DOCSLIB.ORG

Review of Diuretic Use in AKI Julie Pfeifer, DVM Emergency And

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Review of Diuretic Use in AKI Julie Pfeifer, DVM Emergency And What to do When “Urine” Trouble: Review of Diuretic Use in AKI Julie Pfeifer, DVM Emergency and Critical Care Resident Department of Small Animal Clinical Sciences College of Veterinary Medicine Veterinary Medical Center Michigan State University East Lansing, MI 48824-1314 Introduction: Acute kidney injury (AKI) is a commonly encountered condition in both human and veterinary medicine. Homer W. Smith introduced the term “acute renal failure” in a textbook in 1951. Since that time there have been many definitions of acute renal failure, but currently the preferred nomenclature for this clinical syndrome is referred to an Acute Kidney Injury. In an attempt to create a universal and accurate definition of AKI classifications systems were created. Current human classifications/definitions of AKI include the RIFLE (Risk, Injury, Failure, Loss, and End Stage Renal Disease), and AKIN (Acute Kidney Injury Network). Veterinary medicine has also established classification systems including VAKI (Veterinary Acute Kidney Injury) and the IRIS (International Renal Interest Society) staging system of AKI. Pathophysiology: The pathophysiology of acute kidney injury is multifactorial, and greatly depends on the type of insult that has occurred. Acute ischemic kidney injury can be separated into four stages, initiation, extension, maintenance, and recovery. The Initiation stage is characterized by decreased renal blood flow resulting in cellular ATP depletion. Injury in this stage also leads to activation of the inflammatory cascade. Injury occurring at this stage is generally subclinical. The extension phase is characterized by two major events: continued hypoxia and inflammatory response. Cellular injury progresses to cell death, and clinical signs may manifest. During the maintenance phase GFR (glomerular filtration rate) remains low, and cell death and regeneration are occurring simultaneously. Blood flow returns toward normal and cells undergo migration, apoptosis, and proliferation. After several days the recovery phase begins and the epithelium is reestablished. Cellular function and GFR return toward normal. Treatment: The first goal of therapy is to treat the underlying cause. This often entails fluid therapy. The main goal of fluid therapy is to provide adequate replacement, maintain renal perfusion, all while avoiding fluid overload, and oliguria or anuria. This is most often accomplished with the use of isotonic crystalloids, and to much lesser extent colloids. Oliguria/anuria are associated with a higher morbidity and mortality as they can lead to fluid overload, electrolyte disturbances, and the need for renal replacement therapy. Unfortunately, renal replacement therapy is not commonly available in veterinary medicine, and is often financially burdensome. Diuretics are frequently used in the management of anuric/oliguric renal failure and their use has been reported in up to 60% of human cases. However, there is little clinical evidence to support their use. Many diuretics have been evaluated in both human and veterinary medicine including: furosemide, bumetanide, mannitol, diltiazem, dopamine, and fenoldopam. At this time there is limited clinical evidence in human or veterinary medicine to support their use in AKI. Current research: Methods: Medical records from Michigan State University’s Veterinary Medical Center were searched from January 2012 to December 2018 to identify dogs with AKI. Cases were included if they had a clinical diagnosis of AKI, and a urinary catheter placed during hospitalization with documentation of UOP. Exclusion criteria included lack of urinary catheter, incomplete medical records, or diagnosis of a urinary obstruction. Oliguria was defined as UOP between 0.51- 1.0ml/kg/hr, and anuria was defined as UOP of 0-0.5ml/kg/hr. Results: Four hundred and twenty-five dogs were diagnosed with AKI, and 110 met inclusion criteria (25.8%). Sixty-seven cases had documented oliguria (16/67) or anuria (52/67). Twenty-four dogs (21.8%) received furosemide alone, 3 (2.7%) received mannitol alone, 27 (24.5%) received both furosemide and mannitol, and 56 (50.9%) received no diuretics. UOP increased from anuria/oliguria to >1ml/kg/hr within 24 hours in 54.1% (13/24) of dogs receiving furosemide alone, 0 dogs receiving mannitol alone, 18.5% (5/27) of dogs receiving both diuretics, and 50% (8/16) of dogs receiving