if blood is dark or Acetaminophen Toxicity Anemia, brown urine (hemoglobinuria) if severe r r r r chocolate colored. Serum zinc Regenerative Methemoglobinemia Zinc intravascular hemolysis. Signs related to concentration if indicated. Toxicity underlying disease in cats with systemic disease and Heinz bodies. IMAGING ABBREVIATIONS r = r = Physical Examination Findings Abdominal radiographs may reveal HCT hematocrit MCHC mean r r gastrointestinal metal objects in zinc toxicity. corpuscular hemoglobin concentration Pale or icteric mucous membranes. Dark r = or chocolate-colored blood with RBC red blood cell r methemoglobinemia. Tachypnea, Suggested Reading tachycardia. Andrews D. Disorders of red blood cells. In: CAUSES & RISK FACTORS Handbook of Small Animal Practice, 5th ed. r TREATMENT St. Louis: Saunders, 2008, pp. 632–635. Dietary: onions (raw, cooked, dehydrated, r and powdered), garlic (dogs), propylene glycol Immediate identification and removal of Stockham SL, Scott MA. Erythrocytes. In: r (cats), Chinese chives (dog). Drugs: oxidant may be sufficient, though it may take Fundamentals of Veterinary Clinical several days for the severity of anemia to reach Pathology, 2nd ed. Ames, IA: Blackwell, acetaminophen, phenacetin (cats), r phenazopyridine (cats), methylene blue, nadir. Supportive care depends on the 2008, pp. 186–187. Author Jennifer S. Thomas vitamin K1 or K3 (dogs), DL-methionine severity of the hemolytic crisis and includes (cats), benzocaine (topical), phenylhydrazine IV fluids, RBC transfusions, oxygen, and Consulting Editor A.H. Rebar r r (dog), propofol (cats). Miscellaneous: zinc restricted activity. Endoscopy or surgery to (nuts, bolts, pennies, dermatologic creams), remove metallic items in gastrointestinal tract. BLBS078-CF_A45 BLBS078-Tilley June 17, 2011 7:3

76 Blackwell’s Five-Minute Veterinary Consult A Anemia, Immune-Mediated

GENETICS phagocytophilum, Babesia spp., Leishmaniasis, Cocker spaniels are at increased risk. Absence Dirofilaria immitis, Ehrlichia,FeLV,FIP, of dog erythrocyte antigen 7 is associated with chronic bacterial infection). BASICS r increased risk in this breed. Neoplasia (lymphoma, lymphoid leukemia, DEFINITION GEOGRAPHIC DISTRIBUTION hemangiosarcoma, hemophagic histiocytic sarcoma). Accelerated destruction or removal of RBCs Secondary IMHA may have a higher r due to a Type II hypersensitivity reaction. prevalence in areas where associated infectious Drugs (e.g., beta lactam antibiotics, PATHOPHYSIOLOGY diseases are endemic. propylthiouracil, methimazole, sulfonamides). r MISCELLANEOUS CAUSES Anti-RBC antibodies form against SIGNALMENT r SLE endogenous unaltered surface antigens Species r Neonatal isoerythrolysis (primary IMHA) or altered RBC membrane Dogs and cats r antigens (secondary IMHA). Hemolysis due to DEA incompatible blood r Breed Predilections Infectious organisms, drugs, exposure of r transfusion previously unexposed antigens, or adsorption Cocker spaniel is the breed at highest risk. RISK FACTORS Other commonly affected breeds include of preformed antigen—antibody complexes to Exposure to infectious agents, vaccination, miniature poodle, Irish setter, English the RBC membrane can alter RBC membrane chemicals or drugs, surgery, hormonal change, springer spaniel, Old English sheepdog, antigens. or other stressful event is hypothesized as a r Doberman pinscher, collie, bichon frise, Immunoglobulin (IgG or IgM, with or potential trigger for IMHA. miniature pinscher, and Finnish spitz. without complement) deposits on the RBC r membrane, causing either direct intravascular Domestic shorthair cats. hemolysis or accelerated removal by the Mean Age and Range r monocyte/macrophage system (extravascular In dogs, mean age 5–6 years with reported DIAGNOSIS hemolysis). range of 1–13 years. r r Intravascular hemolysis occurs when In cats, mean age 2 years with reported DIFFERENTIAL DIAGNOSIS adsorbed antibodies (usually IgG) activate range of 0.5–9 years. Dogs r complement. Predominant Sex Pyruvate kinase deficiency. r r r In vivo agglutination of RBCs occurs when Females may have a higher risk in dogs. Phosphofructokinase deficiency. r r IgM or high titers of IgG molecules cause Male cats are overrepresented. Toxicity (zinc, onions, garlic, broccoli, bridging of RBCs. copper, naphthalene, skunk musk). r SIGNS r Extravascular removal of RBCs occurs in the Snake/spider evenomation (coral snakes, Historical Findings spleen, liver, bone marrow, or other site of r recluse spiders). Lethargy/weakness/collapse r macrophage activity. r Severe hypophosphatemia. r Anorexia r Nonregenerative IMHA is believed to be r Anemia due to hemorrhage Exercise intolerance/dyspnea caused by immune-mediated destruction of r (immune-mediated thrombocytopenia, Tachypnea RBC precursors in the bone marrow. r rodenticide toxicosis). r Vomiting and/or diarrhea r Rarely cold-acting antibodies cause in vivo r Microangiopathic anemia due to splenic Dark red urine hemolysis and erythrocyte agglutination in r neoplasia, DIC, splenic torsion. peripheral vasculature. Pica (cats) Cats SYSTEMS AFFECTED Physical Examination Findings r r r Toxicity (acetaminophen zinc, onions, Cardiovascular—hypoxia leads to Pale mucous membranes, tachycardia, and garlic). tachypnea. r tachycardia; low blood viscosity and turbulent r Severe hypophosphatemia. Splenomegaly and hepatomegaly. r blood flow may cause a low-grade heart r Congenital feline porphyria. r murmur. Icterus and pigmenturia (hemoglobin or Increased osmotic fragility (Abyssinian, r bilirubin). Hemic/Lymphatic/Immune—immune- r Somali). Fever and lymphadenomegaly. mediated destruction of RBCs, elaboration of r Systolic murmur. CBC/BIOCHEMISTRY/URINALYSIS proinflammatory mediators (e.g., cytokines, r r endothelial-derived substances), DIC. Petechiae, ecchymoses, or melena in animals CBC—anemia, high MCV (3–5 days r with concurrent thrombocytopenia or DIC. post-hemolytic episode), spherocytes, Hepatobiliary—hemolysis leads to r hyperbilirubinemia and icterus as well as Other physical examination findings anisocytosis, polychromasia, nucleated RBCs, bilirubinuria when hepatic function is possible (e.g., joint pain and increased RBC distribution width, marked overwhelmed; hypoxia may cause glomerulonephritis) when IMHA is a leukocytosis with neutrophilia and a left shift. centrilobular necrosis. component of SLE. Anemia is nonregenerative in 30% of dogs r r and 50% of cats. Respiratory—hypoxia causes tachypnea. Necrosis of extremities and ear tips in r Pulmonary thromboembolism may result cold-type IMHA (rare). Serum biochemistry—hyperbilirubinemia, hemoglobinemia, high ALT. from a hypercoagulable state due to increased CAUSES r Urinalysis—hemoglobinuria, bilirubinuria. activity procoagulant factors, presence of free Primary IMHA hemoglobin, decreased concentration of OTHER LABORATORY TESTS Autoimmune (idiopathic) hemolytic anemia r fibrinolytic and anticoagulant factors, due to poorly characterized immune Spontaneous saline agglutination vasculitis, and increased platelet reactivity. r dysregulation. test—before and after washing of red blood Skin—rarely cold-type IMHA may cause cells. Secondary IMHA r necrosis of extremities and ear tips because of r Positive direct antiglobulin test (Coombs’ RBC agglutination in peripheral vessels. Infectious causes (hemotrophic Mycoplasma test)—positive in up to 75% of animals with spp., Ehrlichia canis, Anaplasma IMHA. BLBS078-CF_A45 BLBS078-Tilley June 17, 2011 7:3

Canine and Feline, Fifth Edition 77

(Continued) Anemia, Immune-Mediated A

r Flow cytometric detection of NURSING CARE CONTRAINDICATIONS r r membrane-bound immunoglobulin and Fluid therapy to maintain vascular volume Do not use heparin, enoxaparin, or aspirin complement. and correct dehydration. in dogs with severe thrombocytopenia r r Reticulocytosis—absolute count Careful monitoring for complications such (< 80,000/μl). r > 60,000/μlindogsand> 50,000/μlincats as pulmonary thromboembolism, bleeding Do not use multiple cytotoxic drugs in regenerative IMHA. (especially gastrointestinal), disseminated concurrently. r Thrombocytopenia in 60% of dogs. intravascular coagulation, infection. PRECAUTIONS r r Thrombocytopenia may be severe in animals Cage rest. Do not administer azathioprine to cats with Evans syndrome and DIC. r CLIENT EDUCATION because of risk of bone marrow toxicity. r r Prolonged APTT and PT, increased fibrin IMHA and its complications (e.g., DIC and Prednisone can cause signs of Cushing degradation products, d-dimer, and decreased pulmonary thromboembolism) can be fatal. syndrome and potentially increase risk of antithrombin in animals with DIC. r r Lifelong treatment may be needed, and the pulmonary thromboembolism, pancreatitis, Increased fibrinogen concentration. r disease may recur. secondary infection, and gastric ulcers r Positive ANA titer and LE cell test in Side effects of treatment may be severe. (consider gastric protectants). animals with SLE. r r SURGICAL CONSIDERATIONS Cytotoxic drugs can cause bone marrow Positive serologic titers or PCR in secondary r suppression, secondary infection, pancreatitis IMHA due to infectious causes. Splenectomy can be considered if medical r management fails to control the disease. (azathioprine), cystitis (cyclophosphamide), Evidence of hematologic parasites in blood r and infertility. smears of capillary blood in secondary IMHA Consider blood product administration due to infectious causes. preoperatively. POSSIBLE INTERACTIONS r Increased RBC osmotic fragility. Azathioprine and prednisone have both been IMAGING associated with development of pancreatitis. r Radiographic findings—hepatomegaly and MEDICATIONS ALTERNATIVE DRUG(S) splenomegaly; thorax usually within normal r limits; may see evidence of pulmonary DRUG(S) OF CHOICE Dexamethasone (0.25–0.5 mg/kg/day r thromboembolism in dogs with IMHA Packed RBCs typed or cross-matched for IV)—can be used instead of prednisone in (patchy alveolar pattern, interstitial pattern, naive recipient. Blood should be animals that do not tolerate oral drugs, until oral intake is possible. pleural fluid), but dogs with pulmonary cross-matched for recipients that have r embolism may have normal thoracic received prior transfusions. Chlorambucil—for cats, 0.1–0.2 mg/kg PO radiographs. r = q24h initially, then q48h. r Transfusion volume recipient weight (kg) r Ultrasonographic findings—hepatomegaly × 85(dog)or50(cat)× desired PCV-current Cyclosporine—microemulsion, e.g., and splenomegaly; liver and spleen can be PCV/donor PCV. Atopica—dogs, 5–10 mg/kg/day PO divided mottled and hyperechoic or hypoechoic. r twice daily; cats, 0.5–3 mg/kg q12h. Transfusion rate 0.25 ml/kg/hour for first r 2 DIAGNOSTIC PROCEDURES 30 minutes then 5–10 ml/kg/hour. Cyclophosphamide—dogs, 50 mg/M /day r 2 r Corticosteroids—prednisone 1–2 PO for 4 out of 7 days or 200 mg/M IV once Examination of bone marrow aspirate a week (only in dogs that do not tolerate usually reveals erythroid hyperplasia. mg/kg/day q12h for 2–4 weeks. r r azathioprine or cyclosporine); cats, 2.5 In animals with nonregenerative IMHA, Once the hematocrit increases above 30%, decrease dose to 1 mg/kg q12h. mg/kg/day PO for 4 out of 7 days or 7 mg/kg maturation arrest or erythroid hypoplasia may r IV once a week. be evident. Subsequently the dose is tapered by a r γ r maximum rate of 25–50% per month over a Human -globulin—0.5–1.5 g/kg over In animals with chronic IMHA, 12h, single IV infusion. myelofibrosis may be present. 3- to 6-month period, depending upon the PATHOLOGIC FINDINGS hematocrit and severity of side effects. If after r 6 months the prednisone dose has been Hepatosplenomegaly, centrilobular hepatic tapered to a low every-other-day dose and the necrosis r disease is in remission, discontinuation of FOLLOW-UP Splenic and hepatic extramedullary medication should be attempted. PATIENT MONITORING hematopoiesis r r Add azathioprine (dogs) if there is a poor r Reactive lymphadenomegaly Monitor heart rate, respiratory rate, and r response to prednisone after 5–7 days or if temperature frequently during hospitalization. Pulmonary thromboembolism and DIC r poor prognostic indicators (e.g., intravascular Monitor for adverse reactions to treatment > hemolysis, serum bilirubin 8–10 mg/dl, (e.g., transfusion reactions and persistent autoagglutination, Evans overhydration). syndrome). r TREATMENT r If pulmonary thromboembolism is Azathioprine dose 2 mg/kg/day, can suspected, monitor thoracic radiographs and APPROPRIATE HEALTH CARE decrease to 2 mg/kg every other day if bone arterial blood gases frequently. r r Inpatient during the acute hemolytic crisis; marrow suppression. Monitor for During the first month of treatment, check outpatient when PCV has stabilized, ongoing immunosuppresson, hepatotoxicosis, the PCV weekly until stable and then every pancreatitis. hemolysis has been controlled, and clinical r 2 weeks for 2 months; if still stable, recheck signs of anemia have resolved. For prevention of thromboembolism (dogs) PCV monthly for 6 months and then 2–4 r Inpatient if animal has complications such consider unfractionated heparin 300 U/kg SC times per year; rechecks may need to be more as DIC, pulmonary thromboembolism, q6–8h (with does adjusted based on APTT frequent if patient is on long-term prolongation) or ultralow-dose aspirin medication. thrombocytopenia, gastrointestinal bleeding, r or a need for multiple transfusions. 0.5–1.0 mg/kg/day or enoxaparin A CBC and reticulocyte count should be r Chronic low-grade extravascular hemolysis (low-molecular-weight heparin) 0.8 mg/kg rechecked at least monthly during treatment, q6h or 1.5 mg/kg q12h. can be treated on an outpatient basis if the r especially if cytotoxic drugs are used; if the patient is not exhibiting clinical signs Address underlying cause (e.g., infection neutrophil count falls < 3,000 cells/μL, secondary to anemia. and drugs) if secondary IMHA. BLBS078-CF_A45 BLBS078-Tilley June 17, 2011 7:3

78 Blackwell’s Five-Minute Veterinary Consult

A Anemia, Immune-Mediated (Continued)

r r discontinue cytotoxic drugs until the count Response to treatment may take weeks to IMHA = immune-mediated hemolytic recovers; reinstitute at a lower dosage. months; nonregenerative IMHA may have a anemia r r Coombs’ test can be monitored to assist in more gradual onset than typical IMHA and LE = lupus erythematosus r drug tapering. may be slower to respond to treatment. MCV = mean cell volume r r IMHA may recur despite previous or PCR = polymerase chain reaction PREVENTION/AVOIDANCE r current therapy. PCV = packed cell volume Consider need for vaccination on a r PT = prothrombin time case-by-case basis in dogs in which IMHA r RBC = red blood cell developed after vaccination. r SLE = systemic lupus erythematosus POSSIBLE COMPLICATIONS r MISCELLANEOUS Pulmonary and multiorgan Suggested Reading SYNONYMS Kohn B, Weingart C, Eckmann V, et al. thromboembolism (up to 80% of all cases at r necropsy). Autoimmune hemolytic anemia Primary immune-mediated hemolytic r r Disseminated intravascular coagulation. Immune-mediated anemia anemia in 19 cats: Diagnosis, therapy, and r Centrilobular hepatic necrosis, and renal SEE ALSO outcome (1998–2004). J Vet Intern Med r 2006, 20:159–166. tubular necrosis secondary to hypoxia. Anemia, Regenerative r r Piek CJ, Dekker JA, Slappendel RJ, Teske E. Secondary infection secondary to Chapters on causes of secondary IMHA r Idiopathic immune-mediated hemolytic immunosuppressive therapy. Cold Agglutinin Disease r r anemia: Treatment outcome and prognostic Gastrointestinal ulceration due to high-dose Disseminated Intravascular Coagulation glucocorticoids. factors in 149 dogs. J Vet Intern Med 2008, r ABBREVIATIONS 22:366–373. Iatrogenic hyperadrenocorticism. r ALT = alanine aminotransferase Authors J. Catharine Scott-Moncrieff and EXPECTED COURSE AND PROGNOSIS r ANA = antinuclear antibody Rose E. Raskin r r Mortality ranges from 30 to 80% in dogs, APTT = activated partial thromboplastin Consulting Editor A.H. Rebar 25% in cats. time r r Causes of death include thromboembolism, DEA = dog erythrocyte antigen r infection due to immunosuppression, DIC, DIC = disseminated intravascular Client Education Handout persistent anemia. coagulation available online r > r Hyperbilirubinemia 5mg/dL, FeLV = feline leukemia virus r autoagglutination, intravascular hemolysis, FIV = feline immunodeficiency virus severe thrombocytopenia, hypoalbuminemia are associated with a poorer prognosis. BLBS078-CF_A46 BLBS078-Tilley March 21, 2011 21:34

Canine and Feline, Fifth Edition 79 Anemia, Iron-Deficiency A

detecting iron-deficient erythropoiesis; until features of iron deficiency have resolved. r currently only available on one central Kittens undergo spontaneous recovery and BASICS laboratory hematology system: see Steinberg iron repletion beginning at 5–6 weeks of age, and Olver and Fry and Kirk. coinciding with intake of solid food. r OVERVIEW Changes in erythrocytes may be seen on the Oral Iron Supplements r r Adults—caused by chronic external blood film—hypochromia (indicated by Ferrous sulfate powder—place in food or marked central pallor), oxidative lesions (e.g., drinking water (100–300 mg PO q24h). hemorrhage. r r keratocytes), fragmentation. Ferrous gluconate—one (325 mg) tablet PO Develops when erythrocytes are produced r Decreased MCHC is neither sensitive nor q24h. under the condition of limited iron r specific for iron deficiency. Iron and vitamins—any suitable iron with availability. r r Thrombocytosis may occur. multiple vitamin supplement; as Characteristic changes include erythrocyte r microcytosis, hypochromic appearance caused Hypoproteinemia—consistent finding only recommended or once daily. by thin cell geometry, and keratocyte and if the blood loss is sustained; both albumin CONTRAINDICATIONS/POSSIBLE schistocyte formation. and globulin fractions are low normal or low. r INTERACTIONS Important to recognize—leads clinician to OTHER LABORATORY TESTS r Oral iron supplementation is associated with the underlying disease problem, which is Hypoferremia (serum iron < 70 μg/dL) unexplained death in kittens and should be chronic external blood loss. and low transferrin saturation (< 15%) avoided. SIGNALMENT support the diagnosis. r r Fairly common in adult dogs. Serumironvaluesmaybenormal,evenin r Rare in adult cats. animals with hematologic features of iron r Transient, neonatal iron-deficiency anemia deficiency, if blood loss has ceased and the FOLLOW-UP animal is undergoing iron repletion. occurs at 5–10 weeks of age in about 50% of r r kittens. Fecal flotation to rule out clinically Monitor CBC every 1–4 weeks; if the suspected hookworm disease. anemia is severe, monitor more frequently to SIGNS r r Fecal examination for occult blood or gross follow the animal through recovery from a Signs of anemia (e.g., lethargy, depression, melena to detect gastrointestinal bleeding. life-threatening illness. weakness, anorexia, and tachypnea) and r IMAGING Effective treatment associated with an underlying disease. increase in MCV and reticulocyte volume. r r Intermittent melena with gastrointestinal Imaging studies—gastrointestinal disease that Erythrocyte histogram—effective treatment blood loss. accounts for blood loss. r associated with movement to the right as new, Possible heavy bloodsucking parasite load DIAGNOSTIC PROCEDURES normal cells are produced; subpopulation of (e.g., fleas and hookworms). Complete hemogram and iron measurements microcytes produced under conditions of iron CAUSES & RISK FACTORS as detailed above. deficiency slowly disappear, as these cells r Any form of chronic external blood loss. complete their survival time; may take a few r Blood loss most often occurs through the months in some animals to establish a normal gastrointestinal tract. histogram. r Common causes—GI lymphoma, TREATMENT hookworm infestation, stomach or intestinal r neoplasia. Identify and correct cause of chronic r external blood loss. Less common sites—skin (e.g., severe flea r MISCELLANEOUS infestation) and urinary tract. Administer iron until hematologic features r of iron deficiency resolve. ABBREVIATIONS Overuse of blood donors. r r If unusually severe (i.e., PCV < 15%), Chr = reticulocyte hemoglobin content r transfusion may be required to treat GI = gastrointestinal r life-threatening condition; administer whole MCHC = mean cell hemoglobin blood (10–20 mL/kg IV) or packed red blood concentration r DIAGNOSIS cells. MCV = mean cell volume r DIFFERENTIAL DIAGNOSIS MCVr = mean reticulocyte volume r r = Any cause of anemia, especially hemorrhage. PCV packed cell volume r r = Microcytic anemia in portosystemic shunt RDW red cell distribution width disease may or may not be due to iron MEDICATIONS Suggested Reading deficiency. r DRUG(S) Fry MM, Kirk CA. Reticulocyte indices in a Anemia of chronic inflammatory disease. Iron Supplementation canine model of nutritional iron deficiency. CBC/BIOCHEMISTRY/URINALYSIS Parenteral Iron Supplementation Vet Clin Path 2006, 35:172–181. r r PCV usually but not always decreased, Iron replacement therapy should be Steinberg JD, Olver CS. Hematologic and generally 10–40% in dogs. initiated with injectable iron. biochemical abnormalities indicating iron r r Anemia may be either regenerative or Iron dextran—a slowly released form of deficiency are associated with decreased nonregenerative. reticulocyte hemoglobin content (CHr) and r injectable iron; one injection (10–20 mg/kg Microcytosis—indicated by low normal or IM) followed by oral supplementation. reticulocyte volume (rMCV) in dogs. Vet low MCV, often accompanied by increased Oral Iron Supplementation Clin Path 2005,34:23–27. r heterogeneity, detected by erythrocyte Animals with severe iron deficiency have Thrall MA. Regenerative anemias. In: Thrall histogram widening or increased red cell impaired intestinal absorption of iron, MA, et al., Veterinary Hematology and distribution width (RDW) value. Clinical Chemistry. Baltimore: Lippincott r making oral supplementation of little value Newer erythrocyte indices, mean until partial iron repletion has occurred. Williams & Wilkins, 2004, pp. 95–98. r reticulocyte volume (MCVr) and reticulocyte Follow parenterally injected iron with oral Author Glade Weiser hemoglobin content (CHr), are sensitive for iron supplementation for 1–2 months, or Consulting Editor A.H. Rebar BLBS078-CF_A47 BLBS078-Tilley March 21, 2011 21:38

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

r Normal mean corpuscular volume and CONTRAINDICATIONS/POSSIBLE mean corpuscular hemoglobin concentration INTERACTIONS in most animals. BASICS r Variable according to underlying cause. Normocytic, normochromic, and OVERVIEW nonregenerative. r r Sometimes occurs concomitantly with Polychromasia on blood films only with diffuse diseases of the liver, kidney, and, rarely, accompanying blood loss (as with hepatic FOLLOW-UP spleen. hemangiosarcoma). r r In most animals with liver disease, WBC changes variable, based on underlying Monitor CBC periodically while treating the cause of hepatic or renal pathology. underlying condition. spiculated cells have 2–10 elongated, blunt, r finger-like projections from their surfaces and Inflammatory conditions likely to be are classified as acanthocytes. accompanied by inflammatory leukogram. r r Acanthocytic anemias can be associated Variable findings in liver and kidney with renal disease; anemias of renal disease function tests (serum biochemistry and MISCELLANEOUS more often have oval red cells with irregular urinalysis). SEE ALSO or ruffled membranes (burr cells). Hepatic Diseases r r r Anemia of Chronic Kidney Disease Rarely, acanthocytic anemias can be seen in High ALT, ALP, and γ -glutamyl transferase. r r Hemangiosarcoma, Spleen and Liver association with splenic disease alone. High bile acids, serum ammonia. r r ABBREVIATIONS Pathogenesis not entirely clear; abnormal Possibly low albumin and serum urea r ALP = alkaline phosphatase lipid metabolism with free cholesterol loading nitrogen. r r ALT = alanine aminotransferase of RBC membranes is most frequently Bilirubinuria, bilirubin crystals in urine. r implicated as cause. PCV = packed cell volume r Renal Diseases r r RBC = red blood cell Dogs with disseminated abdominal r High serum urea nitrogen, creatinine, and WBC = white blood cell hemangiosarcoma with liver involvement phosphorus. r often have acanthocytes. Highly variable urinalysis findings, Suggested Reading SIGNALMENT including isosthenuria (urine specific gravity Harvey JW. Atlas of Veterinary Hematology, Dogs and cats (infrequently) 1.008–1.025 in dogs; 1.008–1.035 in cats). Blood and Bone Marrow of Domestic r Tubular and/or protein casts. Animals. Philadelphia: Saunders, 2001, SIGNS r r Pyuria. p. 29. None in most animals (usually mild to r moderate condition). Proteinuria. Rebar AH. Hemogram Interpretation for r r Detection of spiculated RBCs on peripheral Hematuria. Dogs and Cats. Wilmington, DE: Gloyd blood film can be first marker for liver, OTHER LABORATORY TESTS Group for Ralston Purina Co., 1998, pp. 22–23. kidney, or splenic disease. None r In large-breed dogs with vague signs or large Rebar AH, Lewis HB, DeNicola DB, IMAGING Halliwell WH, Boon GD. Red blood cell spleen, suggests possibility of splenic or Abdominal radiographs and ultrasound— hepatic hemangiosarcoma. fragmentation in the dog: An editorial evaluate hepatic, renal, and splenic review. Vet Pathol 1981, 18:415–426. CAUSES & RISK FACTORS structure. r Rebar AH, MacWilliams PS, Feldman BF, Any disease of the liver, kidneys, or possibly DIAGNOSTIC PROCEDURES Metzger FL, Pollock RVH, Roche J. A spleen. r Liver or kidney biopsy if indicated. Guide to Hematology in Dogs and Cats. The likelihood of RBC morphologic Jackson, WY: Teton NewMedia, 2002, abnormalities parallels the severity of organ p. 36. involvement. r Thrall MA, Campbell TW, DeNicola D, Hemangiosarcoma involving the liver is a Fettman MJ, Lassen ED, Rebar A, Weiser frequent cause. TREATMENT r G. Veterinary Hematology and Clinical Observed in cats with fatty liver syndrome. Focus treatment on diagnosis and treatment Chemistry. Baltimore: Lippincott Williams of underlying hepatic, renal, or splenic & Wilkins, 2004, p. 96. disease. Weiser EG. Erythrocyte responses and disorders. In: Ettinger SJ, Feldman EC, eds. DIAGNOSIS Textbook of Veterinary Internal Medicine, 4th ed. Philadelphia: Saunders, 1995, DIFFERENTIAL DIAGNOSIS MEDICATIONS pp. 1864–1891. Determination of renal or hepatic causes Author Alan H. Rebar DRUG(S) based on results of biochemistry profile and Consulting Editor A.H. Rebar urinalysis. Variable according to underlying cause. CBC/BIOCHEMISTRY/URINALYSIS r Mild to moderately low PCV, RBC count, and hemoglobin. BLBS078-CF_A48 BLBS078-Tilley July 15, 2011 5:23

Canine and Feline, Fifth Edition 81 Anemia, Nonregenerative A

(AID)—most common cause of mild secondary to abortifacient therapy and Sertoli r nonregenerative anemia; anemia can be seen cell tumor). Infections—FeLV, FIV, BASICS within 3–10 days of infection, inflammation, ehrlichiosis, babesiosis, and parvoviral tissue injury, immune-mediated processes, infection (although recovery usually precedes r DEFINITION and local or disseminated neoplasia; increased development of anemia). Infiltrative Low RBC mass without evidence of a liver production of hepcidin along with processes— myelodysplasia, regenerative response (increased release of IL-1, interferon, and TNF from myeloproliferative disease, polychromasia or reticulocytosis) in the T-lymphocytes and macrophages lead to lymphoproliferative disease, metastatic peripheral blood. sequestration of iron within tissue neoplasia, myelofibrosis, and osteosclerosis. PATHOPHYSIOLOGY macrophages, decreased intestinal iron RISK FACTORS r r r absorption; low serum iron and transferrin, Renal failure Inflammatory or chronic Key feature is low or inadequate erythroid r r r increased concentration of macrophage (and disease process Liver failure Sertoli cell production or release. Onset of anemia and r r r serum) ferritin, decreased erythropoietin tumor Cancer Chronic blood loss Cats its related signs insidious unless RBC survival production, impaired marrow response to r is concurrently shortened by hemorrhage or from multicat households (FeLV) Lead r anemia and shortened RBC lifespan. r exposure—chronic hemolysis. May be caused by selective Chronic renal failure—kidneys fail to alteration in erythropoiesis or generalized produce adequate amount of erythropoietin; bone marrow injury affecting leukocytes and r uremic toxins shorten RBC lifespan and platelets as well. Mechanisms for selectively impair the response to erythropoietin. r DIAGNOSIS altered erythropoiesis include deficient Chronic liver disease—RBC morphologic hormonal stimulation, nutritional deficiency, changes (target cells and acanthocytes) and DIFFERENTIAL DIAGNOSIS cytokine-mediated sequestration of iron, and shortened RBC survival caused by changes in Regenerative anemia may initially appear disturbed metabolism in or destruction of RBC membrane lipids; decreased transferrin nonregenerative; sudden onset of signs more precursors; generalized bone marrow injury synthesis and impaired mobilization of consistent with regenerative than usually caused by a toxin, infection, or hepatic iron contribute to functional iron nonregenerative anemia; however, the latter r infiltrative process. deficiency. Endocrine disease—thyroid may appear to have an acute onset if SYSTEMS AFFECTED associated with a sudden exacerbation of a r hormones and cortisol stimulate Cardiovascular—heart murmur associated chronic primary condition. r erythropoiesis and facilitate the effect of with low blood viscosity. Hemic/Lymph/ LABORATORY FINDINGS r erythropoietin; mild anemia is commonly Immune. Hepatobiliary—centrilobular associated with hypothyroidism and can Disorders That May Alter Laboratory degeneration associated with hypoxic injury. occasionally be seen in patients with Results hypoadrenocorticism and hypopituitarism. r SIGNALMENT r Factors causing turbidity (lipemia) can r r Immune-mediated destruction of Varies with primary cause. Giant r falsely elevate hemoglobin and MCHC precursors–pure red cell aplasia. Infectious r schnauzers, border collies, beagles— > values. With lead toxicity, increased NRBC congenital cobalamin malabsorption. destruction of precursors (although usually may falsely elevate the WBC count. one cell line is involved), e.g., FeLV and SIGNS Valid If Run in Human Laboratory? ehrlichiosis, Cytauxzoon felis. r r General Comments Dogs—yes. Cats—yes, if lab’s hematology r r Nutritional or Mineral Deficiency Usually a secondary condition. Signs r instrument uses species-specific parameters; Iron deficiency—usually caused by chronic instruments designed strictly for analysis of associated with the primary disease often external blood loss; initially regenerative, but precede signs attributable to anemia. human specimens may under-count small as severity increases, anemia becomes feline RBCs. Historical Findings r r nonregenerative. Cobalamin (vitamin B12) CBC/BIOCHEMISTRY/URINALYSIS Lack of energy, exercise intolerance, and/or folate deficiency—rare in dogs and r CBC and Blood Smear inappetence, and cold intolerance. Other cats but can be caused by dietary insufficiency, r PCV, RBC count, and hemoglobin low. findings reflect the primary condition, such as malabsorption, or chronic drug r polyuria and polydipsia (e.g., CRF), paint administration (e.g., sulfas, methotrexate, and Anemia usually normocytic, normochromic, with normal MCV and exposure from remodeling old houses (e.g., anticonvulsants) that inhibits folate; r lead poisoning), living in multicat households congenital defect in cobalamin absorption MCHC. Macrocytosis (high (e.g., FeLV), and treating female dogs for reported in giant schnauzers, border collies, MCV)—without polychromasia suggests a mismating or urinary incontinence and and beagles; can occasionally cause nuclear maturation defect (cells skip a feminization in male dogs (e.g., normocytic or macrocytic anemia; division); seen in cats with FeLV; occasionally hyperestrogenism). megaloblastic changes may be seen in the caused by vitamin B12 or folate deficiency. r r Physical Examination Findings marrow. Disruption of precursor Microcytosis (low MCV)—suggests a r Pallor, heart murmur (severe anemia), and metabolism—chronic lead toxicity and cytoplasmic maturation defect (cells undergo r possibly tachycardia or polypnea. Signs possibly high concentrations of aluminum an extra division); iron deficiency the most reflecting the primary condition include and cadmium inhibit heme synthesis; common cause; in late stages, concurrent uremic breath and oral ulcerations (e.g., cadmium also reported to cause renal toxicity hypochromasia (low MCHC) common in CRF), cachexia (e.g., cancer), and impaired erythropoietin production. dogs but not in cats; also seen in approximately one-third of patients with lymphadenopathy and/or splenomegaly (e.g., Nonregenerative Anemia with Other hepatic insufficiency or vascular shunting. lymphoma), gastrointestinal or CNS signs Cytopenias r r Specific RBC morphologies-schistocytes (e.g., lead poisoning), symmetrical alopecia Toxicities—drugs or chemicals (e.g., cancer common with iron deficiency; acanthocytes (e.g., hypothyroidism and hyperestrogenism). chemotherapeutics, chloramphenicol, associated with cholestatic liver disease; target phenylbutazone, trimethoprim-sulfadiazine CAUSES cells associated with iron deficiency, liver zonisamide, phenobarbital, griseofulvin, r Nonregenerative Anemia without Other disease, and hypothyroidism. An methimazole, fenbendazole, albendazole, and Cytopenias inflammatory leukogram supports AID. r benzene), hormones (e.g., estrogen toxicity r Anemia of inflammatory disease Thrombocytosis often accompanies iron BLBS078-CF_A48 BLBS078-Tilley July 15, 2011 5:23

82 Blackwell’s Five-Minute Veterinary Consult

A Anemia, Nonregenerative (Continued)

r deficiency. A high number of NRBCs DIAGNOSTIC PROCEDURES CRF (see Anemia of Chronic Kidney r without polychromasia or disproportionate to Cytologic Examination of Bone Marrow Disease). Iron supplementation in patients the degree of anemia and polychromasia seen with iron deficiency anemia (see Anemia, and Core Biopsy r in animals with lead toxicity, extramedullary r Iron-Deficiency). May supplement with Cytologic examination of an aspirate r hematopoiesis, heat stroke, and injury to bone indicated in all patients unless the primary folic acid at a rate of 4–10 mg/kg/day. May marrow stroma by endotoxemia or hypoxia. cause is readily apparent (e.g., AID and CRF). supplement with cobalamin (vitamin B12)ata r r RBC or WBC precursors in the peripheral Bone marrow biopsy—useful in evaluation rate of 100–200 mg/day PO (dogs) or blood without orderly progression to more of bone marrow architecture and overall 50–100 mg/day PO (cats); parenteral mature forms suggest myelodysplasia or cellularity; important for diagnosis of aplastic administration (0.5–1 mg IM weekly to once myeloproliferative disease (leukemia). r every few months) needed in giant r marrow or myelofibrosis. Erythroid Concurrent cytopenia in other cell lines hypoplasia or aplasia confirms the problem, schnauzers, beagles, or border collies with without evidence of marrow responsiveness although history and other tests, as indicated inherited cobalamin malabsorption. (e.g., band neutrophils and macroplatelets) above, may be needed to determine the PRECAUTIONS r suggests generalized bone marrow injury. underlying etiology. Myeloid hyperplasia r Monitor for transfusion reactions in patients Serum Biochemistry and Urinalysis and high iron stores support AID. Absence r receiving multiple transfusions. High BUN and creatinine with inadequate of canine (but not feline) bone marrow iron urine concentration (dogs, < 1.030; cats, stores, which occurs before microcytosis, r < 1.035) support anemia of CRF. High supports iron deficiency; classically, iron ALT, total bilirubin suggest liver disease. deficiency associated with an expanded r FOLLOW-UP High serum cholesterol (> 500 mg/dL) erythron and high numbers of r < r PATIENT MONITORING strongly suggests hypothyroidism. Na/K metarubricytes. Increased r In patients with severe anemia, PCV and 23, lymphocytosis, and eosinophilia in ill erythrophagocytosis suggests injury to cells r (e.g., immune-mediated and toxic causes). blood smear examination every 1–2 days. In dogs suggest hypoadrenocorticism. r OTHER LABORATORY TESTS An incomplete maturation sequence stabilized animals with chronic or slowly r suggests injury to a specific maturation stage improving disease course, reevaluation every Reticulocyte count—value of < 60,000/μL (e.g., immune-mediated and toxic causes) or 1–2 weeks. in dogs or < 50,000/μL in cats accompanied possibly incomplete recovery from a previous by a low PCV confirms nonregenerative r r injury (recheck in 3–5 days). A disorderly anemia. Direct antiglobulin test maturation sequence and atypical cellular (Coombs’)—immune-mediated destruction morphology suggest myelodysplastic MISCELLANEOUS of erythroid precursors can lead to anemia r syndrome. A hypercellular marrow with a without reticulocytosis; spherocytosis, PREGNANCY/FERTILITY/BREEDING high number of blast cells (> 20% of autoagglutination, or positive Coombs’ test nucleated cells) indicates hematopoietic Some pregnant animals have a mildly low provides support for immune-mediated r neoplasia; immunophenotyping and PCV, caused by an expanded blood volume. anemia. Serum iron profile—indicated for cytochemical stains used to identify the patients with microcytic anemia; in patients affected cell line(s); circulating neoplastic cells SYNONYMS with iron deficiency, serum iron is low, total r may or may not be seen. Non-marrow cells Non-responsive anemia iron-binding capacity varies, and serum indicate metastatic neoplasia. ABBREVIATIONS ferritin is low; in patients with AID, serum r ACTH = adrenocorticotropic hormone iron is low but serum ferritin is high (MCV r r AID = anemia of inflammatory disease and MCHC usually normal). Bile acids r r ALT = alanine aminotransferase CNS = measurement—may be indicated for r TREATMENT central nervous system CRF = chronic renal evaluation of microcytic anemia and r r r failure FeLV = feline leukemia virus FIV confirmation of hepatic insufficiency or Nonregenerative anemia usually resolves r r = feline immunodeficiency virus IL-1 = vascular shunting. Serum lead with resolution of the underlying disease. r r interleukin-1 MCHC = mean corpuscular measurement—indicated when NRBCs are Conditions associated with severe anemia or r hemoglobin concentration MCV = mean present, especially when the patient has pancytopenia often carry a guarded-to-poor r cell volume NRBC = nucleated red blood concurrent gastrointestinal or CNS signs; a prognosis and may involve long-term r value > 30 μL/dL (0.3 ppm) strongly treatment without complete resolution. cells PCR = polymerase chain reaction r r r r supports lead intoxication. Serologic Metabolic compensation occurs with slowly TNF = tumor necrosis factor TSH = testing—FeLV test in any cat with developing nonregenerative anemia; thus mild thyroid stimulating hormone nonregenerative anemia; Ehrlichia canis, to moderately severe anemia (PCV > 15%) INTERNET RESOURCES Anaplasma phagocytophilia (E. equi), and generally requires no supportive intervention. Erythrocytes: Overview, Morphology, r < Babesia titers or PCR assays may be indicated For patients with severe anemia (PCV Quantity; A.H. Rebar, P.S. MacWilliams, B.F. in dogs with unexplained anemia, especially 10–15%), the degree of hypoxia will probably Feldman, et. al.: http://www.ivis.org/ when concurrent with thrombocytopenia or r require restricted exercise, transfusions, or advances/Rebar/Chap4/chapter.asp?LA = 1 hyperglobulinemia. Endocrine r both. If blood volume and tissue perfusion Suggested Reading testing—indicated when clinical signs and are compromised by concurrent blood loss or Feldman BF. Nonregenerative anemia. In: laboratory tests suggest a possible endocrine shock, administer lactated Ringer’s solution or Ettinger SJ, Feldman EC, eds., Textbook of disorder; thyroid: T4,freeT4, and TSH colloids. concentrations; adrenal: low-dose Veterinary Internal Medicine: Diseases of dexamethasone suppression test and the Dog and Cat, 6th ed. Philadelphia: ACTH-stimulation test. Elsevier Saunders, 2005, pp. 1908–1917. Author Joyce S. Knoll MEDICATIONS Consulting Editor A.H. Rebar DRUG(S) r Erythropoietin in patients with anemia of BLBS078-CF_A49 BLBS078-Tilley July 15, 2011 5:29

Canine and Feline, Fifth Edition 83 Anemia, Nuclear Maturation Defects (Anemia, Megaloblastic) A

r In cats, anemia can be mild to severe. avoided in patients whose condition results r Anemia classically macrocytic (high mean from other causes. BASICS corpuscular volume) and normochromic (normal mean corpuscular hemoglobin OVERVIEW concentration). r r Nonregenerative anemia characterized by Large, fully hemoglobinized RBC; FOLLOW-UP occasional to numerous megaloblasts, r arrested development of the nuclei of RBC Monitor response to treatment by CBC particularly at the feather edge; minimal to no precursors (as a result of interference with (weekly) and occasional bone marrow polychromasia. DNA synthesis) while the cytoplasm develops r collection and evaluation. In cats with FeLV, anemia may occur in r normally (nuclear-cytoplasmic asynchrony). Closely monitor FeLV-positive cats for r association with a myelodysplastic syndrome Affected RBC precursors fail to divide evidence of onset of other signs of or in conjunction with leukemia of a different normally and thus are larger than hematopoietic dyscrasia in the peripheral cell line. corresponding normal precursors with the blood and bone marrow. r same degree of cytoplasmic maturity OTHER LABORATORY TESTS Prognosis—depends on underlying cause; in (hemoglobinization); because their nuclei are FeLV FeLV-positive cats, prognosis guarded; in deficient in chromatin (DNA), they have a IMAGING animals with drug-associated anemia, distinctive open and stippled appearance; N/A prognosis good when use of offending drug is these giant precursors with atypical, immature interrupted. nuclei are known as megaloblasts. OTHER DIAGNOSTIC PROCEDURES r Although these asynchronous changes are Bone Marrow Biopsy r most prominent in RBC precursors, WBC In dogs, usually hyperplastic, often in all cell and platelet precursors are similarly affected. lines. r MISCELLANEOUS SIGNALMENT In cats, marrow findings are highly variable r SEE ALSO Dogs and cats. and may be hyper- to hypocellular. r r r Anemia, Nonregenerative Spontaneous, clinically unimportant Maturation arrest with nuclear and r occurrence in toy poodles (occasional). cytoplasmic asynchrony in all cell lines. Feline Leukemia Virus Infection r r Breed predilection: giant schnauzers with Many megaloblastic RBC precursors may be ABBREVIATIONS r inherited cobalamin malabsorption. observed. FeLV = feline leukemia virus r r r Defect usually acquired. Macrophagic hyperplasia with active PCV = packed cell volume r SIGNS phagocytosis of nucleated RBCs and RBC = red blood cell r megaloblasts (common). r = In dogs, generally mild, usually not WBC white blood cell clinically important. r Suggested Reading In cats with FeLV-associated nuclear Harvey JW. Atlas of Veterinary Hematology, maturation anemia, FeLV-related signs can be Blood and Bone Marrow of Domestic anticipated. Anemia may be mild to severe. TREATMENT r Animals. Philadelphia: Saunders, 2001, CAUSES & RISK FACTORS Treat by targeting the underlying cause if pp. 135–137. r possible. Infectious—FeLV; retroviral infection the r Rebar AH. Hemogram Interpretation for most common cause of megaloblastic anemia Except for that occurring with FeLV in cats, Dogs and Cats. Wilmington, DE: Gloyd in cats. megaloblastic anemia is a relatively mild Group for Ralston Purina Co., 1998, r condition. p. 23. Nutritional—folic acid and vitamin B12 r deficiencies. Treatmostpatientsonanoutpatientbasis. Rebar AH, MacWilliams PS, Feldman BF, r Toxic—phenytoin (Dilantin) toxicity and Metzger FL, Pollock RVH, Roche J. A methotrexate toxicity (folate antagonist). Guide to Hematology in Dogs and Cats. r Congenital—toy poodles. Jackson, WY: Teton NewMedia, 2002, MEDICATIONS pp. 57–58. Thrall MA, Campbell TW, DeNicola D, DRUG(S) r Fettman MJ, Lassen ED, Rebar A, Weiser In animals with drug toxicity, discontinue G. Veterinary Hematology and Clinical DIAGNOSIS the offending drug. r Chemistry. Baltimore: Lippincott Williams DIFFERENTIAL DIAGNOSIS In all animals, consider supplementation & Wilkins, 2004, pp. 161–162. r with folic acid (4–10 mg/kg/day) or vitamin In dogs, all other mild to moderate Weiser EG. Erythrocyte responses and B (dogs, 100–200 mg/day PO; cats, nonregenerative anemias, including anemia of 12 disorders. In: Ettinger SJ, Feldman EC, eds. 50–100 mg/day PO). inflammatory disease, renal disease, and lead r Textbook of Veterinary Internal Medicine, Giant schnauzers with inherited cobalamin poisoning. 4th ed. Philadelphia: Saunders, 1995, r malabsorption require parenteral treatment Differentiation based on the distinctive pp. 1864–1891. with vitamin B (0.5–1 mg IM weekly to CBC and bone marrow findings listed. 12 Author Alan H. Rebar r every few months). In cats, FeLV infection is the primary Consulting Editor A.H. Rebar differential. CONTRAINDICATIONS/POSSIBLE CBC/BIOCHEMISTRY/URINALYSIS INTERACTIONS r In dogs, mild to moderate anemia (PCV: Drugs known to cause megaloblastic anemia 30–40%). (e.g., methotrexate and phenytoin) should be BLBS078-CF_A50 BLBS078-Tilley July 23, 2011 4:43

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

English sheepdogs, poodles, and Shetland propofol, dl-methionine (cats), phenolic sheepdogs, have a predisposition to compounds (moth balls), and r BASICS immune-mediated syndromes, such as SLE phenazopyridine (cats). In cats, some and immune-mediated hemolytic anemia. systemic diseases (e.g, diabetes mellitus, DEFINITION SIGNS hyperthyroidism, and lymphoma) enhance r r Characterized by a decreased circulating RBC Pallor. Weakness, exercise intolerance. Heinz body formation but do not necessarily r r mass (as indicated by low PCV, hemoglobin, Anorexia. Possible heart murmur, cause anemia. r and total RBC count) accompanied by tachycardia, bounding pulses. Possible Erythrocyte Parasites r r appropriate, compensatory increase in RBC jaundice and hemoglobinuria. Petechiae, Mycoplasma haemofelis (formerly production by the bone marrow (e.g., epistaxis, melena suggest blood loss due to Haemobartonella felis), M. haemominutum, reticulocytosis in the peripheral blood and r M. turicensis,andM. haematoparvum (cats). vasculitis or a platelet problem. Hematomas r RBC hyperplasia in the bone marrow). or cavity bleeds suggest a coagulopathy. Mycoplasma haemocanis (formerly H. canis; r r PATHOPHYSIOLOGY Clinical signs depend on the degree of dogs). Babesia canis and B. gibsoni (dogs). r r r Regenerative anemia caused by blood loss or anemia and rapidity of onset. Rapid loss of Cytauxzoon felis (domestic shorthair and r 15–25% of blood volume or acute hemolysis bobcats). hemolysis. Hemolysis—caused by intrinsic r RBC defects (e.g., congenital RBC membrane results in shock and possible death. With Mechanical RBC Fragmentation r defects or enzyme deficiencies) or extrinsic chronic anemia, compensatory increases in Thromboembolic disease (e.g., DIC). r r r factors such as RBC parasites, oxidative heart rate, and eventually heart size, lessens Heartworm disease. Vasculitis. Liver, r injury, hemolysins, osmotic changes, the RBC circulation time; hemoglobin can kidney or heart disease. Neoplasia (e.g., r immune-mediated RBC destruction, heat drop to as low as 50% of the minimum hemangiosarcoma). Splenic torsion. r stroke, and severe hypophosphatemia. normal value without overt signs of hypoxia. Hemolytic-uremic syndrome. r Intravascular hemolysis may lead to DIC CAUSES Inherited RBC Abnormalities r r and hemoglobinuria. Hemolytic anemia Immune Mediated Pyruvate kinase deficiency—impaired RBC r usually more regenerative than blood loss Antibodies, immune complexes, and/or glucose use and ATP formation, leading to anemia; external blood loss depletes body of complement on the RBC surface shorten premature destruction of RBCs; autosomal r both cells and iron; hemolysis conserves iron, RBC lifespan. Antibodies may target RBC recessive trait. Phosphofructokinase which is readily available for reuse in RBC membrane components or may be directed deficiency—marked alkaline fragility caused production, making hemolytic anemia against tumor antigens, infectious agents, by impaired synthesis of generally more responsive. vaccines, or drugs (e.g., sulfonamides, 2,3-diphosphoglycerate; hemolytic episodes SYSTEMS AFFECTED penicillins, cephalosporins, methimazole, triggered by hyperventilation-induced r amiodarone) that are either directly adherent alkalemia such as occurs after vigorous Cardiovascular—murmurs with marked r anemia; tachycardia with severe rapid-onset to RBC surface or part of immune complexes exercise. Increased RBC osmotic fragility r r anemia. Hemic/Lymph/Immune—marked adherent to RBCs. Hemolysis may be either leads to recurrent severe anemia and intravascular or extravascular. IgG-coated splenomegaly. The responsible RBC defect RBC hyperplasia in the bone marrow; EMH r in the spleen; splenomegaly due to EMH and RBCs are typically engulfed by splenic has not been identified. Spectrin deficiency histiocytic hyperplasia can be a feature of macrophages. IgM-coated RBCs are often leads to destabilization of RBC membranes, r destroyed through activation of complement. leading to increased RBC osmotic fragility; extravascular hemolytic anemia. Hepatic— r anoxia causes centrilobular degeneration of Hemolytic antibodies are generally reactive autosomal dominant trait; unclear if this r r the liver. Renal—severe intravascular at body temperature; rarely cold-acting results in hemolytic anemia. Feline hemolysis can (rarely) lead to renal tubular antibodies cause in vivo hemolysis and/or congential porphyria—deficiency in RBC agglutination in cooler, peripheral uroporphyrinogen III cosynthetase in Siamese necrosis and acute renal failure. r SIGNALMENT vasculature. Transfusion of a blood type B cats causes an inability to produce normal r cat with type A blood can result in rapid, amounts of hemoglobin; coproporphyrin and No breed, age, or sex predilections for the severe, intravascular hemolysis; neonatal uroporphyrin accumulate, causing brown-red broad category of regenerative anemia. r isoerythrolysis seen in kittens born to a blood discoloration of teeth and bones, Pyruvate kinase deficiency—basenjis, type B queen mated to a blood type A tom. photosensitivity, and severe hemolytic anemia; beagles, cairn terriers, Chihuahuas, r Canine blood type DEA 1.1 can cause a second, less severe autosomal dominant trait dachshunds, miniature poodles, pugs, West hemolysis in a DEA 1.1-negative dog, in domestic shorthair cats causes tissue Highland white terriers, and American although a single incompatible transfusion discoloration without anemia or Eskimo; and Somali, Abyssinian, and r can be tolerated. The newly identified blood photosensitivity. domestic shorthair cats. r types Mik (cats) and Dal (dogs) can cause Phosphofructokinase deficiency—English Blood Loss significant hemolytic transfusion reactions in r r springer spaniels, American cocker spaniels, Trauma. Bleeding neoplasms (e.g., animals lacking these common RBC antigens. and mixed breed dogs with spaniel parentage. hemangiosarcoma, intestinal r Oxidant Injury r Spectrin deficiency has been reported in r adenocarcinoma). Coagulopathies (e.g., r Oxidants can cause Heinz body formation warfarin poisoning, hemophilia, and golden retrievers. Marked RBC osmotic r fragility—English springer spaniels and (aggregates of oxidized hemoglobin), thrombocytopenia). Bloodsucking parasites Abyssinian, Somali, Siamese, and domestic eccentrocytes (oxidation of RBC membranes), (e.g., fleas, ticks, and Ancylostoma). r r r shorthair cats. Feline congenital and methemoglobinemia. Damaged RBCs Gastrointestinal ulcers. porphyria—Siamese and domestic shorthair are prematurely removed from the circulation r cats. Some breeds of dogs have a genetic (extravascular hemolysis). Destabilization of RBC membranes causes intravascular predisposition for heritable coagulopathies r such as factor VIII deficiency and von hemolysis. Oxidants include onions and r DIAGNOSIS Willebrand disease. Middle-aged female garlic, acetaminophen (especially in cats), zinc DIFFERENTIAL DIAGNOSIS dogs, especially American cocker spaniels, (from pennies minted after 1982, zinc oxide English springer spaniels, Irish setters, Old ointment, and zinc bolts), acute copper Differentiated from nonregenerative anemia toxicosis, benzocaine, vitamin K3 (dogs), by high reticulocyte count. BLBS078-CF_A50 BLBS078-Tilley July 23, 2011 4:43