no diuretics. Median total dosage for furosemide was 1.0mg/kg (range 0.25mg/kg-5.0mg/kg), and 0.5g/kg (range 0.25g/kg-6.6g/kg) for mannitol administered as either a bolus dose or continuous rate infusion. The change in UOP (delta UOP) at 12h was significantly increased (0.52ml/kg/hr, [range 0.0 – 5.62]) in anuric/oliguric dogs receiving furosemide alone, compared with 0.0ml/kg/hr (range 0- 4.69) in dogs receiving no diuretics (p = 0.0062). No difference in delta UOP was identified between dogs that received both diuretics compared to dogs that received no diuretics. No difference could be determined for dogs receiving mannitol alone due to low number of patients. The overall mortality rate in the evaluated population was 57.2%, which increased to 71.6% in cases with documented oliguria (16/67) or anuria (52/67). Mortality rates in anuric/oliguric dogs that received furosemide alone, mannitol alone, both furosemide and mannitol, or no diuretics were 65.2%, 66.7%, 77.8%, and 81.3%, respectively. No correlation between delta UOP and survival to discharge could be determined. Conclusion: Oliguric and anuric renal failure carry significant mortality rates. Furosemide may increase UOP when administered to oliguric or anuric dogs, however the efficacy of diuretics and association with survival requires further evaluation and prospective studies. Drug Dose Mechanism of action Adverse effects Furosemide 0.25 – 1mg/kg IV Inhibits Na+/K+/2Cl pump Hypovolemia, aciduria, bolus on thick ascending loop of electrolyte losses henle 0.25-1mg/kg/hr CRI Bumetanide 0.01mg/kg IV dogs Inhibits Na+/K+/2Cl pump Hypovolemia, aciduria, (experimental) on thick ascending loop of electrolyte losses henle (transported differently into tubules) Mannitol 0.25 -0.5 g/kg IV over Osmotic diuretic Induces AKI at doses of > 20-30 min or 2-4g/kg/day, and contraindicated in fluid 1mg/kg/min CRI overloaded animals as a large volume is needed Diltiazem 0.1-0.5mg/kg IV bolus Calcium channel blocker Sinus bradycardia, followed by CRI of 1- (benzothiazepines) hyperkalemia, hypotension Reversal of renal 5 mcg/kg/min vasoconstriction Dopamine 0.5-3 mcg/kg/min Dopamine-1 (DA-1) renal Arrhythmias, GI upset afferent arteriole receptor agonist- vasodilation Fenoldopam 0.8mcg/kg/min dogs, Dopamine-1 (DA-1) renal Hypotension, reflex 0.5mcg/kg/min cats afferent arteriole receptor tachycardia, increased agonist- vasodilation intraocular pressure References: 1. Venkataraman R, Kellum JA. Prevention of acute renal failure. Chest. 2007;131:300–308. 2. Venkataraman R, Kellum JA. Acute renal failure in the critically ill. Current Opinion in Anaesthesiology. 2005;18(2):117–122. doi: 10.1097/01.aco.0000162828.51399.1b. 3. Kellum JA. Use of diuretics in the acute care setting. Kidney Int 1998;66:S67-70. 4. Kellum JA, Bellomo R. Ronco C. The concept of acute kidney injury and the RIFLE criteria. Contrib Nephrol 2007;156:10-6. 5. Kellum JA, M. Decker J. Use of dopamine in acute renal failure: A meta-analysis. Critical Care Medicine. 2001;29(8):1526-1531. 6. Kellum JA.The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence. Crit Care 1997;1:53-9. 7. Bagshaw SM, Bellomo R, Kellum JA. Oliguria, volume overload, and loop diuretics. Critical Care Medicine. 2008;36(4):S172-S178. doi: 10.1097/CCM.0b013e318168c92f. 8. Uchino S, Doig GS, Bellomo R, et al. Diuretics and mortality in acute renal failure*. Critical Care Medicine. 2004;32(8):1669-1677. doi: 10.1097/01.CCM.0000132892.51063.2F. 9. Shilliday I, Allison ME. Diuretics in acute renal failure. Ren Fail 1994;16:3-17. 10. Heyman SN, Brezis M, Greenfeld Z, Rosen S. Protective role of furosemide and saline in radiocontrast- induced acute renal failure in the rat. Am J Kidney Dis 1989;14:377-85. 11. Heyman S.N., Rosen S., Epstein F.H., Spokes K., and Brezis M.L.: Loop diuretics reduce hypoxic damage to proximal tubules of the isolated perfused rat kidney. Kidney Int 1994; 45: pp. 981-985 12. Nuutinen L.S., and Tuononen S.: The effect of furosemide on renal blood flow and renal tissue oxygen tension in dogs. Ann Chir Gynaecol 1976; 65: pp. 272-276 13. Englberger L, Suri RM, Li Z, et al. Clinical accuracy of RIFLE and Acute Kidney Injury Network (AKIN) criteria for acute kidney injury in patients undergoing cardiac surgery. Crit Care. 2011;15(1):R16. doi:10.1186/cc9960 14. Brezis M, Rosen S, Silva P, Epstein FH. Transport activity modifies thick ascending limb damage in the isolated perfused kidney. Kidney Int 1984;25:65-72. 