Canine and Feline, Fifth Edition 85

(Continued) Anemia, Regenerative A

LABORATORY FINDINGS 60,000/μL (dogs) suggests regenerative r Disorders That May Alter Laboratory anemia. The reticulocyte% should be Results corrected for the degree of anemia; formula = r MEDICATIONS Lipemia can cause mild in vitro hemolysis, reticulocyte% × (PCV/normal PCV); normal without appreciable anemia, and may falsely PCV: cat 37, dog 45; corrected reticulocyte% DRUG(S) r r r elevate MCHC. Autoagglutination may > 1% suggests a regenerative response. It Blood-loss anemias—administration of iron falsely decrease the RBC count. takes 3–5 days for the bone marrow to mount may benefit animals with chronic blood-loss a peak regenerative response to anemia, so anemia (see Anemia, Iron-Deficiency). Valid If Run in Human Laboratory? r r r reticulocytosis may initially be absent with Hemolytic anemias—varies with cause of Dogs—yes. Cats—yes, if lab’s hematology r acute blood loss or hemolysis. Direct instrument uses species-specific parameters; hemolysis. antiglobulin test (Coombs’ test) indicated instruments designed for analysis of human when immune-mediated hemolytic anemia specimens may under-count small feline r suspected; a positive test and evidence of RBCs. Human labs, unfamiliar with feline spherocytosis and polychromasia in the FOLLOW-UP punctuate reticulocytes, may include them in peripheral blood is confirmatory; both false the reticulocyte count, overestimating the PATIENT MONITORING negatives and false positives are possible, so r regenerative response. Initially, measurement of RBC mass (e.g., the test must be interpreted cautiously. CBC/BIOCHEMISTRY/URINALYSIS PCV, RBC count, and hemoglobin) and r DIAGNOSTIC PROCEDURES PCV, RBC count, and hemoglobin low. r morphologic features on a blood film (i.e., r Bone marrow aspirate—needed only when Total protein is often low with blood loss polychromasia) every 24 hours to monitor there is no evidence of RBC responsiveness in anemia and may be the only sign of effectiveness of treatment and bone marrow the peripheral blood (i.e., no reticulocytosis); r hemorrhage in dogs with acute blood loss; responsiveness. As regeneration becomes RBC hyperplasia confirms a regenerative normal PCV may be maintained through apparent (rising RBC values and r response; absence of RBC hyperplasia means transient splenic contraction. The severity r polychromasia), recheck patients every 3–5 that the anemia is nonregenerative. Bone of acute blood loss may be underestimated days; return to normal values should occur marrow biopsy—useful in evaluation of bone until the plasma volume has been restored by about 14 days after acute hemorrhage but marrow architecture and overall cellularity; fluid administration and/or internal fluid may take longer with an immune-mediated r important for confirmation of a shifts. RBC indices vary depending on the process. nonregenerative process. cause of anemia and degree of regenerative response—MCV, normal to high; MCHC, normal to low in most patients; MCHC, MISCELLANEOUS artificially high with intravascular hemolysis r and hemoglobinemia. With iron deficiency TREATMENT SEE ALSO r r owing to chronic blood loss, dogs may have a r Anemia, Heinz Body Anemia, Emergency if anemia is severe and develops r low MCV, MCH, and MCHC; cats have a r Immune-Mediated Anemia, rapidly. Massive hemorrhage leads to r r low MCV but normal MCH and MCHC. Iron-Deficiency Babesiosis Bartonellosis r hypovolemic shock and anoxia; acute r r Specific RBC morphologies may suggest a r Cytauxzoonosis Lupus Erythematosus, hemolysis leads to anoxia. Cage rest and r cause of hemolysis: marked spherocytosis careful observation indicated, depending on Systemic Zinc Toxicity suggests immune-mediated disease; Heinz severity of clinical signs. ABBREVIATIONS r r bodies or eccentrocytes suggest oxidant BLOOD LOSS ANEMIAS ATP = adenosine triphosphate DIC = injury; and numerous schistocytes suggest r r With major traumatic blood loss leading to disseminated intravascular coagulation microangiopathy. Spherocytes, formed r shock, crystalloid fluids can rapidly correct EMH = extramedullary hematopoiesis through incomplete RBC phagocytosis, r hypovolemia and restore circulation. Colloid MCH = mean corpuscular hemoglobin cannot be as easily detected in cats because r solutions (e.g., dextran 70) can produce a MCHC = mean corpuscular hemoglobin RBCs generally lack central pallor. r r r slightly greater volume expansion. RBC concentration MCV = mean cell volume Agglutinated RBCs indicate anemia is r r replacement (packed RBCs or whole blood) is PCV = packed cell volume RBC = red immune mediated; autoagglutination must be r indicated if PCV is < 15–20% and signs of blood cell SLE = systemic lupus distinguished from rouleaux by generous r hypoxia are severe (i.e., extremely pale erythematosus sample dilution with saline. Hemolysis may mucous membranes, weakness, tachycardia, cause an inflammatory leukogram INTERNET RESOURCES and tachypnea), or oxyhemoglobin (30 (neutrophilia with a left shift and Erythrocytes: Overview, Morphology, mL/kg at rate of 10 mL/kg/hr; OPK Biotech, monocytosis). Acute blood loss may be Quantity; A.H. Rebar, P.S. MacWilliams, Cambridge, MA) can provide both oncotic associated with a stress leukogram (mild r B.F. Feldman, et al.: http://www.ivis.org/ r pressure and an oxygen transporter. Animals neutrophilia and lymphopenia). Blood loss advances/Rebar/Chap4/chapter.asp?LA = 1. with chronic blood loss are normovolemic may be accompanied by either with increased cardiac output, therefore Suggested Reading thrombocytopenia or rebound transfusion volumes and rates should be Giger U. Regenerative anemias caused by thrombocytosis; iron deficiency is often conservative to avoid cardiac failure. Cats are blood loss or hemolysis. In: Ettinger SJ, accompanied by thrombocytosis. r prone to volume overload. Feldman EC, eds., Textbook of Veterinary Hyperbilirubinemia and bilirubinuria Internal Medicine: Diseases of the Dog and accompany marked hemolysis; HEMOLYTIC ANEMIAS Cat, 6th ed. Philadelphia: Elsevier Saunders, hemoglobinemia and hemoglobinuria seen Blood transfusion or oxyhemoglobin may be 2005, pp. 1886–1907. with intravascular hemolysis. indicated; in patients with an Author Joyce S. Knoll OTHER LABORATORY TESTS immune-mediated process, RBCs probably Consulting Editor A.H. Rebar r survive similarly to the patient’s own RBCs, In an anemic animal, an absolute so transfusion should not be withheld if reticulocyte count (RBC count × marked signs of anemia are present. reticulocyte%) > 50,000/μL(cats)or> BLBS078-CF_A51 BLBS078-Tilley July 15, 2011 9:18

86 Blackwell’s Five-Minute Veterinary Consult A Anisocoria

r SIGNALMENT Iris atrophy or hypoplasia r Dogs and cats Posterior synechia r Pharmacologic blockade BASICS SIGNS r Neoplasia Unequal pupils r DEFINITION Spastic pupil syndrome CAUSES Inequality of pupil size. RISK FACTORS Neurologic PATHOPHYSIOLOGY r N/A r See Table 1. r Interruption of sympathetic or Disease affecting optic nerve, optic tract, parasympathetic innervation of the oculomotor nerve, or cerebellum pupil—causes altered pupil size. r Ocular Ocular disease. r DIAGNOSIS See Table 2 SYSTEMS AFFECTED r r Anterior uveitis DIFFERENTIAL DIAGNOSIS Nervous r r r Glaucoma Must determine which pupil is Ophthalmic abnormal—see Figure 1.

Table 1 Neurologic lesions causing anisocoria.

Lesion Neurologic Signs Differential Diagnosis Diagnostic Plan

Optic nerve Ipsilateral mydriasis Optic neuritis neoplasm CT/MRI Ipsilateral monocular anopia (total blindness Infectious, inflammatory disease CSF in one eye) Electroretinogram (ERG) No direct PLR affected eye Consensual PLR affected eye Oculomotor nerve Ipsilateral dilated pupil Neoplasm CT/MRI Parasympathetic Normal vision/no direct PLR No consensual Infectious/inflammatory disease CSF nucleus CN III PLR from opposite eye Trauma Ultrasound orbit Ptosis upper eyelid Brain herniation Ventrolateral strabismus Retrobulbar mass

Cerebellar disease Contralateral mydriasis Neoplasm CT/MRI Normal PLR/normal vision Infectious/inflammatory disease CSF Ipsilateral lack of menace response Trauma Other cerebellar signs

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 Old age change Iris hypoplasia Sluggish/absent PLR, irregular pupil margin, other ocular abnormalities Congenital Pharmacological blockade Mydriasis Atropine Absent direct/consensual PLR Normal vision Spastic pupil syndrome Miosis, normal vision FeLV BLBS078-CF_A51 BLBS078-Tilley July 15, 2011 9:18

Canine and Feline, Fifth Edition 87

(Continued) Anisocoria A

Figure 1.

r r Iris Atrophy Distinguish between neurologic and ocular CONTRAINDICATIONS r causes. N/A Optic Neuritis ABBREVIATIONS CBC/BIOCHEMISTRY/URINALYSIS PRECAUTIONS r CNS = central nervous system N/A N/A r CSF = cerebrospinal fluid OTHER LABORATORY TESTS POSSIBLE INTERACTIONS r CT = computed tomography r N/A N/A ERG = electroretinogram r IMAGING ALTERNATIVE DRUG(S) FeLV = feline leukemia virus r r MRI = magnetic resonance imaging See Table 1. N/A r r PLR = pupillary light reflex Ultrasound—identifying ocular and r retrobulbar lesions. VEP = visual-evoked potential r CT and MRI—localizing and identifying INTERNET RESOURCES CNS lesions. FOLLOW-UP http://www.emedicine.com/oph/topic160 DIAGNOSTIC PROCEDURES .htm. r PATIENT MONITORING See Table 1. r N/A Suggested Reading CSF tap—evaluate CNS disease. r POSSIBLE COMPLICATIONS Neer TM, Carter JD. Anisocoria in dogs and ERG—evaluate retinal function. r cats. Ocular and neurologic causes. VEP—evaluate optic nerve function. N/A r Compend Contin Educ Pract Vet 1987, Pharmacologic testing—see Algorithm 1; 9:817–824. postganglionic lesions cause denervation Scagliotti RH. Comparative supersensitivity; direct-acting MISCELLANEOUS neuro-ophthalmology. In: Gelatt KN, ed., (para)sympathomimetic drugs cause the pupil Veterinary Ophthalmology, 3rd ed. to constrict or dilate. r ASSOCIATED CONDITIONS Philadelphia: Lippincott Williams & Preganglionic lesions—respond to N/A Wilkins, 1999, pp. 1307–1400. indirect-acting (para)sympathomimetics. AGE-RELATED FACTORS Author David Lipsitz Consulting Editor Paul E. Miller N/A ZOONOTIC POTENTIAL TREATMENT N/A Client Education Handout available online Depends on underlying disease. PREGNANCY/FERTILITY/BREEDING N/A SEE ALSO r Anterior Uveitis—Cats r MEDICATIONS Anterior Uveitis—Dogs r Glaucoma DRUG(S) OF CHOICE r Depends on underlying disease. Horner’s Syndrome BLBS078-CF_A52 BLBS078-Tilley March 21, 2011 22:1

88 Blackwell’s Five-Minute Veterinary Consult A Anorexia

r necrosis factor, and interferon. Toxicities and drugs. r r The expected upregulation of dietary intake Pain. r in response to elevated energy expenditure is Endocrine and metabolic disease. BASICS r frequently lost in cancer patients. Neoplasia. r r DEFINITION Decreased appetite associated with aging, Infectious disease. r the so-called anorexia of aging, predisposes Immune mediated disease. The lack or loss of appetite for food; appetite r older patients to protein-energy malnutrition Respiratory disease. is psychological and its existence in animals is r and is probably mediated by CCK and an Gastrointestinal disease. assumed. Hunger is physiologically aroused r enhanced satiating effect of small intestinal Musculoskeletal disease. by the body’s need for food. Anorexia may be r carbohydrates. Neurologic disease. partial or complete. Anorexia results in r r Exogenous and endogenous toxins (e.g., Anorexia of aging. decreased food intake, which then leads to r renal and liver failure) cause anorexia. Miscellaneous (e.g., motion sickness, high weight loss. Pseudoanorexia is associated with r the inability to prehend or swallow food Any disorder that decreases cerebral arousal environmental temperature). rather than actual loss of appetite. will potentially decrease food intake. Pseudoanorexia r r PATHOPHYSIOLOGY Gastroparesis associated with neoplasia, Any disease causing painful or dysfunctional r metabolic disorders, and primary prehension, mastication, and swallowing. The control of appetite is a complex r gastrointestinal disease is associated with Stomatitis, glossitis, gingivitis, pharyngitis, interaction between the central nervous decreased appetite. system and the periphery. r and esophagitis (e.g., physical agents, caustics, r Fear, pain, and stress may decrease appetite. The hypothalamus and brainstem contain bacterial or viral infections, foreign bodies, SYSTEMS AFFECTED immune-mediated diseases, uremia). peptidergic feeding-regulatory neurons that r act as input stations for hormonal and All body systems Retropharyngeal disorders (e.g., gastrointestinal information. These cell SIGNALMENT lymphadenopathy, abscess, hematoma, sialocele). populations project to several brain regions r Species Dental disease or periodontal disease. and interconnect extensively. r r Dogs and cats Retrobulbar abscess. Peripheral signals that affect appetite r include the palatability, texture, and quantity Breed Predilections Oral, glossal, pharyngeal, or esophageal of recently consumed food. N/A neoplasia. r r Satiety is influenced by gastric and duodenal Mean Age and Range Neurologic disorders (e.g., rabies; distention in addition to the presence of N/A neuropathies of cranial nerves V, VII, IX, X, XII; and central nervous system lesions). nutrients in the gastrointestinal tract. Predominant Sex r r Musculoskeletal lesions (e.g., masticatory Hunger is affected by plasma concentrations N/A of glucose and fatty acids, by interacting with myositis, temporomandibular joint disease, SIGNS nutrient-specific receptors in the liver and fractures, craniomandibular osteopathy, gastrointestinal tract. Historical Findings myasthenia gravis, botulism, and r r cricopharyngeal achalasia). Decreased and increased oxidative Refusal to eat is a common complaint r metabolism by the liver leads to hunger and presented by pet owners because poor appetite Salivary gland neoplasia or inflammation. satiety, respectively. is strongly associated with illness. RISK FACTORS r r Learned behavior and circadian rhythms Patients with disorders causing dysfunction N/A modulate appetite and may override other or pain of the face, neck, oropharynx, and signals for satiety and hunger. esophagus may display an interest in food but r Leptin is primarily produced by adipocytes cannot eat. These patients are referred to as being pseudoanorectic. and acts on specific hypothalamic receptors to r DIAGNOSIS decrease metabolism and decrease appetite. Animals lacking a sense of smell (anosmia) r Neuropeptide Y released from the often show no sniffing behavior. DIFFERENTIAL DIAGNOSIS r r gastrointestinal tract induces hunger and Weight loss may be noted. Question owners about the patient’s interest hyperphagia, and decreases energy Physical Examination Findings in food and ability to prehend, masticate, and expenditure after food restriction. r swallow food. r Clinical signs in anorexia vary depending on r Cholecystokinin and bombesin released the underlying cause but include fever, pallor, Perform a thorough ophthalmic, dental, from the gastrointestinal tract decrease icterus, pain, changes in organ size, ocular oropharyngeal, facial, and cervical appetite. r changes, abdominal distention, dyspnea, examination (sedation or anesthesia may be Ghrelin produced by the stomach is a muffled heart and lung sounds, adventitious required) in addition to observing the patient prokinetic and decreases leptin and increases eating to rule out pseudoanorexia. lung sounds, cardiac murmurs, and masses. r neuropeptide Y production. r r Pseudoanorectic patients commonly display Elicit a thorough history regarding the Serotonin is an important and perhaps final weight loss, halitosis, excessive drooling, patient’s environment, diet, changes in mediator centrally via a serotonergic tract that difficulty in prehending and masticating food, routine, people, or other pets to help identify passes near the ventromedial hypothalamus. potential psychological etiologies. r and odynophagia (painful swallowing). r Dopaminergic tracts in the hypothalamus CAUSES A complete physical examination is help regulate food intake and are closely required to determine the presence of associated with the lateral hypothalamus Anorexia systemic disease. r r (classical feeding center). Almost any systemic disease process can A database including a complete blood r cause anorexia. Appetite is stimulated by aldosterone and r count, serum biochemistry panel, urinalysis, corticosterone and suppressed by glucagons Psychological—unpalatable diet, food heartworm serology, retrovirus serology, and somatostatin. aversion, stress, alterations in routine and abdominal and thoracic imaging studies, r environment. Inflammatory and neoplastic disease can r endoscopy, and histologic/cytologic Acid-base disorders. cause anorexia by releasing proinflammatory r examination of tissue/cell samples are often cytokines such as interleukin-1, tumor Cardiac failure. required make a definitive diagnosis. BLBS078-CF_A52 BLBS078-Tilley March 21, 2011 22:1

Canine and Feline, Fifth Edition 89

(Continued) Anorexia A

r Only if the history, physical examination, EXPECTED COURSE AND PROGNOSIS and database strongly suggest psychologic Varies with underlying cause anorexia should further diagnostic work-up be MEDICATIONS forgone; in such cases, daily contact with the pet owner is essential until the anorexia has DRUG(S) OF CHOICE r resolved. Diazepam is a short-acting appetite MISCELLANEOUS CBC/BIOCHEMISTRY/URINALYSIS stimulant with sedative properties dosed at 0.1 r mg/kg IV daily or 1 mg PO once daily in cats. ASSOCIATED CONDITIONS Abnormalities vary with different r N/A underlying diseases and causes of Oxazepam (2 mg/cat PO q12h) is a short-acting appetite stimulant and sedative. AGE-RELATED FACTORS pseudoanorexia and anorexia. r r Can be normal in patients with medical as Cyproheptadine, an antihistamine with Nutritional support and/or well as psychologic causes of anorexia. antiserotonergic properties, has been used as glucose-containing fluids may be necessary to an appetite stimulant with mixed success at a OTHER LABORATORY TESTS treat or prevent hypoglycemia in anorectic dose range of 0.2–0.4 mg/kg PO 10–20 puppies and kittens. Special diagnostic tests may be necessary to minutes prior to feeding. r ZOONOTIC POTENTIAL rule out specific diseases suggested by history, Analgesics may promote appetite in painful physical examination, and preliminary tests. conditions. N/A r Metoclopramide (0.2–0.4 mg/kg SC or PREGNANCY/FERTILITY/BREEDING IMAGING PO), ranitidine (2 mg/kg SC, IV, or PO), or N/A r Thoracic and abdominal imaging erythromycin (0.5–1 mg/kg PO) are useful if SYNONYMS (radiographic and ultrasound) studies are anorexia is associated with gastroparesis or N/A ileus. often included in the minimum database to r SEE ALSO detect anatomic abnormalities. Antiemetics such as prochlorperazine r Fluoroscopy may be indicated to specifically (0.1–0.5 mg/kg PO) or metoclopramide are See “Causes” evaluate pharyngeal and esophageal function. useful to decrease nausea-associated anorexia. ABBREVIATIONS r DIAGNOSTIC PROCEDURES CONTRAINDICATIONS CCK = cholecystokinin r r Vary with underlying condition suspected. Avoid antiemetics if gastrointestinal Suggested Reading r obstruction is present or suspected. Endoscopy may be useful for visualization r Guilford WG. Nutritional management of of the pharyngeal and esophageal structures. Drugs with sedative properties should be gastrointestinal diseases. In: Guilford WG, used with caution in severely debilitated Center SA, Strombeck DR, et al., eds., animals. Strombeck’s Small Animal PRECAUTIONS Gastroenterology, 3rd ed. Philadelphia: TREATMENT N/A Saunders, 1996, pp. 889–910. r POSSIBLE INTERACTIONS Hoover JP, Monroe WE. Anorexia. In: The mainstay of treatment is aimed at Ettinger SJ, Feldman EC, eds., Veterinary N/A identifying and correcting the underlying Internal Medicine, 6th ed. Philadelphia: disease. ALTERNATIVE DRUG(S) r Elsevier Saunders, 2005, pp. 117–119. Symptomatic therapy includes attention to N/A Monroe WE. Anorexia and polyphagia. In: fluid and electrolyte derangements, reduction Ettinger SJ, Feldman EC, eds., Veterinary in environmental stressors, and modification Internal Medicine, 5th ed. Philadelphia: of the diet to improve palatability. r Saunders, 2000, pp. 102–104. Palatability can be improved by adding FOLLOW-UP Remillard RL, Armstrong PJ, et al. Assisted flavored toppings such as chicken and beef feeding in hospitalized patients: Enteral and broth, seasoning with condiments such as PATIENT MONITORING r parenteral nutrition. In: Hand MS, garlic powder, increasing the fat or protein Body weight, body condition score Thatcher CD, Remillard RL, et al., eds., content of the food, and heating the food to assessment, and hydration determination. Small Animal Clinical Nutrition, 4th ed. body temperature. r r Return of appetite. Topeka, KS: Mark Morris Institute, 2000, As a general rule, dogs and cats with PREVENTION/AVOIDANCE pp. 351–399. debilitating disease should not go without Feed highly palatable diet Author Elizabeth M. Streeter food for longer than 3–5 days before enteral Consulting Editor Albert E. Jergens or parenteral feeding is used. POSSIBLE COMPLICATIONS r r The decision to institute enteral or Dehydration, malnutrition, and cachexia parenteral feeding can be influenced by are most likely; these exacerbate the Client Education Handout ≥ underlying disease. several factors. In animals that have 10% r available online body weight loss, hypoalbuminemia, A loss of more than 25–30% of body lymphopenia, lower body condition score, protein compromises the immune system and and chronic disease processes, supplemental muscle strength, and death results from nutrition should be considered. infection and/or pulmonary failure. r r Techniques for providing enteral nutrition Feline hepatic lipidosis is a possible complication of anorexia in obese cats. include forced feeding and placement of a r nasoesophageal, esophagostomy, gastrostomy, Breakdown of the intestinal mucosal barrier or jejunostomy tube. is a concern in debilitated patients. BLBS078-CF_A53 BLBS078-Tilley March 21, 2011 22:2

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

r severely bowed antebrachium and carpal Complete symmetrical closure of distal subluxation. physis—may note straight limb with a BASICS GEOGRAPHIC DISTRIBUTION widened radial carpal joint space; may note caudal bow to radius and ulna. N/A r DEFINITION Asymmetrical closure of medial distal SIGNALMENT Abnormally shaped forelimbs and/or physis—varus angular deformity; occasionally Species inward rotation. malalignments of the elbow or antebrachial r carpal joints that result from maldevelopment Dogs and cats Closure of lateral distal physis—valgus of the radius or ulna in the growing animal. Breed Predilections angular deformity; external rotation. r r Skye terriers—recessive inheritable form. Closure of proximal radial physis with r PATHOPHYSIOLOGY Chondrodysplastic and toy breeds continued ulnar growth—malarticulation of r (especially basset hounds, dachshunds, Lhasa the elbow joint; widened radial to humeral Antebrachium—predisposed to deformities space and humeral to anconeal space. resulting from continual growth of one bone apsos, Pekingese, Jack Russell terriers)—may be predisposed to elbow malalignments. CAUSES after premature growth cessation or decreased r r Giant breeds (e.g., Great Danes, Trauma growth rate of the paired bone. r r wolfhounds)—may be induced by rapid Developmental basis Decreased rate of elongation in one bone r behaves as a retarding strap; the growing growth owing to excessive or unbalanced Nutritional basis paired bone must twist and bow away from nutrition, OCD, HOD. RISK FACTORS the short bone or overgrow at the elbow or Mean Age and Range r r Forelimb trauma carpus; causes joint malalignment. Traumatic—anytime during the active r r Excessive dietary supplementation Normal growth—bones elongate through growth phase. r the process of endochondral ossification, Elbow malarticulations—during growth; which occurs in the physis; physis closure may not be recognized until secondary occurs when the germinal cell layer stops arthritic changes become severe, occasionally DIAGNOSIS producing new cartilage and the existing at several years of age. cartilage hypertrophies, ossifies, and is DIFFERENTIAL DIAGNOSIS Predominant Sex r remodeled into bone. Elbow dysplasia r N/A r Hereditary—premature closure of distal Fragmented medial coronoid process SIGNS r ulnar physis reported as recessive trait in Skye Un-united anconeal process r terriers; may be a component of common General Comments Panosteitis r r elbow joint malalignment in many Longer-limbed dogs—angular deformities Flexor tendon contracture generally more common. r chondrodysplastic breeds (basset hounds and r Hypertrophic osteodystrophy Lhasa apsos). Shorter-limbed dogs—tend to develop more CBC/BIOCHEMISTRY/URINALYSIS r severe joint malalignments. Osteochondrosis or dietary r oversupplementation—possibly associated Age at the time of premature N/A with retardation of endochondral ossification closure—affects relative degree of deformity OTHER LABORATORY TESTS (retained cartilaginous cores) in giant-breed and joint malarticulation; perhaps because of N/A dogs. the variation in stiffness of bone with age and IMAGING r r Hypertrophic osteodystrophy—juvenile the duration of altered growth until maturity. Damage to growth potential of the growth syndrome with physeal and periosteal Historical Findings r physis—commonly cannot be seen at the time inflammation that may impede physeal Traumatic—progressive limb angulation or of trauma; usually 2–4 weeks before growth. r lameness 3–4 weeks after injury; owner may radiographically apparent. Trauma—most common cause; if not be aware of causative event. r r Standard craniocaudal and mediolateral chondroproliferative layer of the physis is Developmental elbow radiographic views—include entire elbow crushed (Salter V fracture), new cartilage malalignments—insidious onset of lameness joint; from mid-humerus proximally extend production and bone elongation are stopped. in one or both forelimbs; most apparent after to digits distally; take same series for SYSTEMS AFFECTED exercise. comparison to normal contralateral limb. r Musculoskeletal Physical Examination Findings Degree of angular deformities and relative GENETICS Premature Distal Ulnar Closure shortening—determined by comparing r r Skye terriers—reported as a recessive Three deformities of the distal relative lengths of radius and ulna within the deformed pair to the normal contralateral pair. inheritable trait. radius—lateral deviation (valgus), cranial r r Chondrodysplastic breeds bowing (curvus), and external rotation Degree of rotational (dogs)—predisposed to elbow malalignment. (supination). deformity—determined by comparing r rotational position of the elbow and carpus on INCIDENCE/PREVALENCE Relative shortening of limb length r compared to the contralateral normally same view, i.e., lateral of elbow and 45-degree Traumatic—may occur after forelimb growing limb. oblique of carpus documents rotatory injuries in up to 10% of actively growing r deformity. Caudolateral subluxation of the radial carpal r animals; uncommon in cats. Elbow and carpal joints—evaluate for r ± joint and malarticulation of the elbow Elbow malalignment syndrome angular joint—may occur; causes lameness and malalignment (treated surgically) and arthritis deformity (chondrodysplastic dog (e.g., osteophytes; influences prognosis). painful joint restriction. r breeds)—fairly common and can be bilateral. Premature Radial Physeal Closure Elbow joint—evaluate for associated r r Nutritionally induced—incidence Affected limb—significantly shorter than un-united anconeal process and fragmented decreasing as nutritional standards are the normal contralateral. medial coronoid process. improved. r r Severity of lameness—depends on degree of DIAGNOSTIC PROCEDURES Congenital agenesis of the radius (cats and joint malarticulation. rarely dogs)—occasionally seen; results in N/A BLBS078-CF_A53 BLBS078-Tilley March 21, 2011 22:2

Canine and Feline, Fifth Edition 91

(Continued) Antebrachial Growth Deformities A

PATHOLOGIC FINDINGS longer bone (radial or ulnar ostectomy as Cartilage of prematurely closed physis indicated). r replaced with bone Significant limb length MISCELLANEOUS discrepancies—distraction osteogenesis; osteotomy of the shortened bone is ASSOCIATED CONDITIONS r progressively distracted at the rate of 1 Osteochondrosis r mm/day with an external fixator system to HOD TREATMENT r create new bone length. UAP APPROPRIATE HEALTH CARE r AGE-RELATED FACTORS Genetic predisposition—do not breed. r The younger the age at the time of Traumatic physeal damage—not seen at traumatically induced physeal closure, the time of injury; revealed 2–4 weeks later. r MEDICATIONS more severe the deformity and Surgical treatment is recommended as soon malarticulation. as possible following diagnosis. DRUG(S) OF CHOICE ZOONOTIC POTENTIAL NURSING CARE Anti-inflammatory drugs—symptomatic treatment of arthritis N/A N/A CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING ACTIVITY Corticosteroids—do not use owing to N/A Exercise restriction—reduces joint potential systemic side effects and cartilage malalignment damage; slows arthritic SYNONYMS damage seen with long-term use. progression. Radius curvus PRECAUTIONS DIET ABBREVIATIONS r Warn client of possible gastrointestinal upset r Decrease nutritional supplementation in HOD = hypertrophic osteodystrophy associated with chronic anti-inflammatory r giant-breed dogs—slows rapid growth; may OCD = osteochondrodysplasia therapy. r reduce incidence. UAP = un-united anconeal process r POSSIBLE INTERACTIONS Avoid excess weight—helps control arthritic Suggested Reading N/A pain resulting from joint malalignment and Balfour RJ, Boudrieau RJ, Gores BR. T-plate overuse. ALTERNATIVE DRUG(S) fixation of distal radial closing wedge CLIENT EDUCATION Neutraceuticals (e.g., glycosamines)—may osteotomies for treatment of angular limb r Discuss heritability in Skye terriers and help minimize cartilage damage and arthritis deformities in 18 dogs. Vet Surg 2000, possibly chondrodysplastic breeds. development; may be anti-inflammatory and 29:207–217. r Explain that damage to physeal growth analgesic. Dismukes DI, Fox DB, Tomlinson JL, potential is not apparent at time of forelimb Essman SC. Use of radiographic measures trauma and that the diagnosis is often made and three-dimensional computed 2–4 weeks following an injury. tomographic imaging in surgical correction r Discuss the importance of joint FOLLOW-UP of an antebrachial deformity in a dog. malalignment and resultant arthritis as JAVMA 2008, 232(1):68–73. PATIENT MONITORING primary causes of lameness. Fox DB, Tomlinson JL, Cook JL, Breshears r r Emphasize that early surgical treatment Post-operative—depends on surgical LM. Principles of uniapical and biapical treatment. leads to a better prognosis. r radial deformity correction using dome SURGICAL CONSIDERATIONS Periodic checkups—evaluate arthritic status osteotomies and the center of rotation of r and anti-inflammatory therapy. Premature distal ulnar physeal closure in a angulation methodology in dogs. Vet Surg < PREVENTION/AVOIDANCE 2006, 35(1):67–77. patient 5–6 months of age (significant r Selective breeding of susceptible breeds. Henney LH, Gambardella PC. Premature amount of radial growth potential r remaining)—treated with a segmental ulnar Avoid dietary oversupplementation in closure of the ulnar physis in the dog: A ostectomy, valgus deformities ≤ 25◦:may rapidly growing giant-breed dogs. retrospective clinical study. JAAHA 1989, spontaneously correct and may not require POSSIBLE COMPLICATIONS 25:573–581. additional surgery; patients and those with Meola SD, Wheeler JL, Rist CL. Validation of Routinely seen with various osteotomy a technique to assess radial torsion in the more severe deformities: often require a fixation techniques (e.g., infection, non-union second definitive correction after maturity. presence of procurvatum and valgus r of osteotomy, fixator pin tract inflammation). Radial or ulnar physeal closure in a mature deformity using computed tomography: A patient (limited or no growth potential) cadaveric study. Vet Surg 2008, EXPECTED COURSE AND PROGNOSIS 37(6):525–529. requires deformity correction, joint r Generally, best results seen with early realignment, or both. QuinnMK,ErhartN,JohnsonAL,Schaeffer r diagnosis and surgical treatment—minimizes Deformity correction—may be DJ. Realignment of the radius in canine arthritis. antebrachial growth deformities treated with accomplished with a variety of osteotomy r Premature ulnar closure—tends to be easier techniques; may be stabilized with several corrective osteotomy and bilateral (Type II) to manage; yields better results. external fixation. Vet Surg 2000, different fixation devices; must correct both r Limb lengthening by distraction rotational and angular deformities; performed 29:558–563. osteogenesis—requires extensive Author at the point of greatest curvature. Peter K. Shires r post-operative management by the Consulting Editor Joint malalignment (particularly Peter K. Shires veterinarian and owner; high rate of elbow)—must correct to minimize arthritic complications. development (primary cause of lameness); Client Education Handout obtain optimal joint alignment via dynamic available online proximal ulnar osteotomy (use triceps muscle traction and joint pressure) or shortening BLBS078-CF_A54 BLBS078-Tilley July 15, 2011 9:21

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

inflammatory cells adherent to corneal edema associated with ulcers is either localized endothelium; most notable ventrally. to, or most severe at, site of ulcer; ocular r BASICS Aqueous flare and cells—cloudiness of discharge often thicker and more copious aqueous humor due to increased protein than with uveitis; discomfort may be r DEFINITION content and suspended cellular debris; best alleviated by topical anesthetic. Horner’s r visualized with a bright, narrow beam of light syndrome—miosis, enophthalmos, and Inflammation of the anterior uveal tissues, r including iris (iritis), ciliary body (cyclitis), or shined through anterior chamber. Ciliary nictitans protrusion are similar in both r flush—injection of deep perilimbal anterior conditions, but Horner’s is non-painful with both (iridocyclitis). May be associated with r concurrent posterior uveal and retinal ciliary vessels. Deep corneal no ocular discharge; ptosis with Horner’s is vascularization—circumcorneal distribution distinguished from blepharospasm, as the inflammation (choroiditis; chorioretinitis). r r (brush border). Miosis and/or resistance to latter is an active process; minor conjunctival May be unilateral or bilateral. r PATHOPHYSIOLOGY pharmacologic dilation. Iridal hyperemia may be noted with Horner’s, but r swelling—may be generalized or nodular. cornea and anterior chamber are clear; clinical r Increased permeability of the blood-aqueous Reduced IOP is consistent with anterior signs of Horner’s syndrome resolve following barrier related to infectious, uveitis but is not a uniform finding. topical application of ophthalmic 1–10% r immune-mediated, neoplastic, traumatic, or Posterior synechia—adhesions between phenylephrine. other causes; allows entrance of plasma posterior iris and anterior lens surface. proteins and blood cellular components into r r CBC/BIOCHEMISTRY/URINALYSIS r Fibrin in anterior chamber. Hypopyon or r aqueous humor. Disruption of CBC—often normal; changes may be hyphema—accumulations of white blood present related to underlying disease. blood-aqueous barrier is initiated and cells or red blood cells, respectively, in the r maintained by numerous chemical mediators, Biochemistry—often normal; most anterior chamber; usually settles horizontally common abnormality in cats with uveitis is including histamine, prostaglandins, in ventral aspect of chamber but may be r elevated serum proteins (usually due to leukotrienes, serotonin, kinins, and diffuse. Chronic changes may include r complement. polyclonal gammopathy). Urinalysis—often rubeosis iridis, iridal hyperpigmentation, normal; changes may be present related to SYSTEMS AFFECTED secondary cataract, lens luxation, pupillary r r underlying disease. Ophthalmic. Other systems may also be seclusion, iris bombe,´ secondary glaucoma, OTHER LABORATORY TESTS affected by underlying disease process. and phthisis bulbi. r r FeLV serum titers. FIV serum titers. INCIDENCE/PREVALENCE CAUSES r r r r Coronavirus titers—not specific for FIP but Relatively common condition. Tr ue Infectious—mycotic (Blastomyces spp., may influence the index of suspicion for this r incidence/prevalence unknown. Cryptococcus neoformans; Coccidiodes immitis; disease. Toxoplasma gondii IgM and IgG GEOGRAPHIC DISTRIBUTION Histoplasma capsulatum); protozoal titers performed on serum and/or aqueous r Geographic location may affect incidence of (Toxoplasma gondii); bacterial (Bartonella spp., humor. Bartonella spp. serology, PCR certain infectious causes of uveitis. Mycobacterium spp. or any bacterial (serum or aqueous humor) and/or blood septicemia); viral (FIV, FeLV, feline SIGNALMENT culture. coronavirus; FHV-1); parasitic Species (ophthalmomyiasis; ocular larval migrans). IMAGING r r Cats Idiopathic—lymphocytic-plasmacytic Thoracic radiography—may show evidence r Mean Age and Range uveitis. Immune-mediated—reaction to lens of causative disease process (e.g., infiltrates r r related to infectious disease; evidence of Mean age—7–9 years. Anyagemaybe proteins (due to cataract or lens trauma). r r metastatic neoplastic disease). Ocular affected. Neoplastic—primary ocular tumors (esp. diffuse iris melanoma, ocular sarcoma); ultrasound—indicated if opacity of ocular Predominant Sex metastasis to uveal tract (esp. lymphoma). media precludes direct examination; may r Males/neutered males more commonly Metabolic—hyperlipidemia; hyperviscosity; reveal intraocular neoplasm or retinal affected than females. systemic hypertension. detachment. r SIGNS Miscellaneous—trauma; ulcerative keratitis; DIAGNOSTIC PROCEDURES r Historical Findings corneal stromal abscess; toxemia of any cause. Tonometry—low IOP consistent with r Cloudy eye—due to corneal edema, aqueous RISK FACTORS uveitis; elevated IOP indicates glaucoma r flare, hypopyon, etc. Painful eye—manifest (primary disease or secondary to uveitis). None specific; immune suppression and r by blepharospasm, photophobia, or rubbing geographic location may increase incidence of Ocular centesis—if retinal detachment is eye; usually less pronounced than in dogs. present, cytology of subretinal aspirate may r certain infectious causes of uveitis. Red eye—due to conjunctival hyperemia reveal causative agents; anterior chamber and ciliary flush; less pronounced than in centesis may be performed for Toxoplasma r dogs in most cases. Vision loss—variable. gondii or Bartonella IgM and IgG titers on Physical Examination Findings DIAGNOSIS aqueous humor. Importance of a thorough physical PATHOLOGIC FINDINGS DIFFERENTIAL DIAGNOSIS r examination in cats presenting with uveitis Gross—see physical examination findings. r r cannot be overstated. Conjunctivitis—redness limited to Histopathologic—corneal edema; Ophthalmic Findings conjunctival hyperemia (i.e., no ciliary flush); r peripheral corneal deep stromal Ocular discomfort—manifest by ocular discharge usually thicker and more r vascularization; keratic precipitates; preiridal blepharospasm and photophobia Ocular copious than in uveitis; discomfort may be fibrovascular membrane; peripheral anterior discharge—usually serous; sometimes mucoid alleviated by topical anesthetic. r r synechia; posterior synechia; entropion or to mucopurulent. Conjunctival Glaucoma—elevated IOP is most consistent ectropion uveae; leukocyte accumulation in hyperemia—bulbar and palpebral conjunctiva distinguishing feature of this disease; others r iris, ciliary body, sclera, choroid both usually affected. Corneal may include dilated pupil, Haab’s striae, and r r (lymphocytic-plasmacytic, suppurative, or edema—diffuse; mild to severe. Keratic buphthalmos. Ulcerative keratitis—corneal granulomatous infiltrates, depending on precipitates—multifocal aggregates of fluorescein staining will detect ulcers; corneal etiology); secondary cataract; with posterior BLBS078-CF_A54 BLBS078-Tilley July 15, 2011 9:21

Canine and Feline, Fifth Edition 93

(Continued) Anterior Uveitis—Cats A

r segment involvement in inflammatory subconjunctival injection. Often not EXPECTED COURSE AND PROGNOSIS r r process, cyclitic membrane; vitreal traction required. Indicated only in severe cases as Guarded prognosis for affected eyes. bands and retinal detachment may be present. one-time injection, followed by topical and/or Depends on underlying disease and response r r Lymphoplasmacytic infiltrate of iris and systemic anti-inflammatories. to treatment. Cats with treatable underlying ciliary body (either diffuse or nodular) is most Systemic disease (e.g., toxoplasmosis) are more likely to r common histopathologic finding. Prednisone 1–3 mg/kg/day initially; taper have a favorable ophthalmic outcome than r dose after 7–10 days. Use only if systemic those with idiopathic lymphocytic- infectious causes of uveitis have been ruled plasmacytic uveitis or untreatable underlying out. condition (e.g., FIP, FIV). TREATMENT Nonsteroidal Anti-inflammatory Drugs Topical APPROPRIATE HEALTH CARE r Flurbiprofen—apply 2–4 times daily, Outpatient medical management generally depending on severity of disease. MISCELLANEOUS sufficient. r Diclofenac—apply 2–4 times daily, AGE-RELATED FACTORS ACTIVITY r depending on severity of disease. Youngercatsmorelikelytobediagnosed No changes indicated in most cases. Systemic r r with infectious etiology. Older cats at higher DIET Meloxicam 0.2 mg/kg IV, SC, PO once, risk of idiopathic lymphocytic-plasmacytic No changes indicated. then 0.05 mg/kg IV, SC, PO q24h x 2 days, uveitis and intraocular neoplastic causes. then 0.025 mg/kg q24–48h. Due to potential CLIENT EDUCATION ZOONOTIC POTENTIAL r renal effects, limit duration of use to 4–6 days. r r Inform of potential systemic diseases Topical Mydriatic/Cycloplegic None in most cases. Some forms of r causing ophthalmic signs and emphasize Atropine sulfate 1%—apply 1–4 times systemic infection causing uveitis may pose a importance of appropriate diagnostic testing. r daily, depending on severity of disease. Use slight risk to immunocompromised owners. In addition to symptomatic uveitis lowest frequency adequate to maintain dilated PREGNANCY/FERTILITY/BREEDING treatment, treatment of underlying disease pupil and ocular comfort; taper medication as Avoid systemic corticosteroids. Because of (when possible) is paramount to a positive r condition resolves. Ointment is preferred over systemic absorption, topical corticosteroids outcome. Inform of potential complications solutionincatsasitcauseslesssalivation. may also pose a risk, especially with frequent and emphasize compliance with treatment CONTRAINDICATIONS application. and follow-up recommendations that will r reduce the likelihood of complications. Avoid the use of miotic medications (e.g., SYNONYM pilocarpine), including topical prostaglandins SURGICAL CONSIDERATIONS Iridocyclitis (e.g., latanoprost), in the presence of uveitis. r r r SEE ALSO None in most cases. Specific instances Topical and subconjunctival corticosteroids r r requiring surgical intervention include are absolutely contraindicated in the presence Horner’s Syndrome Red Eye r removal of ruptured lenses and surgical of ulcerative keratitis. Corticosteroids ABBREVIATIONS r r management of secondary glaucoma. (especially systemic) should be avoided in cats FeLV = feline leukemia virus FHV-1 = r r Chronic uveitis leading to secondary with systemic hypertension. Avoid systemic feline herpsevirus FIP = feline infectious r glaucoma commonly necessitates enucleation NSAIDS in cats with renal disease. peritonitis FIV = feline immunodeficiency r r of affected globes. Enucleation is PRECAUTIONS virus IOP = intraocular pressure recommended in cats with uveitis related to diffuse iris melanoma or other primary Owing to concern for secondary glaucoma, Suggested Reading intraocular tumors. topical atropine should be used judiciously Colitz CM. Feline uveitis: Diagnosis and and IOP should be monitored periodically. treatment. Clin Tech Small Anim Pract POSSIBLE INTERACTIONS 2005, 20:117–120. Systemic corticosteroids and nonsteroidal Cullen C, Webb A. Ocular manifestations of MEDICATIONS anti-inflammatory drugs should not be used systemic diseases. Part 2: The cat. In: Gelatt concurrently. KN, ed., Veterinary Ophthalmology, 4th ed. DRUG(S) Ames, IA: Blackwell, 2007, pp. 1538–1587. Corticosteroids Miller P. Uvea. In: Maggs DJ, Miller PE, Ofri Topical R, Slatter’s Fundamentals of Veterinary r Prednisolone acetate 1%—apply 2–8 times FOLLOW-UP Ophthalmology, 4th ed. St. Louis: daily, depending on severity of disease; taper Saunders, 2008, pp. 203–229. PATIENT MONITORING medication as condition resolves. Stiles J, Townsend WM. Feline r Dexamethasone 0.1%—apply 2–8 times Recheck in 3–7 days, depending on severity of ophthalmology. In: Gelatt KN, ed., daily, depending on severity of disease; taper disease. IOP should be monitored at recheck Veterinary Ophthalmology, 4th ed. Ames, r medication as condition resolves. Other to detect secondary glaucoma. Frequency of IA: Blackwell, 2007, pp. 1095–1164. topical corticosteroids (e.g., betamethasone, subsequent rechecks dictated by severity of Author IanP.Herring hydrocortisone) are considerably less effective disease and response to treatment. Consulting Editor Paul E. Miller in the treatment of intraocular inflammation. POSSIBLE COMPLICATIONS r Taper treatment frequency as condition Systemic Complications improves; stopping topical corticosteroids Client Education Handout Occur as a result of the systemic etiology of available online abruptly may result in rebound of ocular the uveitis. inflammation. Subconjunctival Ophthalmic Complications r r Triamcinolone acetonide 4 mg by Secondary glaucoma—common complication of chronic uveitis in cats. subconjunctival injection. r r r Secondary cataract. Lens luxation. Methylprednisolone 4 mg by r r Retinal detachment. Phthisis bulbi. BLBS078-CF_A55 BLBS078-Tilley June 16, 2011 10:55

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

r Conjunctival hyperemia—bulbar and palpebral conjunctiva both usually affected. r Corneal edema—diffuse; mild to severe. BASICS r DIAGNOSIS Keratic precipitates—multifocal aggregates DEFINITION of inflammatory cells adherent to corneal DIFFERENTIAL DIAGNOSIS r endothelium; most notable ventrally. r Inflammation of the anterior uveal tissues, r Conjunctivitis—redness limited to including iris (iritis), ciliary body (cyclitis), or Aqueous flare and cells—cloudiness of conjunctival hyperemia (i.e., no ciliary flush); r both (iridocyclitis). May be associated with aqueous humor due to increased protein ocular discharge usually thicker and more concurrent posterior uveal and retinal content and suspended cellular debris; best copious than in uveitis; discomfort may be inflammation (choroiditis; chorioretinitis). visualized with a bright, narrow beam of light alleviated with application of topical r r r May be unilateral or bilateral. shined through anterior chamber. Ciliary anesthetic. Glaucoma—elevated IOP is flush—injection of deep perilimbal anterior PATHOPHYSIOLOGY r most consistent feature of this disease; others r ciliary vessels. Deep corneal may include dilated pupil, Haab’s striae, and Increased permeability of the blood-aqueous r vascularization—circumcorneal distribution buphthalmos. Lens luxation—corneal barrier related to infectious, r (brush border). Miosis and/or resistance to edema may be localized to site of lens contact immune-mediated, traumatic, or other causes r pharmacologic dilation. Iridal swelling. with endothelium or may be diffuse as a result allows entrance of plasma proteins and blood r Reduced IOP is consistent with uveitis but of associated uveitis and/or glaucoma; lens cellular components into aqueous humor. r r is not a uniform finding. Posterior luxation is highly breed associated. Disruption of blood-aqueous barrier is r synechia—adhesions between posterior iris Ulcerative keratitis—corneal fluorescein initiated and maintained by numerous r and anterior lens surface. Fibrin in anterior staining will detect ulcers; corneal edema chemical mediators, including histamine, r chamber. Hypopyon or associated with ulcers is either localized to, or prostaglandins, leukotrienes, serotonin, hyphema—accumulations of white blood most severe at, site of ulcer; ocular discharge kinins, and complement. cells or red blood cells, respectively, in the often thicker and more copious than with SYSTEMS AFFECTED anterior chamber; usually settles horizontally r r uveitis; discomfort may be partially alleviated Ophthalmic. Other systems may also be in ventral aspect of chamber but may be r r by topical anesthetic. Corneal endothelial affected by underlying disease process. diffuse. Chronic changes may include dystrophy or degeneration—diffuse corneal INCIDENCE/PREVALENCE rubeosis iridis, iridal hyperpigmentation, edema is present, but IOP is normal; r r secondary cataract, lens luxation, pupillary conjunctival hyperemia and signs of ocular Relatively common condition. Tr ue r incidence/prevalence unknown. seclusion, iris bombe,´ secondary glaucoma, discomfort are generally absent. Horner’s and phthisis bulbi. GEOGRAPHIC DISTRIBUTION syndrome—miosis, enophthalmos, and CAUSES nictitans protrusion are similar in both Geographic location may affect incidence of r conditions, but Horner’s is non-painful with certain infectious causes of uveitis. Infectious—mycotic (Blastomyces dermatitidis, Cryptococcus neoformans, no ocular discharge; ptosis with Horner’s is SIGNALMENT Coccidiodes immitis, Histoplasma capsulatum); distinguished from blepharospasm as the Species protozoal (Toxoplasma gondii, Neospora latter is an active process; minor conjunctival Dogs caninum, Leishmania donovani); rickettsial hyperemia may be noted with Horner’s, but cornea and anterior chamber are clear; clinical Breed Predilections (Ehrlichia canis, Rickettsia rickettsii); bacterial r r (Leptospira spp., Bartonella spp., Brucella 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 canis, Borrelia burgdorferi, any bacterial r (a.k.a. golden retriever uveitis). Increased septicemia); algal (Prototheca spp.); viral CBC/BIOCHEMISTRY/URINALYSIS incidence of uveodermatologic syndrome in (adenovirus, distemper, rabies, herpes); Often normal; changes related to underlying parasitic (ocular filariasis, ocular larval Siberian husky, Akita, Samoyed, and Shetland r disease may be present. sheepdog. migrans). Immune-mediated—reaction to OTHER LABORATORY TESTS lens proteins (due to cataract or lens trauma); r Mean Age and Range Serology for infectious diseases listed under uveodermatologic syndrome; post-vaccinal r r “Causes” may be appropriate, depending on Any age may be affected. Mean age in reaction to canine adenovirus vaccine; r index of suspicion for infectious etiology. uveodermatologic syndrome—2.8 years. vasculitis. Neoplastic—primary ocular r r Clinical signs raising the suspicion of Mean age in golden retriever uveitis— tumors (especially uveal melanoma, systemic disease including lethargy, pyrexia, 8.6 years. iridociliary adenoma/adenocarcinoma); weight loss, coughing, lymphadenopathy, etc., SIGNS metastasis to uveal tract (lymphosarcoma most r warrant serology for infectious diseases. Historical Findings common). Metabolic—hyperlipidemia; r IMAGING Red eye—due to conjunctival hyperemia hyperviscosity; systemic hypertension. r r r and ciliary flush. Cloudy eye—due to Miscellaneous—idiopathic; trauma; golden Thoracic radiography may show evidence of corneal edema, aqueous flare, hypopyon, etc. retriever uveitis; ulcerative keratitis; corneal causative disease process (e.g., systemic r r Painful eye—manifest by blepharospasm, stromal abscess; scleritis; lens mycoses; metastatic neoplasia). Abdominal r ultrasound may be warranted if suspicion for photophobia, or rubbing eye. Vision instability/luxation; dental/periodontal r loss—variable. disease; toxemia of any cause. metastatic neoplastic disease is high. Ocular ultrasound is indicated if opacity of ocular Physical Examination Findings RISK FACTORS media precludes direct examination; may None specific; immune suppression and The importance of a thorough physical reveal intraocular neoplasm or retinal geographic location may increase incidence of examination in dogs presenting with uveitis detachment. cannot be overstated. certain infectious causes of uveitis; breed Ophthalmic Findings predispositions, as listed above, should be DIAGNOSTIC PROCEDURES r r Ocular discomfort—manifest by considered. Tonometry—low IOP consistent with blepharospasm, photophobia, and rubbing uveitis; elevated IOP indicates glaucoma r eye. Ocular discharge—usually serous; (primary disease or secondary to uveitis). sometimes mucoid to mucopurulent. BLBS078-CF_A55 BLBS078-Tilley June 16, 2011 10:55

Canine and Feline, Fifth Edition 95

(Continued) Anterior Uveitis—Dogs A

r Lymph node aspirates—if enlarged nodes daily, depending on severity of disease; taper are palpable, aspiration for cytology is medication as condition resolves. r r indicated. Ocular centesis—if retinal Dexamethasone 0.1%—apply 2–8 times FOLLOW-UP detachment is present, cytology of subretinal daily, depending on severity of disease; taper r aspirate may reveal causative agents; anterior medication as condition resolves. Other PATIENT MONITORING chamber centesis is generally unrewarding. topical corticosteroids (e.g., betamethasone, Recheck in 3–7 days, depending on severity of PATHOLOGIC FINDINGS hydrocortisone) are considerably less effective disease. IOP should be monitored at recheck r in the treatment of intraocular inflammation. to detect secondary glaucoma. Frequency of Gross—see physical examination findings. r r Histopathologic—corneal edema; Taper treatment frequency over several subsequent rechecks dictated by severity of peripheral corneal deep stromal weeks as condition improves; stopping topical disease and response to treatment. vascularization; keratic precipitates; preiridal corticosteroids abruptly may result in PREVENTION/AVOIDANCE fibrovascular membrane; peripheral anterior rebound of ocular inflammation. N/A Subconjunctival synechia; posterior synechia; entropion or r POSSIBLE COMPLICATIONS ectropion uveae; leukocyte accumulation in Triamcinolone acetonide 4–6 mg by r subconjunctival injection. Many systemic complications, including iris, ciliary body, sclera, choroid (lymphocytic, r Methylprednisolone 3–10 mg by death, may occur due to systemic etiology of plasmacytic, suppurative, or granulomatous r r subconjunctival injection. Often not uveitis. Ophthalmic complications include infiltrates, depending on etiology); secondary r required. Indicated only in severe cases as secondary cataract, secondary glaucoma, lens cataract; with posterior segment involvement luxation, retinal detachment, phthisis bulbi. in inflammatory process, cyclitic membrane; one-time injection followed by topical and/or EXPECTED COURSE AND PROGNOSIS vitreal traction bands and retinal detachment systemic anti-inflammatories. Systemic may be present. r Extremely variable; depends on underlying Prednisone 0.5–2.2 mg/kg/day initially; r disease and response to treatment. taper dose after 7–10 days. Use only if systemic infectious causes of uveitis have been TREATMENT ruled out. APPROPRIATE HEALTH CARE Nonsteroidal Anti-inflammatory Drugs MISCELLANEOUS Topical r ZOONOTIC POTENTIAL Outpatient medical management is generally Less effective than topical corticosteroids. r sufficient. Flurbiprofen—apply 2–4 times daily, None in most cases. Some forms of systemic NURSING CARE depending on severity of disease. infection causing uveitis may pose a slight risk r None Diclofenac—apply 2–4 times daily, to immune-compromised owners. ACTIVITY depending on severity of disease. PREGNANCY/FERTILITY/BREEDING r Systemic Avoid systemic corticosteroids. Because of No changes indicated in most cases. r r Reduced exposure to bright light may Do not use concurrently with systemic possibility of systemic absorption, topical corticosteroids; avoid in the presence of corticosteroids may also pose risk, especially alleviate discomfort. r hyphema. Aspirin 10–25 mg/kg PO q12h with frequent application in small dogs. r DIET Carprofen 2.2 mg/kg PO q12h or r SYNONYMS No changes indicated. 4.4 mg/kg PO q24h Tepoxalin 10 mg/kg r Iridocyclitis CLIENT EDUCATION PO q24h Meloxicam 0.2 mg/kg PO q24h r Topical Mydriatic/Cycloplegic SEE ALSO Inform of potential systemic diseases r causing ophthalmic signs and emphasize Atropine sulfate 1%—apply 1–4 times Red Eye importance of appropriate diagnostic testing. daily, depending on severity of disease. Use ABBREVIATIONS r r r In addition to symptomatic uveitis lowest frequency adequate to maintain dilated IOP = intraocular pressure NSAID = treatment, treatment of underlying disease pupil and ocular comfort; taper medication as nonsteroidal anti-inflammatory drug (when possible) is paramount to a positive condition resolves. r Suggested Reading outcome. Inform of potential complications CONTRAINDICATIONS Cullen C, Webb A. Ocular manifestations of and emphasize compliance with treatment r Avoid the use of miotic medications (e.g., systemic diseases. Part 1: The dog. In: Gelatt and follow-up recommendations that will pilocarpine, demecarium bromide), including KN, ed., Veterinary Ophthalmology, 4th ed. reduce the likelihood of complications. topical prostaglandins (e.g., latanoprost), in r Ames, IA: Blackwell, 2007, pp. 1470–1537. SURGICAL CONSIDERATIONS the presence of uveitis. Topical and Hendrix D. Diseases and surgery of the None in most cases. Specific instances subconjunctival corticosteroids are absolutely canine anterior uvea. In: Gelatt KN, ed., contraindicated in the presence of ulcerative requiring surgical intervention include r Veterinary Ophthalmology, 4th ed. Ames, removal of ruptured lenses, removal of keratitis. Avoid systemic corticosteroids in IA: Blackwell, 2007, pp. 812–858. cataracts causing uveitis (if prognosis for dogs with systemic hypertension or systemic Miller P. Uvea. In: Maggs DJ, Miller PE, Ofri successful surgery is otherwise favorable), and infections. R, Slatter’s Fundamentals of Veterinary surgical management of secondary glaucoma. PRECAUTIONS Ophthalmology, 4th ed. St. Louis: Out of concern for secondary glaucoma, Saunders, 2008, pp. 203–229. topical atropine should be used judiciously Author IanP.Herring and IOP should be monitored periodically. Consulting Editor Paul E. Miller MEDICATIONS POSSIBLE INTERACTIONS Systemic corticosteroids and NSAIDS should DRUG(S) OF CHOICE Client Education Handout not be used concurrently. available online Corticosteroids ALTERNATIVE DRUG(S) Topical r N/A Prednisolone acetate 1%—apply 2–8 times BLBS078-CF_A56 BLBS078-Tilley July 23, 2011 9:4

96 Blackwell’s Five-Minute Veterinary Consult A Anticoagulant Rodenticide Poisoning

toxicosis by consumption of poisoned product); bioavailability enhanced by the rodents—unlikely. concurrent feeding of a small amount of fat, r BASICS such as canned dog food. Vitamin K1 administration—continued for 3–4 weeks DEFINITION with suspected second-generation Coagulopathy caused by reduced circulating DIAGNOSIS anticoagulant toxicosis. vitamin K1–dependent clotting factors after CONTRAINDICATIONS DIFFERENTIAL DIAGNOSIS r exposure to anticoagulant rodenticides. r r Vitamin K —not efficacious in the DIC Congenital clotting factor deficiencies 3 PATHOPHYSIOLOGY treatment of anticoagulant rodenticide r CBC/BIOCHEMISTRY/URINALYSIS r Inhibits vitamin K1 epoxide reductase, DT toxicosis; contraindicated. Intravenous diaphorase, and possibly other enzymes Anemia—with marked hemorrhage vitamin K1—reported anaphylactic reactions; involved in the reduction of vitamin OTHER LABORATORY TESTS avoid this route of administration. r r K1–epoxide to vitamin K1. Vitamin ACT > 150 sec—supports coagulopathy. PRECAUTIONS r r K1—required for carboxylation of clotting Prolonged PT and PTT—support exposure Avoid unnecessary surgical procedures and factors II, VI, IX, and X; uncarboxylated to rodenticide; PT affected earlier than is r r parenteral injections. Use the smallest clotting factors do not bind calcium PTT. Analysis of blood or liver—confirm possible needle when giving an injection or sufficiently to participate in clot formation. exposure to a specific product. collecting samples. SYSTEMS AFFECTED IMAGING POSSIBLE INTERACTIONS Hemic/Lymphatic/Immune Thoracic radiography—may detect Sulfonamides and phenylbutazone—may INCIDENCE/PREVALENCE hemothorax or hemopericardium. displace anticoagulant rodenticides from Common—many baits are sold DIAGNOSTIC PROCEDURES plasma binding sites, leading to more free over-the-counter and widely used in homes. Thoracentesis—may confirm hemothorax. toxicant and toxicosis. SIGNALMENT PATHOLOGIC FINDINGS r r r Dogs and cats. No breed or gender Free blood in the thoracic cavity, lungs, and r predilections; younger animals may ingest bait abdominal cavity—common. Hemorrhage FOLLOW-UP more readily. into the cranial vault, gastrointestinal tract, SIGNS and urinary tract—less common; may occur PATIENT MONITORING both subcutaneously and intramuscularly. ACT and PT—assess efficacy of therapy; General Comments monitoring continued 3–5 days after May be slightly more prevalent in the spring discontinuation of treatment. and fall when rodenticide products are used. PREVENTION/AVOIDANCE Historical Findings TREATMENT r Prevent access to anticoagulant rodenticides. Use of anticoagulant rodenticides r r APPROPRIATE HEALTH CARE POSSIBLE COMPLICATIONS Dyspnea—exercise intolerance Bleeding r Inpatient—acute crisis r Physical Examination Findings r May note secondary bacterial pneumonia, r Outpatient—consider once the after intrapulmonary hemorrhage. Hematomas—often ventral and at r r coagulopathy is stabilized Intracranial, intra-articular hemorrhage. venipuncture sites Muffled heart or lung r r NURSING CARE sounds Pale mucous membranes Lethargy EXPECTED COURSE AND PROGNOSIS Fresh whole blood or plasma transfusion CAUSES If the patient survives the first 48 hours of r —may be required with hemorrhaging; acute coagulopathy—the prognosis improves. Exposure to anticoagulant rodenticide r provides immediate access to vitamin First-generation coumarin anticoagulants K–dependent clotting factors; whole blood (e.g., warfarin, pindone)— largely replaced by may be preferred with severe anemia. more potent second-generation products. r ACTIVITY MISCELLANEOUS Second-generation anticoagulants (e.g., brodifacoum, bromadiolone, diphacinone, Confine patient during the early stages; PREGNANCY/FERTILITY/BREEDING and chlorophacinone)—generally more toxic activity enhances blood loss. Warfarin and diphacinone, perhaps others— and some persist longer before excretion than DIET r may pass into amniotic fluid and on to the first-generation agents. Difenthialone No recognized effect fetuses of an exposed pregnant bitch; similar (D-Cease)—less toxic to dogs (LD50 4 CLIENT EDUCATION concerns for feeding affected milk to pups. mg/kg) than are brodifacoum (LD 0.25–2.5 50 Warn client that reexposure could be a serious ABBREVIATIONS mg/kg), bromadiolone (LD 11–20 mg/kg), r r 50 problem. ACT = activated clotting time DIC = chlorophacinone (LD 50–100 mg/kg), and r 50 disseminated intravascular coagulation PT warfarin (LD 20–50 mg/kg); similar to SURGICAL CONSIDERATIONS r 50 r = prothrombin time PTT = partial diphacinone (LD50 3–7.5 mg/kg); cats, LD50 Thoracentesis—may be important for > removing free thoracic blood, which causes thromboplastin time 16 mg/kg; concentration in baits lower r (0.0025%; 25 ppm) than that of other dyspnea and respiratory failure. Must INTERNET RESOURCES second-generation rodenticide baits (0.005%; correct coagulopathy before surgery. http://www.aspcapro.org/animal-poison 50 ppm), so dogs and cats may tolerate higher -control-center-articles.php. intakes. Author Michael J. Murphy RISK FACTORS Consulting Editor Gary D. Osweiler r MEDICATIONS Small doses over several days more dangerous than a single large dose; either type DRUG(S) OF CHOICE r r Client Education Handout of exposure may cause toxicosis. Secondary Vitamin K1 2.5–5.0 mg/kg PO q24h for available online 5 days–6 weeks (depending on the specific BLBS078-CF_A56a BLBS078-Tilley July 23, 2011 5:11

Canine and Feline, Fifth Edition 97 Antidepressants—SSRI Toxicosis A

r CAUSES Tremors: methocarbamol (50–150 mg/kg r SSRI overdose—accidental exposure, IV, titrate up but do not exceed inappropriate administration, or therapeutic 330 mg/kg/day). BASICS r use. Ingestion of an SSRI along with CONTRAINDICATIONS DEFINITION another class of medications that increases r r High risk of serotonin syndrome: other Toxicity secondary to the overdose of an serotonin (TCAs, SNRIs, MAOIs, novel SSRIs, MAOIs, TCAs, amphetamines, SSRI or co-ingestion of two types of antidepressants, tramadol, fentanyl, 5-HTP, clarithromycin, dextromethorphan, r r serotonergic drugs. SSRIs include meperidine, amphetamines, cocaine, lithium, St. John’s wort. Low risk of citalopram (Celexa), escitalopram (Lexapro), dextromethorphan, 5-HTP, buspirone, serotonin syndrome: tramadol, fentanyl, fluoxetine (Prozac), fluvoxamine (Luvox), bupropion, triptans, LSD). amantadine, bupropion, carbamazepine, paroxetine (Paxil), sertraline (Zoloft). RISK FACTORS codeine. r PATHOPHYSIOLOGY Animals on a serotonergic drug r PRECAUTIONS r r SSRIs are a class of antidepressants that Underlying liver or kidney disease Benzodiazepines (e.g., diazepam) are inhibit reuptake of serotonin, a reported by some sources to exacerbate neurotransmitter involved in aggression, serotonin syndrome and their use for SSRI anxiety, appetite, depression, migraine, pain, r toxicosis is not universally recommended. and sleep. Excessive stimulation of serotonin DIAGNOSIS POSSIBLE INTERACTIONS receptors can occur by enhanced serotonin r DIFFERENTIAL DIAGNOSIS Decreased metabolism of SSRIs: cimetidine, synthesis, increased presynaptic serotonin r r release, inhibition of serotonin uptake into Toxicologic: TCAs, SNRIs MAOIs, diuretics, quinidine, lithium. Increased the presynaptic neuron, inhibition of metaldehyde, lead, ethylene glycol, hops, levels of medications (decreased metabolism): anticholinergics, antihistamines. theophylline, coumadin, digoxin. serotonin metabolism, or serotonin agonism. r Serotonin syndrome is characterized in Non-toxicologic: meningitis e.g., (rabies, humans as a combination of symptoms that canine distemper), neoplasia, heat stroke, include at least three of the following: malignant hyperthermia. myoclonus, mental aberration, agitation, CBC/BIOCHEMISTRY/URINALYSIS FOLLOW-UP r hyperreflexia, tremors, diarrhea, ataxia, or CBC/biochemistry: no changes are PATIENT MONITORING r r hyperthermia. Toxic dosage varies widely expected. Urinalysis: myoglobinuria Blood pressure, heart rate, urine color: among commonly available SSRIs and are not secondary to rhabdomyolsis may be seen. monitor hourly, then less frequently as the well defined in veterinary medicine. OTHER LABORATORY TESTS animal remains stable. r SYSTEMS AFFECTED Blood gas: metabolic acidosis may be seen. PREVENTION/AVOIDANCE r r r Cardiovascular—decreased vascular tone Testing for SSRIs can be performed, but the Keep medications out of the reach of (hypotension), increased heart rate and stroke r r tests are not clinically useful. animals. Follow label directions when giving volume (tachycardia). Gastrointestinal— DIAGNOSTIC PROCEDURES serotonergic drugs to animals. increased smooth muscle contractility r POSSIBLE COMPLICATIONS (vomiting, diarrhea). Nervous—stimulation There are no diagnostic tests to confirm (agitation, restlessness, seizures) and altered serotonin syndrome Renal failure secondary to myoglobinuria mental status (vocalization, disorientation). from rhabdomyolysis. DIC secondary to r Neuromuscular—autonomic dysfunction hyperthermia. (hyperactivity) and neuromuscular EXPECTED COURSE AND PROGNOSIS r hyperactivity (hyperreflexia, myoclonus, TREATMENT Prognosis is good in most cases, with r r tremors). Ophthalmic—increased APPROPRIATE HEALTH CARE recovery in 12–24 hours. Patients that autonomic function (mydriasis). r r Emesis (if asymptomatic and recent present in status epilepticus or with severe Respiratory—increased bronchial smooth ingestion) or gastric lavage (if large number of hyperthermia have a guarded prognosis. r muscle contraction (dypsnea). pills ingested). Activated charcoal with INCIDENCE/PREVALENCE cathartics (may need to repeat due to long Increasing in incidence due to increasing use half-life of most of these medications). of serotonergic drugs. NURSING CARE MISCELLANEOUS SIGNALMENT IV fluids to help maintain blood pressure and AGE-RELATED FACTORS Species body temperature, and to protect kidneys Young and elderly animals are more at risk for Dogs and cats from myoglobinuria. developing serious toxicosis. Mean Age and Range CLIENT EDUCATION PREGNANCY/FERTILITY/BREEDING Any age can be affected. If animal appears blind, sight should return SSRIs can cause increased litter mortality and SIGNS possible birth defects. Historical Findings ABBREVIATIONS r r r r Agitation or lethargy Dilated pupils 5-HTP = 5-hydroxytryptophan MAOI r r r MEDICATIONS r Vomiting Tre mor s Hypersalivation = monoamine oxidase inhibitor SNRI = r r r DRUG(S) OF CHOICE serotonin and norepinephrine reuptake Diarrhea Seizures Nystagmus r r ◦ inhibitor SSRI = selective serotonin Physical Examination Findings Agitation: Phenothiazines (acepromazine r r r r r = Agitation Ataxia Mydriasis Tre mor s 0.025–0.05 mg/kg IV, titrate up as needed). reuptake inhibitor TCA tricyclic r r r ◦ Vomiting Disorientation Hyperthermia Cyproheptadine (dog, 1.1 mg/kg; cat, 2–4 antidepressant r r r Vocalization Depression Tachycardia mg PO q4–6h or can be given rectally if Author Tina Wismer r r r ◦ Hypotension Diarrhea Blindness vomiting). Benzodiazepines (diazepam Consulting Editor Gary D. Osweiler r r r Seizures Hypersalivation Death 0.5–2 mg/kg IV) (see “Precautions”). BLBS078-CF_A56b BLBS078-Tilley July 23, 2011 5:15

98 Blackwell’s Five-Minute Veterinary Consult A Antidepressants—Tricyclic Toxicosis

Predominant Sex IMAGING None N/A SIGNS DIAGNOSTIC PROCEDURES BASICS r General Comments ECG to monitor for arrhythmias DEFINITION r r r Signs can be seen at therapeutic doses. Blood pressure monitoring r Toxicity secondary to the acute or chronic Signs of toxicity can be seen within 30–60 PATHOLOGIC FINDINGS ingestion of a tricyclic antidepressant. r minutes or delayed by several hours. TCA medications include amitriptyline, No specific lesions expected Historical Findings amozapine, clomipramine, despiramine, r doxepin, imipramine, maprotiline (tetracyclic Evidence of accidental consumption of the owner’s or another pet’s medication. antidepressant), nortriptyline, protriptyline, r CNS depression (lethargy, ataxia). and trimipramine. r TREATMENT Vocalization. PATHOPHYSIOLOGY r APPROPRIATE HEALTH CARE Vomiting or hypersalivation. r r r TCAs block the reuptake of norepinephrine, Panting. Outpatient—not recommended for r dopamine, and serotonin at the neuronal Agitation or restlessness. symptomatic patients, patients with cardiac r membrane. They also have anticholinergic Tachypnea or dyspnea. disease, or patients ingesting greater than a r activity and are thought to have membrane Tremors. therapeutic dose of TCAs. r r stabilizing effects on the myocardium Seizures. Inpatient—asymptomatic: (particularly inhibiting fast sodium channels ◦ Decontamination with emesis (less than Physical Examination Findings in the ventricular myocardium). They can r 15 minutes of exposure time), gastric lavage CNS depression or stimulation. also have slight alpha-adrenergic blocking r in large exposures, and activated charcoal. Tachycardia. activity and antihistaminic effects. r ◦ Monitor at a clinic for a minimum of r Mydriasis. TCAs are rapidly and well absorbed across r 6 hours after exposure. Hypothermia. r the digestive tract. They can decrease GI r Inpatient—symptomatic—stabilize the Hypertension. motility and delay gastric emptying, resulting r cardiovascular and CNS systems and provide Pallor. in delayed drug absorption. r supportive care. r Cyanosis. They are lipophilic, protein bound, and well r Hyperthermia. NURSING CARE distributed across all tissues. r r r Arrhythmias. Fluid therapy—restore hydration due to They are metabolized by the liver and r Hypotension. vomiting, regulate blood pressure when undergo enterohepatic recirculation. The r hypotension is noted. Urinary retention. r inactive metabolites are eliminated in the r Thermoregulation as needed. Constipation. r urine. Enema with warm water if not defecating SYSTEMS AFFECTED CAUSES r within 6–12 hours. Cardiovascular—anticholinergic effects and Accidental exposure, inappropriate administration, or therapeutic use. ACTIVITY inhibition of norepinephrine reuptake N/A contribute to tachycardia; alpha adrenergic RISK FACTORS r blockade, cardiac membrane stabilization, and Concurrent use of other antipsychotic DIET decreased cardiac contractility contribute to medication NPO if vomiting r hypotension and arrhythmias. Preexisting cardiac disease CLIENT EDUCATION r r Gastrointestinal—anticholinergic effects With a prescribed TCA, instruct client to may cause ileus and delayed gastric emptying. r monitor for adverse or idiosyncratic effects, Nervous—increased dopamine, serotonin, and to stop the medication and contact the and norepinephrine levels in the CNS clinic if they occur. DIAGNOSIS r contribute to CNS signs. Prevent exposure to non-prescribed r DIFFERENTIAL DIAGNOSIS 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 causing cardiac arrhythmias (e.g., quinidine, Species and individual differences in propranolol, albuterol, digoxin). absorption, metabolism, and elimination can r Non-toxicologic differentials include MEDICATIONS be significant. hyperkalemia, cardiac ischemia, DRUG(S) OF CHOICE INCIDENCE/PREVALENCE cardiomyopathy, and other diseases of cardiac Decontamination Incidence is unknown conduction. r GEOGRAPHIC DISTRIBUTION CBC/BIOCHEMISTRY/URINALYSIS Emesis within 15 minutes of ingestion only if asymptomatic; induce emesis with either N/A Expected to be normal hydrogen peroxide or apomorphine. r SIGNALMENT OTHER LABORATORY TESTS Gastric lavage under anesthesia may be r considered with large exposures. Species Blood gases—metabolic acidosis may be r noted. After emesis (or if > 15 minutes of Dogs and cats r Breed Predilections OTC urine drug screen for TCAs—can be exposure), administer activated charcoal used to determine if exposure has occurred. (1–2 g/kg PO) with a cathartic such as None r Serum TCA levels—can be used to sorbitol (70% sorbitol at 3 ml/kg) or sodium Mean Age and Range determine if exposure has occurred; not useful sulfate (0.25 tsp/5 kg) if no diarrhea. None in determining degree of toxicity. BLBS078-CF_A56b BLBS078-Tilley July 23, 2011 5:15

Canine and Feline, Fifth Edition 99

(Continued) Antidepressants—Tricyclic Toxicosis A

r Repeat one-half dose of activated charcoal ALTERNATIVE DRUG(S) ZOONOTIC POTENTIAL in 4–6 hours if patient is still symptomatic. N/A None Other PREGNANCY/FERTILITY/BREEDING r Cyproheptadine: dogs, 1.1 mg/kg q6h PO TCAs cross the placenta and can be found in or rectally; cats, 2–4 mg/cat q6h PO or breast milk; the significance of this is not rectally; used for treatment of serotonin FOLLOW-UP knownatthistime. syndrome. r PATIENT MONITORING SEE ALSO Sodium bicarbonate—used to maintain r r Acid-base status—monitor for acidosis and Antidepressants—SSRI Toxicosis blood pH at 7.55; if not monitoring acid-base if implementing sodium bicarbonate therapy. r r Poisoning (Intoxication) status, start with 2–3 mEq/kg IV over 15–30 Blood pressure—monitor until minutes in a symptomatic patient. ABBREVIATIONS r asymptomatic. r r CNS = central nervous system Diazepam 0.5–1 mg/kg IV, repeat if ECG—monitor until asymptomatic. r ECG = electrocardiogram necessary; for agitation or seizures. r r PREVENTION/AVOIDANCE GI = gastrointestinal Acepromazine 0.02 mg/kg IV, repeat if r Keep medications out of reach of pets. MAOI = monoamine oxidase inhibitor necessary; for agitation or mild hypertension. r r OTC = over-the-counter Phenobarbital—as needed for seizure POSSIBLE COMPLICATIONS r control. Pulmonary edema can occur secondary to TCA-tricyclic antidepressant CONTRAINDICATIONS aggressive fluid therapy. INTERNET RESOURCES r Atropine should not be used because TCAs EXPECTED COURSE AND PROGNOSIS http://www.aspcapro.org/animal-poison- r have anticholinergic effects that are Due to the variable half-lives of the different control-center-articles.php. exacerbated by atropine. TCAs, signs can last 24 hours or longer. r r Magnesium sulfate should not be used as a The prognosis is generally good in patients Suggested Reading cathartic. Ileus or reduced GI motility will exhibiting mild to moderate signs. r Gwaltney-Brant S. Antidepressants: Tricyclic enhance absorption of magnesium and may The prognosis is guarded in patients antidepressants. In: Plumlee KH, ed., result in magnesium toxicity. r exhibiting severe signs such as seizures, Clinical Veterinary Toxicology. St. Louis: Beta-blockers (e.g., propranolol, atenolol) arrhythmias, or hypotension that are poorly Mosby, 2004, pp. 286–288. should not be used for tachycardia because of responsive to therapy. Johnson LR. Tricyclic antidepressant their potential to exacerbate hypotension. r toxicosis. Vet Clin North Am Small Anim Do not induce emesis in a patient already Pract 1990, 20:393–403. showing clinical signs. Volmer PA. “Recreational” drugs: Tricyclic PRECAUTIONS MISCELLANEOUS antidepressants. In: Peterson ME, Talcott N/A ASSOCIATED CONDITIONS PA, eds., Small Animal Toxicology, 2nd ed. St. Louis: Saunders Elsevier, 2006, POSSIBLE INTERACTIONS Serotonin syndrome may occur as a result of r pp. 303–306. TCAs increase risk of hyperthermia, TCA ingestion. seizures, and death with use of MAOIs. Wismer TA. Antidepressant drug overdoses in r AGE-RELATED FACTORS Sympathomimetic and anticholinergic dogs. Vet Med 2000, 95:520–525. None Author medications increase the risk for arrhythmias Cristine L. Hayes or cardiac effects from TCAs. Consulting Editor Gary D. Osweiler r Levothyroxine increases the risk for arrhythmias when used with TCAs. BLBS078-CF_A57 BLBS078-Tilley July 15, 2011 8:22

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

differentiation of mild SAS from this breed anemia, pain, fever, excitement. Systolic variation is problematic. murmurs on the left thorax are commonly BASICS Mean Age and Range caused by patent ductus arteriosus (usually a SAS develops post-natally over the first weeks continuous murmur, but diastolic component DEFINITION to months of life; phenotypic development is may be localized), pulmonic stenosis, mitral Narrowing of the left ventricular outflow complete by 1 year of age. Onset of clinical regurgitation, ventricular septal defect, atrial tract, most commonly seen as a congenital or signs can occur at any age depending on the septal defect, or tetralogy of Fallot in dogs. Some of these conditions may coexist with perinatal disease that worsens over the first severity of obstruction. Signs may be seen on r year of life. Defect can be valvular, subvalvular physical examination without any historical SAS. Weak pulses may occur with other (most common in dogs), or supravalvular evidence of disease. cardiac conditions that reduce stroke volume (e.g., pulmonic stenosis and cardiomyopathy) (most common in cats). As a congenital SIGNS anomaly in dogs, the obstruction is usually or in animals with aortic obstruction distal to Historical Findings caused by fibrous tissue proximal to the valve, r the outflow tract (e.g., aortic coarctation, and the disease is referred to as subaortic Related to the severity of obstruction; range aortic interruption, and aortic from none to CHF, syncope, and sudden stenosis. Less commonly, mitral valve r thromboembolism). dysplasia may cause SAS by tethering the death. Genetic history of affected litters CBC/BIOCHEMISTRY/URINALYSIS from same sire or bitch. mitral valve to the interventricular septum. Typically normal Physical Examination Findings PATHOPHYSIOLOGY r IMAGING Systolic ejection murmur loudest near the Marked aortic obstruction requires an increase Thoracic Radiographic Findings left, fourth intercostal space at the heart base r in intraventricular pressure to maintain May be subtle because myocardial forward blood flow and systemic blood to costochondral junction, which may radiate to the thoracic inlet, carotid arteries, and, if hypertrophy from pressure overload may not pressure. Pressure overload leads to myocyte increase the size of the cardiac silhouette very loud, even to the cranium. Radiation to r hypertrophy and subsequent thickening of the (concentric hypertrophy). Left-sided heart the left apex and right cranial thorax is r heart walls. Coronary artery disease, relative enlargement. Normal lung fields unless cardiac ischemia, arrhythmias, aortic or mitral common. Murmur intensity is roughly correlated with the severity of disease. CHF develops, causing pulmonary venous regurgitation, left-sided congestive heart distention and interstitial or alveolar Murmur may not be present in puppies less r failure, and diminished systemic blood flow pulmonary infiltrates. Mediastinum may be may result. The mechanism of sudden death than 2 months old, becoming more prominent during the first 6 months of age. widened and cranial waist of the cardiac is poorly understood. r Thrill at the left heart base to costochondral silhouette filled as a result of post-stenotic SYSTEMS AFFECTED r dilation of the aorta. r junction in some animals. Diastolic Cardiovascular—pressure overload of the r murmur may be heard at the left apex, if Echocardiographic Findings left ventricle. Pulmonary—if pulmonary r r r aortic regurgitation develops. Holosystolic Spectrum of findings depending on the edema develops. Multisystemic signs may murmur at the left apex may be present, if severity of disease; abnormalities may be r r develop secondary to CHF or low cardiac mitral regurgitation develops. Dyspnea, subtle. Thickening of the left ventricular output. Multisystemic signs with bacterial tachypnea, and crackles with the onset of r r wall and interventricular septum. Echogenic endocarditis. left-sided CHF. Femoral pulses typically ridge and/or gross narrowing of the left GENETICS weak and late rising (pulsus tardus) with ventricular outflow tract may be visible disease severe enough to affect hemodynamics. r Inherited trait in Newfoundland dogs. r proximal to the aortic valve in SAS. Valvular A left ventricular “heave” in animals with Polygenic transmission exhibiting r thickening and increased echogenicity for left ventricular hypertrophy. Arrhythmias. valvular subaortic stenosis, vegetative lesions pseudodominance; a major dominant gene r with modifiers may be involved. Other breeds CAUSES with endocarditis. The anterior mitral valve r r leaflet may also be thickened and echogenic. may exhibit similar inheritance characteristics. Congenital or perinatal disease. Secondary r Post-stenotic dilation of the aorta in some INCIDENCE/PREVALENCE to bacterial endocarditis of the aortic valve in r r animals. Increased echogenicity of the Approximately 1.5–2/1,000 dogs admitted to some dogs. In cats with hypertrophic myocardium in some animals, particularly the veterinary teaching institutions; SAS is cardiomyopathy, functional stenosis (e.g., subendocardial zone and papillary muscles. probably the second most common congenital muscular or subvalvular) is common but r r “Premature closure” of the aortic valve often heart defect in dogs and the most common in significance unknown. “Dynamic” subaortic seen on M-mode echocardiography. large breeds. Approximately 0.2/1,000 cats stenosis reported in dogs in which muscular admitted to veterinary teaching institutions. hypertrophy can contribute to narrowing of Doppler Echocardiographic Findings r r > In one study, aortic stenosis accounted for 6% the aortic outflow tract. As a complication Elevated peak ejection velocity (i.e., 2.25 of congenital cardiac defects in cats. or variant of mitral valve dysplasia. m/s), which may be delayed to a later time in SIGNALMENT RISK FACTORS ejection if severely affected; flow acceleration r Familial history of subaortic stenosis. proximal to the obstruction, and a jet of Species r turbulent blood flow distal to the valve. Dogs and cats Aortic endocarditis is predisposed by r immunosuppression, systemic infection, Transvalvular pressure gradient can be Breed Predilections estimated from the flow velocity (pressure bacteremia, and abnormal intracardiac blood = × SAS is most common in Newfoundlands, flow, including congenital SAS. gradient 4 flow velocity squared) with German shepherds, golden retrievers, Bouvier variable accuracy. Color-flow Doppler allows des Flanders, rottweilers, and boxers. direct visualization of the turbulent jet distal to the obstruction and “flow convergence” Samoyeds, English bulldogs, and Great Danes r proximal. Effective orifice area is decreased. also at higher risk than other breeds; bull DIAGNOSIS terriers predisposed to valvular aortic stenosis, Angiocardiographic Findings/Cardiac typically with concurrent mitral valve DIFFERENTIAL DIAGNOSIS Catheterization r r dysplasia. Boxers exhibit a narrower outflow A systolic ejection murmur may represent Contrast radiography may show thickening tract than other similarly sized breeds; an innocent murmur in a young animal, of the left ventricular wall and septum, BLBS078-CF_A57 BLBS078-Tilley July 15, 2011 8:22

Canine and Feline, Fifth Edition 101

(Continued) Aortic Stenosis A

narrowing of the left ventricular outflow tract resection of SAS in dogs does not currently hypotensive, arrhythmogenic, or cardiac or valve orifice, and post-stenotic dilation of support recommendation, and dogs still may depressant side effects should be avoided. A r r the aorta. Cardiac catheterization allows die suddenly after the procedure. Balloon narcotic (e.g., butorphanol or oxymorphone) determination of the transvalvular pressure dilation of the outflow tract during cardiac with diazepam for sedation can be combined gradient. Pressure gradient categories of mild catheterization results in acute reduction of with low inspired concentrations of isoflurane (< 50 mm Hg), moderate (50–l75 mm Hg), transvalvular gradients and improvement of for anesthesia if necessary. severe (75–100 mm Hg), and very severe clinical signs in some symptomatic dogs. ALTERNATIVE DRUG(S) > r ( 100 mm Hg) are somewhat arbitrary and However, despite reduction in valve gradient, Metoprolol tartrate (0.5–1 mg/kg PO loosely related to clinical course. Pressure a small clinical trial failed to demonstrate q8–12h for dogs; 2–15 mg/cat PO q8h), gradients (by catheterization or Doppler survival advantage of this procedure for cardvedilol (0.5–1.5 mg/kg PO q12h for echocardiography) are greater with increased severely affected dogs, compared with dogs) are among alternative beta-blockers. r ejection volume and, therefore, must be beta-blocker (atenolol) therapy alone. Diltiazem (dogs, 0.5–2 mg/kg PO q8h; cats, interpreted in light of other aspects of cardiac 7.5–15 mg/cat PO q8h) may have similar function. Anesthesia (cardiac catheterization) r theoretical benefits in this disease. may affect gradients. Elevated left ventricular diastolic pressure may accompany MEDICATIONS loss of ventricular compliance, impending or r DRUG(S) OF CHOICE overt CHF. Angiocardiography and cardiac r FOLLOW-UP catheterization allow characterization of Medical management is palliative and uncommon types of stenosis including empirical; no placebo controlled clinical trials PATIENT MONITORING have been published supporting a specific valvular, supravalvular, and “tunnel outflow r Monitor by ECG, thoracic radiography, and tract” and evaluation of concurrent defects. treatment. Beta adrenergic blockers have 2-dimensional and Doppler DIAGNOSTIC PROCEDURES been advocated for dogs with subaortic echocardiography. Treatment of complications stenosis with a history of syncope or collapse, (e.g., CHF and arrhythmias) necessitates Electrocardiographic Findings > r a transvalvular pressure gradient 75 mm careful monitoring to detect renal/ electrolyte, ECG may show signs of left ventricular Hg, or when ventricular arrhythmias or proarrhythmic, negative inotropic, and hypertrophy (e.g., tall R waves, wide QRS ST-segment changes are evident on a hypotensive side effects of drugs. complexes, and shift in mean electrical axis to post-exercise ECG. Potential benefits include r POSSIBLE COMPLICATIONS the left). Slurring of ST segment consistent limitation of myocardial oxygen requirements, with left ventricular hypertrophy or ischemia; protection from ventricular arrhythmias, and CHF, arrhythmias, myocardial infarction, ST-segment deviation after mild exercise slowing of the heart rate. Beta-blockers are aortic regurgitation, mitral regurgitation, strongly suggests coronary insufficiency. sudden death, bacterial endocarditis. r given to effect. Therapy should be initiated Ventricular tachyarrhythmias may occur in with caution at low dosages and titrated EXPECTED COURSE AND PROGNOSIS r severely affected cases and are a potential cause upward over days to weeks. Atenolol (dogs, Mildly affected dogs may live a normal for clinical signs and sudden death. Holter 0.5–1.5 mg/kg PO q12h; cats, 6.25 mg/cat r r lifespan without treatment. Severe disease 24-hour ECG monitoring is appropriate in PO q12–q24h). Specific treatment for typically limits longevity due to CHF or r symptomatic or significantly affected animals. ventricular arrhythmias, atrial fibrillation, or sudden death. CHF, collapse, or syncope left-sided CHF may also be required. r suggests severe disease and an ominous Affected animals are at risk of developing prognosis. bacterial endocarditis. Meticulous treatment TREATMENT of infections is recommended as is chemoprophylaxis for dental or genitourinary APPROPRIATE HEALTH CARE r procedures. Treatment of dynamic stenosis MISCELLANEOUS Management recommendations are in cats with hypertrophic cardiomyopathy is controversial and vary among experts. controversial. AGE-RELATED FACTORS Inpatient management appropriate for CONTRAINDICATIONS Murmur typically not present at birth in SAS; complications including arrhythmias, develops in the first weeks to months syncope, and CHF. Beta-blockers are contraindicated in animals post-natally along with development of ACTIVITY with bronchoconstrictive disorders. stenotic lesion. Continued use in patients with overt CHF is Restrict in animals with more than mild controversial. PREGNANCY/FERTILITY/BREEDING disease. Syncope, collapse, or sudden death PRECAUTIONS Contraindicated may be brought on by exertion in animals r SEE ALSO with severe disease. Beta-blockers limit the ability of the r Cardiomyopathy, Hypertrophic—Cats CLIENT EDUCATION dysfunctional heart to increase cardiac output. r r These drugs should be initiated at a low Cardiomyopathy, Hypertrophic—Dogs Affected animals should be neutered or r r dosage and gradually titrated upward to avoid Congestive Heart Failure, Left-Sided r r otherwise not permitted to breed. Evaluate iatrogenic complications. Overzealous use Endocarditis, Infective closely related dogs for evidence of clinical r of diuretics or venodilators may cause a ABBREVIATIONS disease. Alert owners to potential r r r precipitous drop in cardiac output. Marked CHF = congestive heart failure ECG = complications (e.g., sudden death and CHF) r reduction of systemic blood pressure by ACE electrocardiogram SAS = subaortic stenosis in severely affected animals and increased risk inhibitors, calcium channel blockers, or for endocarditis and anesthetic complications. Author Donald J. Brown arteriolar dilators may worsen outflow Consulting Editor Larry P. Tilley and Francis SURGICAL CONSIDERATIONS obstruction or coronary insufficiency. r r W.K. Smith, Jr. Definitive treatment requires open heart Digitalis glycosides and positive inotropes surgery to resect, repair (valvuloplasty), or such as pimobendan may exacerbate outflow replace (valve replacement) the obstructive obstruction or ventricular arrhythmias. Client Education Handout r lesion. The risk-to-benefit ratio for open Anesthetic agents and sedatives with marked available online BLBS078-CF_A58 BLBS078-Tilley July 15, 2011 8:31

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

r Mean Age and Range Electrolyte derangements, due to low output Age distribution is 1–20 years. The mean age and muscle damage, such as hypocalcemia, BASICS is approximately 8 years. hyponatremia, hyperphosphatemia and hyperkalemia are not uncommon. Predominant Sex r DEFINITION Males > females (2:1) CBC and urinalysis changes are non-specific. Aortic thromboembolism results from a SIGNS thrombus or blood clot that is dislodged OTHER LABORATORY TESTS Historical Findings within the aorta, causing severe ischemia to r Routinely available coagulation profiles Acute onset paralysis and pain are the most the tissues served by that segment of aorta. typically do not reveal significant common complaints. PATHOPHYSIOLOGY r abnormalities because the hypercoagulability Lameness or a gait abnormality. r r results from hyperaggregable platelets. ATE is most commonly associated with Tachypnea or respiratory distress is myocardial disease in cats, most commonly common. IMAGING r hypertrophic cardiomyopathy. It is theorized Vocalization and anxiety are common. Radiographic Findings r r that abnormal blood flow (stasis) and a About 15% of cats may vomit prior to ATE. Cardiomegaly is common in cats. hypercoagulable state contribute to the r Physical Examination Findings Pulmonary edema and/or pleural effusion in formation of a thrombus within the left r approximately 50% of cats. Usually paraparesis or paralysis of the rear r atrium. The blood clot is then embolized Rarely, a mass is seen in the lungs, distally to the aorta. The most common site legs with signs of lower motor neuron injury. Less commonly, monoparesis of a front leg. suggestive of neoplasia. of embolization is the caudal aortic r Pain upon palpation of the legs. Echocardiographic Findings trifurcation (hind legs). Other less common r r sites include the front leg, kidneys, Gastrocnemius muscle often becomes firm Changes consistent with cardiomyopathy. several hours after embolization. gastrointestinal tract, or cerebrum. r Hypertrophic cardiomyopathy is most r Absent or diminished femoral pulses. ATE in dogs typically is associated with r common, followed by restrictive or Cyanotic or pale nail beds and foot pads. neoplasia, sepsis, infectious endocarditis, r unclassified cardiomyopathy and then dilated Tachypnea or dyspnea. Cushing’s disease, protein-losing nephropathy, r cardiomyopathy. Hypothermia is common. r > or other hypercoagulable states. r Most cases ( 50%) have severe left atrial Cardiac murmur, arrhythmias, or gallop SYSTEMS AFFECTED enlargement (i.e., left atrial to aortic ratio of sound (not always present). ≥2). r r Cardiovascular—the majority of affected CAUSES A left atrial thrombus or spontaneous cats have advanced heart disease and left heart r Cardiomyopathy (all types) echocardiographic contrast (smoke) may be failure. r r Hyperthyroidism seen. Nervous/Musculoskeletal—severe ischemia r Neoplasia Abdominal Ultrasonographic Findings to the muscles and nerves served by the r r Sepsis (dogs) May be able to identify the thrombus in the segment of occluded aorta causes variable pain r Hyperadrenocorticism (dogs) caudal aorta. and paresis. Gait abnormalities or paralysis r r results in the leg or legs involved. Protein-losing nephropathy (dogs) Typically not necessary to reach a diagnosis. RISK FACTORS Angiographic Findings GENETICS r Non-selective angiography should identify a Hypertrophic cardiomyopathy, a common It is theorized that a markedly enlarged left negative filling defect in the caudal aorta associated disease, is likely heritable. atrium, spontaneous echocardiographic representing the thrombus. Additionally, a family of domestic shorthair contrast (smoke), or an intracardiac thrombus r Typically not necessary to reach a diagnosis. cats with remodeled hypertrophic observed on an echocardiogram may be risk cardiomyopathy who all died of ATE has been factors. DIAGNOSTIC PROCEDURES reported. Electrocardiography r INCIDENCE/PREVALENCE Sinus rhythm and sinus tachycardia most r common. Less common rhythms include Prevalence is not known in the general DIAGNOSIS population of cats. In two large studies of cats atrial fibrillation, ventricular arrhythmias, with hypertrophic cardiomyopathy, 12–16% DIFFERENTIAL DIAGNOSIS supraventricular arrhythmias, and sinus bradycardia. presented with signs of ATE. In two Hind limb paresis secondary to other causes r retrospective studies of cats with ATE, such as spinal neoplasia, trauma, myelitis, Left ventricular enlargement pattern and left 11–25% of cats had previous evidence of fibrocartilaginous infarction, or intervertebral ventricular conduction disturbances (left heart disease. anterior fascicular block) are common. r disk protrusion. These conditions resulting in Rare in dogs. spinal cord injury present with signs of upper PATHOLOGIC FINDINGS r GEOGRAPHIC DISTRIBUTION motor neuron disease, whereas ATE patients Thrombus typically is identified at the present with signs of lower motor neuron caudal aortic trifurcation. N/A r disease. Occasionally, a left atrial thrombus is seen. SIGNALMENT r CBC/BIOCHEMISTRY/URINALYSIS Emboli of the kidneys, gastrointestinal tract, Species r cerebrum, and other organs also may be seen. Cats, rarely dogs High creatine kinase as a result of muscle injury. r Breed Predilections High aspartate aminotransferase and alanine Mixed-breed cats are most commonly aminotransferase as a result of muscle and affected. Abyssian, Birman, and ragdoll liver injury. TREATMENT r purebred cats were overrepresented in one Hyperglycemia secondary to stress. APPROPRIATE HEALTH CARE study. r Mild increases in blood urea nitrogen and Initially, cats with ATE should be treated as creatinine due to low cardiac output and inpatients because many have concurrent possible renal emboli. congestive heart failure and require injectable BLBS078-CF_A58 BLBS078-Tilley July 15, 2011 8:31