15. Sward K, Valsson F, Sellgren J, Ricksten SE. Differential effects of human atrial natriuretic peptide and furosemide on glomerular filtration rate and renal oxygen consumption in humans. Intensive Care Med 2005;31:79-85. 16. Ludens JH, Hook JB, Brody MJ, Williamson HE. Enhancement of renal blood flow by furosemide. J Pharmacol Exp Ther 1968;163:456-60. 17. Brunton P, Lazo J, Parker K, editors. Goodman and Gillman’s. The Pharmacological Basis of Therapeutics. 11th ed. Milano: McGraw Hill Publishing; 2005. 18. Ponto LL, Schoenwald RD. Furosemide. A pharmacokinetic/pharmacodynamic review (Part II). Clin Pharmacokinet 1990; 18: 460–471. 19. Ponto LL, Schoenwald RD. Furosemide (frusemide). A pharmacokinetic/ pharmacodynamic review (Part I). Clin Pharmacokinet 1990; 18: 381–408. 20. Ludens JH, Hook JB, Brody MJ, et al. Enhancement of renal blood flow by furosemide. J Pharmacol Exp Ther 1968; 163: 456–460. 21. Mehta RL, Pascual MT, Soroko S, et al. Diuretics, mortality, and nonrecovery of renal function in acute renal failure.
Load more

Recommended publications
  • Point-Of-Care Ultrasound to Assess Anuria in Children
    CME REVIEW ARTICLE Point-of-Care Ultrasound to Assess Anuria in Children Matthew D. Steimle, DO, Jennifer Plumb, MD, MPH, and Howard M. Corneli, MD patients to stay abreast of the most current advances in medicine Abstract: Anuria in children may arise from a host of causes and is a fre- and provide the safest, most efficient, state-of-the-art care. Point- quent concern in the emergency department. This review focuses on differ- of-care US can help us meet this goal.” entiating common causes of obstructive and nonobstructive anuria and the role of point-of-care ultrasound in this evaluation. We discuss some indications and basic techniques for bedside ultrasound imaging of the CLINICAL CONSIDERATIONS urinary system. In some cases, as for example with obvious dehydration or known renal failure, anuria is not mysterious, and evaluation can Key Words: point-of-care ultrasound, anuria, imaging, evaluation, be directed without imaging. In many other cases, however, diagnosis point-of-care US can be a simple and helpful way to assess urine (Pediatr Emer Care 2016;32: 544–548) volume, differentiate urinary retention in the bladder from other causes, evaluate other pathology, and, detect obstructive causes. TARGET AUDIENCE When should point-of-care US be performed? Because this imag- ing is low-risk, and rapid, early use is encouraged in any case This article is intended for health care providers who see chil- where it might be helpful. Scanning the bladder first answers the dren and adolescents in acute care settings. Pediatric emergency key question of whether urine is present.
    [Show full text]
  • Hemorrhagic Anuria with Acute Kidney Injury After a Single Dose of Acetazolamide: a Case Study of a Rare Side Effect
    Open Access Case Report DOI: 10.7759/cureus.10107 Hemorrhagic Anuria With Acute Kidney Injury After a Single Dose of Acetazolamide: A Case Study of a Rare Side Effect Christy Lawson 1 , Leisa Morris 2 , Vera Wilson 3 , Bracken Burns Jr 4 1. Surgery, Quillen College of Medicine, East Tennesse State University, Johnson City, USA 2. Trauma, Ballad Health Trauma Services, Johnson City, USA 3. Pharmacy, Ballad Health Trauma Services, Johnson City, USA 4. Surgery, Quillen College of Medicine, East Tennessee State University, Johnson City, USA Corresponding author: Bracken Burns Jr, [email protected] Abstract Acetazolamide (ACZ) is a relatively commonly used medication in critical illness, glaucoma and altitude sickness. ACZ is sometimes used in the intensive care unit to assist with the treatment of metabolic alkalosis in ventilated patients. This is a case report of a patient who received two doses of ACZ, one week apart, for metabolic alkalosis and subsequently developed renal colic and dysuria that progressed to hemorrhagic anuria and acute kidney injury. This is an incredibly rare side effect of ACZ therapy, and has been reported in a few case reports in the literature, but usually is associated with a longer duration of therapy. This case resolved entirely within 24 hours with aggressive fluid therapy. Clinicians using ACZ therapy for any reason should be aware of this rare but significant side effect. Categories: Trauma Keywords: acetazolamide, hemorrhagic anuria, acute kidney injury Introduction Acetazolamide (ACZ) is a carbonic anhydrase inhibitor. It works to cause an accumulation of carbonic acid in the proximal kidney, preventing its breakdown, and causes lowering of blood pH and resorption of sodium, bicarbonate, and chloride with their subsequent excretion into the urine [1].