Canine and Feline, Fifth Edition 103

(Continued) Aortic Thromboembolism A

drugs, in addition to being in considerable activation of the coagulation cascade. Give an PRECAUTIONS r pain and distress. initial dose of 100–200 units/kg IV and then Anticoagulant therapy with heparin, NURSING CARE 200–300 units/kg SC q8h. Alternatively, warfarin, or the thrombolytic drugs may cause r heparin can be administered as a CRI, if there bleeding complications. Fluid therapy is cautiously used as most cats r have advanced myocardial disease. If in is concern about adequate bioavailability via Avoid a non-selective beta-blocker such as congestive heart failure, IV fluid therapy may the SC route, at a dose of 25–35 propranolol as it may enhance peripheral not be necessary. units/kg/hour. Titrate the dose to prolong the vasoconstriction. r Supplemental oxygen therapy or activated partial thromboplastin time POSSIBLE INTERACTIONS approximately two-fold. thoracocentesis may be beneficial if in r Warfarin may interact with other drugs, which congestive heart failure. Aspirin is theoretically beneficial during and may enhance its anticoagulant effects. r Initially, minimally handle the affected legs. after an episode of thromboembolism because of its antiplatelet effects. The dose in cats is an ALTERNATIVE DRUG(S) However, as reperfusion occurs, physical N/A therapy (passive extension and flexion of the 81-mg tablet PO q48–72h. Vomiting and legs) may speed full recovery. diarrhea are not uncommon. Some specialists r Do not perform venipuncture on the advocate a mini dose of 5 mg/cat q72h. affected legs. Antithrombotic dose recommendations for r FOLLOW-UP These cats may have difficulty posturing to dogs range from 0.5–2 mg/kg q24h. Always give aspirin with food. urinate and may need to have their bladders r PATIENT MONITORING Clopidogrel is an antiplatelet aggregation r expressed to prevent overdistention or urine ECG monitoring while the cat is in hospital drug. Cat dose is 18.75 mg/cat (one-fourth of scald. is helpful to detect reperfusion injury and 75 mg tablet) PO q24h. Dog dose is ACTIVITY hyperkalemia related ECG changes. approximately 1 mg/kg q24h. Clopidogrel r Monitoring electrolytes and renal Restrict activity and stress can be used either in combination or instead parameters periodically may be helpful to DIET of aspirin. r optimize management of the cardiac disease. Buprenorphine is used for analgesia and r Initially, most cats are anorexic. Tempt these Examine the legs frequently to assess clinical sedation at a dose of 0.005–0.02 mg/kg IV, cats with any type of diet to keep them eating response. Initially, APTT should be SC, or PO q6–8h. For stronger analgesia, use and avoid hepatic lipidosis. performed once daily to titrate the heparin fentanyl or hydromorphone. CLIENT EDUCATION r dose. Acepromazine may be cautiously used for its r r If warfarin is used, PT or INR is measured Short- and long-term prognosis is poor. sedative and vasodilatory properties at a dose r approximately 3 days after initiation of Most cats will reembolize. Most cats that of 0.01–0.02 mg SC q8–12h. r therapy and then weekly until the desired survive an initial episode will be on some type Warfarin, a vitamin K antagonist, is the anticoagulant effect is reached. Thereafter, of anticoagulant therapy that may require anticoagulant most widely used in humans measure three to four times yearly or when frequent reevaluations and an indoor lifestyle. and has been proposed for prevention of r drug regimen is altered. Most cats that survive an initial episode will reembolization in cats surviving an initial recover complete function to the legs; episode. The initial dose is 0.25–0.5 mg/cat PREVENTION/AVOIDANCE however, if ischemia was severe and PO q24h. Overlap with heparin therapy for Because of the high rate of reembolization, prolonged, sloughing of parts of the distal 3 days. The dose is then adjusted to prolong prevention with either aspirin, clopidogrel, extremities or persistent neurological deficits the prothrombin time approximately two warfarin, or LMWH is strongly may result. In one study, approximately 15% times its baseline value or to attain an recommended. of cats had permanent neuromucscular international normalized ratio of 2 to 4. POSSIBLE COMPLICATIONS abnormalities after surviving the initial r Long-term management with warfarin can be Bleeding with the anticoagulant therapy. embolic event. r challenging because of frequent monitoring Permanent neurological deficits or muscular SURGICAL CONSIDERATIONS and dose adjustments in addition to bleeding r abnormalities in the hind limbs may arise Surgical embolectomy typically is not complications. with prolonged ischemia. r r recommended because these patients are high Low molecular weight heparin has recently Recurrent congestive heart failure or sudden risk for surgery because of severe heart disease. been proposed for the long-term prevention death. r r Rheolytic thrombectomy has been used of feline ATE. LMWH has a more predictable Reperfusion injury and death usually with limited success in a small number of cats relationship between dose and response than associated with hyperkalemic arrhythmias. with ATE. warfarin and does not need monitoring or EXPECTED COURSE AND PROGNOSIS dose adjustments. It also has a lower risk of r bleeding complication. The main Expected course is days to weeks for full recovery of function to the legs. disadvantage of LMWH is high drug cost and r the injectable route of administration. The Prognosis in general is poor. In two large MEDICATIONS ∼ two LMWHs that have been used in feline studies, 60% of cats were euthanized or DRUG(S) OF CHOICE died during the initial thromboembolic r ATE are: dalteparin (100 units/kg SC Thrombolytic therapy such as streptokinase, q12–24h) and enoxaparin (1 mg/kg SC episode. Long-term prognosis varies between urokinase, and tissue plasminogen activator is q12–24h). Best dose unknown. LMWH 2 months to several years; however, the used extensively in humans and infrequently usually started q24h due to cost. Some studies average is a few months with treatment. in cats. These drugs are expensive and carry a suggest q6h dosing necessary for stable blood Predictors of poorer prognosis include < ◦ significant risk for bleeding complications; levels, but may increase bleeding risk. hypothermia ( 99 F) and congestive heart they have not demonstrated improved CONTRAINDICATIONS failure. One study demonstrated a median treatment efficacy and thus are rarely used in survival time of 77 days in cats with general practice. N/A congestive heart failure and 223 days in cats r Unfractionated heparin is the preferred drug without congestive heart failure. in general practice. It has no effect on the established clot; however, it prevents further BLBS078-CF_A58 BLBS078-Tilley July 15, 2011 8:31

104 Blackwell’s Five-Minute Veterinary Consult

A Aortic Thromboembolism (Continued)

r Predictors of better prognosis include SEE ALSO Laste NJ, Harpster NK. A retrospective study r normothermia, single leg affected, and Cardiomyopathy, Dilated—Cats of 100 cats with feline distal aortic r presence of motor function on initial exam. Cardiomyopathy, Hypertrophic—Cats thromboembolism: 1977–1993. JAAHA r r Recurrence of ATE is common. Cardiomyopathy, Restrictive—Cats 1995, 31:492–500. ABBREVIATIONS Smith CE, et al. Use of low molecular weight r APTT = activated partial thromboplastin heparin in cats: 57 cases (1999–2003). time JAVMA 2004, 225:1237–1241. r MISCELLANEOUS ATE = aortic thromboembolism Smith SA. Feline arterial thromboembolism: r CRI = constant rate infusion An update. Vet Clin North Am Small Anim ASSOCIATED CONDITIONS r ECG = electrocardiogram Pract 2004, 34:1245–1271. See “Causes” and “Risk Factors” r INR = international normalized ratio Smith SA. Arterial thromboembolism in cats: AGE-RELATED FACTORS r LMWH = low molecular weight heparin Acute crisis in 127 cases (1992–2001) and r N/A PT = prothrombin time long-term management with low dose ZOONOTIC POTENTIAL aspirin in 24 cases. J Vet Intern Med 2003, Suggested Reading 17:73–83. None Cole SG, Drobatz KJ. Emergency Author Teresa C. DeFrancesco PREGNANCY/FERTILITY/BREEDING management and critical care. In: Tilley LP, Consulting Editor Larry P. Tilley and Francis N/A Smith FWK, Oyama MA, Sleeper MM, W.K. Smith, Jr. SYNONYMS eds., Manual of Canine and Feline r Saddle thromboembolism Cardiology, 4th ed. St. Louis: Saunders r Client Education Handout Systemic thromboembolism Elsevier, 2008, pp. 342–355. available online BLBS078-CF_A59 BLBS078-Tilley March 22, 2011 7:27

Canine and Feline, Fifth Edition 105 Apudoma A

r r Iron-deficiency anemia secondary to Omeprazole—a proton pump inhibitor; the gastrointestinal bleeding. most potent inhibitor of gastric acid secretion r Increased BUN secondary to available; highly effective and expensive. BASICS r gastrointestinal bleeding. Sucralfate—adheres to ulcerated gastric r OVERVIEW Hypoproteinemia. mucosa and protects it from acid; promotes r r Tumors of endocrine cells that are capable Electrolyte abnormalities with chronic healing by binding pepsin and bile acids and of amine precursor uptake and vomiting. stimulating local prostaglandins. decarboxylation and secretion of peptide OTHER LABORATORY TESTS CONTRAINDICATIONS/POSSIBLE r hormones; the tumors are named after the Serum gastrin concentration normal or INTERACTIONS hormone they secrete. high-normal in patients with gastrinoma. r r Because sucralfate may be less effective in an APUD cells are generally found in the Provocative test of gastrin alkaline environment, and may reduce the gastrointestinal tract and CNS. r secretion—increased gastrin concentration absorption of other drugs, it should be given Gastrin- and pancreatic after intravenous calcium gluconate or secretin 1–2 hours prior to antacid drugs. polypeptide-secreting tumors are discussed administration suggests gastrinoma; see here; insulinoma and glucagonoma are Appendix II for protocol and interpretation. discussed separately. r IMAGING Hypergastrinemia from gastrin-secreting tumors causes gastritis and duodenal Abdominal ultrasound sometimes FOLLOW-UP hyperacidity, which can cause gastric demonstrates a pancreatic mass but is usually PATIENT MONITORING normal. r ulceration, esophageal dysfunction from Physical examination and clinical signs are chronic reflux, and intestinal villous atrophy. DIAGNOSTIC PROCEDURES r r the most useful measures of treatment High concentration of pancreatic Endoscopy with gastric and duodenal effectiveness and disease progression. polypeptide also causes gastric hyperacidity biopsy. r r Gastroscopy can monitor progression of and its consequences. Aspirate any detectable masses because of gastritis but is not necessary. r SIGNALMENT suspicion of mast cell disease. Abdominal radiography or ultrasound may r r Gastrinoma—rare in dogs and cats; age If no detectable masses exist, examine a detect development of abdominal masses. range 3–12 years, mean 7.5 years (dogs). buffy coat smear for mast cells. EXPECTED COURSE AND PROGNOSIS r PATHOLOGIC FINDINGS r Pancreatic polypeptide—extremely rare in Difficult to predict r r dogs. Endoscopic biopsy reveals gastrointestinal Patients with gastrinoma have been SIGNS ulceration. controlled on medical management for r r Vomiting Histopathologic examination of pancreatic months to years. r r Weight loss tumors reveals findings consistent with islet No cure available. r Anorexia cell tumor but not specific for hormone type. r r Diarrhea Immunocytochemical staining can aid in r Lethargy, depression the specific diagnosis. r r Polydipsia Histopathologic examination also can reveal MISCELLANEOUS r Melena metastasis to liver and regional lymph nodes. r SEE ALSO Abdominal pain r Hematemesis Gastroduodenal Ulcer Disease r Hematochezia ABBREVIATIONS r r Fever TREATMENT APUD = amine precursor uptake and r CAUSES & RISK FACTORS Tell owner that most APUDomas are decarboxylation r = malignant and have metastasized by the time CNS central nervous system Unknown r = of diagnosis and that long-term control is NSAID nonsteroidal anti-inflammatory often difficult. drug r Aggressive medical management can Suggested Reading sometimes palliate signs for months to years. DIAGNOSIS r Lurye JC, Behrend EN. Endocrine tumors. Surgical exploration and excisional biopsy of Vet Clin North Am Small Anim Pract 2001, DIFFERENTIAL DIAGNOSIS a pancreatic mass are important both r 31(5):1083–1110, ix–x. Other conditions associated with diagnostically and therapeutically. r Zerbe CA. Islet cell tumors secreting insulin, hypergastrinemia, gastric hyperacidity, and Medical management is useful for gastric pancreatic polypeptide, gastrin, or glucagon. gastrointestinal ulceration. hyperacidity. r In: Kirk RW, Bonagura JD, eds., Current Uremia. r Veterinary Therapy XI. Philadelphia: Hepatic failure, r Saunders, 1992, pp. 368–375. Drug-induced ulceration (e.g., NSAIDs or Author Thomas K. Graves steroids). r MEDICATIONS Consulting Editor Deborah S. Greco Inflammatory gastritis. r Stress-induced ulceration. DRUG(S) r r Mast cell disease. Histamine H2-receptor CBC/BIOCHEMISTRY/URINALYSIS antagonists—cimetidine, ranitidine, and r famotidine; decrease acid secretion by gastric Normal or reflect the chronic effects of parietal cells. general disease. BLBS078-CF_A60 BLBS078-Tilley March 22, 2011 7:28

106 Blackwell’s Five-Minute Veterinary Consult A Arsenic Poisoning

r OTHER LABORATORY TESTS Signs of toxicosis (pain at injection site, Arsenic concentration—test urine, vomitus, vomiting, tremors, convulsions) subside as or stomach contents (acute poisoning), BAL is excreted over 3–4 hours. BASICS r kidney, liver (subacute), hair (chronic); Releases arsenic, which may worsen signs; OVERVIEW decreases dramatically in urine, kidney, and give additional BAL. r Caused by herbicides, insecticides, wood liver 1–2 days after exposure; unreliable in Other Drugs preservatives, and treatments for blood blood. DMSA (succimer)—less toxic than BAL; parasites. IMAGING r effective oral treatment for lead poisoning in Leads to disruption of many important N/A small animals. Potentially useful for arsenic metabolic reactions. r DIAGNOSTIC PROCEDURES poisoning but controlled studies for treatment Exposure—oral most common; of arsenic-poisoned dogs and cats not found N/A percutaneous exposure may cause systemic in the literature. toxicosis. PATHOLOGIC FINDINGS r SIGNALMENT Peracute poisoning—death without lesions. r r Cats and dogs Gastrointestinal tract lesions—common and r Any breed, age, or sex severe; reddening of the gastric mucosa and FOLLOW-UP proximal small intestine; watery SIGNS r gastrointestinal content; blood and sloughed Prognosis is grave with high-dose exposure, Acute Exposure mucosa in feces. unless the diagnosis is made and treatment is r r Abdominal pain Liver—soft, yellow liver. started early. r r r Vomiting Lungs—congested; edematous. Monitor closely for signs of BAL toxicosis. r r Weakness Skin lesions (cutaneous r Diarrhea exposure)—blistering; edema; cracking; r Hematochezia bleeding; secondary infections. r Rapid weak pulse MISCELLANEOUS r Prostration r SEE ALSO Subnormal temperature r Collapse Poisoning (Intoxication) r TREATMENT ABBREVIATIONS Death r Remove arsenic source. r = Subchronic to Chronic Oral Exposure r BAL British anti-Lewisite r Emetics followed by gastric lavage—if r = Anorexia DMSA 2,3-dimercaptosuccinic acid r vomiting has not occurred. r Weight loss Promote excretion. Suggested Reading r CAUSES & RISK FACTORS Dialysis in cases of renal failure. Garland T. Arsenic. In: Gupta RC, ed., r r Oral, percutaneous, or therapeutic exposure Appropriate fluid therapy. Veterinary Toxicology: Basic and Clinical r to arsenic-containing compounds. Kaolin-pectin soothes gastrointestinal tract. Principles. New York: Academic Press, r r Toxicity varies greatly. 2007, pp. 418–421. r Keep patient warm and comfortable. Weak and debilitated animals more DIET National Research Council. Arsenic. In: susceptible. Mineral Tolerance of Animals, 2nd ed. When patient is able to keep food down, Washington, DC: National Academies provide small amounts of high-quality food; Press, 2005, pp. 31–45. increase as tolerated. Neiger RD. Arsenic. In: Peterson ME, Talcott DIAGNOSIS PA, eds., Small Animal Toxicology, 2nd ed. Philadelphia: Saunders, 2006, pp. 592–602. DIFFERENTIAL DIAGNOSIS Author Regg D. Neiger r Heavy metal toxicosis MEDICATIONS Consulting Editor Gary D. Osweiler r Ingestion of caustic agents r DRUG(S) Ingestion of irritating plants r Dimercaprol(BAL) Canine or feline parvovirus r Give 2.5–5 mg/kg in oil by deep IM CBC/BIOCHEMISTRY/URINALYSIS injection q4h for 2 days; q8h on day 3; q12h Serum biochemical analysis—evidence of liver for up to 10 days; 5 mg/kg in only acutely and renal damage. affected patients on day 1. BLBS078-CF_A61 BLBS078-Tilley March 22, 2011 7:29

Canine and Feline, Fifth Edition 107 Arteriovenous Fistula A

(liver), seizures (brain), paresis (spinal cord), clinical signs related to the arteriovenous and dyspnea (lung). fistula, since lesions may increase in size. r CAUSES & RISK FACTORS Surgery can be difficult and labor-intensive BASICS r Rarely, a congenital lesion. and may require blood transfusion; OVERVIEW r Acquired arteriovenous fistula typically delineation of lesion before surgery by angiography is advised. An abnormal, low-resistance connection results from local damage to vasculature r between an artery and vein. A large secondary to trauma, surgery, venipuncture, Although surgery is often successful, arteriovenous fistula allows a significant perivascular injection (e.g., barbiturates), or arteriovenous fistula may recur. In some fraction of the total cardiac output to bypass tumor. animals, amputation of the affected part may be necessary. the capillary bed. The resulting increase in r cardiac output may lead to (high-output) Transcatheter embolization with congestive heart failure. Location of vaso-occlusive coils is a newer treatment option. Potential advantages include relatively arteriovenous fistula varies. Reported sites DIAGNOSIS include the head, neck, ear, tongue, limbs, non-invasive treatment and intravascular flank, spinal cord, cerebrum, lung, liver, vena DIFFERENTIAL DIAGNOSIS access to remote lesions. r cava, and gastrointestinal tract. Usually seen The lesion may look like an aneurysm or as an acquired lesion. false aneurysm. r SIGNALMENT Bizarre clinical findings, depending on r Dogs and cats (rare in both) location of arteriovenous fistula, may suggest MEDICATIONS r No specific age, breed, or sex predilections other disease processes; arteriovenous fistula DRUG(S) may be a late diagnostic consideration. r known Concurrent medical treatment depends on SIGNS CBC/BIOCHEMISTRY/URINALYSIS the site of the arteriovenous fistula and Historical Findings May reflect damage to systems in the vicinity secondary clinical features. r of the lesion, i.e., biochemical abnormalities r Animals with acquired disease often have a Medical treatment for congestive heart history of trauma to the affected area. suggesting hepatic, renal, or other organ failure may be required before surgery. r Owner may notice a warm, non-painful dysfunction are possible. CONTRAINDICATIONS/POSSIBLE swelling at the site. OTHER LABORATORY TESTS INTERACTIONS r History consistent with impending or overt N/A Avoid excessive fluid administration; animals CHF is possible depending on shunt size and IMAGING with arteriovenous fistula are volume duration. r Thoracic Radiographic Findings overloaded. Other historical findings depend on the r location of the lesion. Cardiac enlargement and pulmonary r The shunt may cause local organ overcirculation in some animals with dysfunction. hemodynamically significant arteriovenous fistula. FOLLOW-UP Physical Examination Findings r Echocardiographic Findings Post-operative reevaluation is needed to Vary and depend on location of the r arteriovenous fistula. May allow imaging of the arteriovenous determine whether arteriovenous fistula r fistula depicting its cavernous nature. recurred. Signs of CHF (e.g., coughing, dyspnea, r tachypnea, and exercise intolerance) may Doppler ultrasound may demonstrate develop in animals with long-standing disease high-velocity, turbulent flow within the lesion. and high blood flow. Angiography r r Bounding pulses are present in some Selective angiography outlines the lesion, MISCELLANEOUS animals because of high ejection volume and may be necessary for definitive diagnosis, and SEE ALSO rapid runoff through the arteriovenous fistula. is highly desirable for presurgical evaluation. r Congestive Heart Failure, Left-Sided Continuous murmur (bruit) at the site Placement of the catheter close to the lesion ABBREVIATIONS caused by blood flow through the lesion. and rapid injection is necessary; high-volume r = Cautious compression of the artery blood flow dilutes the contrast medium CHF congestive heart failure proximal to the lesion abolishes the bruit. quickly. Suggested Reading When blood flow is high, this compression DIAGNOSTIC PROCEDURES Fox PR, Petrie J-P, Hohenhaus AE. Peripheral may also elicit an immediate reflex decrease in N/A vascular disease. In: Ettinger SJ, Feldman heart rate (Branham’s sign). r EC, eds., Textbook of Veterinary Internal Edema, ischemia, and congestion of organs Medicine, 6th ed. St. Louis: Elsevier, 2005. and tissues caused by high venous pressure in Author Donald J. Brown the proximity of the lesion. r TREATMENT Consulting Editors LarryP.TilleyandFrancis If the lesion is on a limb, pitting edema, r W.K. Smith, Jr. lameness, ulceration, scabbing, and gangrene Historically definitive treatment has may result. required surgery to divide and remove r Lesion near vital organs may cause signs abnormal vascular connections. Definitive associated with organ failure such as ascites treatment is recommended in animals with BLBS078-CF_A62 BLBS078-Tilley March 22, 2011 7:31

108 Blackwell’s Five-Minute Veterinary Consult A Arteriovenous Malformation of the Liver

r Abdominal effusion—pure transudate Multi-Sector CT r (ascites; protein-losing nephropathy, Non-invasive contrast imaging of hepatic BASICS protein-losing enteropathy, liver disease); vasculature; 3-dimensional reconstruction modified transudate (congenital cardiac illustrates malformation. OVERVIEW malformations, right-sided heart failure, Echocardiography r r Intrahepatic arteriovenous fistulae are pericardial tamponade, supradiaphragmatic Rule out right-sided heart disease, communications between proper hepatic vena caval obstruction, neoplasia, portal vein pericardial disease, and vena caval occlusion. thrombosis); hemorrhage. arteries and intrahepatic portal veins that r DIAGNOSTIC PROCEDURES impose hepatofugal splanchnic circulation. Portal hypertension—chronic hepatic r r Exploratory laparotomy for lobectomy/AV Blood flows from the hepatic artery to the disease, juvenile fibrosing liver disease, fistula resection. portal system retrograde into the vena cava non-cirrhotic or idiopathic portal r Liver biopsy—collect samples from affected through multiple APSS. hypertension, cirrhosis, portal thrombi. r and unaffected liver lobes; “normal” liver AV fistulae are uncommon, usually CBC/BIOCHEMISTRY/URINALYSIS often has severe vascular arterialization (more congenital, but may be acquired (surgical r Erythrocyte microcytosis (APSS), target severe than associated with PSVA or injury, trauma, neoplasia). cells. r non-cirrhotic portal hypertension). SIGNALMENT Hypoalbuminemia, serum globulin normal r Dogs,lesscommonincats or low; ALP and ALT activity normal or r Age-related presentation (congenital): moderately increased; variable low BUN and < hypocholesterolemia. 2yrs r r Hyposthenuria or isosthenuria. TREATMENT No sex or breed predilection r SIGNS Ammonium biurate crystalluria. APPROPRIATE HEALTH CARE OTHER LABORATORY TESTS Inpatient for HE and treatment of ascites General Comments r r prior to surgical AV fistula resection or Vague or acute illness; present for signs of Coagulation tests—variable abnormalities but may be normal; low protein C. percutaneous selective embolization. portal hypertension and APSS: ascites, HE. r Peritoneal fluid—pure transudate (total NURSING CARE Historical Findings r r protein < 2.5 g/dL) or modified transudate. Dogs may have a normal transition to r Diet—restrict nitrogen intake to ameliorate Total serum bile acids—fasting values HE and hyperammonemia; restrict sodium growth foods, unlike PSVA that demonstrate usually high; post-prandial values always high; (ascites). HE. r r shunting pattern. HE—resolve endoparasitism and electrolyte Acute onset of ascites or HE. r r Plasma ammonia—usually high. Lethargy, anorexia, vomiting, diarrhea, and hydration disturbances, treat infections, IMAGING weight loss, polydipsia, dementia, abdominal initiate treatments to alter enteric uptake and distention. Radiography formation of HE toxins (see Hepatic r Encephalopathy). Physical Examination Findings Abdominal effusion. r r r Ascites—mobilize by restricting activity and Lethargic, poor body condition, ascites; Microhepatica or normal size due to large liver lobe associated with AV fistulae. sodium intake; abdominocentesis for tense enlarged liver segment containing AV r Renomegaly. ascites impairing ventilation or nutrition; and fistula(e) rarely palpated. combined use of furosemide and r Abdominal Ultrasonography Hepatic bruit rarely auscultated. r spironolactone (see Hypertension, Portal and Abdominal effusion. CAUSES & RISK FACTORS r below). r Liver lobe with AV fistula—large compared Usually reflect congenital vascular SURGICAL CONSIDERATIONS to most other lobes that are atrophied due to malformations (single or multiple vessels) r portal hypoperfusion. Resection of liver lobe containing AV fistula reflecting failed differentiation of common r Tortuous anechoic tubular structures (AV is complicated by other vascular malformation embryologic anlage. r fistulae) with unidirectional pulsating or within the liver; recurrent illness may occur; Rarely secondary to abdominal trauma, turbulent flow with color-flow Doppler. percutaneous selective acrylamide vascular inflammation, neoplasia, surgical r Hepatic artery and/or portal vein branches embolization may result in interventions, or diagnostic procedures (e.g., may appear tortuous. thromboembolism, improvement (may be liver biopsy). r r Hepatofugal portal flow through APSS. temporary), or continued clinical signs. Portal hypertension establishes APSS. r r Renomegaly. Multiple microscopic vascular r Calculi or sand-like uroliths: urinary malformations continue portal hypertension bladder or renal pelvis. and APSS. r r Rule out portal thrombosis. Do not ligate APSS nor band the vena cava. DIAGNOSIS Radiographic Contrast Angiography r DIFFERENTIAL DIAGNOSIS Not indicated in most cases. r r Venous portography—confirms APSS. CNS signs—infectious disorders (e.g., r MEDICATIONS distemper); toxicity (e.g., lead); Hepatic arteriography—required to hydrocephalus; idiopathic epilepsy; metabolic demonstrate AV communication (celiac trunk DRUG(S) disorders (e.g., hypoglycemia, or anterior mesenteric artery contrast Hepatic Encephalopathy hypo-/hyperkalemia); HE (e.g., acquired liver injection). See Hepatic Encephalopathy disease or PSVA). BLBS078-CF_A62 BLBS078-Tilley March 22, 2011 7:31

Canine and Feline, Fifth Edition 109

(Continued) Arteriovenous Malformation of the Liver A

Ascites CONTRAINDICATIONS r Furosemide (0.5–2 mg/kg PO IM or IV Avoid drugs that rely on hepatic q12–24h)—best used combined with biotransformation and drugs that react with MISCELLANEOUS spironolactone. GABA-benzodiazepine receptors. r Spironolactone (0.5–2 mg/kg PO SEE ALSO r q12h)—initiate double dose as loading dose Ascites r one time. Hepatic Encephalopathy r r Chronic diuretic therapy individualized to Hypertension, Portal FOLLOW-UP r response, 4- to 7-day intervals. Portosystemic Shunting, Acquired r PATIENT MONITORING r Diuretic resistant ascites may require Portosystemic Vascular Anomaly, therapeutic abdominocentesis to initiate Biochemistry—initially bimonthly to Congenital monthly until stabilized, thereafter quarterly; diuresis or use of vasopressin V2 receptor ABBREVIATIONS antagonist. monitor for hypoalbuminemia, infection, and r ALP = alkaline phosphatase optimal management of HE. r Bleeding Tendencies ALT = alanine aminotransferase EXPECTED COURSE AND PROGNOSIS r See Coagulopathy of Liver Disease APSS = acquired portosystemic shunt r r Prognosis fair if patient survives surgical AV = atrioventricular Gastrointestinal Hemorrhage r r resection of AV fistula. CNS = central nervous system Histamine type-2 receptor antagonists r r Most patients require indefinite nutritional CT = computed tomography (famotidine 0.5 mg/kg PO, IV, or SC r and medical management (HE, ascites) GABA = gamma-aminobutyric acid q12–24h); give indefinitely, GI bleeding and r because of co-existing microscopic vascular GI = gastrointestinal ulceration are common, long-term problems. r r lesions (all liver lobes); APSS persists HE = hepatic encephalopathy Gastroprotectant—sucralfate 0.25-0.5 g/ r 10 kg PO q8–12h. requiring continued management of HE. PSVA = portosystemic vascular anomalies r Eliminate endoparasitism. Author Sharon A. Center Consulting Editor Sharon A. Center BLBS078-CF_A63 BLBS078-Tilley March 22, 2011 7:32

110 Blackwell’s Five-Minute Veterinary Consult A Arthritis (Osteoarthritis)

r evidence of DJD on radiographs. Clinical and Rickettsia to evaluate for infectious problems are more prevalent in larger, arthritis. overweight, and very active animals. IMAGING BASICS r r Primary DJD is rare. Radiographic changes—include joint DEFINITION SIGNALMENT capsular distention, osteophytosis, Osteoarthritis or degenerative joint disease is Species enthesiophytosis, soft-tissue thickening, and the progressive and permanent deterioration Dogs and cats narrowed joint spaces; in severely affected of the articular cartilage of diarthrodial Mean Age and Range patients: subchondral sclerosis, subchondral (synovial) joints due to primary (idiopathic) r bone cysts, attrition of subchondral bone, Secondary DJD due to congenital disorders and secondary causes. mineralization of joint soft tissues, and (OCD, hip dysplasia) seen in immature PATHOPHYSIOLOGY intra-articular calcified bodies (joint mice). animals; some present with DJD signs when r r r Radiographic severity often does not DJD is initiated by mechanical older (hip and elbow dysplasia). Secondary r correlate with clinical severity. Stress stress—traumatic injury, instability, abnormal to trauma—any age. conformation, abnormal activity, etc. radiography may identify underlying r SIGNS Metalloproteinases, serine proteases, and instability and accentuate joint incongruity cysteine protease enzymes are released from Historical Findings (e.g., distraction index, passive hip laxity of r the coxofemoral joint is predictive of hip damaged chondrocytes, causing collagen Dogs—decreased activity level, unwilling to r degradation and loss of collagen cross-linking perform certain tasks; intermittent lameness DJD). Bone nuclear scintigraphy can assist r in cartilage. Collagen synthesis is altered, or stiff gait that slowly progresses; possible in localizing subtle DJD. resulting in decreased collagen/proteoglycan history of joint trauma, OCD, or DIAGNOSTIC PROCEDURES r interaction and reduced hydrophyllic matrix developmental disorders; may be exacerbated Arthrocentesis and synovial fluid r by exercise, long periods of recumbency, and properties. Cartilage matrix is further r analysis—cell counts are normal or slightly compromised by increased breakdown of cold weather. Cats—overt lameness may not increased (< 2,000–5,000 cells/mL) PGAs and manufacture of poorer-quality be seen. May have difficulty grooming, r predominantly mononuclear (macrophages) PGAs. Nitric oxide is released, which jumping onto furniture, or accessing the litter and occasional synovial lining cells. r mediates cartilage breakdown and supports box; increased irritability. Bacterial culture of synovial fluid—negative. r chronic inflammation. Chondrocyte Physical Examination Findings Biopsy of synovial tissue to rule out apoptosis is facilitated by cyclooxygenase-2 r r Stiff-legged or altered gait (e.g., bunny neoplasia or immune-mediated arthridites enzymes. Synovial membrane inflammation hopping in hip dysplasia) or non-use of leg. (lymphocytic plasmacytic synovitis, SLE). r r r results in decreased viscosity of the synovial Decreased range of motion. Crepitus. Force plate analysis or static load bearing r r fluid, reducing lubrication. Poorer-quality Joint swelling (effusion and/or thickening of allows quantification of reduced limb loading. synovial fluid reduces oxygen and nutrient r r r the joint capsule). Joint pain. Joint PATHOLOGIC FINDINGS supply to the chondrocytes. Subchondral r r instability. Gross joint deformity. Fibrillation or erosion of articular cartilage. bone becomes sclerotic, worsening loading r CAUSES Eburnation and sclerosis of subchondral qualities of the bone and overlying cartilage. r r r Primary—no known cause. bone. Thickening and fibrosis of the joint Pain of DJD results from stimulation of r r pain receptors in the tendons, ligament, Secondary—results from an initiating capsule. Synovial fluid can be grossly r cause: abnormal wear on normal cartilage normal to thin and watery, usually increased subchondral bone, and joint capsule. The r (e.g., joint instability, joint incongruity, volume. Synovial villous hypertrophy and result of these processes is progressive cartilage r degradation ranging from fibrillation to deep trauma to cartilage or supporting soft tissues) hyperplasia. Osteophytes and fissuring of cartilage. Full-thickness cartilage or normal wear on abnormal cartilage (e.g., enthesiophytes at joint capsule attachments r osteochondral defects). and adjacent to the joint. loss can eventually occur. Peri-articular r fibrosis occurs to reduce joint motion (and RISK FACTORS Neovascularization or pannus in severe cases r pain), leading to poorer vascularity of the Working, athletic, and obese dogs place over joint surfaces. r r synovial membrane. Osteophytes and more stress on their joints. Dogs with enthesiophytes develop around and within the disorders that affect collagen or cartilage joint to increase the load-bearing surface area. (Cushing’s disease, diabetes mellitus, r These changes reduce functionality and hypothyroidism, hyperlaxity, prolonged, TREATMENT eventually lead to ankylosis. steroids). APPROPRIATE HEALTH CARE r r SYSTEMS AFFECTED Medical—usually tried initially. Surgical Musculoskeletal—diarthrodial joints options—to improve joint geometry or GENETICS remove bone-on-bone contact areas. r DIAGNOSIS Primary DJD is rare—once associated with NURSING CARE r r a colony of beagles. Dogs—causes of DIFFERENTIAL DIAGNOSIS Physical therapy—very beneficial. r r secondary DJD are varied, including hip and Neoplastic (synovial cell sarcoma; rarely, Maintaining or increasing joint r elbow dysplasias, osteochondrosis dissecans, chondrosarcoma; osteosarcoma). Septic motion—passive range of motion exercises, r patellar luxations, congenital shoulder arthritis (caused by bacteria; spirochetes; L massage, cavaletti, swimming. Pain luxation, Legg-Perthes, and cranial cruciate forms in cats; Mycoplasma; Rickettsia; management—cold and heat therapy. r r ligament rupture. Cats—causes of Ehrlichia; viruses, such as feline calicivirus; Muscle tone/strengthening—swimming r secondary DJD are patellar luxation, hip fungi, and protozoa). Immune-mediated (aerobic exercise with minimal weight dysplasia, and arthropathy. arthritis (erosive vs. non-erosive). bearing); controlled leash walks up hills or on INCIDENCE/PREVALENCE OTHER LABORATORY TESTS soft surfaces, such as sand or dry or r r Dogs—very common; 20% of dogs older Coombs’ test, ANA, and rheumatoid factor underwater treadmill. than 1 year have some degree of DJD. may help to rule out immune-mediated r r Cats—90% of cats over 12 years of age had arthritis. Serum titers for Borrelia, Ehrlichia, BLBS078-CF_A63 BLBS078-Tilley March 22, 2011 7:32

Canine and Feline, Fifth Edition 111

(Continued) Arthritis (Osteoarthritis) A

ACTIVITY CONTRAINDICATIONS Suggested Reading r Limited to a level that minimizes aggravation NSAIDs must not be given with steroids Aragon CL, Hofmeister EH, Budsberg SC. r of clinical signs Acetaminophen must not be given to cats Systematic review of clinical trials of DIET PRECAUTIONS treatments for osteoarthritis in dogs. r r Weight reduction for obese NSAIDs—may cause gastric ulceration. JAVMA 2007, 230(4):514–521. r patients—decreases stress placed on arthritic COX-2 selective drugs may interfere with Baime MJ. Glucosamine and chondroitin r r joints. Omega n-6 and n-3 fatty acids liver function. When switching sulphate did not improve pain in decrease the production of certain NSAIDs—wait 3 days for washout before osteoarthritis of the knee. Evid Based Med prostaglandins and modulate inflammation. starting new drug. 2006, 11(4):115. Beale BS, Goring RL. Degenerative joint CLIENT EDUCATION POSSIBLE INTERACTIONS r disease. In: Bojrab MJ, ed., Disease Medical therapy is palliative and the Steroids and NSAIDS r Mechanisms in Small Animal Surgery. condition is likely to progress. Discuss ALTERNATIVE DRUG(S) Philadelphia: Febiger, 1993, pp. 727–736. r treatment options, activity level, and diet. Free-radical scavengers. Budsberg SC, Bartges JW. Nutrition and r SURGICAL CONSIDERATIONS Glucocorticoids—inhibit inflammatory osteoarthritis in dogs: Does it help? Vet r Arthrotomy—used to remove aggravating mediators and cytokines; however, chronic Clin North Am Small Anim Pract 2006, causes (e.g., fragmented coronoid process, use delays healing and initiates damage to 36(6):1307–1323. un-united anconeal process, osteochondral articular cartilage; potential systemic side Glass GG. Osteoarthritis. Dis Mon 2006, r flaps). Arthroscopy—used to diagnose and effects documented; goal is low-dose (dogs, 52(9):343–362 (human review). remove aggravating causes; flushing the joint 0.5–2 mg/kg; cats, 2–4 mg/kg), alternate-day Hampton T. Efficacy still uncertain for widely r r may be beneficial. Reconstructive therapy. Prednisone—initial dose 1–2 used supplements for arthritis. JAMA 2007 procedures—used to eliminate joint mg/kg PO q24h for dogs and 4 mg/kg PO 297(4):351–352. r instability and correct anatomic problems q24h for cats. Triamcinolone Herrero-Beaumont G, Ivorra JA, et al. r (patella luxation, angular deformity). Joint hexacetonide—intra-articular injection of Glucosamine sulfate in the treatment of removal—femoral head and neck ostectomy, 5mgindogsshowedaprotectiveand knee osteoarthritis symptoms: A r temperomandibular joint arthroplasty. Joint therapeutic effect in one model. randomized, double-blind, replacement—total hip replacement is widely placebo-controlled study using used, total elbow replacement still acetaminophen as a side comparator. r experimental. Joint fusion (arthrodesis)—in Arthritis Rheum 2007, 56(2):555–567. selected chronic cases and for joint instability, FOLLOW-UP Johnston SJ. Osteoarthritis joint anatomy, complete or partial; carpus: generally excellent physiology and pathobiology. Vet Clin outcome; shoulder, elbow, stifle, hock: less PATIENT MONITORING North Am 1997, 27:699–723. predictable outcome. Clinical deterioration—indicates need to Mlacnik E, Bockstahler BA, Muller M, change drug selection or dosage; may indicate Tetrick MA, Nap RC, Zentek J. Effects of need for surgical intervention. caloric restriction and a moderate or intense PREVENTION/AVOIDANCE physiotherapy program for treatment of MEDICATIONS Early identification of predisposing causes and lameness in overweight dogs with osteoarthritis. JAVMA 2006, DRUG(S) OF CHOICE prompt treatment to help reduce progression of secondary conditions, e.g., surgical removal 229(11):1756–1760. NSAIDs Pederson NC. Joint diseases of dogs and cats. r of osteochondral lesions. Inhibit prostaglandin synthesis through In: Ettinger SJ, ed., Textbook of Veterinary r EXPECTED COURSE AND PROGNOSIS cyclooxygenase enzymes. Deracoxib (3–4 r r Internal Medicine, 5th ed. Philadelphia: r mg/kg PO q24h, chewable). Carprofen (2.2 Slow progression of disease likely. Some Saunders, 2000, pp. 1862–1886. r mg/kg PO q12h or q24h). Etodolac (10–15 form of medical or surgical treatment usually Van Der Kraan PM, Van Den Berg WB. r mg/kg PO q24h). Meloxicam (load 0.2 allows a good quality of life. Osteophytes: Relevance and biology. mg/kg PO, then 0.1 mg/kg PO q24h: liquid). Osteoarthritis Cartilage 2007, r Tepoxalin (load 20 mg/kg, then 10 mg/kg 15(3):237–244. r PO q24h). Cats—meloxicam (0.1 mg/kg Author Peter K. Shires PO q24h: liquid). MISCELLANEOUS Consulting Editors Peter K. Shires Acknowledgement The author and editors Chondroprotective/Regenerative SYNONYMS acknowledge the contributions of Brian S. Supplements r r r Degenerative arthritis Degenerative joint Beale and Jennifer J. Warnock in an earlier Supply PSGAG molecules to repair and r r r disease Osteoarthritis Osteoarthrosis edition. regenerate cartilage. Host of products, many ABBREVIATIONS with little production oversight so effects vary r r r ANA = antinuclear antibody COX-2 = widely. Glucosamine and chondroitin r cyclooxygenase-2 DJD = degenerative joint Client Education Handout sulphate—injectable Adequan, oral Cosequin, r disease OCD = osteochondrodysplasia available online oral MSM, mixtures (Glycoflex II, SynFlex, r r r PGA = proteoglycan PSGAGs = etc.). Adequan—clinical study in dogs with r polysulfated glycosaminoglycans NSAID = hip dysplasiam; 4.4 mg/kg IM every 3–5 days r nonsteroidal anti-inflammatory drug SLE = for 8 injections had a positive, temporary r systemic lupus erythematosus effect. Cosequin—trials showed positive effects. BLBS078-CF_A64 BLBS078-Tilley July 15, 2011 9:33

112 Blackwell’s Five-Minute Veterinary Consult A Arthritis, Septic

r r Localized joint heat Make slides immediately; if additional fluid r Decreased range of motion is obtained, place in EDTA tube. r r > BASICS Fever Elevated WBC count— 80% neutrophils CAUSES with > 40,000/mm3 (normal joint fluid < DEFINITION r 10% neutrophils and < 3,000/mm3). Aerobic bacterial organisms—most r Pathogenic microorganisms within the closed common: staphylococci, streptococci, Neutrophils in synovial fluid may show space of one or more synovial joints. coliforms, and Pasteurella degenerative changes (chromatolysis, r PATHOPHYSIOLOGY Anaerobic organisms—most common: vacuolation, nuclear swelling, loss of r Propionibacterium, Peptostreptococcus, segmentation). However, toxic neutrophils are Usually caused by contamination associated not necessary for diagnosis. Fusobacterium,andBacteroides r with traumatic injury (e.g., a direct r Spirochete—Borrelia burgdorferi Definitive diagnosis—neutrophils with penetrating injury such as a bite, gunshot r Mycoplasma phagocytosed bacteria (observed in wound, or foreign object); a sequela to r approximately half of cases) or bacteria in the surgery, arthrocentesis, or joint injection; Fungal agents—Blastomyces, Cryptococcus, and Coccidioides synovial fluid. hematogenous spread of microorganisms r Ehrlichia Synovial Fluid Culture from a distant septic focus; or the extension of r r primary osteomyelitis. Leishmania Positive culture is definitive but not r r necessary for diagnosis. Primary sources of hematogenous Feline calicivirus r infection—urogenital, integumentary RISK FACTORS Must be collected aseptically; requires heavy r sedation or general anesthesia. (including ears and anal sacs), respiratory, Predisposing factors for hematogenous r Place fluid sample in aerobic and anaerobic cardiac, and gastrointestinal systems. infection—diabetes mellitus; culturettes and in blood culture medium. SYSTEMS AFFECTED hypoadrenocorticism (Addison’s disease); r Use 1:9 dilution of synovial fluid to blood immunosuppression. Musculoskeletal—usually affects one joint r culture media. Penetrating trauma to the joint including r GENETICS Culturette samples—cultured immediately surgery. N/A r upon arrival to the laboratory. Existing osteoarthritis or other joint r Blood culture medium—reculturing after INCIDENCE/PREVALENCE damage. r 24 hours of incubation increases accuracy by Relatively uncommon cause of monoarticular Intra-articular injection, particularly if 50% and is the preferred method. arthritis in dogs and cats. steroid injected. r Mycoplasma, bacterial L-forms, and protozoa GEOGRAPHIC DISTRIBUTION require specific culture procedures—contact May be an increased incidence in Lyme laboratory prior to sample collection. disease-endemic areas. Other DIAGNOSIS r SIGNALMENT Synovial biopsy—to rule out Species DIFFERENTIAL DIAGNOSIS immune-mediated joint disease; no more r r Mostcommonindogs Osteoarthritis effective than incubated blood culture r r Trauma medium for growing bacterial organisms. Rare in cats r r Immune-mediated arthropathy Blood and urine cultures if hematogenous Breed Predilections r Post-vaccinal transient polyarthritis source is suspected. Medium to large breeds—most commonly r Greyhound polyarthritis PATHOLOGIC FINDINGS German shepherd dogs, Dobermans, and r Feline progressive polyarthritis r Labrador retrievers. r Synovium—thickened; discolored; often Crystal-induced joint disease r very proliferative. Mean Age and Range Synovial cell sarcoma r Any age; usually between 4 and 7 years Histology—evidence of hyperplastic CBC/BIOCHEMISTRY/URINALYSIS synoviocytes. Predominant Sex r r Hemogram—inflammatory left shift in Increased numbers of neutrophils, Male some cases macrophages, and fibrinous debris. r r SIGNS Other results normal Cartilage—loss of proteoglycan, destruction General Comments OTHER LABORATORY TESTS of articular surface, pannus formation. Always consider the diagnosis in patients with Serologic testing for specific pathogens monoarticular lameness associated with soft IMAGING tissue swelling, heat, and pain. Radiography Historical Findings r TREATMENT r Early disease—may reveal thickened and Lameness—acute onset most common, but APPROPRIATE HEALTH CARE dense periarticular tissues; may see evidence of can present as chronic lameness. r r joint effusion. Often difficult to diagnose Inpatient—initial stabilization; initiate Lethargy r early disease radiographically. systemic antibiotic therapy as soon as fluid is Anorexia r r Late disease—reveals bone destruction, obtained for bacterial culture; consider joint May report previous trauma—dog bite, osteolysis, irregular joint space, discrete drainage/lavage as soon as possible to penetrating injury, prior surgery or other minimize intra-articular injury. erosions, and periarticular osteophytosis. r invasive procedure of the joint. Identify and treat source if hematogenous DIAGNOSTIC PROCEDURES Physical Examination Findings spread is suspected. r Synovial Fluid Analysis r Monoarticular lameness, rarely r Outpatient—long-term management. Increased volume. pauciarticular (four or fewer joints) or r NURSING CARE Turbid fluid. r polyarticular (five or more joints) r Alternating heat and cold Decreased viscosity. involvement. r packing—beneficial in promoting increased r Decreased mucin clot reaction. Joint pain and swelling—commonly carpus, blood flow and decreased swelling. stifle, hock, shoulder, or cubital joint. BLBS078-CF_A64 BLBS078-Tilley July 15, 2011 9:33

Canine and Feline, Fifth Edition 113

(Continued) Arthritis, Septic A

r r Joint immobilization may enhance patient NSAIDs and other analgesics—may help ZOONOTIC POTENTIAL comfort but should not be prolonged due to decrease pain and inflammation. N/A risk of worsening cartilage damage. CONTRAINDICATIONS PREGNANCY/FERTILITY/BREEDING ACTIVITY Avoid fluorinated quinolones in pediatric N/A Restricted until resolution of symptoms patients; they induce cartilage lesions SYNONYMS r DIET experimentally. Infectious arthritis r N/A PRECAUTIONS Joint ill CLIENT EDUCATION Failure to respond to conventional antibiotic SEE ALSO r r Discuss probable cause. therapy—may indicate anaerobic disease or Osteomyelitis r r Warn client about the need for long-term other unusual cause (fungal, spirochete). Polyarthritis, Erosive, Immune-Mediated r antibiotics and the likelihood of residual POSSIBLE INTERACTIONS Polyarthritis, Non-erosive, degenerative joint disease. N/A Immune-Mediated SURGICAL CONSIDERATIONS ALTERNATIVE DRUG(S) ABBREVIATIONS r r Acute disease with minimal radiographic N/A EDTA = ethylene diamine tetra-acetate r changes—general recommendation for initial NSAID = nonsteroidal anti-inflammatory joint decompression via arthrocentesis, and drug r possibly joint lavage via needle arthrocentesis, WBC = white blood cell arthroscopic lavage, or arthrotomy. An FOLLOW-UP Suggested Reading irrigation catheter (ingress/egress) can be PATIENT MONITORING Bennett D, Taylor DJ. Bacterial infective placed in larger joints. Considerable debate r arthritis in the dog. J Small Anim Pract exists regarding superiority of repeated needle Observation for clinical signs of joint pain 1988, 29:207–230. arthrocentesis, arthroscopic lavage, or open and swelling. r Benzioni H, Shahar R, Yudelevitch S, lavage. Repeated synovial fluid cytology to assess r Milgram J. Bacterial infective arthritis of the Chronic disease—may require arthroscopy response to treatment. r coxofemoral joint in dogs with hip or arthrotomy with debridement of the Duration of antibiotic therapy—2 weeks dysplasia. Vet Comp Orthop Traumatol synovium and copious lavage; if appropriate, following resolution of clinical signs. Total 2008, 21:262–266. an irrigation catheter (ingress/egress) may be treatment may be 4–8 weeks or longer Clements DN, Owen MR, Mosely JR, et al. placed to lavage the joint post-operatively. depending on clinical signs and pathogenic r Retrospective study of bacterial infective Lavage—use warmed physiologic saline or organism. r arthritis in 31 dogs. J Small Anim Pract lactated Ringer’s solution (2–4 ml/kg q8h) Persistent synovial inflammation without 2005, 46:171–176. until effluent is clear. Do not add viable bacterial organisms (dogs)—may be Ellison RS. The cytologic examination of povidone/iodine or chlorhexidine to lavage caused by antigenic bacterial fragments or synovial fluid. Semin Vet Med Surg Small fluid. antigen antibody deposition. r r Anim 1988, 3:133–139. Effluent fluid—cytologically monitored Physical therapy—may be needed to Fitch RB, Hogan TC, Kudnig ST. daily for existence and character of bacteria prevent muscle contracture, maintain cartilage Hematogenous septic arthritis in the dog: and neutrophils. health, and maximize normal joint dynamics. r Results of five patients treated nonsurgically Removal of catheters—when effluent fluid PREVENTION/AVOIDANCE with antibiotics. JAAHA 2003, has no bacteria and the neutrophils are If clinical signs recur, early (within 39:563–566. cytologically healthy. r 24–48 hours) treatment provides the greatest Hodgin EC, Michaelson F, Howerth EW. Arthroscopy allows for visual assessment of benefit. Anaerobic bacterial infections causing articular cartilage, lavage, and biopsy, and is a POSSIBLE COMPLICATIONS osteomyelitis/arthritis in a dog. JAVMA less-invasive method of thorough joint lavage r Chronic disease—severe degenerative joint 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 arthritis in 19 dogs. Australian Vet J 1999, 77:233–237. MEDICATIONS 24–48 hours) responds well to antibiotic therapy. MacWilliams PS, Friedrichs KR. Laboratory DRUG(S) OF CHOICE r evaluation and interpretation of synovial r Delayed diagnosis or resistant or highly Pending culture susceptibility virulent organisms—guarded to poor fluid. Vet Clin North Am Small Anim Pract data—bactericidal antibiotics, such as prognosis. 2003, 33:153–178. first-generation cephalosporin or Author Sherisse A. Sakals and Spencer A. amoxicillin-clavulanic acid, preferred. Johnston r Choice of antimicrobial drugs—primarily Consulting Editors Peter K. Shires depends on in vitro determination of MISCELLANEOUS susceptibility of microorganisms; toxicity, Client Education Handout frequency, route of administration, and ASSOCIATED CONDITIONS available online expense also considered; most penetrate the N/A synovium well; need to be given for a AGE-RELATED FACTORS minimum of 4–8 weeks. N/A BLBS078-CF_A65 BLBS078-Tilley March 22, 2011 7:38

114 Blackwell’s Five-Minute Veterinary Consult A Ascites

r Ultrasonography of the liver, spleen, pancreas, kidney, bladder, and abdomen can often determine cause. BASICS DIAGNOSIS r Stages of ascites: DEFINITION DIFFERENTIAL DIAGNOSIS ◦ Stage I: minimal ascites. Detected by The escape of fluid, either transudate or Differentiating Abdominal Distension ultrasound only. ◦ exudate, into the abdominal cavity between without Effusion Stage II: moderate ascites. Abdominal r the parietal and visceral peritoneum. Organomegaly—hepatomegaly, distention visible and/or noted on PATHOPHYSIOLOGY splenomegaly, renomegaly, and hydrometra. ballottement. r ◦ r Abdominal neoplasia. Stage III: significant ascites. Marked Ascites can be caused by the following: r ◦ Pregnancy. abdominal distention. Patient CHF and associated interference in r Bladder distension. uncomfortable, possibly with labored venous return r ◦ Obesity. breathing. Depletion of plasma proteins associated r with inappropriate loss of protein from Gastric dilatation. DIAGNOSTIC PROCEDURES renal or gastrointestinal disease—protein- Differentiating Diseases Ascitic Fluid Evaluation r losing nephropathy or enteropathy, Transudate—nephrotic syndrome, cirrhosis Exfoliative cytologic examination and respectively of liver, right-sided CHF, hypoproteinemia, bacterial culture and antibiotic ◦ Obstruction of the vena cava or portal and ruptured bladder. sensitivity—remove approximately 3–5 mL of r vein, or lymphatic drainage due to Exudate—peritonitis, abdominal neoplasia, abdominal fluid via aseptic technique. neoplastic occlusion and hemorrhage. Transudate ◦ r Overt neoplastic effusion CBC/BIOCHEMISTRY/URINALYSIS Clear and colorless. ◦ r Peritonitis—infective or inflammatory r Protein < 2.5 g/dL. ◦ Neutrophilic leukocytosis occurs in patients r Electrolyte imbalance, especially with systemic infection. Specific gravity < 1.018. hypernatremia r r < 3 ◦ Albumin is low in patients with impaired Cells 1,000/mm —neutrophils and Liver cirrhosis. liver synthesis, gastrointestinal loss, or renal mesothelial cells. SYSTEMS AFFECTED loss. Modified Transudate r r r Cardiovascular Cholesterol is low in patients with impaired Red or pink; may be slightly cloudy. r r Gastrointestinal liver synthesis. Protein 2.5–5 g/dL. r r Hemic/Lymph/Immune Liver Enzymes Specific gravity > 1.018. r r r Renal/Urologic Low to normal in patients with impaired Cells < 5,000/mm3—neutrophils, SIGNALMENT liver synthesis. mesothelial cells, erythrocytes, and r r Dogs and cats High in patients with liver inflammation, lymphocytes. r No species or breed predisposition hyperadrenocorticism, gallbladder Exudate (Non-septic) r SIGNS obstruction, and chronic passive congestion. Pink or white; cloudy. r r Episodic weakness Total and Direct Bilirubin Protein 2.5–5 g/dL. r r r > Lethargy Low to normal in patients with impaired Specific gravity 1.018. r r 3 Abdominal fullness liver synthesis. Cells 5,000–50,000/mm —neutrophils, r r Abdominal discomfort when palpated High in patients with biliary obstruction mesothelial cells, macrophages, erythrocytes, r Dyspnea from abdominal distension or caused by tumor, gallbladder distension, or and lymphocytes. associated pleural effusion obstruction. Exudate (Septic) r r Anorexia BUN and Creatinine Red, white, or yellow; cloudy. r r Vomiting r Protein > 4.0 g/dL. r High in patients with renal failure. r Weight gain r Specific gravity > 1.018. r BUN low in patients with impaired liver r Scrotal or penile edema Cells 5,000–100,000/mm3—neutrophils, r synthesis or hyperadrenocorticism. Groaning when lying down Glucose mesothelial cells, macrophages, erythrocytes, r CAUSES Low in patients with impaired liver lymphocytes, and bacteria. r Nephrotic syndrome synthesis. Hemorrhage r r Cirrhosis of liver Red; spun supernatant clear and sediment r OTHER LABORATORY TESTS Right-sided CHF r red. r To detect hypoproteinemia—protein r Hypoproteinemia Protein > 5.5 g/dL. r electrophoresis and immune profile. r Ruptured bladder r Specific gravity 1.007–1.027. r To detect proteinuria—urinary r Peritonitis Cells consistent with peripheral blood. r protein:creatinine ratio (normal < 0.5:1). r Abdominal neoplasia Does not clot. r IMAGING Abdominal hemorrhage r Chyle r RISK FACTORS Thoracic and abdominal radiography is Pink, straw, or white. sometimes helpful. r N/A Protein 2.5–7 g/dL. BLBS078-CF_A65 BLBS078-Tilley March 22, 2011 7:38

Canine and Feline, Fifth Edition 115

(Continued) Ascites A

r r Specific gravity 1.007–> 1.040. For exudate ascites control, address the POSSIBLE COMPLICATIONS r Cells < 10,000/mm3—neutrophils, underlying cause; corrective surgery is often Aggressive diuretic administration may cause mesothelial cells, and large population of indicated, followed by specific therapeutic hypokalemia, which could predispose to small lymphocytes. management (e.g., patient with splenic metabolic alkalosis and exacerbation of r Other—fluid in tube separates into tumor: tumor removed, abdominal bleeding hepatic encephalopathy in patients with cream-like layer when refrigerated; fat controlled, blood transfusion administered). underlying liver disease; alkalosis causes a shift droplets stain with Sudan III. LARGE-VOLUME PARACENTESIS from NH4 to NH3. Pseudochyle r r Stage III treatment. White. r r Pretreat patient with hetastarch (6%) @ Protein > 2.5 g/dL. 1–2 ml/kg for 2 hours. r r Specific gravity 1.007–1.040. Abdominal tap (paracentesis), until drainage MISCELLANEOUS r < 3 Cells 10,000/mm —neutrophils, slows. ASSOCIATED CONDITIONS mesothelial cells, and small lymphocytes. r r Post-treat patient with hetastarch (6%) @ N/A Other—fluid in tube does not separate into 1–2 ml/kg for 4 hours. cream-like layer when refrigerated; does not AGE-RELATED FACTORS stain with Sudan III. N/A Urine ZOONOTIC POTENTIAL r Clear to pale yellow. MEDICATIONS N/A r Protein > 2.5 g/dL. r DRUG(S) OF CHOICE PREGNANCY/FERTILITY/BREEDING Specific gravity 1–> 1.040. r r N/A Cells 5,000–50,000/mm3—neutrophils, Patients with liver insufficiency or erythrocytes, lymphocytes, and macrophages. CHF—restrict sodium and give a diuretic SYNONYMS r Other—if the urinary bladder ruptured combination of hydrochlorothiazide Abdominal effusion < 12 hours before, urinary glucose and (2–4 mg/kg q12h PO) and spironolactone SEE ALSO (1–2 mg/kg q12h PO); if control is r protein could be negative; if bladder ruptured Cirrhosis and Fibrosis of the Liver > inadequate, furosemide (1–2 mg/kg q8h PO) r 12 hours before, urine becomes a dialysis Congestive Heart Failure, Right-Sided can be substituted for the thiazide with r medium with ultrafiltrate of plasma, and Hypoalbuminema urine contains glucose and protein. spironolactone continued; must monitor r serum potassium concentration to prevent Nephrotic Syndrome Bile r potassium imbalances. ABBREVIATIONS Slightly cloudy and yellow. r r Patients with hypoproteinemia, nephrotic CHF = congestive heart failure Protein > 2.5 g/dL. r > syndrome, and associated ascitic fluid Suggested Reading Specific gravity 1.018. accumulation—can treat as above with the r 3 Kramer RE, Sokol RJ, Yerushalmi B, Liu E, Cells 5,000–750,000/mm —neutrophils, addition of hetastarch (6% hetastarch in 0.9% MacKenzie T, Hoffenberg EJ, Narkewicz erythrocytes, macrophages, and lymphocytes. NaCl); administer an IV bolus (dogs, r MR. Large-volume paracentesis in the Other—bilirubin confirmed by urine 20 mL/kg; cats, 10–15 mL/kg) slowly over management of ascites in children. J Ped dipstick; non-icteric patient may have ∼1 hour; hetastarch increases plasma oncotic Gastro Nutr 2001; 33:245–249. gallbladder rupture, biliary tree leakage, or pressure and pulls fluid into the intravascular Lewis LD, Morris ML Jr,, Hand MS. Small rupture in the proximal bowel. space for up to 24–48 hours. r Animal Clinical Nutrition, 3rd ed. Topeka, Systemic antibiotic therapy is dictated by KS: Mark Morris Associates, 1987. bacterial identification and sensitivity testing Li MK. Management of ascites. Hong Kong in patients with septic exudate ascites. Med Di 2009, 14:27–29. TREATMENT CONTRAINDICATIONS r Runyon BA. Management of adult patients Can design treatment on an outpatient N/A with ascites due to cirrhosis. Hepatol 2004, basis, with follow-up or inpatient care, 39:1–16. depending on physical condition and Author Jerry A. Thornhill underlying cause. r Consulting Editors LarryP.TilleyandFrancis If patients are markedly uncomfortable FOLLOW-UP W.K. Smith, Jr. when lying down or become more dyspneic PATIENT MONITORING with stress, consider removing enough ascites r to reverse these signs. Varies with the underlying cause. Client Education Handout r r Dietary salt restriction may help control Check sodium, potassium, BUN, creatinine, available online transudate fluid accumulation due to CHF, and weight fluctuations periodically if the cirrhosis, or hypoproteinemia. patient is maintained on a diuretic. BLBS078-CF_A66 BLBS078-Tilley June 16, 2011 11:0

116 Blackwell’s Five-Minute Veterinary Consult A Aspergillosis—Disseminated

r r Geographic/environmental Pulmonary involvement rare, mixed conditions—may be a factor, as some regions interstitial/alveolar pattern, enlarged sternal BASICS have a higher incidence (e.g., California, and/or tracheobronchial lymph nodes, pleural Louisiana, Michigan, Georgia, Florida, and effusion; productive and destructive lesions of OVERVIEW Virginia in the United States; western sternebrae. r Opportunistic fungal infection caused by Australia; Barcelona; and Milan). Ultrasonographic Findings r r Aspergillus spp., common molds that are Cats—associated with FIP, FePLV, FeLV, Kidneys—commonest site to detect ubiquitous in the environment, forming diabetes mellitus, and chronic corticosteroid changes; changes seen include renal pelvis numerous spores in dust, straw, grass or antibiotic administration. dilation ± echogenic debris within pelvis; loss clippings, and hay. r of corticomedullary distinction; renal Disseminated disease does not appear to be distortion and mottled appearance of the related to the nasal form of the disease, parenchyma; dilation of proximal ureter; although one report of a dog developing DIAGNOSIS renalomegaly; nodules or masses; fungal osteomyelitis 6 months after treatment DIFFERENTIAL DIAGNOSIS hydronephrosis. for nasal aspergillosis raises the possibility. r r Spleen—hypoechoic, lacy, sharply Disseminated disease—usually A. terreus; Bacterial osteomyelitis/diskospondylitis; demarcated areas with no doppler signal A. deflectus and A. fumigatus also associated; spinal neoplasia; intervertebral disk disease; suggestive of infarct are most significant portal of entry not definitively established but skeletal neoplasia; bacterial pyelonephritis; finding in spleen; other findings include possibly through the respiratory tract or bacterial pneumonia; other causes of nodules/masses, mottled parenchyma, splenic gastrointestinal tract, with subsequent vestibular signs/seizures; other causes of venous thrombosis. r hematogenous spread. uveitis (see Anterior Uveitis—Cats, Anterior Other—abdominal lymphadenomegaly; SIGNALMENT Uveites—Dogs). diffuse hepatic hypoechogenicity. CBC/BIOCHEMISTRY/URINALYSIS Dogs r MRI Findings r Non-specific. Morecommonindogsthanincats. r Useful for further defining brain lesions in r Dogs—often have mature neutrophilic German shepherds overrepresented but animals with CNS signs; changes similar to leukocytosis and lymphopenia. reported sporadically in many breeds; average r other infectious and non-infectious Cats—may have nonregenerative anemia age 3 years (range of 1–9 years); slight bias inflammatory brain diseases. and leucopenia. toward females. r DIAGNOSTIC PROCEDURES Biochemistry—may see high globulins, Cats Choice of diagnostic procedure as indicated r creatinine, phosphate, BUN and calcium. Persians—marginally increased incidence. r by clinical presentation but may include CSF r Urinalysis—may see isosthenuria, Disseminated cases mostly affect the lungs hematuria, pyuria, and possible fungal hyphae tap, joint aspirates, intervertebral disc space and/or gastrointestinal tract. in the sediment; detection of the fungal aspirates, abdominocentesis/thoracocentesis, SIGNS hyphae can be improved by allowing the aspirate of various organs (spleen, liver, renal). Dogs sample to incubate at room temperature for r PATHOLOGIC FINDINGS May develop acutely or slowly over a period 24–48 hours; sediment samples may be of several months. examined unstained as wet preparations or Histopathology—most likely to render a r may be air dried and stained with Diff-Quick definitive diagnosis; special stains may be Often associated with spinal pain (fungal ◦ diskospondylitis) or lameness (fungal (the hyphae that branch at 45 stain purple). required; granulomas and multiple organ osteomyelitis). OTHER LABORATORY TESTS infarcts noted with disseminated disease r r Neurologic—spinal cord damage. (kidneys, liver, spleen, and vertebrae). r Positive fungal serology (agar gel double CNS—vestibular signs, seizures, diffusion, counterimmunoelectrophoresis, hemiparesis, mental dullness, ataxia, and ELISA) support the diagnosis; false paraparesis, vision impairment, circling. r negatives with agar gel immunodiffusion Polyuria/polydipsia and hematuria—renal reported; false positives and cross-reactivity TREATMENT involvement. with Penicillium spp. reported. r r DOGS Uveitis—ocular involvement. Interpret serology in conjunction with other r r Treatment rarely curative; may halt Non-specific—fever, weight loss, vomiting, diagnostic tests. r progression of clinical signs. lymphadenopathy, and anorexia. Cats—test for FeLV and FIV because they r Fluid therapy—indicated by the degree of affect prognosis. Cats r renal compromise and azotemia. r Positive fungal culture from normally sterile Usually non-specific signs (e.g., lethargy, CATS depression, vomiting, and diarrhea). body fluids and tissues, e.g., urine, bone, CSF, r Ocular—exophthalmos. blood, lymph node, pleural effusions, Disseminated—likely difficult to treat; data are limited. CAUSES & RISK FACTORS intervertebral disc aspirates, kidney, spleen. r IMAGING Caused by Aspergillus species, most Radiographic Findings commonly A. terreus, A. deflectus and less r commonly A. fumigatus, A. niger, A. flavipes. Spinal views may show end-plate lysis, r MEDICATIONS German shepherds at higher risk. attempted bony intervertebral bridging, and r Immune deficiency—may play a factor lysis of vertebral bodies consistent with DRUG(S) r because the organism is widespread but the diskospondylitis; productive and destructive Itraconazole 5–10 mg/kg PO q24h (can be lesions of the vertebral bodies. disease is uncommon; breed-related immune r divided)—drug of choice; dogs; unlikely to be defect proposed in German shepherds and Bony proliferation and lysis and periosteal curative, though the disease may be contained their crosses. reaction typical of osteomyelitis of the with continued use. diaphyseal region of long bones. BLBS078-CF_A66 BLBS078-Tilley June 16, 2011 11:0

Canine and Feline, Fifth Edition 117

(Continued) Aspergillosis—Disseminated A

r r Other drug combinations reported but Oral azoles—nausea, intermittent anorexia, ABBREVIATIONS r none have ultimately resulted in reported cure liver enzyme elevation. CNS = central nervous system r r of disease. Some of the combinations reported Combination of flucytosine and CSF = cerebrospinal fluid r include amphotericin B—cutaneous drug eruptions ELISA = enzyme-linked immunosorbent ◦ Lipid complex amphotericin B (dogs, in dogs. assay r r 2–3 mg/kg IV 3 days per week for a total of Avoid midazolam and cisapride with FeLV = feline leukemia virus r 9–12 treatments, to cumulative dose of azoles—fatal drug reactions noted in humans. FePLV = feline panleukopenia virus r r 24–27 mg/kg) + itraconazole 5 mg/kg PO High dose (10 mg/kg) itraconazole FIP = feline infectious peritonitis r q24h. associated with ulcerative dermatitis in FIV = feline immunodeficiency virus r ◦ Itraconazole (5 mg/kg PO q24h) + 5–10% dogs—recognize early and MRI = magnetic resonance imaging terbinafine (5–10 mg/kg PO q24h). discontinue, then reinstitute at a reduced Suggested Reading ◦ New triazoles, voriconazole (5 mg/kg dosed, or severe cutaneous and subcutaneous Maddison JE, Page SW, Church DB. Small POq12h) and posaconazole (5 mg/kg PO sloughing can occur. Animal Clinical Pharmacology, 2nd ed. q24h), are potential alternatives to cases Edinburgh: Saunders, 2008, pp. 186–197. poorly responsive to itraconazole. Reported Schultz RM, Johnson EG, Wisner ER, Brown used in combination with lipid complex NA, Byrne BA, Sykes JE. Clinicopathologic amphotericin B. FOLLOW-UP and diagnostic imaging characteristics of ◦ β-glucan synthase inhibitors caspofungin, Disseminated—monitor serial radiographs systemic aspergillosis in 30 Dogs. J Vet micafungin, anidulafungin—may prove every 1–2 months, renal function, and urine Intern Med 2008, 22:851–859. useful but very limited clinical information. cultures; prognosis poor, especially in German Author Tania N. Davey ◦ Combination therapy with flucytosine shepherds. Consulting Editors Stephen C. Barr (25–50 mg/kg PO q6—dogs) and amphotericin B may prove successful, but no published reports. Client Education Handout CONTRAINDICATIONS/POSSIBLE MISCELLANEOUS available online INTERACTIONS r ZOONOTIC POTENTIAL Amphotericin B—contraindicated in dogs with preexisting renal compromise or failure; None amphotericin B lipid complex significantly reduced nephrotoxicity. BLBS078-CF_A66a BLBS078-Tilley June 1, 2011 12:41

118 Blackwell’s Five-Minute Veterinary Consult A Aspergillosis, Nasal

Physical Examination Findings Skull Radiography r r Unilateral or bilateral nasal discharge. Intraoral dorsoventral radiograph of the r Increased nasal airflow on the affected side. nasal cavity shows turbinate lysis. BASICS r r Depigmentation with ulceration of the nasal Rostrocaudal or skyline frontal sinus view DEFINITION planum—∼40% of dogs. may show increased soft tissue density in the r r Facial pain. frontal sinus. Nasal disease caused by Aspergillus spp., r r primarily A. fumigatus. Ipsilateral mandibular lymphadenopathy. Cannot evaluate cribriform plate. r r Saprophytic fungus that is ubiquitous in the Stertor, exophthalmos, hard palate DIAGNOSTIC PROCEDURES environment. ulceration, loss of nasal airflow—cats. r Rhinoscopy Opportunistic pathogen. CAUSES r r Flexible rhinoscopy in dogs allows PATHOPHYSIOLOGY No underlying cause identified, although examination of the nasopharynx and possibly r Inhalation of fungus leads to disease in the preexisting foreign body or trauma is the frontal sinus if the opening of the occasionally implicated. nasal cavity with destruction of turbinates and r nasofrontal duct is destroyed by fungal overproduction of mucus causing clinical Likely due to inhalation of a large bolus of infection. r signs of nasal disease. fungus that is ubiqutous in the environment. Rigid rhinoscopy—examination of the nasal r r Rarely may be associated with underlying Species—most commonly A. fumigatus; cavity alone; good visualization is possible due foreign body or previous trauma. others—A. niger, A. flavus. to large airspaces caused by turbinate lysis; r Causes a locally aggressive and invasive RISK FACTORS excessive mucus and bleeding can make full disease but does not result in systemic examination difficult. Unknown r mycosis. Visualization of fungal plaques (white, r Confined to nasal cavity and frontal yellow, black, or light-green) on the mucosa of sinus—sinonasal form (most common in the nasal cavity and/or frontal sinus confirms dogs). fungal infection. r DIAGNOSIS May also extend to the orbit in cats and PATHOLOGIC FINDINGS rarely in dogs—sino-orbital form. DIFFERENTIAL DIAGNOSIS r r Biopsies obtained of affected area under SYSTEMS AFFECTED Foreign body. r direct rhinoscopic visualization using cup Oronasal fistula. Respiratory—nasal cavity, sinus, orbit (cats, r biopsy instruments. Lymphoplasmacytic rhinitis. r rare in dogs) r Samples immersion-fixed in buffered 10% Neoplasia. GENETICS r formalin, routinely processed. Nasopharyngeal polyp, nasal tumor, or r Unknown Evidence supportive of a diagnosis of cryptococcus—cats only. aspergillosis—identification of septate, INCIDENCE/PREVALENCE CBC/BIOCHEMISTRY/URINALYSIS branching hyphae and conidia on r Unknown, but a common diagnosis in dogs Often normal histopathology. Surrounding inflammation is r with nasal discharge in many locations. Possible inflammatory leukogram commonly neutrophilic or GEOGRAPHIC DISTRIBUTION lymphoplasmacytic, rarely eosinophilic. OTHER LABORATORY TESTS r Worldwide Blind biopsies in an unaffected area of the Serology r nasal cavity may result in a false diagnosis of SIGNALMENT Detects fungi-specific serum antibodies. r inflammation. Species AGID—commercially available; 98% Dogs and cats (less common) specificity, 67% sensitivity in dogs; serial Breed Predilections serology does not appear to correlate with r clinical status. Dogs—dolichocephalic and mesocephalic r TREATMENT breeds ELISA—88% sensitivity, 96.8% specificity. r r APPROPRIATE HEALTH CARE Cats—brachycephalic breeds may be Counter-immunoelectrophoresis—85% specificity in dogs. overrepresented r Overnight hospitalization required after Serum galactomannan—shown to be topical treatment or surgery. Mean Age and Range r unreliable. Dogs—predominantly young to NURSING CARE middle-aged Culture Maintain the nares free of nasal discharge r r Cats—no predilection Tissue fungal culture of affected area; ACTIVITY visualized biopsy sample taken from a region Predominant Sex of suspected fungal growth showed 100% Restriction of activity is not required None identified specificity, 81% sensitivity. DIET r SIGNS Culture of nasal discharge is less specific and N/A Historical Findings insensitive. CLIENT EDUCATION r r Unilateral or bilateral nasal IMAGING Dogs—inform client that multiple topical discharge—typically mucoid, mucopurulent, Computed Tomography treatments are usually necessary to cure the r or serosanguinous but may be primarily Imaging method of choice. disease; follow-up with rhinoscopy is highly epistaxis. r r Cavitated turbinate lysis. recommended to ensure resolution. Sneezing. r r r Thickening of the mucosa along the nasal No established protocols for treatment in Typically chronic signs—several months. turbinates. cats. r r Many patients will have been treated with Frontal sinus proliferative mass effect. SURGICAL CONSIDERATIONS antibiotics for a possible bacterial infection r Soft tissue mass in the choana or Trephination of the Frontal Sinus before presentation with variable response. nasopharynx—cats. r r Recommended for dogs with frontal sinus Necessary for evaluation of the cribriform involvement. plate before topical antifungal treatment. BLBS078-CF_A66a BLBS078-Tilley June 1, 2011 12:41

Canine and Feline, Fifth Edition 119

(Continued) Aspergillosis, Nasal A

r Performed using a Jacob’s chuck and triazole drugs. POSSIBLE COMPLICATIONS r r intramedullary pin. Fluconazole is not recommended due to Topical therapy—monitor after treatment r Allows direct visualization of the frontal resistance. for any complications such as swelling of sinus with a rigid rhinoscope and local CONTRAINDICATIONS oropharynx, neurologic signs, debridement of fungal plaques. r infection/swelling of trephine site. r Breach in the cribriform plate can allow r Allows for lavage and topical treatment of contact of antifungal medication with brain Triazoles can cause anorexia and can be the area using a red rubber catheter. hepatoxic. resulting in neurologic signs and possible r Surgical Debridement and Exenteration death. Amphotericin B can be nephrotoxic. r r Used in some cats with sino-orbital disease. Sino-orbital disease necessitates the use of EXPECTED COURSE AND PROGNOSIS r Endoscopic Debridement systemic therapy. Studies have shown an 87% response rate to r Extensive curettage and removal of fungal PRECAUTIONS topical therapy in dogs after one to three r treatments. material from the nose and frontal sinus are Topical clotrimazole and enilconazole are r essential to allow efficacy of topical caustic to all mucosal surfaces—protective A newer study showed that recurrence or medication. gear (gloves, goggles) should be worn by all reinfection is more common than previously staff that are in close contact. thought and can occur years after supposedly r successful therapy. Enilconazole can be associated with tissue r swelling and upper airway obstruction. The prognosis for cats with sinonasal MEDICATIONS aspergillosis is better than with the POSSIBLE INTERACTIONS sino-orbital form. DRUG(S) OF CHOICE N/A Topical Clotrimazole or Enilconazole ALTERNATIVE DRUG(S) Therapy Enilconazole r r 1-hour infusion into nasal cavity under Also active in the vapor phase. MISCELLANEOUS anesthesia. r Combined Clotrimazole Irrigation and ASSOCIATED CONDITIONS Treatment is usually performed during the Depot Therapy N/A same anesthesia as diagnostics. r r Clotrimazole (1%) is flushed through a Treatment of choice in dogs; reported AGE-RELATED FACTORS trephine hole in the frontal sinus over 5 efficacy 85–89% with multiple treatments. N/A r minutes; 50 ml in each side in dogs > 10 kg; Foley catheters are used to occlude the nares 25 ml in each side in dogs <10 kg. ZOONOTIC POTENTIAL and nasopharynx. r r Clotrimazole cream (1%) is then introduced There are no documented cases of human Dose—Clotrimazole: 1 gram of in 100 ml into the front sinuses; 20 g in each side in dogs infection from an affected dog or cat. of polyethylene glycol 200 (1% solution) > 10 kg, 10 g in each side in dogs < 10 kg. PREGNANCY/FERTILITY/BREEDING evenly divided between two 60-ml syringes r Reported efficacy similar to topical slowly infused over 1 hour into each side for N/A Clotrimazole or Enilconazole alone (86%). large dogs; if trephination is used, divide the ABBREVIATIONS r amount between the nasal cavity and sinus on AGID = agar gel immunodiffusion r the same side; less volume in smaller dogs. CT = computed tomography r Enilconazole: 100 mls of 1%, 2%, or 5% ELISA = enzyme-linked immunosorbent solution. FOLLOW-UP r assay Dog is placed in dorsal recumbency with PATIENT MONITORING Suggested Reading head turned to each side every 15 minutes Dogs during the infusion. r Barrs VR. Feline sino-orbital aspergillosis: An r Monitor clinical signs, although reduction Dog is placed in sternal recumbency with emerging clinical syndrome. ACVIM of clinical signs does not establish resolution Forum Proceedings 2009, pp. 395–397. head down at the end of the procedure to of disease. allow all of the medication to drain. r Friend E, Anderson DM, White RAS. r Follow-up rhinoscopy is recommended in Has been used in cats without orbital Combined clotrimazole irrigation and depot all cases to establish response to treatment, therapy for canine nasal aspergillosis. J Small involvement in combination with oral regardless of clinical signs—histopathology antifungal therapy with varying success. Anim Pract 2006, 47(6):312–315. and culture can help establish response. Mathews KG, Davidson AP, Koblik PD, et al. Systemic Therapy r r Serial serology (AGID) appears not to Comparison of topical administration of Antifungal triazole drugs should be correlate with clinical status. r clotrimazole through surgically placed versus considered if the cribriform plate is not intact; Repeat CT scan should be considered for nonsurgically placed catheters for treatment also used as primary therapy in some cats. r reassessment of the cribriform plate before of nasal aspergillosis in dogs: 60 cases Canalsobeusedincombinationwith repeat topical treatment if a worsening clinical (1990–1996). JAVMA 1998, 213:501–506. topical therapy. r signs are seen. McLellan GJ, Aquino SM, Mason DR, Myers May be cost-prohibitive. r r Monitor liver enzymes in animals on RK. Use of posaconazole in the Itraconazole 5 mg/kg PO q12h in dogs with triazole therapy. management of invasive orbital aspergillosis a reported efficacy of 60–70%; 10 mg/kg PO Cats in a cat. JAAHA 2006, 42:302–307. q24h in cats. r r Monitor clinical signs for improvement or PomrantzJS,JohnsonLR,NelsonRW, Voriconazole 5 mg/kg PO q12h; efficacy as resolution. Wisner ER. Comparison of serologic sole therapy has not been established. r r Monitor liver enzymes in animals on evaluation via agar gel immunodiffusion Posaconazole 5 mg/kg PO q24h; efficacy as triazole therapy. and fungal culture of tissue for diagnosis of sole therapy has not been established. r r Monitor renal parameters in animals on nasal aspergillosis in dog. JAVMA 2007, Amphotericin B (deoxycholate) 0.8 mg/kg Amphotericin B. 230:1319–1323. SC in 400 ml of warmed 2.5% PREVENTION/AVOIDANCE Author Jill S. Pomrantz dextrose/0.45% saline q 3–4 days; cumulative Consulting Editors Lynelle R. Johnson dose 10–14 mg/kg in combination with N/A BLBS078-CF_A67 BLBS078-Tilley March 22, 2011 7:45

120 Blackwell’s Five-Minute Veterinary Consult A Aspirin Toxicity

r r Preexisting painful condition—question Sodium bicarbonate 1 mEq/kg IV owner about aspirin administration. alkalinizes urine CBC/BIOCHEMISTRY/URINALYSIS CONTRAINDICATIONS/POSSIBLE BASICS r Cats—prone to Heinz body formation INTERACTIONS OVERVIEW r r Hyponatremia and hypokalemia N/A Given by owners to relieve minor pain and OTHER LABORATORY TESTS discomfort; now less commonly used owing r to increasing popularity of other Initial respiratory alkalosis followed by over-the-counter pain-relieving drugs. metabolic acidosis. r r Gastric irritation and hemorrhage occur in Salicylic acid concentrations in serum or FOLLOW-UP r 10–20% of cases. urine. r r Maintaining renal function and acid-base Repeated doses may produce High ketones and pyruvic, lactic, and amino balance is vital. r gastrointestinal ulceration and perforation. acid levels. r r Severe acid-base disturbances, severe Toxic hepatitis, suppression of bone marrow Decreased sulfuric and phosphoric acid dehydration, toxic hepatitis, bone marrow activity, and anemia may occur, especially in renal clearance. depression, and coma are poor prognostic cats. IMAGING indicators. SIGNALMENT N/A Cats and less commonly dogs DIAGNOSTIC PROCEDURES SIGNS N/A r MISCELLANEOUS Depression r Vomiting—vomitus may be blood-tinged Be sure that history of “aspirin” medication r Tachypnea does not refer to other available pain r Fever TREATMENT medications. r Muscular weakness and ataxia r r Inpatient—following general principles of Suggested Reading Comaanddeathin1ormoredays poisoning management. Oehme FW. Aspirin and acetaminophen. In: r CAUSES & RISK FACTORS Correction of acid-base Kirk RW, ed., Current Veterinary Therapy r balance—continuous intravenous fluids. IX: Small Animal Practice. Philadelphia: Owners employing human dosage r guidelines to medicate cats—most common. Induced gastric emptying—gastric lavage or Saunders, 1986, pp. 188–189. r induced emesis. Author Frederick W. Oehme Deficiency in glucuronide conjugation r capability (cats). Peritoneal or hemodialysis or Consulting Editors Gary D. Osweiler r Biological half-life—cats, 44.6 hours; dogs, hemoperfusion—heroic procedures. 7.5 hours; responsible for higher risk in cats.

MEDICATIONS DIAGNOSIS DRUG(S) r DIFFERENTIAL DIAGNOSIS No specific antidote available r r Clinical signs—uncharacteristic. Activated charcoal—2 g/kg PO r History of aspirin ingestion or decontaminates gut medication—important; within 5 days of signs should raise concern. BLBS078-CF_A68 BLBS078-Tilley March 22, 2011 7:46

Canine and Feline, Fifth Edition 121 Asthma, Bronchitis—Cats A

r CAUSES BAL performed to collect airway fluids from Triggers of airway inflammation unknown most severely affected areas. RISK FACTORS Cytology BASICS r r Cigarette smoke, dusty cat litter, hair sprays, Eosinophils and neutrophils are most DEFINITION and air fresheners may exacerbate disease. prominent cell types. A mixed cell population r r r Chronic bronchitis—inflammation in the Parasitic lung infections are more common occurs in about 21% of cats. Up to 20% airways (bronchi and bronchioles); chronic in outdoor cats in certain geographic eosinophils on BAL cytology can be found in daily cough of greater than 2 months in r r locations. Use of potassium normal cats. duration. Asthma—acute or chronic airway bromide—implicated in causing signs of Bacterial Cultures r inflammation associated with increased bronchitis/asthma in some cats. Quantitated cultures recommended; airway responsiveness to various stimuli, bacterial colony counts > 100–300 cfu/ml r airway narrowing due to smooth muscle uncommon. Specific Mycoplasma culture hypertrophy or constriction, reversibility of may be needed. airway constriction, and presence of DIAGNOSIS eosinophils, lymphocytes, and mast cells Biopsy r r within the airways. Feline bronchitis or DIFFERENTIAL DIAGNOSIS Keyhole biopsy—can differentiate between r bronchopulmonary disease is used to describe Rule out infectious pneumonia idiopathic pulmonary fibrosis and bronchitis. the clinical syndrome of acute or chronic (Mycoplasma, Toxoplasma, bacterial or fungal PATHOLOGIC FINDINGS coughing and/or wheezing due to lower pneumonia), Dirofilaria immitis and primary Hyperplasia/hypertrophy of goblet cells, airway inflammation. lung parasites (Aelurostrongylus abstrusus, hypertrophy of airway smooth muscle, PATHOPHYSIOLOGY Capillaria aerophilia, Paragonimus kellicotti). epithelial erosion, and inflammatory r r Noxious or allergic stimuli initiate Primary or metastatic neoplasia can have infiltrates. inflammation within the lower airways. similar clinical and radiographic appearance. r r Bronchiolar smooth muscle constriction— Idiopathic pulmonary fibrosis may appear reversible spontaneously or with treatment. similar to feline bronchitis. r Smooth muscle hypertrophy implies CBC/BIOCHEMISTRY/URINALYSIS r TREATMENT chronicity—usually not reversible. Increase ∼ Frequently normal, 40% of cats with APPROPRIATE HEALTH CARE in mucosal goblet cells, mucus production, bronchial disease have peripheral r r Remove patient from inciting environment and edema of bronchial wall. Excessive eosinophilia. r mucus can cause bronchiolar obstruction, Hospitalize for acute respiratory distress r OTHER LABORATORY TESTS atelectasis, or bronchiectasis. Chronic r NURSING CARE Fecal exams—flotation for Capillaria, inflammation may lead to fibrosis. Oxygen therapy and sedatives in an acute sedimentation for Paragonimus, Baermann for SYSTEMS AFFECTED crisis. Minimize manipulation in order to Aelurostrongylus. False-negative tests common. r r r lessen stress and oxygen needs of the Respiratory Cardiac—pulmonary Heartworm antigen and antibody testing. r animal. hypertension rarely Radioallergosorbent testing or intradermal GEOGRAPHIC DISTRIBUTION skin testing—no correlation between skin and ACTIVITY Worldwide. Parasitic causes more common in respiratory allergies currently documented. Usually self-limited by patient southern and midwest U.S. states. IMAGING DIET Paragonimus kellicotti found in Great Lakes Radiography Calorie restriction for obese cats area. Heartworm disease more prevalent in r Classically, diffuse bronchial wall CLIENT EDUCATION southern United States. r thickening; interstitial or patchy alveolar Most causes are chronic and progressive. SIGNALMENT r r patterns possible. Severity of radiographic Do not discontinue medical therapy when Species changes may not correlate with clinical r clinical signs have resolved—subclinical Cats severity or duration. Hyperinflation of lung inflammation is common and can lead to Breed Predilections fields—flattened and caudally displaced progression of disease. Lifelong medication Siamese overrepresented diaphragm, increased distance between the and environmental changes usually heart and diaphragm, extension of lungs to r Mean Age and Range r necessary. Some clients can be taught to give Any age; more common between 2 and 8 the first lumbar vertebrae. Collapse of right terbutaline subcutaneously and corticosteroid middle lung lobe reported in 11% of cases. years r injections at home for a crisis situation. Predominant Sex Pulmonary lobar arterial enlargement is One study shows females overrepresented suspicious for heartworm disease. SIGNS Echocardiography Useful to document heartworm disease or MEDICATIONS Historical Findings r secondary pulmonary hypertension. Coughing (80%), sneezing (60%), labored DRUG(S) OF CHOICE r DIAGNOSTIC PROCEDURES breathing or wheezing (40%). Signs are Emergency Treatment Transoral Tracheal Wash r typically episodic and can be acute or chronic. r Oxygen and a parenteral bronchodilator. Physical Examination Findings Use a sterile endotracheal tube and Injectable terbutaline (0.01 mg/kg IV or SC); r Severely affected cats present with open- polypropylene catheter to collect airway fluids repeat if no clinical improvement (decrease in mouth breathing, tachypnea, and cyanosis. at the level of the carina. respiratory rate or effort) in 20–30 minutes. r r Increased tracheal sensitivity is common. Bronchoscopy/Bronchoalveolar Lavage A sedative can aid in decreasing anxiety r r Chest auscultation may reveal crackles Allows visualization of trachea and bronchi. (butorphanol tartrate at 0.2–0.4 mg/kg IV or and/or expiratory wheezes, or may be normal. IM, buprenorphine at 0.01 mg/kg IV or IM, r Excessive amounts of thick mucus are r Labored breathing with an abdominal push common with bronchitis. Mucosa of the or acepromazine at 0.01–0.05 mg/kg SC). A on expiration, increase in expiratory effort. airways is typically hyperemic and edematous. short-acting parenteral corticosteroid may also BLBS078-CF_A68 BLBS078-Tilley March 22, 2011 7:46

122 Blackwell’s Five-Minute Veterinary Consult

A Asthma, Bronchitis—Cats (Continued)

r be required. Dexamethasone sodium cytology in an appropriate geographic therapy appropriately adjusted. Afewcats r phosphate (0.25–0.5 mg/kg, IV or SC). Can location. Consider fenbendazole, will be refractory to treatment; these carry a repeat if no improvement noted within 20–30 ivermectin, or praziquantel. much worse prognosis. minutes. Prednisolone sodium succinate Antibiotics r (Solu-Delta-Cortef) can also be used (50–100 Use based on a positive quantitative culture mg IV). and susceptibility testing. Long-Term Management CONTRAINDICATIONS MISCELLANEOUS Corticosteroids r r Beta-2 antagonists (e.g., propranolol) are ASSOCIATED CONDITIONS Decrease inflammation. Oral treatment is contraindicated because of their ability to Cor pulmonale can be a sequela to chronic preferred over injectable for closer monitoring r block sympathetically mediated lower airway disease. of dose and duration. Prednisolone: 0.5–1 bronchodilation. PREGNANCY/FERTILITY/BREEDING mg/kg PO q12h. Begin to taper dose (50% PRECAUTIONS each week) after 1–2 weeks if clinical signs r Glucocorticoids are contraindicated in the Long-term use of steroids increases risk of have improved. Maintenance therapy = pregnant animal. Bronchodilators should be r development of diabetes mellitus and 0.5–1 mg/kg PO q24–48h. Longer-acting r used with caution. predisposes to immunosuppression. Use of parenteral steroids (Vetalog or Depomedrol) corticosteroids in cats may precipitate SYNONYMS should be reserved only for situations where r congestive heart failure. Bronchodilators Allergic bronchitis, chronic obstructive owners are unable to administer oral may exacerbate underlying cardiac disease. pulmonary disease, asthmatic bronchitis, medication on a routine basis. POSSIBLE INTERACTIONS feline lower airway disease, extrinsic asthma, Inhaled Corticosteroids eosinophilic bronchitis, immune-mediated r Fluoroquinolones decrease metabolism of Requires a form-fitting facemask, spacer, airway disease. methylxanthines in dogs; effect has not been and metered-dose inhaler. Veterinary brands investigated in cats. SEE ALSO include Aerokat (Trudell medical) or Nebulair r r r ALTERNATIVE DRUG(S) Heartworm Disease—Cats Respiratory (DVM pharmaceuticals). The most Parasites common corticosteroid used as an MDI is Cyproheptadine μ ABBREVIATIONS fluticasone propionate (Flovent). 220- gor Serotonin antagonist. Inhibits airway smooth r μ BAL = bronchoscopy/bronchoalveolar 110- g Flovent MDI is recommended (1–2 muscle constriction in vitro, unknown effects r lavage FBD = feline bronchopulmonary actuations, 7–10 breaths q12h) along with in cats with asthma/bronchitis. r disease MDI = metered-dose inhaler bronchodilators and oral corticosteroids, r Cyclosporine (Neoral or Gengraf) PU/PD = polyuria/polydipsia depending on the severity of clinical signs. In Give 2.5–5.0 mg/kg PO q12h—monitor μ INTERNET RESOURCES one study, use of 44- g Flovent decreased cyclosporine levels. May be helpful in patients BAL eosinophil counts in experimental cats. r r refractory to bronchodilator and www.Aerokat.com: for ordering facemasks Flovent is used for long-term control of and spacers for inhalant therapy. corticosteroid therapy. r airway inflammation. Takes 10–14 days to www.fritzthebrave.com: source for clients to reach peak effect; use oral steroids Leukotriene Inhibitors or Receptor r research use of inhaled medications. concurrently. Results in some suppression of Blockers the hypothalamic-pituitary axis but systemic No evidence to support use. Suggested Reading side effects appear to be reduced. Cohn LA, DeClue AE, Cohen RL, Reinero Bronchodilators CR. Effects of fluticasone propionate dosage r Methylxanthines: sustained-release in an experimental model of feline asthma. theophylline formulations recommended, and FOLLOW-UP J Feline Med Surg 2010, 12(2):91–96. Dye JA, McKiernan BC, Rozanski EA, et al. pharmacokinetics can vary greatly. Only PATIENT MONITORING generic currently available. Dose at r Bronchopulmonary disease in the cat: Owners should report any increase in 10–20 mg/kg PO once daily in the evening. Historical, physical, radiographic, r coughing, sneezing, wheezing, or respiratory Beta-2 agonists (terbutaline, albuterol)— clinicopathologic, and pulmonary distress. Medications should be increased inhibit smooth muscle constriction. Oral functional evaluation of 24 affected and appropriately if clinical signs worsen. terbutaline dose is 1/4 of a 2.5 mg tablet r 15 healthy cats. J Vet Intern Med 1996, Follow-up radiographs may be helpful to q12h. Initial albuterol dose is 20 μg/kg PO r 10:385–399. evaluate response to medical therapy. Owner q12h; can increase to 50 μg/kg PO q8h. Kirschvink J, Leemans J, Delvaux F, et al. should watch for signs of PU/PD that could Inhaled fluticasone reduces bronchial Inhaled Bronchodilators r indicate diabetes mellitus or renal disease. responsiveness and airway inflammation in Albuterol—preferred inhalant Monitor blood glucose and urine cultures. cats with mild chronic bronchitis. J Feline bronchodilator, effect lasts less than 4 hours. PREVENTION/AVOIDANCE Med Surg 2006, 8(1):45–54. Long-term use of traditional racemic form of Eliminate any environmental factors that may Reinero CR, Delgado C, Spinka C, DeClue inhaled albuterol (R and S-enantiomers) has trigger a crisis situation (see “Risk Factors”). AE, Dhand R. Enantiomer-specific effects been associated with worsened airway Change furnace and air-conditioner filters on of albuterol on airway inflammation in inflammation. Enantiomer specific a regular basis. Consider dust-free litters. healthy and asthmatic cats. Int Arch Allergy R-albuterol should be used if the drug is Immunol 2009, 150(1):43–50. POSSIBLE COMPLICATIONS needed in moderately to severely affected cats r Author Carrie J. Miller (q12–24h) or during respiratory distress. Acute episodes can be life-threatening. r r Consulting Editors Lynelle R. Johnson Ipratropium bromide: inhaled Right-sided heart disease may develop as a anticholinergic; can provide bronchodilation result of long-term bronchitis. and may act synergistically with albuterol to EXPECTED COURSE AND PROGNOSIS Client Education Handout r provide maximal bronchodilation. Long-term therapy should be expected. available online Anthelminthics r r Most cats do well if recurrence of clinical Empirical therapy is indicated for cats with signs is carefully monitored and medical clinical signs of FBD and eosinophilic airway BLBS078-CF_A69 BLBS078-Tilley June 16, 2011 11:3

Canine and Feline, Fifth Edition 123 Astrocytoma A

r tissue chemical properties so infarcts and Chemotherapy may be toxic, and seeking edema can be detected in an earlier stage. advice from a veterinary oncologist before r BASICS CT of brain with and without contrast can initiating treatment is recommended. be useful for lesion confirmation but is not as OVERVIEW sensitive for soft tissue lesion imaging r Categorized as a glial cell neoplasm, which compared to MRI. most commonly affects the brain but rarely DIAGNOSTIC PROCEDURES FOLLOW-UP r the spinal cord. Neoplastic cells are of r r r Neurologic exam. Ophthalmic exam. PATIENT MONITORING astrocyte origin. This tumor is the most r r Advanced imaging such as MRI or CT. Blood phenobarbital concentration should common intra-axial (situated inside of the r r CSF analysis. Brain biopsy is rarely done be assessed after 7–10 days of treatment, with brain parenchyma) intracranial neoplasm of r because of procedural induced morbidity; modifications to dosages for achieving target dogs but is rarely diagnosed in cats. Tumors r however, may provide a definitive diagnosis plasma concentrations. Serial CT or MRI areoftenlocatedinthepyriformareaofthe and aid in treatment planning and prognosis. maybe considered for documenting response temporal lobe, the cerebral hemispheres, the if clinically indicated and economically thalamus, hypothalamus, or midbrain. r r feasible. Serial CBC and platelet counts Biologic behavior of this tumor is dictated should be performed to document bythedegreeofanaplasia(gradedI–IV,from r TREATMENT myelotoxicity associated with chemotherapy. best to worst prognosis). Tumors typically r r r Surgery. Chemotherapy. Radiation EXPECTED COURSE AND PROGNOSIS do not penetrate the ventricular system or r r metastasize outside of the cranial vault. therapy can be very effective in some cases, Long-term prognosis—guarded. Survival SIGNALMENT and consultation with a veterinary radiation time with no treatment is variable and r oncologist is recommended. dependent upon tumor and host factors. Dogs—often brachycephalic breeds r Median survival after chemotherapy plus > 5 years of age; no sex predilection reported. r medical management may be up to 7 months. Cats—usually old (> 9 years); no sex or r Median survival after radiation therapy has breed predilection reported. MEDICATIONS been reported to be as high as 12 months. SIGNS r Location and growth kinetic dependent DRUG(S) r r Seizures Behavioral changes Seizure Control r r Disorientation Loss of conscious r r Status epilepticus—diazepam (0.5–1 mg/kg MISCELLANEOUS proprioception Cranial nerve abnormalities r IV given up to three times to achieve effect); if Upper motor neuron tetraparesis no response to diazepam, use pentobarbital PREGNANCY/FERTILITY/BREEDING CAUSES & RISK FACTORS (5–15 mg/kg IV slowly to effect). Do not breed animals undergoing r chemotherapy Unknown Long-term management—phenobarbital (1–4 mg/kg PO q12h) with or without SEE ALSO r adjuvant potassium bromide (20 mg/kg PO Seizures (Convulsions, Status r q24h). Epilepticus)—Cats Seizures (Convulsions, Tumor Control Status Epilepticus)—Dogs DIAGNOSIS r Radiation therapy may be effective, and ABBREVIATIONS DIFFERENTIAL DIAGNOSIS r r r consultation with a radiation oncologist is CSF = cerebrospinal fluid CT = Other primary tumors arising from tissues r r recommended. Stereotactic radiosurgery or computed tomography MRI = magnetic of the central nervous system. Metastatic intensity modulated radiation therapy should resonance imaging neoplasia with brain tropism. be considered first-line treatment options. r r Granulomatous meningoencephalitis. Suggested Reading r r Chemotherapy may be effective for treating Trauma. Cerebrovascular infarction. Bley CR, Sumova A, Roos M, Kaser-Hotz B. r dogs. Potential drugs that may exert Meningitis. measurable anticancer effects include Irradiation of brain tumors in dogs with CBC/BIOCHEMISTRY/URINALYSIS lomustine (70 mg/m2 PO every 3 weeks) or neurologic disease. J Vet Intern Med 2005, carmustine (50 mg/m2 IV every 6 weeks). 19:849–854. Usually normal r Prednisone (0.5–1 mg/kg q24h), although Meyerholz DG, Haynes JS. Solitary retinal OTHER LABORATORY TESTS not cytotoxic to cancer cells, may be effective astrocytoma in a dog. Vet Pathol 2004, CSF analysis may show albuminocytologic in controlling peri-tumoral edema and 41:177–178. dissociation (high protein with few cells). improving clinical signs. Morrison WB. Cancer affecting the nervous Analysis should include the characterization CONTRAINDICATIONS/POSSIBLE system. In: Morrison WB, ed., Cancer in of the fluid including color, turbidity, protein Dogs and Cats: Medical and Surgical INTERACTIONS concentration, total nucleated cell count, r Management. Jackson, WY: Teton cytologic evaluation, and titers for antibodies Prednisone and phenobarbital may cause NewMedia, 2002, pp. 631–640. polyphagia, polydipsia, and polyuria. against infectious agents; and culturing. r Snyder JM, Shofer FS, Van Winkle TJ, et al. IMAGING Phenobarbital may cause sedation for up to Canine intracranial primary neoplasia: 173 r 2 weeks after initiation of treatment, and may cases (1986-2003). J Vet Intern Med 2006, MRI of brain is ideal for mass lesion cause increase in hepatic enzymes on serum confirmation. Unlike CT scanning, r 20:669–675. biochemical panel. CBC and platelet count Troxel MT, Vite CH, Van Winkle TJ, et al. beam-hardening artifacts originating from is recommended 7–10 days after thick compact bone do not occur with MRI, Feline intracranial neoplasia: Retrospective chemotherapy and immediately before each review of 160 cases (1985-2001). J Vet and therefore MRI is superior for detecting dose of chemotherapy to monitor r Intern Med 2003, 17:850–859. lesions in the middle and caudal fossae. myelosuppression. Carmustine has the Additionally, MRI is more sensitive than CT Author Wallace B. Morrison potential of causing pulmonary toxicity at Consulting Editors Timothy M. Fan for the detection of subtle changes in soft cumulative doses of 1,400 mg/m2. BLBS078-CF_A70 BLBS078-Tilley June 1, 2011 12:47

124 Blackwell’s Five-Minute Veterinary Consult A Astrovirus Infection

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 r Kittens show more severe signs. enteritis, rotavirus, or coronavirus enteritis. MISCELLANEOUS r May be severe and acute enough to cause ZOONOTIC POTENTIAL dehydration and anorexia. Sequence analysis of human and animal CAUSES & RISK FACTORS r astroviruses suggests human-to-animal A small, non-enveloped, RNA virus of the TREATMENT transmission does not occur. genus Astrovirus. r r Control diarrhea. Suggested Reading Details of the incidence, prevalence, and r predisposing factors unknown. Reestablish fluid and electrolyte balance. Barr MC, Olsen CW, Scott FW. Feline viral diseases. In: Ettinger SJ, Feldman EC, eds., Veterinary Internal Medicine. Philadelphia: Saunders, 1995, pp. 409–439. MEDICATIONS Lukashov VV, Goudsmit J. Evolutionary DIAGNOSIS relationships among Astroviridae. J Gen DIFFERENTIAL DIAGNOSIS DRUG(S) Virol 2002, 83:1397–1405. r Many causes of gastroenteritis. No specific antiviral drugs. Author Fred W. Scott r Food allergy. CONTRAINDICATIONS/POSSIBLE Consulting Editor Stephen C. Barr r Toxin ingestion. r INTERACTIONS Inflammatory bowel disease. r None Neoplasia. r Intestinal parasites. r Viral infections—panleukopenia, rotavirus, enteric coronavirus, enteric calicivirus. r FOLLOW-UP Bacterial infections—salmonellosis, coliforms. PATIENT MONITORING r Protozoal infections—Giardia, Monitor fluid and electrolytes. cryptosporidiosis. BLBS078-CF_A71 BLBS078-Tilley March 22, 2011 11:20

Canine and Feline, Fifth Edition 125 Ataxia A

r Cerebellar Toxic—metronidazole. r The cerebellum regulates, coordinates, and Vestibular—Peripheral Nervous System r modulates motor activity. Infectious—otitis media interna; BASICS r Proprioception is normal because the Cryptococcus granuloma (cats). r DEFINITION ascending proprioceptive pathways to the Idiopathic—geriatric vestibular disease r A sign of sensory dysfunction that produces cortex are intact; weakness does not occur (dogs); idiopathic vestibular syndrome (cats); because the upper motor neurons are intact. nasopharyngeal (middle ear) polyps (cats). incoordination of the limbs, head, and/or r r trunk. Inadequacy in the performance of motor Metabolic—hypothyroidism. r r Three clinical types—sensory activity; strength preservation; no Neoplastic—squamous cell carcinoma, bone proprioceptive deficits. tumors. (proprioceptive), vestibular, and cerebellar; all r r produce changes in limb coordination, but Affected animal shows uncoordinated Traumatic. motor activity of limbs, head, and neck; Spinal Cord vestibular and cerebellar ataxia also produce r changes in head and neck movement. hypermetria; dysmetria; head tremors; Degenerative—degenerative myelopathy intention tremors; and truncal sway. (old German shepherds, Welsh corgis). PATHOPHYSIOLOGY r SYSTEMS AFFECTED Vascular—fibrocartilaginous embolic Sensory (Proprioceptive) r myelopathy. Proprioceptive pathways in the spinal cord Nervous—spinal cord (and brainstem and r cortex), cerebellum, vestibular system. Anomalous—hemivertebrae; dens (i.e., fasciculus gracilis, fasciculus cuneatus, hypoplasia with atlantoaxial and spinocerebellar tracts) relay limb and SIGNALMENT subluxation-luxation; Chiari-like trunk position to the brain. Any age, breed, or sex r malformation; other spinal cord and vertebral When the spinal cord is slowly compressed, SIGNS malformation; spinal arachnoid cyst. r r proprioceptive deficits are usually the first Important to define the type of ataxia to Neoplastic—primary bone tumors; multiple signs observed, because these pathways are localize the problem. myeloma and metastatic tumors that infiltrate r located more superficially in the white matter Only one limb involved—consider a the vertebral body; meningioma; and their larger sized axons are more lameness problem. others. r r susceptible to compression than are other Only hind limbs affected—likely a spinal Infectious—diskospondylitis; myelitis. tracts. r r cord disorder affecting the spinocerebellar Traumatic—intervertebral disk herniation; Generally accompanied by weakness owing tracts. fracture or luxation; cervical r to early concomitant upper motor neuron All or both ipsilateral limbs spondylomyelopathy; atlantoaxial involvement; weakness not always obvious affected—cerebellar. subluxation-luxation. early in the course of the disease. r r Head tilt—vestibular. Metabolic Ataxia can occur with spinal cord, r CAUSES Anemia. brainstem, and cerebral lesions; mild with r Polycythemia. unilateral brainstem lesions, and subtle to Neurologic r Electrolyte disturbances—especially absent with unilateral cerebral Cerebellar r hypokalemia, hypocalcemia, and lesion. Degenerative—abiotrophy (Kerry blue hypoglycemia. Vestibular terriers, Gordon setters, rough-coated collies, r Miscellaneous Changes in head and neck position are Australian kelpies, Airedales, Bernese r Drugs—acepromazine; antihistamines; relayed through the vestibulo-cochlear nerve mountain dogs, Finnish harriers, Brittany antiepileptic drugs. to the brainstem. spaniels, border collies, beagles, Samoyeds, r r Respiratory compromise. Vestibular receptors or the nerve in the wirehaired fox terriers, Labrador retrievers, r Cardiac compromise—reverse PDA, aortic inner ear are considered part of the peripheral Great Danes, chow chows, Rhodesian thromboembolism. nervous system, whereas nuclei in the ridgebacks, domestic shorthair cats); storage brainstem are part of the central nervous diseases often have cerebellomedullary RISK FACTORS involvement. r system. r Intervertebral disk disease—dachshunds, r Anomalous—hypoplasia secondary to poodles, cocker spaniels, and beagles. Localize the vestibular signs to peripheral or r central vestibular nervous system because perinatal infection with panleukopenia virus Cervical spondylomyelopathy—Doberman (cats); malformed cerebellum due to pinschers and Great Danes. prognosis and rule-outs differ for these two r locations. herpesvirus infection (newborn puppies); Fibrocartilaginous embolism—young, r Both locations of vestibular disease cause arachnoid or epidermoid cyst located near large-breed dogs and miniature schnauzers. fourth ventricle. r various degrees of disequilibrium with r Dens hypoplasia and atlantoaxial ensuing vestibular ataxia. Neoplastic—any CNS tumor (primary or luxation—small-breed dogs, poodles. r secondary) localized to the cerebellum. r Affected animal leans, tips, falls, or even r Chiari-like malformation—Cavalier King rolls toward the side of the lesion; Infectious—canine distemper virus; FIP; Charles spaniels, small-breed dogs. accompanied by head tilt. and any other CNS infection affecting the r cerebellum. Central vestibular signs usually have r changing types of nystagmus or vertical Inflammatory, idiopathic, nystagmus; somnolence, stupor, or coma (due immune-mediated—granulomatous DIAGNOSIS meningoencephalomyelitis. to involvement of the nearby reticular r Toxic—metronidazole. DIFFERENTIAL DIAGNOSIS activating system); multiple cranial nerve r Vestibular—Central Nervous System Differentiate the types of ataxia. signs; proprioceptive deficits and r r quadriparesis or hemiparesis. Infectious—FIP; canine distemper virus; Differentiate from other disease processes r rickettsial diseases. Peripheral vestibular signs do not include r that can affect gait—musculoskeletal, Inflammatory, idiopathic, metabolic, cardiovascular, respiratory. changes in mental status, vertical nystagmus, r proprioceptive deficits, quadriparesis or immune-mediated—granulomatous Musculoskeletal disorders—typically meningoencephalomyelitis. hemiparesis. r produce lameness, pain, and a reluctance to Nutritional—thiamine deficiency. move; degenerative joint disease often BLBS078-CF_A71 BLBS078-Tilley March 22, 2011 11:20

126 Blackwell’s Five-Minute Veterinary Consult

A Ataxia (Continued)

r r improves with increased movements. CT or MRI—if cerebellar disease suspected; Hypoglycemia—seizures. r r Systemic illness and endocrine, evaluate potential brain disease. MRI superior Cerebellar disease—head tremors and cardiovascular, and metabolic disorders—can to CT. bobbing. r r cause intermittent ataxia, especially of the Abdominal ultrasonography—if hepatic, Brainstem disease—stupor, coma, death. pelvic limbs; with fever, weight loss, renal, adrenal, or pancreatic dysfunction murmurs, arrhythmias, hair loss, or collapse suspected. with exercise, suspect a non-neurologic cause; DIAGNOSTIC PROCEDURES obtain minimum data from hemogram, Cerebrospinal fluid—helps confirm nervous MISCELLANEOUS biochemistry, and urinalysis. r system etiology. Head tilt or nystagmus—likely vestibular. AGE-RELATED FACTORS r Intention tremors of the head or N/A hypermetria—likely cerebellar. SEE ALSO r r All four limbs affected: lesion is in the See specific causes TREATMENT r cervical area or is multifocal to diffuse; only Cerebellar Degeneration r r pelvic limbs affected: lesion is anywhere below Usually outpatient, depending on severity Head Tilt the second thoracic vertebra. and acuteness of clinical signs. r r Paralysis CBC/BIOCHEMISTRY/URINALYSIS Exercise—decrease or restrict if spinal cord ABBREVIATIONS disease. r Normal unless metabolic cause (e.g., r CNS = central nervous system Client should monitor gait for increasing r hypoglycemia, electrolyte imbalance, anemia, CT = computed tomography dysfunction or weakness; if paresis worsens or r polycythemia). FIP = feline infectious peritonitis paralysis develops, other testing is warranted. r OTHER LABORATORY TESTS r MRI = magnetic resonance imaging r Avoid drugs that could contribute to the Hypoglycemia—determine serum insulin problem; may not be possible in patients on INTERNET RESOURCES concentration on the same sample (rule out antiepileptic drugs for seizures. IVIS: www.ivis.org insulinoma). r Anemia—differentiate as nonregenerative or Suggested Reading regenerative on the basis of the reticulocyte Davies C, Shell L. Neurological problems. In: count. Common Small Animal Medical Diagnoses: r MEDICATIONS Electrolyte imbalance—correct the An Algorithmic Approach. Philadelphia: problem; see if ataxia resolves. DRUG(S) OF CHOICE Saunders, 2002, pp. 36–59. r Antiepileptic drugs—if being administered, Not recommended until the source or cause Lorenz MD, Kornegay JN. Handbook of evaluate serum concentration for toxicity. of the problem is identified. Veterinary Neurology, 4th ed. Philadelphia: IMAGING Saunders, 2004, pp. 219–244. r Thomas WB. Vestibular dysfunction. Vet Spinal radiography, myelography, CT or Clin North Am Small Anim Pract 2000, MRI—if spinal cord dysfunction suspected. r 30:227–249. Bullae radiography—if peripheral vestibular FOLLOW-UP Author Linda G. Shell disease suspected; CT or MRI superior; for PATIENT MONITORING Consulting Editor Joane M. Parent inner ear disease, MRI superior to CT. r Thoracic radiography—for older patients Periodic neurologic examinations to assess condition. and patients suspected to have neoplasia or Client Education Handout systemic fungal infection. POSSIBLE COMPLICATIONS r available online Spinal cord—progression to weakness and possibly paralysis. BLBS078-CF_A72 BLBS078-Tilley June 24, 2011 13:9

Canine and Feline, Fifth Edition 127 Atherosclerosis A

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 T3 and T4. r arterial change characterized by loss of r Monitor blood triglyceride and cholesterol High values for alpha-2 and beta fractions levels. elasticity, luminal narrowing, and r on protein electrophoresis. 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 MISCELLANEOUS Higher prevalence in miniature schnauzer, DIAGNOSTIC PROCEDURES Doberman pinscher, poodle, and Labrador Electrocardiography ASSOCIATED CONDITIONS r r retriever. Conduction abnormalities and notched Hypothyroidism r r Geriatric patients (> 9 years). QRS complexes. Diabetes r r Atrial fibrillation. Mitral valve disease (myxomatous) SIGNS r r ST segment elevation or depression with Glomerulonephritis Historical Findings r myocardial infarction. AGE-RELATED FACTORS None in some animals r > Lethargy Geriatric patients ( 9 years) r Anorexia SEE ALSO r Weakness r Myocardial Infarction Dyspnea TREATMENT r r INTERNET RESOURCES Collapse Treat the underlying disorder and clinical r www.vetgo.com/cardio Vomiting r signs (e.g., dyspnea if congestive heart failure Diarrhea develops). Suggested Reading r Physical Examination Findings Diet—low-fat diet, weight loss program, Drost WT, Bahr RJ, Henay GA, Campbell r Dyspnea and high soluble fiber intake to control GA. Aortoiliac thrombus secondary to a r Irregular rhythm hyperlipidemia. mineralized arteriosclerotic lesion. Vet r Heart failure Radiol Ultrasound 1999, 40:262–266. r Disorientation Hamlen HJ. Sinoatrial node arteriosclerosis in r Blindness two young dogs. JAVMA 1994, 204:751. r Circling MEDICATIONS Hess RS, Kass PH, Van Winkle JV. r Coma Association between diabetes mellitus, r DRUG(S) Episodic lameness r hypothyroidism or hyperadrenocorticism Treat conduction disturbances and CAUSES & RISK FACTORS and atherosclerosis in dogs. J Vet Intern r arrhythmias if clinically indicated. Med 2003, 17:489–494. Severe hypothyroidism r r Thyroid replacement if hypothyroidism is Kidd L, Stepien RL, Amrheiw DP. Clinical Increasing age r confirmed. findings and coronary artery disease in dogs Hyperlipidemia in miniature schnauzers r r Antihypertensive therapy if hypertension is and cats with acute and subacute myocardial Male gender (male dogs may have documented. necrosis: 28 cases. JAAHA 2000, predisposition) r r Blood cholesterol-reducing medications if 36:199–208. High total cholesterol r hyperlipidemic. Liu SK, Tilley LP, Tappe JP, Fox PR. Clinical Diabetes r r Tre at di abe t e s . and pathologic findings in dogs with Glomerulonephritis CONTRAINDICATIONS/POSSIBLE atherosclerosis: 21 cases (1970–1983). INTERACTIONS JAVMA 1986, 189:227–232. Author Larry P. Tilley N/A Consulting Editors LarryP.TilleyandFrancis DIAGNOSIS W.K. Smith, Jr. DIFFERENTIAL DIAGNOSIS Arteriosclerosis BLBS078-CF_A73 BLBS078-Tilley June 26, 2011 8:34

128 Blackwell’s Five-Minute Veterinary Consult A Atlantoaxial Instability

closely monitored until they are capable of maintaining normal head and neck BASICS DIAGNOSIS carriage. OVERVIEW DIFFERENTIAL DIAGNOSIS r r Results from malformation or disruption of Differential diagnoses are consistent with the articulation between the first and second various causes of cervical myelopathies, TREATMENT r cervical vertebrae (atlas and axis, respectively); including: Prior to treatment, consultation with a causes spinal cord compression. ◦ Other congenital malformation. r ◦ board-certified neurologist or surgeon should AA instability can result in spinal cord Trauma. be pursued. ◦ r trauma or compression at the junction Meningitis or meningomyelitis (i.e., Improper treatment can lead to irreversible between the atlas and axis—may cause neck infectious or non-infectious deterioration in neurologic function. pain and/or varying degrees of general (granulomatous MEDICAL proprioceptive (GP) ataxia /upper motor meningoencephalomyelitis). r neuron (UMN) tetraparesis, tetraplegia (with ◦ Fibrocartilaginous embolic myelopathy. Neck brace (splint) to stabilize the cervical or without nociception), and death from ◦ Disk herniation. vertebral column in extension. respiratory arrest. ◦ Neoplasia. ◦ Fiberglass cast material is positioned Etiology CBC/BIOCHEMISTRY/URINALYSIS ventrally from the rostral aspect of r mandible to the xiphoid and incorporated Congenital: anomaly of the dens (aplasia, Normal into bandage material, which immobilizes hypoplasia, or malformation [dorsal IMAGING the head and neck. angulation] of the dens) and its ligamentous r Plain radiography of the cervical vertebral ◦ Strict exercise restriction (cage attachments. r column: Acquired: may be a consequence of confinement) for a minimum of 8 weeks. ◦ Lateral view—caudal and dorsal ◦ traumatic injury. Frequent bandage/splint changes are displacement of the axis in relationship to needed. SIGNALMENT r r the atlas, resulting in an increased distance Adjunctive medication (see below). Congenital—toy-breed dogs (Yorkshire between vertebrae. Overall Prognosis ◦ r terriers, miniature or toy poodles, Ventral dorsal or oblique view—may Successful outcome observed in 62.5% of Chihuahuas, Pekingese, and Pomeranians). r reveal absence, hypoplasia, or malformation dogs. Age at onset—usually before 12 months of (dorsal angulation) of the dens. r r Improved prognosis was associated with an age. Cross-sectional imaging: r > ◦ acute onset and short duration of clinical Uncommon in larger-breed dogs, dogs 1 MRI. signs (< 30 days). year old, and cats. ◦ Imaging modality of choice. r r ◦ Surgery is recommended to treat animals No sex predilection. Diagnosis based on observation of caudal that fail to improve or experience recurrence SIGNS and dorsal displacement of the axis in of signs following medical treatment. r relationship to the atlas as evidenced by the Intermittent or progressive ambulatory SURGERY following features of the atlantoaxial r tetraparesis, usually with neck pain—most Treatment of choice in the majority of cases. common. articulation: r r ᭿ Surgical approach; ventral method is Signs vary from mild to moderate Dorsal: displacement of the spinous process of the axis. preferred. GP/UMN ambulatory tetraparesis to ◦ ᭿ Ventral approach—variety of methods: non-ambulatory GP/UMN tetraparesis, or Ventral: increased size of the ᭿ Transarticular pinning or lag screw tetraplegia depending on degree of spinal cord occipito-atlas-axis joint cavity. ◦ Allows identification of spinal cord technique; ventral tips of the pins compression and secondary pathology (i.e., incorporated in polymethylmethacrylate edema, hemorrhage, or gliosis). compression. r ◦ to prevent pin migration. Neck pain without concurrent neurologic Allows recognition of secondary spinal ᭿ Transarticular pinning and ventral deficits. cord pathology such as edema, r cortical screws or K-wires in the bodies Episodes of collapse secondary to weakness. hemorrhage, or gliosis, which may impact r of the atlas and axis +/− K-wires Spinal reflexes are normal to exaggerated prognosis. r applied longitundinally and wired to the with normal to increased muscle tone in all Computed tomography: ◦ screws; screw heads and K-wires are four limbs. May provide detailed visualization of r incorporated in polymethylmethacrylate Acute death may occur when accompanied bony structures, which allows for the to provide fixation. by trauma and respiratory arrest creation of three-dimensional reconstructed image to help surgical planning. ᭿ Dorsal approach—use wire or (uncommon). r Precautions: synthetic suture material to fix the CAUSES & RISK FACTORS ◦ r Proper positioning may require sedation spinous process of the axis to the dorsal Usually caused by abnormal development of or general anesthesia. arch of the atlas; provides less rigid the dens or ligamentous support structures, ᭿ Sedation or general anesthesia carries fixation and may be associated with resulting in subluxation of the atlantoaxial greater implant failure. significant risk for iatrogenic r joint. r trauma. Strict exercise restriction is required for the Fracture of the axis. ᭿ r Care needs to be exercised when first month post-operatively, followed by a Clinical signs often occur as a result of mild positioning animals. gradual return to activity over an additional or insignificant trauma (e.g., jumping or ᭿ month. AVOID FLEXION OF THE NECK. r playing). ᭿ Adjunctive medication (see below). r Flexion may exacerbate compression, r Clinical signs may be exacerbated by activity which may worsen clinical signs or cause Overall prognosis ranges from 63% to 91% such as flexion of the neck. death due to spinal cord trauma. success: improved prognosis was associated r < Toy-breed dogs—at risk for congenital ᭿ To protect against neck flexion during with young ( 24 months) dogs, duration of malformation of the dens. recovery, affected animals should be BLBS078-CF_A73 BLBS078-Tilley June 26, 2011 8:34

Canine and Feline, Fifth Edition 129

(Continued) Atlantoaxial Instability A

r clinical signs < 10 months, and mild All dogs should be reevaluated at 1 and 3 Havig ME, Cornell KK, Hawthorne JC, neurologic deficits. months (post-operatively or after neck brace McDonnell JJ, Selcer BA. Evaluation of r Complications: removal) and monthly until neurological nonsurgical treatment of atlantoaxial ◦ Failure to improve/worsening of deficits resolve or remain static over 2–3 subluxation in dogs: 19 cases (1992–2001). neurological deficits. months. JAVMA 2005, 227(2):257–262. r ◦ Implant failure/infection. More frequent rechecks may be needed for McCarthy RJ, Lewis DD, Hosgood G. ◦ Respiratory—dyspnea, cough, and dogs experiencing complications or recurrence Atlantoaxial subluxation in dogs. Compend aspiration pneumonia. of signs. Contin Educ Pract Vet 1995, 17:215–226 r ◦ Death. Untreated animals may experience Platt SR, Chambers JN, Cross A. A modified deterioration in neurologic function, ventral fixation for surgical management of catastrophic acute spinal cord trauma, atlantoaxial subluxation in 19 dogs. Vet respiratory arrest, and death. Surg 2004, 33(4):349–354. MEDICATIONS Sanders SG, Bagley RS, Silver GM, Moore M, Tucker RL. Outcomes and complications DRUG(S) r associated with ventral screws, pins, and Anti-inflammatory medication: MISCELLANEOUS polymethyl methacrylate for atlantoaxial ◦ Corticosteroids: prednisone 0.5–1.0 r instability in 12 dogs. JAAHA 2004, Rehabilitation may play a significant role in mg/kg PO divided twice daily for 2 weeks, 40:204–210. the ultimate neurologic functional level of the followed by a tapering regime. Suggested Schulz KS, Waldron DR, Fahie M. patient. protocol following initial dose: 0.5 mg/kg r Application of ventral pins and Rehabilitation should only be considered in PO daily for 5 days, followed by 0.5 mg/kg polymethylmethacrylate for the dogs > 30 days post-operatively or after neck PO every other day for 5 days. management of atlantoaxial instability: ◦ NSAID: 1- to 4-week course. brace (splint) removal. r Results in nine dogs. Vet Surg 1997, Analgesia: ABBREVIATIONS r 26(4):317–325. ◦ Tramadol 2.0–4.0 mg/kg PO q6–8h. GP = general proprioceptive r Shires PK. Atlantoaxial instability. In: Slatter ◦ Gabapentin 10–20 mg/kg PO q6–8h. MRI = magnetic resonance imaging r D, ed., Textbook of Small Animal Surgery, CONTRAINDICATIONS/POSSIBLE NSAID = nonsteroidal anti-inflammatory 3rd ed. Philadelphia: Saunders, 2003. drug INTERACTIONS r Tomlinson J. Surgical conditions of the r UMN = upper motor neuron Corticosteroid—use caution when given in 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 and http://www.acvs.org/AnimalOwners/Health Authors Mathieu M. Glassman and Marc spinal cord trauma. Conditions/SmallAnimalTopics/Atlantoaxial Kent r Avoid NSAIDs in combination with Instability/. Consulting Editor Peter K. Shires 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). JAVMA 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. BLBS078-CF_A74 BLBS078-Tilley July 23, 2011 5:20

130 Blackwell’s Five-Minute Veterinary Consult A Atopic Dermatitis

r Highland white terrier, wirehaired fox terrier, and elimination of other causes. Sarcoptic r and golden retriever. Feline—none reported. mange—often occurs in young or stray dogs; BASICS Mean Age and Range causes severe pruritus of the ventral chest, Canine—mean age at onset 1–3 years; range lateral elbows, lateral hocks, and pinnal DEFINITION 3 months–6 years; signs may be mild the first margins; differentiation by multiple skin r scrapings and/or complete response to a trial Hypersensitivity reaction to normally year but usually progress and become r innocuous substances, such as pollens clinically apparent before 3 years of age. of miticidal therapy. Secondary pyoderma—usually caused by Staphylococcus (grasses, weeds, and trees), molds, house dust Predominant Sex mites, epithelial allergens, and other pseudintermedius; characterized by follicular r None reported papules, pustules, crusts, and epidermal environmental allergens. Manifests as an r inflammatory, chronically relapsing, SIGNS collarettes. Secondary yeast non-contagious and pruritic skin disease. General Comments infections—caused by Malassezia r PATHOPHYSIOLOGY Pruritus—itching, scratching, rubbing, pachydermatis; characterized by erythematous, r r scaly, crusty, greasy, and very malodorous Susceptible animals become sensitized to licking. Most cutaneous changes caused by self-induced trauma; primary lesions usually body folds and intertriginous areas; environmental allergens by producing differentiation by demonstration of numerous allergen-specific IgE (mediated through unrecognized. r budding yeast organisms by skin cytology and Langerhans cells). Allergen-specific IgE Historical Findings r r obtaining a favorable response to antifungal binds to receptor sites on cutaneous mast Facial, pedal, or axillary pruritus Early age r r r therapy. Contact dermatitis (allergic or cells. Allergen reexposure, primarily by of onset History in related individuals r r irritant)—may cause severe erythema and percutaneous absorption, causes mast cell May be initially seasonal Recurring skin or r pruritus of the feet and thinly haired areas of degranulation (type I immediate ear infection Temporary response to r the ventrum. hypersensitivity reaction) and results in the glucocorticosteroids Symptoms release of histamine, proteolytic enzymes, progressively worsen with time CBC/BIOCHEMISTRY/URINALYSIS cytokines, chemokines, and many other Physical Examination Findings Eosinophilia—rare in dogs without r r chemical mediators. Th2-type cytokine Areas most commonly affected—interdigital concurrent flea infestations; common in response predominates in the acute phase. cats. r spaces, carpal and tarsal areas, muzzle, In chronic (intrinsic) atopic dermatitis, a periocular region, axillae, groin, and pinnae. OTHER LABORATORY TESTS r Th1-type cytokine response predominates. Lesions—vary from none to broken hairs or Serologic Allergy Tests r Bacterial superantigens, auto-antigens released salivary discoloration to erythema, papular Tests to measure the amount of via keratinocyte damage, and Malassezia may reactions, crusts, alopecia, allergen-specific IgE antibody in the patient’s play a role in perpetuating the inflammation. hyperpigmentation, lichenification, serum are commercially available. r SYSTEMS AFFECTED excessively oily or dry seborrhea, and Advantages over IDT—availability; large r r r hyperhidrosis (apocrine sweating). Ophthalmic Respiratory Skin/Exocrine r areas of hair do not have to be shaved; Secondary bacterial and yeast skin infections GENETICS r sedation is not required. r (common). Chronic relapsing otitis externa. r r Disadvantages—frequent false-positive or Dogs—inherited predisposition; mode of Conjunctivitis may occur. inheritance is unknown and environmental false-negative reactions; limited number of r CAUSES allergens tested; inconsistent assay validation, influences are important. Cats—unclear. r r Pollens (grasses, weeds, and trees) Mold quality control, and reliability (may vary with INCIDENCE/PREVALENCE r r spores (indoor and outdoor) Malassezia the laboratory used). r r r Canine—true prevalence is unknown; House dust mite Animal dander Insects DIAGNOSTIC PROCEDURES estimated at 3–15% of the canine population; r (controversial) Cytokine dysregulation Intradermal Test (Preferred) reported to be the second most common r RISK FACTORS Diagnosis of atopy is made by the history, allergic skin disease in the past; however, with r Temperate environments with long allergy physical examination, and ruling out of the availability of effective flea control r seasons and high pollen and mold spore levels. differential diagnoses. Intradermal testing is measures, atopic dermatitis may now be more r r Concurrent pruritic dermatoses, such as flea used to formulate an immunotherapy prevalent. Feline—unknown; generally r believed to be much lower than that for dogs. bite hypersensitivity and adverse food reaction prescription. Small amounts of test allergen (summation effect). are injected intradermally; wheal formation is GEOGRAPHIC DISTRIBUTION r measured and evaluated subjectively. Results Canine—recognized worldwide; local more difficult to interpret in cats owing to the r environmental factors (temperature, relatively small wheals produced. False humidity, and flora) influence the seasonality, DIAGNOSIS positive and false negative reactions may severity, and duration of signs. occur. SIGNALMENT DIFFERENTIAL DIAGNOSIS r PATHOLOGIC FINDINGS Adverse food reaction—may cause identical r Species Gross lesions—see “Physical Examination lesion distribution and physical examination r Dogs and cats Findings.” Skin biopsy—may help rule out findings but should be non-seasonal; may Breed Predilections other differential diagnoses; results are usually r occur concurrently with atopic dermatitis; Canine—any breed, including mongrels; not pathognomonic. differentiation is made by noting response to r recognized more frequently in certain breeds r Dermatohistopathologic r hypoallergenic diet. Flea bite changes—acanthosis, mixed mononuclear or families (can vary geographically). United hypersensitivity—most common cause of superficial perivascular dermatitis, sebaceous States—Boston terrier, cairn terrier, seasonal pruritus in appropriate geographical gland metaplasia, with secondary superficial Dalmatian, English bulldog, English setter, regions; may occur concurrently with atopic bacterial folliculitis. Irish setter, Lhasa apso, miniature schnauzer, dermatitis; differentiation is made by noting pug, Sealyham terrier, Scottish terrier, West lesion distribution, response to flea control, BLBS078-CF_A74 BLBS078-Tilley July 23, 2011 5:20

Canine and Feline, Fifth Edition 131

(Continued) Atopic Dermatitis A

Antihistamines significant impact on the level of r r Less effective than are corticosteroids. pruritus. Minimizing other sources of r Evidence of efficacy is poor. pruritus (e.g., flea infestation, adverse food TREATMENT r Dogs—hydroxyzine (1–2 mg/kg PO q12h), reaction, and secondary skin infection) may APPROPRIATE HEALTH CARE chlorpheniramine (0.2–0.4 mg/kg PO q12h), reduce the level of pruritus. Outpatient diphenhydramine (2.2 mg/kg PO q12h), and POSSIBLE COMPLICATIONS r ACTIVITY clemastine (0.04–0.10 mg/kg PO q12h). Secondary bacterial folliculitis or Malassezia r r Avoid offending allergens when possible Cats—chlorpheniramine (0.5 mg/kg PO dermatitis. Concurrent flea bite q12h); efficacy estimated at 10–50%. DIET hypersensitivity and/or adverse food reaction. PRECAUTIONS Diets rich in essential fatty acids may be r EXPECTED COURSE AND PROGNOSIS r beneficial Corticosteroids—use judiciously in dogs to Not life-threatening unless intractable avoid iatrogenic hyperglucocorticism and r CLIENT EDUCATION pruritus results in euthanasia. Untreated, r associated problems, aggravation of the degree of pruritus worsens and the Explain the progressive nature of the pyoderma, and induction of demodicosis. r r duration of signs last longer each condition. Inform client that it rarely goes r r Antihistamines—can produce drowsiness, year. Some cases spontaneously resolve. into remission and cannot be cured. Inform anorexia, vomiting, diarrhea, and even client that some form of therapy may be increased pruritus; use with caution in necessary to maintain quality of life. patients with cardiac arrhythmias. POSSIBLE INTERACTIONS MISCELLANEOUS Concurrent use of cyclosporine and ASSOCIATED CONDITIONS ketoconazole requires a dose reduction of r r MEDICATIONS Flea bite hypersensitivity Adverse food cyclosporine. r reaction/ food hypersensitivity Bacterial DRUG(S) OF CHOICE ALTERNATIVE DRUG(S) r r r folliculitis Malassezia dermatitis Otitis Immunotherapy (Hyposensitization) Frequent bathing in cool water with r externa Administration of subcutaneous injections antipruritic shampoos is very beneficial. r AGE-RELATED FACTORS of gradually increasing doses of the causative Diets rich in fatty acids may benefit pruritic r allergens to reduce sensitivity. Allergen patients; some studies have indicated that ω-3 Severity worsens with age selection—based on allergy test results, (eicosapentaenoic acid 66 mg/kg/day) may be PREGNANCY/FERTILITY/BREEDING r patient history, and/or knowledge of local more effective than ω-6 (linoleic acid 130 Corticosteroids—contraindicated during r r r exposure. Immunotherapy formulation mg/kg/day) fatty acids. Tricyclic pregnancy Affected animals should not be procedures and administration protocols are antidepressants (doxepin 1–2 mg/kg PO used for breeding not standardized and vary widely between q12h; or amitriptyline 1–2 mg/kg PO q12h) r SYNONYMS clinicians. Indicated when it is desirable to have been given to dogs as antipruritics but r r Atopy Canine atopic disease avoid or reduce the amount of corticosteroids their overall effectiveness and mode of action SEE ALSO required to control signs, when signs last is unclear; not extensively studied in the cat. r r Flea Bite Hypersensitivity and Flea Control longer than 4–6 months per year, or when Topical triamcinolone spray .015% (Genesis r r non-steroid forms of therapy are ineffective. Virbac) can be used over large body surfaces Food Reactions, Dermatologic Otitis r r Successfully reduces pruritus in 60–80% of to control pruritus with minimal side effects. Externa and Media Pyoderma r dogs and cats. Response is usually slow, ABBREVIATIONS r often requiring 3–6 months and up to 1 year, IDT = intradermal test for full effect. Cyclosporine FOLLOW-UP Suggested Reading r Reedy LM, Miller WH, Willemse T. Allergic Cyclosporine (Atopica 5 mg/kg/day) PATIENT MONITORING Skin Diseases of Dogs and Cats, 2nd ed. effective in controlling pruritus associated r r Examine patient every 2–8 weeks when a Philadelphia: Saunders, 1997. with chronic atopic dermatitis. Response is r new course of therapy is started. Monitor Author Alexander H. Werner similar to that of glucocorticosteroids. r pruritus, self-trauma, development of Consulting Editor Alexander H. Werner Onset of activity is slower (1–4 weeks is r bacterial folliculitis, and possible adverse drug r typical). Many patients can be adequately reactions. Once an acceptable level of controlled long term with less frequent dosing r control is achieved, examine patient every Client Education Handout r (every 2–4 days). Frequent patient 3–12 months. CBC, serum chemistry available online monitoring is recommended. profile, and urinalysis—recommended every Corticosteroids r 3–12 months for patients on chronic May be given for short-term relief and to r corticosteroid or cyclosporine therapy. break the itch-scratch cycle. Should be PREVENTION/AVOIDANCE tapered to the lowest dosage that adequately r r If the offending allergens have been controls pruritus. Prednisolone or identified through allergy testing, the owner methylprednisolone tablets (0.2–0.5 mg/kg r should undertake to reduce the animal’s PO q48h). Cats—infrequent exposure as much as possible; seldom makes a methylprednisolone acetate by injection (4 mg/kg). BLBS078-CF_A75 BLBS078-Tilley March 22, 2011 12:7

132 Blackwell’s Five-Minute Veterinary Consult A Atrial Fibrillation and Atrial Flutter

into the AV junctional tissue but are not only heard on beats with effective ejection, robust enough to penetrate the entire length. not on every beat. r BASICS Blocked impulses affect the conduction Third heart sounds (gallop sounds) may be properties of the AV junctional tissue and present. r DEFINITION alter conduction of subsequent electrical Patients with atrial fibrillation have pulse r impulses; electrical impulses are conducted deficits and variable pulse quality. Atrial fibrillation—rapid, irregularly r irregular supraventricular rhythm. Two forms through the AV junction irregularly, Signs of CHF often present (e.g., cough, producing an irregular ventricular rhythm. dyspnea, cyanosis). recognized: primary atrial fibrillation, an r uncommon disease that occurs mostly in large Atrial flutter—probably originates from CAUSES r dogs with no underlying cardiac disease, and one site of reentry that moves continuously Chronic valvular disease r secondary atrial fibrillation, which occurs in throughout the atrial myocardium Cardiomyopathy r dogs and cats secondary to underlying cardiac and frequently and regularly stimulates Congenital heart disease r disease. the AV node. When the atrial rate becomes Digoxin toxicity r r Atrial flutter is similar to atrial fibrillation, sufficiently fast, the refractory period of the AV Idiopathic r but the atrial rate is generally slower and is node exceeds the cycle length (P to P interval) Ventricular preexcitation (atrial flutter) characterized by saw-toothed flutter waves in of the SVT, and some atrial depolarizations the baseline of the ECG. The ventricular are blocked from traversing the AV response is generally rapid but may be regular node (functional second-degree AV block). or irregular. SYSTEMS AFFECTED DIAGNOSIS ECG FEATURES Cardiovascular DIFFERENTIAL DIAGNOSIS Atrial Flutter Loss of atrial contraction may result in r r Frequent atrial (supraventricular) premature Atrial rhythm usually regular; rate decreased stroke volume and cardiac output depolarizations approximately 300–400 bpm. depending on heart rate; high heart rate may r r Supraventricular tachycardia with AV block P waves usually discerned as either discrete result in deterioration in myocardial function P waves or a “saw-toothed” baseline. (tachycardia-induced myocardial failure). CBC/BIOCHEMISTRY/URINALYSIS r Ventricular rhythm and rate generally GENETICS N/A depend on the atrial rate and AV nodal No breeding studies available OTHER LABORATORY TESTS conduction, but are generally regular or INCIDENCE/PREVALENCE N/A regularly irregular and rapid. r N/A IMAGING Conduction pattern to the ventricles is r variable—in some cases every other atrial GEOGRAPHIC DISTRIBUTION Echocardiography and radiography may depolarization produces a ventricular N/A characterize type and severity of the depolarization (2:1 conduction ratio), giving a SIGNALMENT underlying cardiac disease; moderate to severe left atrial enlargement common. regular ventricular rhythm; other times the r conduction pattern appears random, giving Species Typically normal in patients with primary an irregular ventricular rhythm that can Dogs and cats atrial fibrillation, although mild left atrial mimic atrial fibrillation. Breed Predilections enlargement may accompany the hemodynamic alterations imposed by the Secondary Atrial Fibrillation Large- and giant-breed dogs are more prone r arrhythmia. No P waves present—baseline may be flat or to primary atrial fibrillation. may have small irregular undulations Mean Age and Range DIAGNOSTIC PROCEDURES (“f” waves); some undulations may look like P N/A N/A waves. PATHOLOGIC FINDINGS r Predominant Sex Ventricular rate high—usually 180–240 N/A N/A bpm in dogs and > 220 bpm in cats. r SIGNS Interval between QRS complexes is General Comments irregularly irregular; QRS complexes usually r Generally relate to the underlying disease appear normal. TREATMENT Primary Atrial Fibrillation process and/or CHF rather than the arrhythmia itself, but previously stable Similar to secondary atrial fibrillation except APPROPRIATE HEALTH CARE animals may decompensate. r ventricular rate usually in the normal range. r Patients with fast (secondary) atrial Patients with primary atrial fibrillation are fibrillation are treated medically to slow the generally asymptomatic but may demonstrate PATHOPHYSIOLOGY ventricular rate. Converting the atrial r mild exercise intolerance. fibrillation to sinus rhythm would be ideal, Atrial fibrillation—caused by numerous Historical Findings but such attempts in patients with severe small reentrant pathways creating a rapid r Coughing/dyspnea/tachypnea. underlying heart disease or left atrial (> 500 depolarizations/minute) and r Exercise intolerance. enlargement are generally futile because of a disorganized depolarization pattern in the r Rarely syncope. low success rate and high rate of recurrence. atria that results in cessation of atrial r Dogs with primary atrial fibrillation are Consider quinidine or electrical cardioversion contraction. Depolarizations continuously typically asymptomatic. to sinus rhythm for a dog with primary atrial bombard the AV nodal tissue, which acts as a fibrillation. filter and does not allow all depolarizations to Physical Examination Findings r r Patients with primary atrial fibrillation may conduct to the ventricles. Many atrial On auscultation, patients with atrial be converted back to normal sinus rhythm. depolarizations activate only a part of the atria fibrillation have an erratic heart rhythm that The success rate depends on chronicity. because the rapid rate renders portions of the sounds like “tennis shoes in a dryer.” r Patients that have been in atrial fibrillation atria refractory, and thus they cannot reach the First heart sound intensity in atrial for > 4 months generally have a lower success AV junction. Other atrial impulses penetrate fibrillation is variable; second heart sound BLBS078-CF_A75 BLBS078-Tilley March 22, 2011 12:7

Canine and Feline, Fifth Edition 133

(Continued) Atrial Fibrillation and Atrial Flutter A

r rate and a higher rate of recurrence. In these the maintenance dose can be doubled for the Using high-dose oral quinidine for patients, rate control, if necessary, is the first day. If digoxin is administered alone and conversion into sinus rhythm carries a risk of recommended treatment. the heart rate remains high, check the digoxin quinidine toxicity (e.g., hypotension, r Electrical (DC) cardioversion—application level and adjust the dose to bring the level weakness, ataxia, and of a transthoracic electrical shock at a specific into the therapeutic range. If the heart rate seizures)—administration of diazepam time in the cardiac cycle; requires special remains high, consider adding a calcium intravenously controls seizures; other signs equipment, trained personnel, and general channel blocker or a β-adrenergic blocker. abate within several hours of discontinuing r anesthesia. A small (10 joules) electrical shock Diltiazem—initially administered at a dose quinidine administration. may suffice, but most require higher power of 0.5 mg/kg PO q8h, then titrated up to a POSSIBLE INTERACTIONS (50–150 joules). Biphasic DC cardioversion maximum of 1.5 mg/kg PO q8h or until an Quinidine raises the digoxin level, generally consistently cardioverts with lower power adequate response is obtained. r necessitating a digoxin dose reduction. (< 50 joules). Either high-dose oral quinidine or electrical ALTERNATIVE DRUG(S) NURSING CARE cardioversion can be used to convert primary Propranolol—initially administered at a dose As indicated for CHF atrial fibrillation into sinus rhythm. Quinidine doses as high as 20 mg/kg PO q2h of 0.1–0.2 mg/kg PO q8h, then titrated ACTIVITY can be used safely if monitored closely; doses upward until an adequate response is Restrict activity until tachycardia is lower than 12.5 mg/kg q6h are generally obtained. We do not exceed a dose of controlled ineffective. 0.5 mg/kg PO q8h. Propranolol is poorly r DIET Therapy for atrial fibrillation is aimed at tolerated when used chronically and also β Mild to moderate sodium restriction if suppressing the atrial reentry circuit using affects 2 receptors and is therefore rarely CHF sotalol, amiodarone, or procainamide. The used. CLIENT EDUCATION conversion to normal sinus rhythm is usually r unsuccessful. Secondary atrial fibrillation is usually Cats associated with severe underlying heart r FOLLOW-UP disease; goal of therapy is to lower heart rate Diltiazem (1–2.5 mg/kg PO q8h) or and control clinical signs. atenolol (6.25–12.5 mg/cat PO q12–24h) are PATIENT MONITORING r r Sustained conversion to sinus rhythm is the drugs of choice in most cats. Monitor heart rate and ECG closely. r r unlikely with secondary atrial fibrillation. If the heart rate is not sufficiently slowed As heart rates in the hospital and those SURGICAL CONSIDERATIONS with these drugs or if myocardial failure is measured on the surface ECG may be present, digoxin (0.005 mg/kg PO q24–48h) N/A inaccurate (due to patient anxiety and other can be added. environmental factors), Holter monitoring CONTRAINDICATIONS provides a more accurate means for assessing r Digoxin, diltiazem, propranolol, and the need for heart rate control and/or the MEDICATIONS atenolol should not be used in patients with efficacy of medical therapy for heart rate preexisting AV block. control. r DRUG(S) OF CHOICE Use of calcium channel blockers in POSSIBLE COMPLICATIONS β Digoxin, -adrenergic blockers, esmolol, and combination with beta blockers should be Worsening of cardiac function with onset of calcium channel blockers (diltiazem) are avoided because clinically significant arrhythmia bradyarrhythmias and/or AV block can frequently used to slow conduction through EXPECTED COURSE AND PROGNOSIS the AV node; definition of an adequate heart develop. r rate response varies among clinicians, but in PRECAUTIONS Secondary atrial fibrillation—associated dogs is generally 140–160 bpm. r β with severe heart disease, so a guarded-to-poor Calcium channel blockers and -adrenergic prognosis. Dogs blockers, both negative inotropes, should be r r Primary atrial fibrillation with normal Digoxin—maintenance oral dose used cautiously in animals with myocardial ultrasound findings—generally a good 0.005–0.01 mg/kg PO q12h; to achieve a failure. prognosis. therapeutic serum concentration more rapidly,

Figure 1. Atrial flutter with 2:1 conduction at ventricular rate of 330/minute in a 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.) BLBS078-CF_A75 BLBS078-Tilley March 22, 2011 12:7

134 Blackwell’s Five-Minute Veterinary Consult

A Atrial Fibrillation and Atrial Flutter (Continued)

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.)

Suggested Reading Tilley LP, Smith FWK Jr. Kittleson MD. Electrocardiography. In: Electrocardiography. In: Tilley LP, Smith MISCELLANEOUS Kittleson MD, Kienle RD, eds., Small FWK, Oyama MA, Sleeper MM, eds., Animal Cardiovascular Medicine. St Louis: Manual of Canine and Feline Cardiology, AGE-RELATED FACTORS Mosby, 1998, pp. 72–94. 4th ed. St. Louis: Saunders Elsevier, 2008, N/A Kraus MS, Gelzer ARM, Moise S. Treatment pp. 49–77. PREGNANCY/FERTILITY/BREEDING of cardiac arrhythmias and conduction Author Richard D. Kienle Consulting Editors LarryP.TilleyandFrancis N/A disturbances. In: Tilley LP, Smith FWK, Oyama MA, Sleeper MM, eds., Manual of W.K. Smith, Jr. ABBREVIATIONS r Canine and Feline Cardiology, 4th ed. St. AV = atrioventricular r Louis: Saunders Elsevier, 2008, CHF = congestive heart failure Client Education Handout r pp. 315–332. ECG = electrocardiogram available online r SVT = supraventricular tachycardia BLBS078-CF_A76 BLBS078-Tilley March 22, 2011 12:8

Canine and Feline, Fifth Edition 135 Atrial Premature Complexes A

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

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.) BLBS078-CF_A76 BLBS078-Tilley March 22, 2011 12:8

136 Blackwell’s Five-Minute Veterinary Consult

A Atrial Premature Complexes (Continued)

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 in rhythm disappeared after the anesthetic was stopped. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.)

CLIENT EDUCATION PRECAUTIONS AGE-RELATED FACTORS APCs may not cause hemodynamic Use digoxin, diltiazem, atenolol, or Typically occurs in geriatric dogs abnormalities; may be precursors of serious propranolol cautiously in animals with ZOONOTIC POTENTIAL arrhythmias. underlying atrioventricular block or N/A hypotension. SURGICAL CONSIDERATIONS PREGNANCY/FERTILITY/BREEDING POSSIBLE INTERACTIONS N/A N/A N/A SYNONYMS ALTERNATIVE DRUG(S) Atrial extrasystoles, atrial premature N/A MEDICATIONS contractions, atrial premature impulses. SEE ALSO DRUG(S) OF CHOICE Supraventricular Tachycardia Treat CHF and correct any electrolyte or FOLLOW-UP ABBREVIATIONS acid/base imbalances. r APC = atrial premature complex Dogs PATIENT MONITORING r r AV = atrioventricular Digoxin (0.005–0.01 mg/kg PO q12h, r Monitor heart rate and rhythm with serial CHF = congestive heart failure maintenance dosage), diltiazem (0.5–1.5 ECG. INTERNET RESOURCES mg/kg PO q8h), or atenolol (0.25–1 mg/kg PREVENTION/AVOIDANCE PO q12h) are used to treat clinically www.vetgo.com/cardio. N/A significant arrhythmias. r POSSIBLE COMPLICATIONS Suggested Reading Digoxin—treatment of choice; also Tilley LP, Smith FWK Jr. Frequent APCs may further diminish cardiac indicated to treat the cardiac decompensation Electrocardiography. In: Tilley LP, Smith output in patients with underlying heart that is usually present. FWK, Oyama MA, Sleeper MM, eds., r disease and worsen clinical symptoms. CHF is treated with appropriate dosage of Manual of Canine and Feline Cardiology, diuretic and angiotensin converting enzyme EXPECTED COURSE AND PROGNOSIS 4th ed. St. Louis: Saunders Elsevier, 2008, inhibitor; appropriate management of CHF Even with optimal antiarrhythmic drug pp. 66–67. may reduce APC frequency. therapy some animals have an increased Authors Larry P. Tilley and Naomi L. Cats frequency of APCs or deteriorate to more r Burtnick Cats with hypertrophic severe arrhythmia as the underlying disease Consulting Editors LarryP.TilleyandFrancis cardiomyopathy—diltiazem (1–2.5 mg/kg progresses. W.K. Smith, Jr. PO q8h) or atenolol (6.25–12.5 mg PO q12–24h). r Cats with dilated cardiomyopathy—digoxin Client Education Handout (one-fourth of a 0.125-mg digoxin tablet MISCELLANEOUS available online q24h or q48h). ASSOCIATED CONDITIONS CONTRAINDICATIONS None Negative inotropic agents (e.g., propranolol) should be avoided in animals with CHF. BLBS078-CF_A77 BLBS078-Tilley March 22, 2011 12:9

Canine and Feline, Fifth Edition 137 Atrial Septal Defect A

IMAGING Radiographic Findings r None in patients with small defects. BASICS r Right-sided heart and pulmonary vessel OVERVIEW enlargement in patients with large defects. r Congenital cardiac anomaly allowing Echocardiographic Findings r communication between the atria through a Right atrial and right ventricular dilation. r r defect in the interatrial septum. Defects May reveal the defect—septal dropout. r occur in 1 of 3 locations: ostium primum Doppler useful in documenting flow defect, lower atrial septum; ostium secundum through the defect and high ejection velocity defect, near fossa ovalis; and sinus venous r through the pulmonary artery. defect, craniodorsal to fossa ovalis. Blood OTHER DIAGNOSTIC PROCEDURES usually shunts into the right atrium, causing a Electrocardiography volume overload to the right atrium, right r ventricle, and pulmonary vasculature, Right heart enlargement pattern (right axis, sometimes leading to pulmonary deep S waves in Lead II, tall P waves) on ECG r in some patients with large defects. hypertension. If right-sided pressures are r high, shunting may occur right to left, Arrhythmias and intraventricular r causing generalized cyanosis. Comprises conduction disturbances possible. 0.7% of congenital heart defects in dogs and 9% of congenital heart defects in cats. Recent Figure 1. study from France suggests higher incidence Atrial septal defect. Defect involves the lower- with ASD accounting for 37.7% of congenital TREATMENT most part of the atrial septum, known as os- cardiac defects in pooled data from dogs and r tium primum defect. Note the left dominant r Hospitalize patients with CHF until stable. cats. Secundum-type defects most common r r left-to-right shunt. RV = right ventricle, LV = Restrict activity. A low-sodium diet if in = = (98.7% in one study). r left ventricle, RA right atrium, Ao aorta, congestive heart failure. Amplatzer device = SIGNALMENT PT pulmonary trunk. (From: Roberts W. r r can be implanted via transvenous or Adult Congenital Heart Disease. Philadelphia: Dogs and cats. Boxers, standard poodles, transatrial placement to close some FA Davis Co., 1987, with permission.) r Newfoundlands, Doberman pinschers, Old secundum-type defects. Surgical correction English sheepdogs, and Samoyeds may be requires open heart surgery with bypass and is overrepresented. prohibitively expensive for most owners. A SIGNS hybrid approach involving active device MISCELLANEOUS fixation following temporary venous occlusion General Comments ASSOCIATED CONDITIONS If defect is small, may be none. In one study, after transatrial device placement was recently r r Pulmonic stenosis and tricuspid dysplasia 73.7% asymptomatic. described. Pulmonary artery banding may r be palliative in patients with severe disease. Endocardial cushion defects Historical Findings SEE ALSO Variable degrees of exercise intolerance (7%), syncope (5.3%), cough (2.3%), and dyspnea Congestive Heart Failure, Right-Sided (2.3%) ABBREVIATIONS MEDICATIONS r r ASD = atrial septal defect CHF = Physical Examination Findings r r DRUG(S) AND FLUIDS congestive heart failure ECG = Soft systolic murmur over the pulmonic r valve due to relative pulmonic stenosis (20%). CHF—diuretics; furosemide 1–2 mg/kg electrocardiogram r r Rarely a diastolic murmur over tricuspid PO q6–12h. Vasodilators may help reduce Suggested Reading valve due to relative tricuspid stenosis. signs of CHF (e.g., enalapril 0.5 mg/kg PO r Bonagura JD, Lehmkuhl LB. Congenital Systolic mitral murmur may be heard if q12–24h, or benazepril 0.25–0.5 mg/kg PO heart disease. In: Fox PR, Sisson D, Moise endocardial cushion defect and cleft mitral q24h). r ND, eds., Textbook of Canine and Feline valve are present. Cyanosis if right-to-left r Cardiology, 2nd ed. Philadelphia: Saunders, shunt. Ascites if right heart failure develops. r 1999, pp. 471–535. Fixed splitting of the second heart sound. Chetboul V, Charles V, Nicolle A, et al. CAUSES & RISK FACTORS FOLLOW-UP Retrospective study of 156 atrial septal Unknown; genetic basis not documented PATIENT MONITORING defects in dogs and cats (2001–2005). J Vet Med A Physiol Pathol Clin Med 2006, Recheck when decompensation or other 53(4):179–184. clinical signs develop. Gordon SG, Miller MW, Roland RM, et al. EXPECTED COURSE AND PROGNOSIS DIAGNOSIS r Transcatheter atrial septal defect closure Depends on size of the defect and with the Amplatzer atrial septal occluder in DIFFERENTIAL DIAGNOSIS co-existing abnormalities; small, isolated 13 dogs: short- and mid-term outcome. r Pulmonic stenosis—murmur of pulmonic defects unlikely to cause signs or to progress. J Vet Intern Med 2009, 23(5):995–1002. r stenosis usually harsh and loud. Anomalous Primum-type defects typically larger with Gordon SG, Nelson DA, Achen SE, et al. worse prognosis. Defects > 12 mm may pulmonary venous return to the right atrium. r Open heart closure of an atrial septal defect CBC/BIOCHEMISTRY/URINALYSIS develop heart failure. Progressive, by use of an atrial septal occluder in a dog. right-sided CHF expected if the defect is large JAVMA 2010, 236(4):434–439. Polycythemia in some patients with or associated with an endocardial cushion Author Francis W.K. Smith, Jr. right-to-left shunt r defect. Prognosis in cats often guarded to Consulting Editors LarryP.TilleyandFrancis poor. W.K. Smith, Jr. BLBS078-CF_A78 BLBS078-Tilley July 15, 2011 8:57

138 Blackwell’s Five-Minute Veterinary Consult A Atrial Standstill

Predominant Sex case of only left atrial involvement was Hypoadrenocorticism more common in reported. r BASICS females (69%). Severe scapular and brachial muscle wasting in some dogs. SIGNS r DEFINITION Marked fibrosis, fibroelastosis, chronic Historical Findings r mononuclear cell inflammation, and steatosis ECG rhythm characterized by absence of P Vary with underlying cause. r throughout the atria and interatrial septum. waves; condition can be temporary (e.g., Lethargy common; syncope may occur. r associated with hyperkalemia or Patients with persistent atrial standstill may drug-induced), terminal (e.g., associated with show signs of congestive heart failure. severe hyperkalemia or dying heart), or Physical Examination Findings persistent. r TREATMENT Vary with underlying cause. ECG Features r Bradycardia common. APPROPRIATE HEALTH CARE Persistent Atrial Standstill r r Patients with persistent atrial standstill may Persistent Atrial Standstill P waves absent. r have skeletal muscle wasting of the Heart rate usually slow (< 60 bpm). Not life-threatening condition; animal can be r antebrachium and scapula. Rhythm regular with supraventricular type treated as an outpatient. CAUSES Hyperkalemic Atrial Standstill QRS complexes. r r Hyperkalemia. Potentially life-threatening; often requires Heart rate does not increase with atropine r administration. Atrial disease, often associated with atrial aggressive treatment. Hyperkalemic Atrial Standstill distension (e.g., cats with cardiomyopathy). NURSING CARE r r Heart rate normal or slow. Atrial myopathy (persistent atrial standstill). r Aggressive fluid therapy with 0.9% saline Rhythm regular or irregular. RISK FACTORS r often required to correct hypovolemia and QRS complexes tend to be wide and Hyperkalemic Atrial Standstill lower serum potassium levels (see r become wider as the potassium level rises; Hypoadrenocorticism. Hyperkalemia) in patients with hyperkalemic > r with severe hyperkalemia (potassium 10 Conditions leading to obstruction or atrial standstill. mEq/L), the QRS complexes are replaced by a rupture of the urinary tract. ACTIVITY smooth biphasic curve. r r Oliguric or anuric renal failure. Heart rate may increase slightly with Restrict activity in patients with persistent atropine. atrial standstill and signs of CHF or syncope. PATHOPHYSIOLOGY DIET Persistent Atrial Standstill DIAGNOSIS N/A Caused by an atrial muscular dystrophy; DIFFERENTIAL DIAGNOSIS CLIENT EDUCATION skeletal muscle involvement common. r Slow atrial fibrillation Hyperkalemic Atrial Standstill r Persistent Atrial Standstill Sinus bradycardia with small P waves lost in Generally occurs with serum potassium levels Clinical signs generally improve after the baseline > 8.5 mEq/L; value influenced by serum pacemaker implantation; signs of CHF may sodium and calcium levels and acid-base CBC/BIOCHEMISTRY/URINALYSIS develop, and weakness and lethargy may status. Hyperkalemic patients with atrial Persistent Atrial Standstill persist even after heart rate and rhythm are r standstill have sinus node function, but Normal. corrected with the pacemaker. impulses do not activate atrial myocytes; thus, Hyperkalemic Atrial Standstill SURGICAL CONSIDERATIONS r the associated rhythm is termed a Hyperkalemia. Persistent Atrial Standstill r sinoventricular rhythm. Since the sinus node Hyponatremia and sodium:potassium ratio Implant permanent ventricular pacemaker to is functional, an irregular rhythm may be due < 27 if atrial standstill secondary to regulate rate and rhythm. to sinus arrhythmia. hypoadrenocorticism. Hyperkalemic Atrial Standstill SYSTEMS AFFECTED r Azotemia and hyperphosphatemia with Hyperkalemia secondary to urinary tract Cardiovascular hypoadrenocorticism, renal failure, and obstruction or rupture may require surgery. GENETICS rupture or obstruction of the urinary tract. None OTHER LABORATORY TESTS INCIDENCE/PREVALENCE ACTH stimulation test if Rare rhythm disturbance hypoadrenocorticism suspected MEDICATIONS GEOGRAPHIC DISTRIBUTION IMAGING None Echocardiogram and electromyography if DRUG(S) OF CHOICE persistent atrial standstill SIGNALMENT Persistent Atrial Standstill suspected—cardiomegaly and depressed Treat with diuretics and ACE inhibitor (e.g., Species contractility may be seen. enalapril or benazepril) if CHF develops. Dogs and cats DIAGNOSTIC PROCEDURES Hyperkalemic Atrial Standstill Breed Predilections Skeletal muscle biopsy in animals with r Persistent atrial standstill—most common in Treat the underlying cause (e.g., oliguric persistent atrial standstill. renal failure, hypoadrenocorticism). English springer spaniels; other breeds PATHOLOGIC FINDINGS r occasionally affected. Aggressive fluid therapy with 0.9% saline Persistent Atrial Standstill and possibly sodium bicarbonate or insulin Mean Age and Range r Greatly enlarged and paper-thin atria; with dextrose as discussed under Most animals with persistent atrial standstill usually biatrial involvement, although one Hyperkalemia. are young; animals with hypoadrenocorticism are usually young to middle-aged. BLBS078-CF_A78 BLBS078-Tilley July 15, 2011 8:57

Canine and Feline, Fifth Edition 139

(Continued) Atrial Standstill A

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 PREGNANCY/FERTILITY/BREEDING r Calcium gluconate—counters the cardiac CHF in patients with persistent atrial N/A effects of hyperkalemia; can be used in standstill SYNONYMS life-threatening situations to reestablish a EXPECTED COURSE AND PROGNOSIS Silent atrial sinus rhythm while instituting treatment to Persistent Atrial Standstill SEE ALSO lower potassium concentration. r Clinical signs generally improve after Digoxin Toxicity CONTRAINDICATIONS r pacemaker implantation. Signs of CHF may Hyperkalemia Avoid potassium-containing fluids or r develop, and weakness and lethargy persist Hypoadrenocorticism (Addison’s Disease) medications that increase potassium r even after heart rate and rhythm are corrected Urinary Tract Obstruction concentration in hyperkalemic patients. with the pacemaker. There may be persistence ABBREVIATIONS PRECAUTIONS of signs related to muscular dystrophy. r ACE = angiotensin converting enzyme Diuretics lower preload and may worsen r Hyperkalemic Atrial Standstill ACTH = adrenocorticotropic hormone weakness in dogs with persistent atrial r Long-term prognosis is excellent if underlying CHF = congestive heart failure standstill and CHF unless a pacemaker has r cause can be corrected and hyperkalemia ECG = electrocardiogram been implanted. reversed. POSSIBLE INTERACTIONS Suggested Reading N/A Kraus MS, Gelzer ARM, Moise S. Treatment of cardiac arrhythmias and conduction ALTERNATIVE DRUG(S) MISCELLANEOUS disturbances. In: Tilley LP, Smith FWK, N/A Oyama MA, Sleeper MM, eds., Manual of ASSOCIATED CONDITIONS Canine and Feline Cardiology, 4th ed. St. Diseases causing hyperkalemia (e.g., Louis: Saunders Elsevier, 2008, hypoadrenocorticism, urethral obstruction or pp. 315–332. FOLLOW-UP urinary tract tear, acidosis, and drugs). Tilley LP, Smith FWK Jr. PATIENT MONITORING AGE-RELATED FACTORS Electrocardiography. In: Tilley LP, Smith r FWK, Oyama MA, Sleeper MM, eds., Monitor ECG during treatment of Persistent atrial standstill—usually diagnosed Manual of Canine and Feline Cardiology, hyperkalemia and periodically in animals with in young animals; 4th ed. St. Louis: Saunders Elsevier, 2008, a permanent ventricular pacemaker. hypoadrenocorticism—usually diagnosed in r pp. 49–77. Monitor electrolytes in patients with young to middle-aged animals. Author Francis W.K. Smith, Jr. hyperkalemic atrial standstill. ZOONOTIC POTENTIAL r Consulting Editors LarryP.TilleyandFrancis Monitor patients with persistent atrial None W.K. Smith, Jr. standstill for signs of CHF. PREVENTION/AVOIDANCE N/A Client Education Handout available online BLBS078-CF_A79 BLBS078-Tilley June 16, 2011 11:8

140 Blackwell’s Five-Minute Veterinary Consult A Atrial Wall Tear

cardiopulmonary arrest; episode may follow a alveolar pulmonary infiltrates if concomitant r period of increased excitement or activity. left-sided CHF is present. Small volume r BASICS History of long-standing cardiac disease pleural effusion, ascites, hepatomegaly, and with signs of CHF described in most patients. large caudal vena cava may be seen due to r DEFINITION Acute worsening of cough or dyspnea are right-sided CHF. r r Endocardial splitting is a linear defect commonly observed. Possible history of Echocardiographic Findings r limited to the endocardial layer of the atrium blunt trauma. Pericardial effusion is evidenced by a (typically the left atrium) resulting from Physical Examination Findings hypoechoic space between the heart and r r r distension of the atrial wall beyond its elastic Collapse. Tachycardia. Weak arterial pericardial sac; the volume of pericardial r r limits. An atrial tear may result if the split pulses or pulsus paradoxus. Pale, muddy, or effusion identified may be relatively small as extends through the myocardium and ashen mucous membranes; prolonged CRT. the pericardium remains inelastic due to the r epicardium, resulting in a full thickness defect Other signs of significant cardiac disease acute nature of the bleed; a characteristic in the atrial wall and hemorrhage into the (e.g., murmur, gallop rhythm, arrhythmia, linear, hyperechoic blood clot may be seen r pericardial space. cough, or dyspnea) are typically present. within the pericardial sac. The actual tear is r PATHOPHYSIOLOGY Signs of right heart failure (e.g., ascites and often not identified though an associated r jugular venous distension) may also be seen in thrombus is occasionally visualized within the Endocardial splitting typically results from r r increased left atrial pressure secondary to some patients. Heartsoundsmaybe left atrium. Cardiac tamponade is evidenced severe mitral regurgitation; endocardial muffled, or if a murmur was heard before the by diastolic collapse of the right atrium and/or r r degeneration may also play a role. If the atrial wall tear occurred, it may be reduced in ventricle. Signs of advanced mitral split is incomplete, fibrin may seal the defect intensity. endocardiosis, including mitral valve temporarily; this either heals as a linear CAUSES thickening and prolapse, moderate to severe r depression in the endocardial surface or Mitral valve endocardiosis—chronic mitral regurgitation, moderate to severe left r subsequently extends through the valvular heart disease. Dilated atrial enlargement and often one or more r myocardium resulting in a complete left atrial cardiomyopathy. Patent ductus arteriosus. ruptured chordae tendineae. r r tear. A left atrial tear results in peracute Cardiac neoplasia, most commonly DIAGNOSTIC PROCEDURES r r bleeding into the pericardial sac and severe, hemangiosarcoma. Chest trauma. Cardiac Electrocardiographic Findings r r life-threatening hemodynamic compromise catheterization. Sinus tachycardia Atrial or ventricular r r secondary to acute cardiac tamponade . If a RISK FACTORS arrhythmias Dampened QRS complexes tear occurs in the interatrial septum, an r r r Severe mitral regurgitation, left atrial Electrical alternans ST-segment acquired atrial septal defect may form. r r r enlargement. May be precipitated by an abnormalities Possible left ventricular or left Tearing of either atria may also rarely occur episode of excitement, stress, or activity. atrial enlargement pattern secondary to blunt trauma. PATHOLOGIC FINDINGS SYSTEMS AFFECTED r r r Endocardial splitting is noted grossly as a Cardiovascular Respiratory pale or white linear depression in the atrial r GENETICS DIAGNOSIS endocardium. Atrial wall tears appear as full thickness defects extending through the atrial Predisposition to endocardiosis has been DIFFERENTIAL DIAGNOSIS shown to have a heritable component in some r endocardium, myocardium and epicardium; Other causes of acute cardiovascular breeds. r an associated thrombus may or may not be collapse. Pericardial effusion from other INCIDENCE/PREVALENCE present. The caudolateral aspect of the left causes (e.g., neoplastic and idiopathic). atrium is most commonly affected, with many Atrial tear is a rare cause of hemorrhagic r r Heart failure. Severe cardiac arrhythmias. tears occurring at the atrio-auricular pericardial effusion in the dog encompassing r r r Myocardial infarction. Pulmonary junction. Hemorrhagic pericardial effusion approximately 2% of pericardial effusion r thromboembolism. Other causes of or pericardial thrombus is seen with acute cases. r hypotension. tears. Mitral endocardiosis characterized by SIGNALMENT CBC/BIOCHEMISTRY/URINALYSIS thickened mitral valve leaflets with rolled Species r edges; chordae tendinae rupture may be seen; Anemia is uncommon unless r Dogs;uncommonincats pericardiocentesis is performed since volume atrial jet lesions are possible. Cardiomegaly r of blood loss is relatively small. Elevations in with severe left atrial enlargement expected. Breed Predilections r r serum lactate, metabolic acidosis. Increased Same as endocardiosis breeds; more r common in small- to medium-sized dogs. ALT, AST in some patients. Prerenal r Poodles, dachshunds, cocker spaniels, and azotemia; hyponatremia or other electrolyte Shetland sheepdogs may be overrepresented. derangements may be seen. TREATMENT r If trauma is the cause, any breed may be OTHER LABORATORY TESTS APPROPRIATE HEALTH CARE r represented. NT-proBNP and TnI levels may be elevated If a left atrial tear is strongly suspected, Mean Age and Range perform pericardiocentesis only if the effusion Middle-aged to older dogs are predisposed. IMAGING is causing symptomatic, life-threatening Predominant Sex Radiographic Findings cardiac tamponade, since further hemorrhage r A higher incidence of both endocardiosis and Moderate to severe left atrial enlargement is into the pericardial sac or exsanguination may r r left atrial tear is noted in male dogs. expected. Comparison with previous occur once pericardial fluid is removed. If SIGNS thoracic radiographs may show rounding and pericardiocentesis is performed, remove only enough fluid to improve clinical signs. Historical Findings further enlargement of cardiac silhouette; r r characteristic globoid cardiac silhouette Pericardiocentesis will likely be difficult Acute onset of weakness and collapse that associated with pericardial effusion may be given the small volume of effusion typically may progress quickly to respiratory or r more obvious on the DV view. Interstitial to identified, severe cardiac enlargement, and the small size of most dogs with left atrial rupture; BLBS078-CF_A79 BLBS078-Tilley June 16, 2011 11:8

Canine and Feline, Fifth Edition 141

(Continued) Atrial Wall Tear A

ultrasound guidance and continuous ECG pressure monitoring is recommended and the PREVENTION/AVOIDANCE r monitoring are highly recommended. Best dose may be uptitrated as necessary every Recommend avoidance of strenuous physical practices for management of left atrial tears 15–30 minutes up to a maximum of 10 activity and excitement. have not been clearly established; however, ug/kg/min to achieve an improvement in POSSIBLE COMPLICATIONS aggressive medical management to lower left clinical signs and/or a reduction in blood r r Even if the tear seals, the patient is prone to atrial pressure using afterload and preload pressure of 10–15 mm Hg. Alternatively, further tears because of underlying cardiac reducers is recommended based on the amlodipine may be started at 0.1–0.2 mg/kg r r disease. Most dogs have or will develop author’s clinical experience. If a fibrin clot PO q24h; chronic amlodipine therapy may be concurrent CHF. forms over the defect, the patient may implemented in normotensive or hypertensive stabilize and recover. animals to reduce regurgitant fraction and EXPECTED COURSE AND PROGNOSIS r NURSING CARE lower left atrial pressure. Diuretics should Prognosis for survival is guarded to poor; r be used cautiously if needed to treat dyspnea however, some animals can do well for several Administer oxygen to dogs with dyspnea or months or longer with close monitoring, signs of hemodynamic instability. associated with concomitant congestive heart r failure (e.g., 1–2 mg/kg of furosemide IV as exercise restriction and optimal medical Administer IV fluids or blood products only management of cardiac disease. if evidence of hypovolemia is present; most needed); signs of left-sided congestive heart dogs remain in a volume overloaded state and failure may worsen as cardiac tamponade further intravascular volume expansion will resolves due to augmentation of preload; more aggressive diuretic therapy may then be increase left atrial pressure and potentially r MISCELLANEOUS worsen tamponade. required. Pimobendan (0.2–0.3 mg/kg PO q12h) may result in a further reduction in left ACTIVITY ASSOCIATED CONDITIONS atrial pressure though studies have not r r CHF Mainstem bronchial compression Strict cage rest in the acute period should be specifically examined its use in the setting of r r Pulmonary hypertension followed by chronic exercise restriction. left atrial rupture. Once the patient is stable, CLIENT EDUCATION SYNONYMS ACE inhibitors (e.g., enalapril 0.5 mg/kg r r Left atrial tear typically accompanies q12–24h) should be implemented for chronic Atrial rupture Atrial splitting advanced cardiac disease and chronic medical management of accompanying heart failure. SEE ALSO r r therapy will be necessary; though the PRECAUTIONS Chapters on CHF Pericardial Effusion r prognosis is guarded for surviving the acute Aggressive fluid therapy is not warranted in ABBREVIATIONS event some dogs with left atrial tear have lived r these patients; further volume expansion may ACE = angiotensin converting enzyme more than a year after the incident. r r increase left atrial pressure, worsen cardiac ALT = alanine aminotransferase AST = SURGICAL CONSIDERATIONS tamponade, and contribute to hemodynamic r = r r aspartate aminotransferase CHF Exploratory thoracotomy may be compromise. Best practices for management Congestive heart failure of left atrial tear have not been clearly considered if hemorrhage persists or recurs INTERNET RESOURCES but should be undertaken cautiously given the established; the choice of whether to perform James Buchanan Cardiology Library: advanced state of cardiac disease typically pericardiocentesis, and whether to administer r http://www.vin.com/MEMBERS/CMS/Misc/ present. Transcatheter septal puncture and preload and/or afterload reducers should be Default.aspx?id=7703. balloon tear of the fossa ovalis may also be made based on assessment of the volume considered to decompress the left atrium; status, blood pressure and clinical stability of Suggested Reading however, right heart failure or hypoxemia due the patient. Fox PR, Sisson D, Moise S. Textbook of to right-to-left shunting may result. POSSIBLE INTERACTIONS Canine and Feline Cardiology. Philadelphia: Sodium nitroprusside should never be Saunders, 1999. administered concurrently with Reineke EL, Burkett DE, Drobatz KJ. Left phosphodiesterase-V inhibitors (e.g., sildenafil atrial rupture in dogs: 14 cases MEDICATIONS or tadalafil) due to the potential for (1990–2005). J Vet Emerg Crit Care 2008, 18:158–164. DRUG(S) OF CHOICE life-threatening systemic hypotension. r Rush JR. Chronic valvular disease in dogs. In: Atrial tears occur secondary to elevated left Bonagura JD, Twedt DC, eds., Kirk’s atrial pressure; thus medical therapy should be Current Veterinary Therapy XIV. St. Louis: focused on lowering of left atrial pressures in FOLLOW-UP Saunders Elsevier, 2009, pp. 780–786. order to reduce continued hemorrhage into Sadanaga KK, MacDonald MJ, Buchanan the pericardial space and permit fibrin clot PATIENT MONITORING r JW. Echocardiography and surgery in a dog formation at the site of the tear; this may be Recommend close monitoring of respiratory with left atrial rupture and accomplished with preload (e.g., diuretics, rate and effort, mucous membrane color and hemopericardium. J Vet Intern Med 1990, nitroglycerin paste) and/or afterload reducers r CRT, pulse quality, and heart rate; blood 4:216–221. (arterial vasodilators). Preload and afterload pressure monitoring is recommended if Author Suzanne M. Cunningham reduction must be undertaken cautiously to arterial vasodilators are implemented. Consulting Editors LarryP.TilleyandFrancis avoid worsening of hemodynamic r r Follow-up examination with W.K. Smith, Jr. compromise. Afterload reduction may be echocardiography helps determine resolution achieved by conservative doses of sodium of pericardial effusion and resorption of an r nitroprusside; a low starting CRI dose of atrial or pericardial clot. Close follow-up 0.5–1 ug/kg/min is recommended to achieve every 2–3 months thereafter is recommended a decrease in LA pressure without for repeat pericardial fluid checks and precipitating significant hypotension; blood medication adjustments as deemed appropriate. BLBS078-CF_A80 BLBS078-Tilley March 22, 2011 12:42

142 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Block, Complete (Third Degree)

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” Dogs and cats DIFFERENTIAL DIAGNOSIS pacemaker site (junctional or ventricular) Breed Predilections r stimulates the ventricles. r Advanced second-degree AV block r Cocker spaniels—can have idiopathic r Atrial rate normal. fibrosis. Atrial standstill r r r Idioventricular escape rhythm slow. Pugs and Doberman pinschers—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 Mean Age and Range r complexes)—ventricular escape rhythm Geriatric animals, except congenital heart High WBC with left shift in animals with (idioventricular) usually < 40 bpm; disease patients. Median age for cats—14 bacterial endocarditis. junctional escape rhythm (idiojunctional) years. OTHER LABORATORY TESTS 40–60 bpm in dogs and 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 r 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 Myocarditis Cardiovascular r APPROPRIATE HEALTH CARE Endocarditis GENETICS r r Electrolyte disorder Temporary or permanent cardiac Can be an isolated congenital defect r Myocardial infarction pacemaker—only effective treatment in 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 branch block pattern. 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.) BLBS078-CF_A80 BLBS078-Tilley March 22, 2011 12:42

Canine and Feline, Fifth Edition 143

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

r Carefully monitor asymptomatic patients CONTRAINDICATIONS without a pacemaker for development of Avoid digoxin, xylazine, acepromazine, beta clinical signs. blockers (e.g., propranolol and atenolol), and MISCELLANEOUS NURSING CARE calcium channel blockers (e.g., verapamil and ASSOCIATED CONDITIONS Cage rest prior to pacemaker implantation; diltiazem); ventricular antiarrhythmic agents when the pulse generator is put into a are dangerous because they suppress lower None subcutaneous pocket, a non-constricting escape foci. AGE-RELATED FACTORS bandage is required around the ventral neck PRECAUTIONS N/A or abdomen for 3–5 days to prevent seroma Vasodilators—may cause hypotension in ZOONOTIC POTENTIAL formation or pacemaker movement. animals with complete AV block; monitor N/A ACTIVITY closely if used, especially prior to pacemaker PREGNANCY/FERTILITY/BREEDING Restrict if symptomatic implantation. N/A DIET POSSIBLE INTERACTIONS ABBREVIATIONS No modifications unless required to manage N/A r AV = atrioventricular underlying condition (e.g., low-salt diet). ALTERNATIVE DRUG(S) r CHF = congestive heart failure N/A r CLIENT EDUCATION ECG = electrocardiogram r r Temporary or permanent cardiac WBC = white blood cell pacemaker—only effective treatment in INTERNET RESOURCES symptomatic patients. r www.vetgo.com/cardio Asymptomatic patients without a FOLLOW-UP pacemaker—must be carefully monitored for PATIENT MONITORING Suggested Reading r development of clinical signs. Monitor—pacemaker function with serial Bright JM. Pacemaker therapy. In: Tilley LP, SURGICAL CONSIDERATIONS ECGs. Smith FWK, Oyama MA, Sleeper MM, r r Most patients—at high anesthetic Radiographs—following pacemaker eds., Manual of Canine and Feline cardiopulmonary risk; usually paced implantation, to confirm the position of the Cardiology, 4th ed. St. Louis: Saunders preoperatively with a temporary external lead and generator. Elsevier, 2008, pp. 386–397. pacemaker system. Kellum HB, Stepien RL. Third-degree r PREVENTION/AVOIDANCE atrioventricular block in 21 cats The small size of cats makes pacemaker N/A implantation more difficult than in dogs. (1997–2004). J Vet Intern Med 2006, POSSIBLE COMPLICATIONS 20:97–103. Pulse generators—broad range of clinical life; Schrope DP, Kelch WJ. Signalment, clinical pacemaker replacement necessary when signs, and prognostic indicators associated MEDICATIONS battery is depleted, pulse generator with high-grade second or third-degree malfunction occurs, or exit block develops; atrioventricular block in dogs: 124 cases DRUG(S) OF CHOICE pacemaker leads can become dislodged and (January 1, 1997–December 31, 1997). r Treatment with drugs—usually of no value. infected. JAVMA 2006, 228:1710–1717. Traditionally used to treat complete AV block: EXPECTED COURSE AND PROGNOSIS Authors Larry P. Tilley and Naomi L. Burtnick atropine, isoproterenol, corticosteroids, and Poor long-term prognosis if no cardiac dobutamine. Consulting Editors LarryP.TilleyandFrancis r pacemaker implanted, especially when the W.K. Smith, Jr. Intravenous isoproterenol infusion may help animal has clinical signs. Cats can sometimes increase the rate of the ventricular escape survive > 1year. rhythm to stabilize hemodynamics. r Client Education Handout If CHF—diuretic and vasodilator therapy available online may be needed before pacemaker implantation.

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 bundle branchblock pattern. (From: Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd ed. Blackwell Publishing, 1992, with permission.) BLBS078-CF_A81 BLBS078-Tilley July 15, 2011 9:34

144 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Block, First Degree

r Mean Age and Range Hypertrophic cardiomyopathy. r r May occur in young, otherwise healthy dogs Myocarditis (especially Trypanosoma cruzi, as a manifestation of high vagal tone. Borrelia burgdorferi, Rickettsia rickettsii). BASICS r r Intra-atrial conduction delay involving the Infiltrative diseases (tumors, amyloid). r DEFINITION right atrium may be seen with congenital Atropine administered intravenously may Refers to a delay in conduction that occurs heart disease, especially atrioventricular septal briefly prolong the PR interval. defects. between atrial and ventricular activation. r RISK FACTORS ECG Features May be noted in aged patients with Any condition or intervention that raises r degenerative conduction system disease, Rate and rhythm—usually normal. vagal tone 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. Prolonged, consistent PR intervals—dogs, DIAGNOSIS > 0.13 sec; cats, > 0.09 sec (Figures 1 and 2). SIGNS DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY Historical Findings r r Most animals are asymptomatic. P waves superimposed upon preceding T Virtually never causes clinical signs. r r If drug-induced, may have a history of waves because of first-degree AV block should May become a more severe AV conduction be differentiated from bifid T waves. disturbance in some animals. clinical signs related to drug r toxicity—anorexia, vomiting, and diarrhea CBC/BIOCHEMISTRY/URINALYSIS Normally the PR interval tends to shorten r with rapid heart rates. with digoxin; weakness with calcium channel Serum electrolytes—hypokalemia and r β May be the result of intra-atrial conduction blockers or -adrenergic antagonists. hyperkalemia may predispose to AV delay (prolongation of the PA interval on Physical Examination Findings conduction disturbances. r r surface ECG and simultaneous His bundle Normal—unless also signs of more Leukocytosis—may be noted with bacterial electrogram) or delay of conduction within generalized myocardial disease, drug toxicity, endocarditis or myocarditis. the AV node itself (prolongation of the AH or non-cardiac disease. OTHER LABORATORY TESTS r interval on His bundle electrogram). CAUSES Serum digoxin concentration—may be r SYSTEMS AFFECTED May occur in normal animals. high. r r Cardiovascular Enhanced vagal stimulation resulting from T. cruzi, B. burgdorferi, R. rickettsii titers—may be high. GENETICS non-cardiac diseases—usually accompanied r T —may be high in cats if associated with N/A by sinus arrhythmia, sinus arrest, and/or 4 Mobitz type I second-degree AV block. thyrotoxic myocardial disease. INCIDENCE/PREVALENCE r Pharmacologic agents (e.g., digoxin, IMAGING β Common -adrenergic antagonists, calcium channel Echocardiographic examination—may reveal GEOGRAPHIC DISTRIBUTION blocking agents, propafenone, amiodarone, hypertrophic or infiltrative myocardial α None 2-adrenergic agonists, disorder. SIGNALMENT parasympathomimetic agents [bethanechol, DIAGNOSTIC PROCEDURES physostigmine, pilocarpine] and severe Species procainamide or quinidine toxicity). May be needed to identify causes of high r Dogs and cats Degenerative disease of the conduction vagal tone—upper airway disease, cervical and Breed Predilections system. thoracic masses, gastrointestinal disorders, and high intraocular pressure. American cocker spaniels, dachshunds, brachycephalic dogs, Persian cats

Figure 1. Lead II ECG rhythm strip recorded from a cat with hypertrophic cardiomyopathy. There is sinus bradycardia (120 bpm) and first-degree atrioventricularconduction block. The PR interval is 0.12 second (paper speed = 50 mm/s). BLBS078-CF_A81 BLBS078-Tilley July 15, 2011 9:34

Canine and Feline, Fifth Edition 145

(Continued) Atrioventricular Block, First Degree A

Figure 2. Lead II ECG rhythm strip recorded from a dog showing sinus tachycardia (175 bpm) and first-degree atrioventricular conduction block. Because the heart rate is 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).

PATHOLOGIC FINDINGS agents, β-adrenergic antagonists, α PREGNANCY/FERTILITY/BREEDING Variable—depend on underlying cause 2-adrenergic agonists, amiodarone, propafenone). N/A SEE ALSO PRECAUTIONS r Drugs with vagomimetic action (e.g., digoxin, Atrioventricular Block, Complete (Third Degree) TREATMENT bethanechol, physostigmine, pilocarpine) may r potentiate first-degree block. Atrioventricular Block, Second APPROPRIATE HEALTH CARE Degree—Mobitz Type I r POSSIBLE INTERACTIONS r Remove or treat underlying cause(s). Atrioventricular Block, Second r N/A Hospitalization may be necessary to manage Degree—Mobitz Type II the underlying cause (e.g., cardiomyopathy, ALTERNATIVE DRUG(S) ABBREVIATIONS r gastrointestinal disease, airway disease). N/A AV = atrioventricular r NURSING CARE ECG = electrocardiogram r = N/A T4 thyroxine ACTIVITY FOLLOW-UP Suggested Reading Unrestricted; unless restriction required for an Miller MS, Tilley LP, Smith FWK, Fox PR. underlying condition. PATIENT MONITORING Electrocardiography. In: Fox PR, Sisson D, DIET Except in healthy young animals, monitor Moise NS, eds., Textbook of Canine and ECG to detect any progression in conduction Feline Cardiology. Philadelphia: Saunders, No modifications or restrictions unless disturbance. 1999, pp. 67–106. required to manage an underlying condition. PREVENTION/AVOIDANCE Podrid PJ, Kowey PR. Cardiac N/A arrhythmia—mechanisms, diagnosis, and CLIENT EDUCATION management. Baltimore: Williams & POSSIBLE COMPLICATIONS Generally unnecessary Wilkins, 1995. SURGICAL CONSIDERATIONS N/A Tilley LP. Essentials of Canine and Feline EXPECTED COURSE AND PROGNOSIS Electrocardiography, 3rd ed. Baltimore: None unless required to manage an r Depends on underlying cause. Williams & Wilkins, 1992. underlying condition. r Prognosis usually excellent if no significant Tilley LP, Smith FWK Jr. underlying disease is present. Electrocardiography. In: Tilley LP, Smith FWK, Oyama MA, Sleeper MM, eds., MEDICATIONS Manual of Canine and Feline Cardiology, 4th ed. St. Louis: Saunders Elsevier, 2008, DRUG(S) OF CHOICE MISCELLANEOUS pp. 49–77. Medications used only if needed to manage Author Janice McIntosh Bright ASSOCIATED CONDITIONS an underlying condition. Consulting Editors LarryP.TilleyandFrancis CONTRAINDICATIONS None W.K. Smith, Jr. r AGE-RELATED FACTORS Avoid hypokalemia—increases sensitivity to PR interval—tends to lengthen with vagal tone; may potentiate AV conduction Client Education Handout delay. advancing age r available online Avoid drugs likely to impair impulse ZOONOTIC POTENTIAL conduction further (calcium channel blocking None BLBS078-CF_A82 BLBS078-Tilley July 15, 2011 9:51

146 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Block, Second Degree—Mobitz Type I

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 block occurs when AV transmission is Historical Findings r IMAGING progressively delayed prior to a blocked P Most animals are asymptomatic. r wave. If drug-induced, owner may report signs of N/A ECG Features drug toxicity—anorexia, vomiting, and DIAGNOSTIC PROCEDURES r r PR interval—becomes progressively longer diarrhea with digoxin; weakness with calcium May be necessary to identify specific causes prior to the appearance of a P wave that is not channel blockers or β-adrenergic antagonists. of enhanced vagal tone (e.g., upper airway followed by a QRS complex (Figure 1). r r If heart rate is abnormally slow, syncope or disease, cervical and thoracic masses, Heart rate and QRS morphology—usually weakness may occur. gastrointestinal disorders, and high normal. r Physical Examination Findings intraocular pressure). r r Often cyclical. May be normal unless signs of Atropine response test—administer 0.04 PATHOPHYSIOLOGY more-generalized myocardial disease or mg/kg atropine IM and repeat ECG in 20–30 r Frequently associated with high resting non-cardiac disease are present. minutes; may be used to determine whether r vagal tone and sinus arrhythmia in dogs. Intermittent pauses in the cardiac rhythm. AV block is due to vagal tone; resolution of r r AV block with atropine supports 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 r INCIDENCE/PREVALENCE RISK FACTORS 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 8–12 Generally unnecessary weeks of age. ACTIVITY GEOGRAPHIC DISTRIBUTION DIAGNOSIS Unrestricted N/A DIET SIGNALMENT DIFFERENTIAL DIAGNOSIS r Modifications or restrictions only to manage Species Non-conducted P waves from an underlying condition. supraventricular premature impulses or Dogs;uncommonincats supraventricular tachycardias should be Breed Predilections distinguished from second-degree AV block. N/A

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 longest PR intervals preceding non-conducted P waves (typical Wenkebach phenomenon) (paper speed = 50 mm/s). BLBS078-CF_A82 BLBS078-Tilley July 15, 2011 9:51

Canine and Feline, Fifth Edition 147 Atrioventricular Block, Second Degree—Mobitz Type I A

CLIENT EDUCATION PREVENTION/AVOIDANCE Suggested Reading Explain that any treatment is directed toward N/A Branch CE, Robertson BT, Williams JC. reversing or eliminating an underlying cause. POSSIBLE COMPLICATIONS Frequency of second-degree atrioventricular N/A heart block in dogs. Am J Vet Res 1975, SURGICAL CONSIDERATIONS 36:925–929. N/A except to manage an underlying Mangrum JM, DiMarco JP. The evaluation condition and management of bradycardia. N Engl J MISCELLANEOUS Med 2000, 342:703–709. Podrid PJ, Kowey PR. Cardiac ASSOCIATED CONDITIONS Arrhythmia—Mechanisms, Diagnosis, and MEDICATIONS N/A Management. Baltimore: Williams & AGE-RELATED FACTORS Wilkins, 1995. DRUG(S) Tilley LP, Smith FWK Jr. N/A Only as needed to manage an underlying Electrocardiography. In: Tilley LP, Smith PREGNANCY/FERTILITY/BREEDING condition FWK, Oyama MA, Sleeper MM, eds., N/A CONTRAINDICATIONS Manual of Canine and Feline Cardiology, SYNONYMS 4th ed. St. Louis: Saunders Elsevier, 2008, Drugs with vagomimetic action (e.g., digoxin, r Wenckebach periodicity pp. 49–77. bethanechol, physostigmine, pilocarpine) may r Wenckebach phenomenon Tilley LP. Essentials of Canine and Feline potentiate block. Electrocardiography, 3rd ed. Baltimore: SEE ALSO PRECAUTIONS r Williams & Wilkins, 1992. Hypokalemia increases the sensitivity to vagal Atrioventricular Block, Complete (Third Author Janice McIntosh Bright Degree) tone and may potentiate AV conduction r Consulting Editors LarryP.TilleyandFrancis Atrioventricular Block, First Degree delay. r W.K. Smith, Jr. Atrioventricular Block, Second POSSIBLE INTERACTIONS Degree—Mobitz Type II N/A ABBREVIATIONS Client Education Handout r AV = atrioventricular available online r ECG = electrocardiogram FOLLOW-UP PATIENT MONITORING Typically not necessary BLBS078-CF_A83 BLBS078-Tilley July 15, 2011 9:46

148 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Block, Second Degree—Mobitz Type II

r Central nervous or musculoskeletal systems blocking agents, propafenone, α2-adrenergic if inadequate cardiac output. agonists, muscarinic cholinergic agonists, or severe procainamide or quinidine toxicity). BASICS GENETICS r May be heritable in pugs Infiltrative myocardial disorders (neoplasia, DEFINITION amyloid). INCIDENCE/PREVALENCE r Second-degree AV block refers to failure of Endocarditis (particularly involving the Unknown aortic valve). one or more P waves but not all P waves to be r conducted. Mobitz Type II second-degree AV GEOGRAPHIC DISTRIBUTION Myocarditis (viral, bacterial, parasitic, idiopathic). block occurs when one or more P waves are N/A r Cardiomyopathy (especially in cats). blocked without a preceding progressive delay SIGNALMENT r in AV transmission. Trauma. Species r ECG Features Atropine administered intravenously may r Dogs and cats cause a brief period of first- or second-degree One or more P waves not followed by a heart block before increasing the heart rate. QRS complex; PR interval is constant but Breed Predilections may be either normal or consistently American cocker spaniels, pugs, dachshunds, RISK FACTORS prolonged (Figure 1). Airedale terriers, Doberman pinschers. Any condition or intervention that enhances r Ventricular rate—usually slow. Mean Age and Range vagal tone r Fixed ratio of P waves to QRS complexes Generally occurs in older animals may occur (e.g., 2:1, 3:1, 4:1 AV block). r Predominant Sex High-grade (advanced) second-degree AV N/A block is characterized by two or more SIGNS DIAGNOSIS consecutive blocked P waves. r Historical Findings DIFFERENTIAL DIAGNOSIS In second-degree AV block with a 2:1 r r conduction ratio or higher, it is impossible to Presenting complaint may be syncope, High-grade (advanced) form must be collapse, weakness, or lethargy. distinguished from complete AV block. observe prolongation of the PR interval before r r Some animals are asymptomatic. Non-conducted P waves arising from the block, so a designation of Mobitz is not r appropriate. Animals may show signs of the underlying refractoriness of the conduction system r QRS complexes may appear normal but disease process. during supraventricular tachycardias must be may also be wide or have an abnormal Physical Examination Findings differentiated from pathologic conduction r morphology due to aberrant intraventricular ± weakness. block. r conduction or to ventricular enlargement. Bradycardia common. CBC/BIOCHEMISTRY/URINALYSIS r r r Abnormally wide QRS complexes may May be intermittent pauses in the cardiac Serum electrolytes—hypokalemia and indicate serious, extensive cardiac disease. rhythm. hyperkalemia may predispose to AV. r r PATHOPHYSIOLOGY An S4 may be audible in lieu of the Conduction disturbances. r r Rare in healthy animals. normally expected heart sounds (i.e., S1, S2) Leukocytosis—may be noted with bacterial r when the block occurs. endocarditis or myocarditis. May be hemodynamically important when r r ventricular rate is abnormally slow. If associated with digoxin intoxication, there Electrolyte abnormalities (e.g., severe r may be vomiting, anorexia, and diarrhea. Frequently progresses to complete AV block, r hypokalemia, hyperkalemia, or particularly when accompanied by wide QRS May be other abnormalities reflecting the hypercalcemia) may predispose to AV block. complexes. underlying etiology. OTHER LABORATORY TESTS r Typically this type of AV block results from CAUSES r r Serum digoxin concentration—may be conduction delay within the AV node itself Heritable in pugs. high. (rather than delay in another segment of the r r Enhanced vagal stimulation from High T4 in cats—if associated with AV conducting system) that is characterized non-cardiac diseases. hyperthyroidism. r r by normal or prolonged AH intervals with Degenerative change within the cardiac High arterial blood pressure—if associated intermittent block between A and H conduction system—replacement of AV nodal with hypertensive heart disease. r deflections on a His bundle electrogram). cells and/or Purkinje fibers by fibrotic and Positive Borrelia, Rickettsia, or Trypanosoma SYSTEMS AFFECTED adipose tissue in old cats and dogs. cruzi titers—if associated with one of these r r Cardiovascular. Pharmacologic agents (e.g., digoxin, infectious agents. β-adrenergic antagonists, calcium channel

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 with both 2:1 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). BLBS078-CF_A83 BLBS078-Tilley July 15, 2011 9:46

Canine and Feline, Fifth Edition 149 Atrioventricular Block, Second Degree—Mobitz Type II A

r Blood cultures may be positive in patients with vegetative endocarditis. IMAGING MEDICATIONS MISCELLANEOUS Echocardiographic examination may reveal DRUG(S) OF CHOICE ASSOCIATED CONDITIONS structural heart disease (e.g., endocarditis, r neoplasia, or cardiomyopathy). Atropine (0.02–0.04 mg/kg IV, IM) or May be noted in cats with primary or glycopyrrolate (0.005–0.01 mg/kg IV, IM) secondary myocardial disease. DIAGNOSTIC PROCEDURES r may be used short term if positive atropine AGE-RELATED FACTORS Atropine response test—administer response. r N/A 0.04 mg/kg atropine IM and repeat ECG in Chronic anticholinergic therapy ZOONOTIC POTENTIAL 20–30 minutes; may be used to determine (propantheline 0.5–2 mg/kg PO q8–12h or whether AV block is due to high vagal tone. N/A r hyoscyamine 0.003–0.006 mg/kg Electrophysiologic testing is generally q8h)—indicated for symptomatic patients if PREGNANCY/FERTILITY/BREEDING unnecessary but can be done to confirm this improved AV conduction with atropine N/A type of AV block if surface ECG findings are response test. r SEE ALSO equivocal. Isoproterenol (0.04–0.09 μg/kg/minute IV r Atrioventricular Block, Complete (Third PATHOLOGIC FINDINGS to effect) or dopamine (2–5 μg/kg/minute IV Degree) r to effect) may be administered in acute, r Variable—depend on underlying cause. Atrioventricular Block, Second r life-threatening situations to enhance AV Old animals with degenerative change of Degree—Mobitz Type I the conduction system may have focal conduction and/or accelerate an escape focus. ABBREVIATIONS mineralization of the interventricular septal CONTRAINDICATIONS r r AV = atrioventricular crest visible grossly; chondroid metaplasia of Drugs with vagomimetic action (e.g., r ECG = electrocardiogram the central fibrous body and increased fibrous digoxin, bethanechol, physostigmine, r T = thyroxine connective tissue in the AV bundle is noted pilocarpine) may potentiate block. 4 r histopathologically. Avoid drugs likely to impair impulse Suggested Reading conduction further or depress a ventricular Kittleson MD. Electrocardiography. In: escape focus (e.g., procainamide, quinidine, Kittleson MD, Kienle RD, eds., Small lidocaine, calcium channel blocking agents, Animal Cardiovascular Medicine. St. Louis: TREATMENT β-adrenergic blocking agents). Mosby, 1998, pp. 72–94. APPROPRIATE HEALTH CARE PRECAUTIONS Mangrum JM, DiMarco JP. The evaluation r Hypokalemia—increases sensitivity to vagal and management of bradycardia. N Engl J Treatment—may be unnecessary if heart Med 2000, 342:703–709. rate maintains adequate cardiac output. tone and may potentiate AV conduction r delay. Podrid PJ, Kowey PR. Cardiac Positive dromotropic interventions are Arrhythmia—Mechanisms, Diagnosis, and indicated for symptomatic patients. POSSIBLE INTERACTIONS r Management. Baltimore: Williams & Treat or remove underlying cause(s). N/A Wilkins, 1995. NURSING CARE ALTERNATIVE DRUG(S) Tilley LP, Smith FWK Jr. Generally unnecessary N/A Electrocardiography. In: Tilley LP, Smith ACTIVITY FWK, Oyama MA, Sleeper MM, eds., Cage rest advised for symptomatic patients Manual of Canine and Feline Cardiology, 4th ed. St. Louis: Saunders Elsevier, 2008, DIET FOLLOW-UP pp. 49–77. Modifications or restrictions only to manage Tilley LP. Essentials of Canine and Feline an underlying condition. PATIENT MONITORING Electrocardiography, 3rd ed. Baltimore: CLIENT EDUCATION Frequent ECG because often progresses to Williams & Wilkins, 1992. r Need to seek and specifically treat complete (third-degree) AV block. Author Janice McIntosh Bright underlying cause. PREVENTION/AVOIDANCE Consulting Editors LarryP.TilleyandFrancis r Pharmacologic agents may not be effective N/A W.K. Smith, Jr. long term. POSSIBLE COMPLICATIONS SURGICAL CONSIDERATIONS Prolonged bradycardia may cause secondary Client Education Handout Permanent pacemaker may be required for congestive heart failure or inadequate renal available online long-term management of symptomatic perfusion. patients. EXPECTED COURSE AND PROGNOSIS Variable—depends on cause. If degenerative disease of the cardiac conduction system, often progresses to complete (third-degree) AV block. BLBS078-CF_A84 BLBS078-Tilley July 15, 2011 9:55

150 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Valve Dysplasia

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 DIFFERENTIAL DIAGNOSIS Dogs and cats r abnormalities of the ipsilateral outflow tract With the noted exception of the age of Breed Predilections (e.g., valvular or subvalvular aortic or r onset, congenital AV valvular insufficiency pulmonic stenosis). It is not uncommon for Tricuspid valve dysplasia—increased risk for resembles acquired degenerative AV valve mitral and tricuspid valve dysplasia to occur Labrador retrievers, German shepherd dogs, insufficiency with respect to historical r Great Pyrenees, possibly Old English together in the same patient. Valvular r findings, physical examination abnormalities, r insufficiency results in dilation of the sheepdogs. Also common in cats. Mitral and clinical sequelae. The right-sided ipsilateral atrium, eccentric hypertrophy of valve dysplasia—increased risk in bull terriers, murmur of tricuspid insufficiency is the associated ventricle, and, if sufficiently Newfoundlands, Labrador retrievers, Great sometimes confused with the right-sided severe, signs of CHF. Cardiomyopathy of Danes, golden retrievers, Dalmatians, and murmur of a ventricular septal defect. r chronic volume overload and elevated atrial Siamese cats. Perhaps the most common Ascites caused by silent tricuspid pressures are the end result culminating in congenital heart defects of cats. Mitral valve regurgitation or tricuspid valve stenosis is pulmonary congestion if the mitral valve is malformations often are noted in cats with often attributed to pericardial effusion, affected and systemic congestion if the hypertrophic cardiomyopathy. 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 producing outflow tract obstruction and the congestion if pressures exceed 15–20 mm Hg. failure. obstructive form of cardiomyopathy. If the Right-to-left shunting may occur if there is an SIGNS obstruction can be abolished with a beta atrial septal defect or patent foramen ovale. blocker and left ventricular hypertrophy Historical Findings Mitral valve stenosis results in elevated r resolves, it is likely that the primary pulmonary capillary pressure and pulmonary Exercise intolerance is the most common abnormality was mitral valve dysplasia. problem in dogs and cats with AV valve edema if pressures exceed 25–30 mm Hg. r CBC/BIOCHEMISTRY/URINALYSIS Pulmonary hypertension is a common dysplasia. Abdominal distention, weight complicating condition in animals with mitral loss, and stunting may be observed with Usually normal r r valve stenosis. Outflow tract obstruction severe tricuspid valve dysplasia. Labored IMAGING respiration is common in dogs or cats with may develop from defects that translocate the r Radiographic Findings anterior leaflet to a position closer to the mitral valve dysplasia. Syncope and collapse Mitral Valve Dysplasia r interventricular septum. Concentric left if critical mitral or tricuspid valve stenosis, Left atrial and left ventricular enlargement ventricular hypertrophy develops in severe outflow tract obstruction, an associated with valvular insufficiency. Isolated left atrial proportion to the severity of the obstruction. arrhythmia, or heart failure from AV valvular enlargement with valvular stenosis. Mild left SYSTEMS AFFECTED insufficiency. atrial enlargement with dynamic outflow r r Cardiovascular—inflow obstruction due to Physical Examination Findings obstruction. Evidence of left heart Mitral Valve Dysplasia failure—distended pulmonary veins, valvular stenosis and chronic volume overload r from valvular insufficiency result in elevated A holosystolic murmur is heard over the interstitial or alveolar edema in severe cases. Tricuspid Valve Dysplasia pulmonary (left AV valve) or systemic (right cardiac apex on the left. With severe disease r AV valve) venous pressures. Signs of low the murmur is accompanied by a thrill or Right atrial and right ventricular cardiac output develop if the lesion is gallop heart sounds. A soft diastolic murmur enlargement with valvular insufficiency. sufficiently severe. Concentric left ventricular may be present in the same location in Cardiac silhouette may appear globoid with hypertrophy develops secondary to dynamic animals with mitral stenosis but many pronounced enlargement. Isolated right atrial outflow obstruction. affected animals have no audible murmur. A enlargement with valvular stenosis. r r Respiratory—pulmonary edema may systolic ejection murmur that intensifies with Evidence of right heart failure—dilated develop secondary to mitral stenosis or mitral exercise or excitement is audible in animals caudal vena cava, hepatosplenomegaly, or with dynamic outflow tract obstructions. ascites in severe cases. valve insufficiency. Pulmonary hypertension is r a common complication in animals with Evidence of left heart failure—tachypnea, Echocardiography r mitral stenosis. Neurologic—collapse and increased respiratory efforts, pulmonary Mitral Valve Dysplasia r loss of consciousness, most often during crackles, and cyanosis in animals with severe Valvular insufficiency results in left atrial physical exertion, may occur with severe defects. dilation and eccentric hypertrophy of the left Tricuspid Valve Dysplasia disease due to low cardiac output and r ventricle. The papillary muscles are typically hypotension. Collapse in animals with A holosystolic murmur is heard over the flattened and displaced dorsally. Chordae dynamic outflow obstruction is most often cardiac apex on the right. With severe disease tendineae are often short and thickened. due to ventricular arrhythmia. the murmur is accompanied by a thrill or Doppler echocardiography demonstrates a BLBS078-CF_A84 BLBS078-Tilley July 15, 2011 9:55

Canine and Feline, Fifth Edition 151

(Continued) Atrioventricular Valve Dysplasia A

high velocity retrograde systolic transmitral jet Severe defects may be accompanied by a PREVENTION/AVOIDANCE and modestly increased transmitral inflow variety of arrhythmias, particularly atrial Do not breed affected animals. r velocities. Mitral stenosis results in left atrial premature beats, supraventricular tachycardia, POSSIBLE COMPLICATIONS r dilation while the left ventricular dimensions or atrial fibrillation. Congestive heart failure—left-sided with are normal or small. The valve leaflets are mitral valve dysplasia; right-sided with r often thickened, relatively immobile, and tricuspid valve dysplasia. Collapse or r often fused. Doppler echocardiography syncope with exercise. Paroxysmal demonstrates a high velocity transmitral TREATMENT supraventricular tachycardia or atrial diastolic jet with a reduced EF slope. There fibrillation with severe disease. may also be evidence of concurrent mitral APPROPRIATE HEALTH CARE Inpatient treatment required for CHF. EXPECTED COURSE AND PROGNOSIS insufficiency and/or secondary pulmonary r hypertension. Exclude the possibility of cor CLIENT EDUCATION Depends on severity of underlying defect r r triatriatum sinister. Dynamic left ventricular Owners should be informed of heritability Guarded to poor with serious defects outflow obstruction is characterized by and advised against breeding. systolic motion of the anterior mitral valve ACTIVITY leaflet toward the interventricular septum, increased LV outflow tract velocities, and Restricted in accordance with severity. MISCELLANEOUS DIET concentric left ventricular hypertrophy. ASSOCIATED CONDITIONS Tricuspid Valve Dysplasia Sodium-restricted if overt or pending CHF. r r Mitral valve dysplasia commonly Valvular insufficiency results in right atrial accompanies valvular or subvalvular aortic dilation and eccentric hypertrophy of the SURGICAL CONSIDERATIONS r stenosis as well as TVD. Tricuspid valve right ventricle. The papillary muscles and r Valve repair or replacement is available in a dysplasia commonly accompanies pulmonic chordae tendineae may be fused, creating a r few centers. Balloon valvuloplasty is stenosis as well as MVD. curtain-like appearance of the tricuspid valve. sometimes effective for valvular stenosis. Doppler echocardiography demonstrates a PREGNANCY/FERTILITY/BREEDING high velocity retrograde systolic trans- Should be avoided—heritable defect and tricuspid jet and modestly increased possibility of causing decompensated or r trans-tricuspid inflow velocities. Tricuspid MEDICATIONS worsening heart failure. stenosis results in right atrial dilation with SEE ALSO DRUG(S) OF CHOICE r normal or small right ventricular dimensions. Congestive Heart Failure, Left-Sided r r The valve leaflets do not open completely. Mitral or tricuspid dysplasia with Congestive Heart Failure, Right-Sided Doppler echocardiography demonstrates a insufficiency—diuretics, angiotensin ABBREVIATIONS high velocity diastolic trans-tricuspid jet with converting enzyme inhibitors, and r = r = a reduced EF slope. There may be evidence of pimobendan (0.3 mg/kg q12h) for patients AV atrioventricular AVVD r = concurrent tricuspid valve insufficiency with imminent or overt congestive heart atrioventricular valve dysplasia CHF r = and/or right-to-left shunting across a patent failure. Furosemide (2–4 mg/kg q12–24h), congestive heart failure ECG r = foramen ovale or associated atrial septal enalapril (0.5 mg/kg q12h) are used to control electrocardiogram MVD mitral valve r = defect. Exclude the possibility of cor congestion. Digoxin (0.002–0.004 mg/kg dysplasia TVD tricuspid valve dysplasia q12h) is used to control supraventricular triatriatum dexter. r Suggested Reading Cardiac Catheterization tachyarrhythmias. Mitral or tricuspid Bonagura JD, Lehmkuhl LB. Congenital r Indicated only in those cases in which the stenosis—diuretics to control edema. heart disease. In: Fox PR, Sisson D, Moise diagnosis cannot be confirmed by Furosemide (2–4 mg/kg q12–24h) dose NS. Textbook of Canine and Feline echocardiography or if surgical correction is adjusted to resolve congestion. Heart rate Cardiology: Principles and Clinical Practice, r anticipated. Mitral dysplasia— should be maintained near 150 bpm using 2nd ed. Philadelphia: Saunders, 1999, pp. hemodynamic measurements should include digoxin (0.002–0.004 mg/kg q12h), a 520–526. left ventricular pressures, pulmonary capillary calcium channel blocker such as diltiazem Oyama MA, Sisson DD, Thomas WP, wedge pressure or direct measurement of LA (1–1.5 mg/kg q8h), or a beta-receptor Bonagura JD. Congenital heart disease. In: blocking drug, such as atenolol (0.5–1.5 pressure, pulmonary artery pressures, and, in r Ettinger SJ, Feldman EC, eds., Textbook of cases of dynamic obstruction, simultaneous mg/kg q12–24h). Dynamic outflow tract Veterinary Internal Medicine, 6th ed. St. recording of aortic and left ventricular obstruction—titrate a beta-receptor blocking Louis: Elsevier, 2005. pressures with medical provocation. Contrast drug, such as atenolol (0.5–1.5 mg/kg Strickland KN. Congenital heart disease. In: studies are best accomplished with a left q12–24h), to abolish or diminish severity of Tilley LP, Smith FWK, Oyama MA, Sleeper ventricular injection in cases of valvular outflow obstruction. MM, eds., Manual of Canine and Feline insufficiency, and direct left atrial injection via PRECAUTIONS Cardiology, 4th ed. St. Louis: Saunders trans-septal catheterization in cases of valvular Standard patient monitoring for cardiac Elsevier, 2008, pp. 215–239. r stenosis. Tricuspid dysplasia— medication side effects (e.g., digitalis toxicity, Author David Sisson hemodynamic measurements should include azotemia). Consulting Editor Larry P. Tilley and Francis right ventricular and right atrial pressures. W.K. Smith, Jr. Contrast studies are best accomplished with a right ventricular injection in cases of valvular insufficiency, and right atrial injection in cases FOLLOW-UP Client Education Handout of valvular stenosis. available online PATIENT MONITORING DIAGNOSTIC PROCEDURES r Recheck yearly if no signs of heart failure. r Electrocardiographic Findings Recheck at a minimum of every 3 months if Usually reflect pattern of chamber signs of CHF (thoracic radiographs, ECG, enlargement. and echocardiography advisable). BLBS078-CF_A85 BLBS078-Tilley July 15, 2011 9:57

152 Blackwell’s Five-Minute Veterinary Consult A Atrioventricular Valve Endocardiosis

Cavalier King Charles spaniels typically affected much earlier (6–8 years). BASICS Predominant Sex DIAGNOSIS Males—male: female ratio, 1.5:1 DEFINITION DIFFERENTIAL DIAGNOSIS SIGNS r A chronic degenerative disease affecting the Dilated cardiomyopathy Signs depend on the stage of disease. Various r mitral and tricuspid valves, leading to valvular Congenital heart disease grading schemes have been developed to r insufficiency and heart failure. Chronic airway or interstitial lung disease categorize patients based on the severity of r Pneumonia PATHOPHYSIOLOGY their disease and the signs they are showing. r r Pulmonary embolism Proliferation and deposition of These grades are then used to facilitate r Pulmonary neoplasia mucopolysaccharide within the therapeutic decision making. The descriptions r Heartworm disease subendothelial spongiosa layer leads to here align with the grading system described thickening, distortion, and stiffening of the CBC/BIOCHEMISTRY/URINALYSIS in the ACVIM consensus statement on valve r AV valves; initially, swellings are nodular, but disease and the modified NYHA classification Prerenal azotemia secondary to impaired coalescence occurs until the entire valve and scheme. renal perfusion; urinary specific gravity is high often the attached chordae are involved. unless complicated by underlying renal r Asymptomatic Valve Disease AV valve incompetence causes regurgitation, r disease or previous diuretic administration. Systolic murmur is heard best at the left r high atrial pressure, reduced cardiac output, fifth intercostal space (mitral) or right fourth High liver enzyme activity in many patients activation of compensatory mechanisms with passive congestion. intercostal space (tricuspid). r r (sympathetic nervous system, Murmurs may vary from a low-frequency, A “stress leukogram” may be seen. renin-angiotensin-aldosterone system, and holosystolic, band shaped sound to a shorter, OTHER LABORATORY TESTS natriuretic peptides), and CHF. r high-frequency, midsystolic murmur; Elevation in N-Terminal Pro BNP has been Volume overload leads to progressive occasionally only a midsystolic click is documented in patients with both disease and ventricular dilation, advancing ventricular detected. failure. Studies show levels correlate with r stiffness, and impaired ventricular function; As the disease progresses, the murmur severity of disease, the presence of heart congestive and low-output (forward) failure typically gets louder and radiates more widely; failure as a cause for clinical signs and a result. r with severe disease, the volume of possible decrease in response to therapy. With atrial tear, acute cardiac tamponade regurgitation becomes so large that the Elevations in NTproBNP may also help may result. r murmur may decrease in frequency and predict which asymptomatic patients are Degenerative changes in the chordae loudness. likely to progress to heart failure, and assess r tendineae lead to distortion, weakening, and Initially patients will have no obvious prognosis in those that do. rupture, causing valvular instability and radiographic or echocardiographic evidence of IMAGING increased regurgitation. “remodeling” (changes in cardiac chambers or Radiographic Findings SYSTEMS AFFECTED muscular components) (ACVIM stage 2a). As r r Cardiovascular—both AV valves are the disease progresses, evidence of Heart size ranges from normal to left-sided or generalized cardiomegaly. affected, but 1 study found the distribution in cardiomegaly will be seen, often before r necropsy specimens to be mitral alone, 62%; obvious clinical signs of heart failure are Left atrial enlargement in the lateral tricuspid alone, 1%; and both, 33%. recognized (ACVIM stage 2b). Any animal projection exhibits elevation of the distal r Hepatobiliary—passive congestion. with signs of heart failure (regardless of fourth of the trachea and splitting of the r Renal/Urologic—prerenal azotemia. severity) is ACVIM stage C, but varies in its mainstem bronchi; dorsoventral projection r Respiratory—if edema develops. NYHA class depending on severity. shows accentuation of the angle between the mainstem bronchi, a double shadow at the six GENETICS Mild Heart Failure (NYHA Class II) r o’clock position, where the caudal edge of the Some breeds (Cavalier King Charles spaniels, Coughing, exercise intolerance and dyspnea atrium extends beyond the left ventricle, and dachshunds) appear to have an inherited with strenuous exercise; occasionally, syncope bulging of the left atrial appendage in the one component to their disease. may be the only owner complaint. to three o’clock position. r INCIDENCE/PREVALENCE Moderate Heart Failure (NYHA Class III) Left-sided heart failure—the pulmonary r Chronic valvular disease increases from about Coughing, exercise intolerance and dyspnea vein is larger than the associated pulmonary 5% in middle-aged dogs (5–7 years) to > most of the time. artery; an increased interstial pattern ± air 35% in old dogs (12 years). Severe Heart Failure (Requires bronchograms are typical of, but not SIGNALMENT Hospitalization—NYHA Class 4) pathognomonic for, cardiogenic pulmonary r edema; initially, congestion and edema are Species Severe dyspnea, profound weakness, abdominal distention, productive coughing perihilar, with all lung fields eventually Mainly dogs, but may be seen in old cats (i.e., pink, frothy fluid), orthopnea, cyanosis, showing changes. The right lung may be Breed Predilections affected before the left. r and syncope. Typically small breeds (< 20 kg but seen Refractory Heart Failure Echocardiographic Findings less frequently in larger dogs). r r r Clinical signs that persist despite Thickening and distortion of the mitral Highest prevalence—Cavalier King Charles valve; septal leaflet is most severely affected. conventional therapeutic management. r spaniels, Chihuahuas, miniature schnauzers, Elongation and rupture of the chordae CAUSES Maltese, Pomeranians, cocker spaniels, tendineae, causing mitral valve prolapse. r Pekingese, fox terriers, Boston terriers, Idiopathic, although the role of a number of Large left atrium. r miniature poodles, toy poodles, miniature inflammatory modulators is being The left ventricle may be distended and is pinschers, and whippets. investigated in either the onset or propagation hyperdynamic if the regurgitant flow is high Mean Age and Range of the disease. and myocardial function intact; as the Heart failure onset at 10–12 years, although RISK FACTORS ventricle becomes more grossly distended, it may detect a murmur several years earlier; N/A BLBS078-CF_A85 BLBS078-Tilley July 15, 2011 9:57

Canine and Feline, Fifth Edition 153

(Continued) Atrioventricular Valve Endocardiosis A

r may become hypodynamic because of Stable patients receiving medical Chronic Congestive Heart Failure myocardial failure. treatment—restrict exercise to leash walking; (Typically Treated as an Outpatient) r r Pericardial effusion in some patients. avoid sudden, explosive exercise. Diuretics—furosemide (1–2 mg/kg r Doppler studies document a jet of DIET q8–12h). r r regurgitation into the left atrium and the area Preventing cardiac cachexia by ensuring ACE inhibitors enalapril (0.5 mg/kg of the regurgitant jet on color flow. q12–24h), benazepril (0.25–0.5 mg/kg q24h). r adequate calorie intake should be the primary r Doppler indices, including regurgitant objective in the dietary management of Pimobendan, an inodilator, has a rapid fraction, are used to assess severity. onset of action (30–60 minutes) and is r patients with chronic valve disease. r Doppler evaluation for the presence of A salt-restricted diet is recommended, if recommended for the management of heart pulmonary hypertension should be a routine failure. tolerated, for a patient in heart failure; r component of any echocardiographic monitor sodium concentration closely. Spironolactone, while typically used for its r evaluation in patients with chronic valve Hyponatremia may develop as CHF diuretic effect in combination with other disease. progresses and in patients fed severely diuretics, has been shown to have a positive DIAGNOSTIC PROCEDURES sodium-restricted diets in conjunction with influence on deleterious remodeling that r Abdominocentesis/pleurocentesis—a loop diuretics and angiotensin converting occurs as heart disease progresses. It is used modified transudate is characteristic of CHF. enzyme inhibitors. initially at 0.5–1 mg/kg PO q24h. The dose r r Arterial/venous blood gases have been used If hyponatremia develops, switch to a less can be raised to 1–2 mg/kg PO q12h for refractory heart failure. to quantify hypoxemia and monitor treatment sodium-restricted diet (e.g., renal or geriatric r response. diet). Nitroglycerin—2% percutaneous ointment r (0.125–1 inch q6h until patient is stable). Systemic blood pressure should be evaluated CLIENT EDUCATION r r Digoxin—especially if supraventricular to check for concurrent systemic hypertension Discuss the progressive nature of the disease. in all patients with chronic valve disease. r arrhythmias, including atrial fibrillation, are Emphasize the importance of consistent documented (0.005 mg/kg or 0.22 mg/m2 Electrocardiographic Findings dosing of all medications and exercise PO q12h). r r Sinus tachycardia is common in animals management. Sodium restriction if tolerated. r r with CHF. Emphasize the importance of avoiding Antiarrhythmics—as needed. r r May show evidence of left atrial cardiac cachexia by paying close attention to Calcium channel blockers—to treat atrial enlargement (P mitrale) or left ventricular appetite and using the appropriate diet. arrhythmias. enlargement (tall and wide R waves). r r r Highlight the signs of digoxin toxicity, and Beta blockers—to treat atrial and ventricular Atrioventricular arrhythmias may develop. advise the owner to stop treatment and notify arrhythmias. Some cardiologists advocate the PATHOLOGIC FINDINGS the veterinarian immediately should any use of beta blockers in patients with intact r develop. Gross valvular changes are divided into four r myocardial function to negate the negative Education of owners in simple techniques, effects of excessive beta receptor stimulation. types—type I shows only a few discrete r nodules at the line of closure; type IV shows like monitoring the patient’s respiratory rate, Class 1 antiarrhythmics—procainamide, gross distortion of the valve by gray-white or heart rate at rest, helps engage them in their mexiletine, and tocainide; to treat clinically pet’s care and may detect increases suggestive important ventricular arrhythmias. nodules and plaques causing contraction of r the cusps and rolling of the free edge; the of developing or recurring congestive failure. Class III antiarrhythmics—sotalol, SURGICAL CONSIDERATIONS amiodarone for intractable arrhythmias. chordae are irregularly thickened, with r regions of tapering and rupture. PDE 5 inhibitors (sildenafil) should be r Surgical valve replacement and purse-string Jet lesions—irregular thickening and suture techniques to reduce the area of the considered if pulmonary hypertension is opacity of the atrial endocardium. present. r mitral valve orifice have been used; experience Recent and healed left atrium splits or tears with these techniques is limited, but surgical Acute Congestive Heart Failure (Often in some patients; full-thickness tears lead to repair may be an option when access to a Treated as an Inpatient) r hemopericardium (free wall) or acquired atrial cardiovascular surgeon and cardiopulmonary Oxygen—40% in O2 cage (can go as high septal defect (septum). r bypass are available. as 100%) up to 24 hours; use nasal O2 in Left atrium and left ventricle dilation in large-breed dogs, 50–100 mL/kg/minute many patients. through humidifier. r r The degree of left ventricular hypertrophy Diuretics—furosemide (2–4 mg/kg IV may be apparent only on weighing the heart. r MEDICATIONS q4–8h). Small thrombi in the left atrium rare in Vasodilators dogs—more common and extensive in cats. DRUG(S) OF CHOICE r Benazepril (0.25–0.5 mg/kg q24h). Recommended treatment depends on the r Enalapril (0.5 mg/kg q12h–24h). stage of the disease; these recommendations r follow the guidelines set by the consensus Pimobendan (0.25 mg/kg PO q12h) used statement developed by the ACVIM. alone or in combination with other TREATMENT vasodilators and/or digoxin. Asymptomatic Patients r APPROPRIATE HEALTH CARE r Hydralazine (0.5 mg/kg q12h titrated up to If no cardiac enlargement, no treatment is 2 mg/kg if necessary)—used in acute stages to Treat patients that need oxygen support as recommended. inpatients; if stable, patients may be less r decrease afterload rapidly; may cause Administering ACE inhibitors to hypotension. stressed at home. r asymptomatic patients showing progressive Nitroglycerin—ointment (one-fourth NURSING CARE cardiomegaly is advocated in patients with inch/5 kg up to 2 inches percutaneously) or Oxygen therapy as needed for hypoxemia. significant left sided cardiomegaly by some injectable (1–5 μg/kg/minute CRI). r ACTIVITY cardiologists. Administration of pimobendan Sodium nitroprusside (1–10 μg/kg/ r to asymptomatic patients is of unknown value minute)—monitor blood pressure. Absolute exercise restriction for r symptomatic patients. at this time but studies are ongoing to Pulmonary arterial vasdilators such as evaluate this. sildenafil (PDE 5 inhibitors) should be BLBS078-CF_A85 BLBS078-Tilley July 15, 2011 9:57

154 Blackwell’s Five-Minute Veterinary Consult

A Atrioventricular Valve Endocardiosis (Continued)

considered in patients with pulmonary place of nitroglycerin ointment in patients hypertension. requiring long-term nitrate administration. Positive Inotropes MISCELLANEOUS r Pimobendan (0.25 mg/kg PO q12h). r 2 SYNONYMS Digoxin (0.005 mg/kg or 0.22 mg/m PO r Acquired valvular insufficiency q12h). FOLLOW-UP r r Chronic valve disease Dobutamine (dogs, 1–10 μg/kg/minute; PATIENT MONITORING r cats, 1–5 μg/kg/minute)—may cause seizures. r Degenerative valve disease r Take a baseline radiograph when a murmur r Dopamine (1–10 μg/kg/minute). Valve fibrosis r is first detected and every 6–12 months Agents with β-blocking properties (e.g., SEE ALSO thereafter to document progressive r carvedilol) are being investigated for their Atrial Wall Tear cardiomegaly. r ability to upregulate β-receptors in patients r Congestive Heart Failure, Left-Sided Evidence suggests that NTproBNP may be r with severe myocardial dysfunction. used in a similar way. A baseline is taken when Congestive Heart Failure, Right-Sided Carvedilol (0.1–0.4 mg/kg PO q12h) is an the murmur is first heard, and then the test is ABBREVIATIONS alpha- and beta blocker with antioxidant r run serially to assess for significant change. ACE = angiotensin converting enzyme activity. Start at the low end of the dose range r r After an episode of CHF, check patients AV = atrioventricular and gradually raise dose if tolerated. r weekly during the first month of treatment; CHF = congestive heart failure PRECAUTIONS may repeat thoracic radiographs and an ECG r Use digoxin, diuretics, and ACE inhibitors at the first weekly checkup and on subsequent Suggested Reading with caution in patients with renal disease. visits if any changes are seen on physical Abbott JA. Acquired valvular disease. In: r Nitrate tolerance may develop if appropriate examination. Tilley LP, Smith FWK, Oyama MA, Sleeper r 12-hour nitrate-free intervals are omitted Monitor BUN and creatinine when MM, eds., Manual of Canine and Feline from the dosing schedule. diuretics and ACE inhibitors are used in Cardiology, 4th ed. St. Louis: Saunders r Beta blockers are negative inotropes and combination. Monitor serum potassium levels Elsevier, 2008, pp. 2110–2138. may have an acute adverse effect on when spironolactone and ACE inhibitors are Atkins C, et al. Guidelines for the diagnosis myocardial function, although their long-term used concurrently, especially when combined and treatment of canine chronic valvular use may improve myocardial function. with digoxin. heart disease. J Vet Intern Med 2009, 23:1142–1150. POSSIBLE INTERACTIONS POSSIBLE COMPLICATIONS Kvart C, Haggstrom J, Pedersen HD, et al. Monitor digoxin concentration in patients Endocarditis because of bacterial colonization Efficacy of enalapril for prevention of receiving concurrent calcium channel blockers of the diseased mitral valve has been suggested congestive heart failure in dogs with or quinidine. although the evidence remains controversial. myxomatous valve disease and ALTERNATIVE DRUG(S) EXPECTED COURSE AND PROGNOSIS asymptomatic mitral regurgitation. J Vet r Diuretics—add thiazide and potassium Progressive degeneration of both valve Intern Med 2002, 16(1):80–88. sparing diuretic (e.g., spironolactone) in changes and myocardial function occurs, Author Andrew Beardow refractory animals. necessitating increasing drug dosages; Consulting Editors LarryP.Tilleyand r Bumetanide is an alternative to furosemide. long-term prognosis depends on response to Francis WK. Smith, Jr. r Vasodilators—other ACE inhibitors include treatment and stage of heart failure. lisinopril; isosorbide dinitrate can be used in Client Education Handout available online BLBS078-CF_A86 BLBS078-Tilley July 23, 2011 5:25

Canine and Feline, Fifth Edition 155 Atrioventricular Valvular Stenosis A

r r Syncope Two-dimensional echocardiography reveals r Exertional dyspnea or tachypnea a markedly dilated atrium and attenuated r Cough—MS valve excursion during diastole, often with BASICS r Cyanosis thickened, irregular AV valve leaflets; valve r DEFINITION Abdominal distention—TS leaflets may appear to “dome” during diastole. r Acute posterior paresis—cats with MS A supravalvular obstructing ring also may be Atrioventricular valvular stenosis is a r Stunted growth evident as well as other lesions (see “Causes” pathologic narrowing of the mitral or r Hemoptysis from rupture of above). tricuspid valve orifice. r PATHOPHYSIOLOGY intrapulmonary vessels—MS M-mode studies show an enlarged atrium r Physical Examination Findings and concordant motion of the AV valve Ventricular filling in clinically significant r Soft diastolic murmur with point of leaflets indicating commissural fusion; the disease requires a persistent diastolic pressure E-to-F slope is decreased. gradient between atrium and ventricle. maximal intensity over the left apex (MS) or r r right hemithorax (TS). Color-flow imaging reveals a turbulent Concomitant valvular regurgitation is r diastolic jet that originates at the stenotic valve common. Holosystolic murmur of mitral or tricuspid r regurgitation is common. and projects toward the apex of the ventricle; The increased atrial pressure can lead to r AV valve regurgitation is often present. Crackles, tachypnea, dyspnea with MS. r atrial dilation, venous congestion, and CHF. r Spectral Doppler studies show increased Pulmonary edema occurs with mitral stenosis; Jugular distention, jugular pulses, ascites, hepatomegaly with TS. diastolic transvalvular flow velocities; ascites, pleural effusion and chylothorax can r prolonged calculated pressure half-time is a develop in cases of severe tricuspid stenosis. Cyanosis from right to left shunt with TS. r hallmark feature; E-wave/A-wave amplitude The foramen ovale may remain patent CAUSES r reversal may be seen in cases still in normal (PFO) in patients with tricuspid stenosis, Usually due to congenital dysplasia of the sinus rhythm. r allowing right-to-left shunting with signs of mitral or tricuspid valve. Right-sided chamber enlargements in MS cyanotic heart disease. r r Supravalvular obstructing rings of tissue with pulmonary hypertension. Cardiac output and exercise capacity are have been associated with atrioventricular Angiography limited with atrioventricular valvular stenosis. stenosis r r r Mitral stenosis can lead to exertional Infective endocarditis, intracardiac Right atrium: injection demonstrates a dyspnea from transient pulmonary edema. markedly dilated atrium; with TS and usually r neoplasia, hypertrophic cardiomyopathy in Pulmonary hypertension can develop cats are potential causes of acquired stenosis. a PFO or an ASD; opacification of the left r consequent to MS, leading to exercise Tricuspid stenosis has been observed with atrium may be observed following right atrial injection. intolerance and right ventricular hypertrophy. fibrous scarring of the tricuspid valve in dogs r This can be severe, especially in cats with with transvenous pacing leads. May visualize thickened, irregular valve leaflets or a stenotic valve funnel. mitral stenosis. RISK FACTORS r SYSTEMS AFFECTED Ventricular injection typically reveals See “Risk Factors” for Endocarditis, Infective; valvular regurgitation. r r Respiratory—with MS—bronchial permanent transvenous pacing. There may be delayed opacification of the compression from enlarged left atrium, ventricle and great vessels. pulmonary edema; pleural effusion with Cardiac Catheterization atelectesis in tricuspid stenosis. r r A diastolic pressure gradient is identified Hepatobiliary—with TS—hepatic DIAGNOSIS congestion, ascites. between the atrium and ventricle. A large “A” wave is common if atrial function is preserved. GENETICS DIFFERENTIAL DIAGNOSIS r High left atrial, pulmonary capillary wedge, Uncertain Atrioventricular valvular stenosis must be differentiated from the more common causes and pulmonary artery pressures occur in MS. INCIDENCE/PREVALENCE r of mitral and tricuspid regurgitation in the High right atrial and central venous pressures are present in TS. Rare absence of stenosis. These include both r GEOGRAPHIC DISTRIBUTION congenital and acquired lesions of the Ventricular pressure may be normal in the absence of concurrent defects. Worldwide atrioventricular valves and support DIAGNOSTIC PROCEDURES SIGNALMENT apparatus. CBC/BIOCHEMISTRY/URINALYSIS Electrocardiography Species r There may be variable enlargement patterns. Dogs and cats May be normal or reflect changes related to r CHF or drug therapy for CHF. Ectopic rhythms, especially of atrial origin, Breed Predilections r IMAGING are often observed. Atrial fibrillation is the MS is overrepresented in bull terriers and most important rhythm disturbance as atrial Newfoundlands, and possibly Siamese cats. Thoracic Radiography r r contribution to filling is lost. TS has been reported most often in Old Atrial enlargement is the most consistent PATHOLOGIC FINDINGS English sheepdogs and Labrador retrievers. and outstanding feature; may see generalized r cardiomegaly. The atrioventricular valve is abnormal, with Mean Age and Range r thickened leaflets and fused commissures. Most patients are presented at a young age, MS—may see pulmonary venous congestion and pulmonary edema; Other lesions may be identified such as a though exceptions occur, especially in cats. supra-mitral ring (see “Causes”). intrapulmonary hemorrhage can be r Predominant Sex misinterpreted as pneumonia or another Many cases also have abnormal chordae tendineae and papillary muscles. N/A parenchymal disease. r r SIGNS TS—may see hepatomegaly; increased Atrial dilation and hypertrophy are common. Historical Findings diameter of caudal vena cava. r Exercise intolerance Echocardiography r Diagnostic test of choice. BLBS078-CF_A86 BLBS078-Tilley July 23, 2011 5:25

156 Blackwell’s Five-Minute Veterinary Consult

A Atrioventricular Valvular Stenosis (Continued)

r PO q24–48h; adjust dosage based on serum 0.8–1.5 ng/mL. Renal function, electrolyte r concentrations. Beta-blockers such as status, and arterial blood pressure when on r TREATMENT atenolol or the calcium channel blocker diuretic and/or ACE inhibitor. Standard diltiazem for suppression of frequent atrial rhythm ECG or Holter (ambulatory ECG) if APPROPRIATE HEALTH CARE premature complexes and for heart rate arrhythmias are present. Patients in overt CHF should be treated with control in atrial tachyarrhythmias such as POSSIBLE COMPLICATIONS r r r inpatient medical management. Surgical or atrial tachycardia/flutter/fibrillation. Beware: CHF Atrial fibrillation Syncope catheter-based interventions may be using these drugs in uncontrolled CHF. r r Arterial thromboembolism—cats r considered once heart failure has been Typical atenolol dosages: dogs, 0.25–1.0 Pulmonary hemorrhage with MS stabilized. Control of heart rhythm mg/kg q12h; cats, 6.25–12.5 mg/cat disturbances, especially AF, is also important. q12–24h; start low and titrate to effect. EXPECTED COURSE AND PROGNOSIS r r These patients are typically complicated and Diltiazem dosages: dogs, 2–6 mg/kg daily in Morbidity is high; except for mild cases, consultation with a cardiologist is two (long-acting diltiazem) or three divided prognosis is generally poor. However, some recommended. dosages; start low and titate to effect); cats, animals will live for 6–8 years even with relatively severe stenosis of the mitral valve. NURSING CARE 7.5 mg diltiazem HCl PO q8h, 15–30 mg r Dilacor XR q12–24h, or 10 mg/kg Cardizem Surgical intervention or balloon Oxygen therapy should be administered to r valvuloplasty may alter course of disease, but the patient with dyspnea or hypoxemia from CD q24h. Sotalol for intractable arrhythmias—dogs, 1–2 mg/kg PO q12h; data are limited. left-sided congestive heart failure. Fluid r therapy is typically contraindicated in the cats, 10–20 mg/cat q12h. Dogs can be patient with overt CHF except in cases of referred for electrocardioversion to convert AF to sinus rhythm (with follow-up therapy with concurrent moderate to severe azotemia, renal MISCELLANEOUS compromise, or severe dehydration. sotalol or amiodarone); however, reversion Therapeutic paracentesis may be considered back to AF is common owing to marked atrial ASSOCIATED CONDITIONS dilatation. in the patient with pleural effusions or Concurrent congenital defects are common Pulmonary Hypertension tympanic ascites. Sedation with butorphanol r (e.g., subaortic stenosis in MS, PFO in TS). is appropriate for dyspneic patients. Sildenafil—dogs, 0.5–3 mg/kg PO q8–12 PREGNANCY/FERTILITY/BREEDING hours. ACTIVITY The possibility that this may be a heritable PRECAUTIONS Exercise restriction is recommended for any r defect must be considered in assessing animal with this condition. Cage rest is ideal As a general rule pimobendan should not be suitability of the animal for breeding, for patients with CHF. used with pure valvular stenosis; however, particularly in breeds with a predilection for DIET some dogs and cats with advanced CHF have this defect. The additional hemodynamic been treated with this drug with apparent Feed a low-sodium diet to patients in CHF. burden of gestation may be poorly tolerated success, especially when there is combined CLIENT EDUCATION r by an already compromised heart. stenosis/regurgitation of the valve. Use ACE SYNONYMS The client must be advised of symptoms inhibitors or other vasodilators judiciously in associated with CHF and the urgency of patients with CHF; cardiac output is limited Atrioventricular valve dysplasia with stenosis treatment, particularly with left-sided CHF. and vasodilation may induce hypotension. SEE ALSO r The likelihood of recurrent bouts of CHF Monitor arterial blood pressure and renal Atrioventricular Valve Dysplasia r should also be discussed. function. Endocarditis, Infective SURGICAL CONSIDERATIONS POSSIBLE INTERACTIONS ABBREVIATIONS r r r Surgical valve replacement or repair requires Furosemide and ACE inhibitors can affect ACE = angiotensin converting enzyme r cardiopulmonary bypass or hypothermia; cost kidney function, alter blood electrolytes, and AF = atrial fibrillation r and availability are greatly limiting factors. reduce blood pressure; these parametersshould AV = atrioventricular r r Balloon valvuloplasty is an alternative be monitored. CHF = congestive heart failure r r referral treatment and has been used Sildenafil can also reduce systemic blood ECG = electrocardiogram r successfully for managing AV stenosis. pressure and should not be used with MS = mitral stenosis r nitroglycerin paste or another nitrate. PFO = patent foramen ovale r ALTERNATIVE DRUG(S) TS = tricuspid stenosis Spironolactone (2 mg/kg PO q12–24h) may Suggested Reading MEDICATIONS be considered as an ancillary diuretic and for Brown WA, Thomas WP. Balloon DRUG(S) OF CHOICE its antifibrotic benefit (as an aldosterone valvuloplasty of tricuspid stenosis in a antagonist). CHF Labrador Retriever. J Vet Intern Med 1995, r Furosemide—dogs, 2–6 mg/kg IV, IM, SC, 9:419–424. PO q8–24h; cats, 1–4 mg/kg IV, IM, SC, PO Lehmkuhl LB, Ware WA, Bonagura JD. r q8–24h. Enalapril—dogs, 0.25–0.5 mg/kg Mitral stenosis in 15 dogs. J Vet Intern Med PO q12h; cats, 0.25–0.5 mg/kg PO FOLLOW-UP 1994, 8:2–17. q12–24h; see below under “Follow-Up” for PATIENT MONITORING Stamoulis ME, Fox PR. Mitral valve stenosis r r in three cats. J Small Anim Pract 1993, patient monitoring. Nitroglycerin paste Thoracic radiographs for pulmonary edema r 34:452–456. (1/4–1 inch topically q12h) to reduce or pleural effusion. Echocardiography with pulmonary venous pressures, but this has not Authors Lora S. Hitchcock and Doppler studies—to estimate pulmonary John D. Bonagura been evaluated critically. pressures and subjectively assess right heart r Consulting Editors LarryP.Tilleyand Atrial Tachyarrhythmias function if on sildenafil. Digoxin r Francis W.K. Smith, Jr. Digoxin—dogs, 0.003–0.005 mg/kg PO level—check 7–10 days following institution q12h; cats, one-fourth of a 0.125-mg tablet of therapy; 8- to 12-hour trough should be BLBS078-CF_A87 BLBS078-Tilley July 15, 2011 21:2

Canine and Feline, Fifth Edition 157 Azotemia and Uremia A

SIGNALMENT Dogs and cats BASICS SIGNS DIAGNOSIS DEFINITION General Comments DIFFERENTIAL DIAGNOSIS Azotemia may not be associated with r r Dehydration, poor peripheral perfusion, Azotemia is an excess of urea, creatinine, or historical or physical abnormalities. Unless low cardiac output, history of recent fluid other non-protein nitrogenous substances in patient has uremia, clinical findings are r loss, high protein diet, or black, tarry stools— blood, plasma, or serum. Uremia is the limited to the disease responsible for r rule out prerenal azotemia. Recent onset of polysystemic toxic syndrome that results from azotemia. Findings described here are those altered urine output (high or low), clinical marked loss in kidney functions. Uremia of uremia. occurs simultaneously in animals with signs consistent with uremia, exposure to Historical Findings increased quantities of urine constituents in r r possible nephrotoxicants or ischemic renal Weight loss Declining appetite or anorexia blood. r r r injury, or kidney size normal or enlarged— Reduced activity Depression Fatigue r PATHOPHYSIOLOGY r r r r rule out acute renal failure. Progressive r Weakness Vomiting Diarrhea Halitosis weight loss, polyuria, polydipsia, small Azotemia can be caused by (1) increased r r Constipation Changes in urine volume kidneys, pallor, and signs of uremia that have production of non-protein nitrogenous r (increase or decrease) Poor haircoat or developed over several weeks to months—rule substances, (2) decreased glomerular filtration r unkempt appearance out chronic renal failure. Abrupt decline in rate, or (3) reabsorption of urine that has Physical Examination Findings urine output and onset of signs of uremia; escaped from the urinary tract into the r r Muscle wasting: cachexia Mental occasionally dysuria, stranguria, and bloodstream. High production of non-protein r r r depression Dehydration Weakness Pallor hematuria; large urinary bladder or fluid-filled nitrogenous waste substances may result from r r Petechiae and ecchymoses Dull and abdomen—rule out post-renal azotemia. high intake of protein (diet or gastrointestinal r r unkempt haircoat Uremic breath Uremic bleeding) or accelerated catabolism of r CBC/BIOCHEMISTRY/URINALYSIS stomatitis Scleral and conjunctival injection endogenous proteins. Glomerular filtration r CBC Relative hypothermia r rate may decline because of reduced renal Nonregenerative anemia (normocytic, perfusion (prerenal azotemia), acute or CAUSES normochromic)—often present with chronic r chronic kidney disease (renal azotemia), or Prerenal Azotemia renal failure. Hemoconcentration—often r urinary obstruction (post-renal azotemia). Reduced renal perfusion due to low blood present with prerenal azotemia; can also be r Reabsorption of urine into the systemic volume or low blood pressure. Accelerated seen with acute renal failure and post-renal circulation may result from leakage of urine production of nitrogenous waste products azotemia. from the excretory pathways (also a form of r because of enhanced catabolism of tissues in Biochemistry post-renal azotemia). Pathophysiology of association with infection, fever, trauma, r r Serial determinations of serum urea uremia—incompletely understood; may be corticosteroid excess, or burns. Increased nitrogen and creatinine concentrations may related to (1) metabolic and toxic systemic gastrointestinal digestion and absorption of help differentiate the cause of azotemia. effects of waste products retained because of protein sources (diet or gastrointestinal Appropriate therapy to restore renal perfusion renal excretory failure, (2) deranged renal hemorrhage). typically yields a dramatic reduction in regulation of fluids, electrolytes, and acid-base Renal Azotemia azotemia in patients with prerenal azotemia balance, and (3) impaired renal production r Acute or chronic kidney diseases (primary (typically within 24–48 hours). Correcting and degradation of hormones and other kidney disease affecting glomeruli, renal obstruction to urine flow or a rent in the substances (e.g., erythropoietin and tubules, renal interstitium, or renal excretory pathway typically is followed by a 1,25-dihydroxycholecalciferol). rapid reduction in the magnitude of azotemia. vasculature) that impair at least 75% of r SYSTEMS AFFECTED Concurrent hyperkalemia may be consistent r kidney function. Uremia affects virtually every body system. with post-renal azotemia, primary renal r Post-renal Azotemia r Cardiovascular—arterial hypertension, left Urinary obstruction; rupture of the azotemia due to oliguric renal failure, or ventricular hypertrophy, heart murmur, prerenal azotemia associated with excretory pathway. r cardiomegaly, cardiac rhythm disturbances. hypoadrenocorticism. Increased serum r RISK FACTORS Endocrine/Metabolic—renal secondary r albumin and globulin concentration suggest hyperparathyroidism, inadequate production Medical conditions—kidney disease, prerenal azotemia or a prerenal component. of 1,25-dihydroxycholecalciferol and hypoadrenocorticism, low cardiac output, Urinalysis hypotension, fever, sepsis, polyuria, liver r erythropoietin, hypergastrinemia, weight loss. A urine specific gravity value ≥ 1.030 in r disease, pyometra, hypoalbuminemia, Gastrointestinal—anorexia, nausea, dogs and ≥ 1.035 in cats supports a diagnosis dehydration, acidosis, exposure to vomiting, diarrhea, uremic stomatitis, of prerenal azotemia. Administration of fluid nephrotoxic chemicals, gastrointestinal xerostomia, uremic breath, constipation. therapy before urine collection may interfere r hemorrhage, urolithiasis, urethral plugs in Hemic/Lymph/Immune—anemia and with interpretation of low specific gravity r cats, urethral trauma, and neoplasia. r immunodeficiency. Neuromuscular— r values. Azotemic patients that have not been Advanced age may be a risk factor. dullness, drowsiness, lethargy, fatigue, r treated with fluids and have urine specific Drugs—potentially nephrotoxic drugs, irritability, tremors, gait imbalance, flaccid gravity < 1.030 in dogs and < 1.035 in cats nonsteroidal anti-inflammatory drugs, muscle weakness, myoclonus, behavioral typically have primary renal azotemia. A diuretics, antihypertensive medications; changes, dementia, isolated cranial nerve notable exception to this rule is dogs and cats failure to adjust dosage of drugs primarily deficits, seizures, stupor, coma, impaired with glomerular disease. Glomerulopathy is r eliminated by the kidneys to correspond with thermoregulation. Ophthalmic—scleral and r sometimes characterized by glomerulotubular conjunctival injection, retinopathy, decline in renal function. Toxins—ethylene r imbalance in which adequate urine- acute-onset blindness. Respiratory— glycol, grapes (dogs), lilies (cats). r concentrating ability may persist despite dyspnea. Skin/Exocrine— pallor, bruising, sufficient renal glomerular damage to cause increased shedding, unkempt appearance, loss primary renal azotemia; these patients are of normal sheen to coat. recognized by moderate to marked BLBS078-CF_A87 BLBS078-Tilley July 15, 2011 21:2

158 Blackwell’s Five-Minute Veterinary Consult

A Azotemia and Uremia (Continued)

proteinuria in the absence of hematuria and solute diuresis that follows correction of concentrations 24 hours after initiating fluid r r pyuria. Urine specific gravity is not useful in post-renal azotemia. Fluid therapy— administration; also urine production, body identifying post-renal azotemia. indicated for most azotemic patients; weight, and hydration status. OTHER LABORATORY TESTS preferred fluids include 0.9% saline or POSSIBLE COMPLICATIONS r Endogenous or exogenous creatinine, iohexol, lactated Ringer’s solution. Determine fluid Failure to correct prerenal azotemia caused or inulin clearance tests or other specific tests volume to administer on the basis of severity by renal hypoperfusion rapidly could result in r of glomerular filtration rate may be used to of dehydration or volume depletion. If no ischemic primary kidney disease. Primary confirm that azotemia is caused by reduced clinical dehydration is evident, cautiously renal azotemia can progress to uremia. r glomerular filtration rate. assume that the patient is less than 5% Failure to restore normal urine flow in dehydrated and administer a corresponding IMAGING patients with post-renal azotemia can result in r volume of fluid. Generally provide 50 to 75% Abdominal radiographs—used to determine progressive renal damage or death due to of volume replacement over 2–6 hours, except hyperkalemia and uremia. kidney size (small kidneys consistent with in patients with overt or suspected cardiac r chronic kidney disease; mild-to-moderate failure. Mannitol (0.5–1 g/kg IV q8h or enlargement of kidneys may be consistent 0.25–0.5 mg/kg/hr as CRI) may be used in with acute renal failure or urinary obstruction) polyuric patients to promote diuresis and MISCELLANEOUS and to rule out urinary obstruction (marked enhance elimination of nitrogenous waste. r dilation of the urinary bladder or mineral Treat patients in shock appropriately. ASSOCIATED CONDITIONS densities within the excretory pathway). r r Consider feeding diets formulated for An association may exist between Ultrasonography—may detect changes in kidney disease to reduce the magnitude of hypokalemia and azotemia in cats. echogenicity of the renal parenchyma and size azotemia, hyperphosphatemia, and acidosis. Preliminary findings suggest that and shape of kidneys that support a diagnosis hypokalemia may be associated with of primary renal azotemia; useful to rule out functional or structural renal changes leading post-renal azotemia characterized by to azotemia. distension of the excretory pathway and MEDICATIONS AGE-RELATED FACTORS uroliths or masses within or impinging on the DRUG(S) OF CHOICE Primary renal failure may occur in animals of excretory pathway and intra-abdominal fluid r accumulation (with rupture of the excretory Symptomatic therapy may be indicated for any age, but geriatric dogs and cats appear to r uremia in patients with kidney disease. be at substantially higher risk for both acute pathway). Excretory urography, r pyelography, or cystourethrography—may Famotidine (0.5–1.0 mg/kg PO, SC, IM, IV and chronic kidney disease. However, do not help establish the diagnosis of post-renal q12–24h) or other H2-receptor antagonists assume that azotemia in geriatric dogs and may be used to reduce gastric hyperacidity cats indicates primary kidney disease; these azotemia due to urinary obstruction or r rupture of the excretory pathway. and nausea. Antiemetics such as maropitant patients are also at higher risk for prerenal and × DIAGNOSTIC PROCEDURES (1 mg/kg q24h PO or SC 5 days). post-renal causes for azotemia. ZOONOTIC POTENTIAL Renal biopsy can be used to confirm the CONTRAINDICATIONS diagnosis of primary kidney disease, to Administration of nephrotoxic drugs Leptospirosis differentiate acute from chronic kidney PRECAUTIONS PREGNANCY/FERTILITY/BREEDING r r disease, and to attempt to establish the Use caution when administering drugs Data on azotemia and pregnancy in dogs underlying disease process responsible for requiring renal excretion. Consult appropriate and cats are very limited. Humans may primary kidney disease. references concerning dose-reduction tolerate minimal renal disease well during schedules or adjustments of maintenance pregnancy; however, ability to sustain a viable r pregnancy declines as renal function declines. intervals. Use caution in administering r fluids to patients that are oliguric or anuric. Pregnant azotemic animals—pharmacologic TREATMENT Monitor urine production rates and body agents excreted by non-renal pathways are r weight during fluid therapy to minimize the preferred. Prerenal azotemia caused by impaired renal r likelihood of inducing overhydration. Use SEE ALSO perfusion—correct the underlying cause of r caution in administering drugs that may Chapters on acute and chronic kidney renal hypoperfusion; aggressiveness of r treatment depends on the severity of the promote hypovolemia or hypotension (e.g., disease Urinary Tract Obstruction diuretics); carefully monitor the response to underlying condition and the probability that INTERNET RESOURCES persistent renal hypoperfusion will lead to such drugs by assessing hydration status, r International Renal Interest Society (IRIS): primary renal injury or failure. Primary peripheral perfusion, and blood pressure, with serial evaluation of renal function tests. www.iris-kidney.com. renal azotemia and associated uremia—(1) r specific therapy directed at halting or Corticosteroids may worsen azotemia by Suggested Reading reversing the primary disease process affecting increasing catabolism of endogenous proteins. Polzin D. Chronic kidney disease. In: Ettinger the kidneys, and (2) symptomatic, supportive, ALTERNATIVE DRUG(S) SJ, Feldman EC, eds., Textbook of and palliative therapies that ameliorate clinical Azodyl, a probiotic, may enhance Veterinary Internal Medicine, 7th ed. signs of uremia; minimize the clinical impact gastrointestinal excretion of nitrogenous Philadelphia: Saunders, 2010, of deficits and excesses in fluid, electrolyte, wastes, thereby reducing the magnitude of pp. 2036–2067. acid-base balances; minimize the effects of azotemia and possibly ameliorating some Ross L. Acute renal failure. In: Bonagura JD, inadequate renal biosynthesis of hormones uremic signs. Twedt DC, Kirk’s Veterinary Therapy XIV. and other substances, and maintain adequate Philadelphia: Saunders, 2009, pp. 879–882. r nutrition. Post-renal azotemia—eliminate Author David J. Polzin urinary obstruction or repair rents in the Consulting Editor Carl A. Osborne excretory pathway; supplemental fluid FOLLOW-UP administration is often required to prevent PATIENT MONITORING dehydration that may develop during the Serum urea nitrogen and creatinine