    [Show full text]
  • Current Current
    CP_0406_Cases.final 3/17/06 2:57 PM Page 67 Current p SYCHIATRY CASES THAT TEST YOUR SKILLS Chronic enuresis has destroyed 12-year-old Jimmy’s emotional and social functioning. The challenge: restore his self-esteem by finding out why can’t he stop wetting his bed. The boy who longed for a ‘dry spell’ Tanvir Singh, MD Kristi Williams, MD Fellow, child® Dowdenpsychiatry ResidencyHealth training Media director, psychiatry Medical University of Ohio, Toledo CopyrightFor personal use only HISTORY ‘I CAN’T FACE MYSELF’ during regular checkups and refer to a psychia- immy, age 12, is referred to us by his pediatri- trist only if the child has an emotional problem J cian, who is concerned about his “frequent secondary to enuresis or a comorbid psychiatric nighttime accidents.” His parents report that he wets disorder. his bed 5 to 6 times weekly and has never stayed con- Once identified, enuresis requires a thorough sistently dry for more than a few days. assessment—including its emotional conse- The accidents occur only at night, his parents quences, which for Jimmy are significant. In its say. Numerous interventions have failed, including practice parameter for treating enuresis, the restricting fluids after dinner and awakening the boy American Academy of Child and Adolescent overnight to make him go to the bathroom. Psychiatry (AACAP)1 suggests that you: Jimmy, a sixth-grader, wonders if he will ever Take an extensive developmental and family stop wetting his bed. He refuses to go to summer history. Find out if the child was toilet trained and camp or stay overnight at a friend’s house, fearful started walking, talking, or running at an appro- that other kids will make fun of him after an acci- priate age.
    [Show full text]
  • Topic Objectives Physical Examination
    LECTURE MODULE 3; PHYSICAL EXAMINATION OF URINE Topic Objectives 1. Identify the colors which commonly associated with abnormal urine. 2. State two possible causes for urine turbidity in a sample that is not fresh. 3. Identify possible causes for abnormal urinary foam. 4. Identify the odors commonly associated with abnormal urine. 5. Differentiate between the following abnormalities of urine volume: Polyuria Oliguria Anuria Nocturia 6. Define specific gravity of urine. 7. Define refractive index of a solution. 8. Identify possible causes of abnormal specific gravities of urine. 9. Compare and contrast Diabetes Mellitus with Diabetes Insipidus. Physical Examination Appearance Color Transparency Foam Odor Specific Gravity Volume 1 Color • When an examiner first receives a urine specimen, color is observed and recorded. • Normal urine usually ranges from a light yellow to a dark amber color. • The normal metabolic products which are excreted from the body contribute to this color. • Urochrome is the chief urinary pigment. • Urinary color may vary, depending on concentration, dietary pigments, drugs, metabolites, and the presence or absence of blood. • A pale color generally indicates dilute urine with low specific gravity. • Occasionally, a pale urine with high specific gravity is seen in a diabetic patient. Color In many diseases, urinary color may drastically change. In liver disease, bile pigments may produce a yellow-brown or greenish tinge in the urine. Pink, red, or brown urine usually indicates the presence of blood, but porphyrins may also cause a pink or red urine. Since drugs, dyes and certain foods may alter urine color, the patient’s drug list and diet intake should be checked.
    [Show full text]
  • Download PDF (Inglês)
    ORIGINAL ARTICLE Vol. 47 (1): 73-81, January - February, 2021 doi: 10.1590/S1677-5538.IBJU.2019.0448 A comparison of the effi cacy and tolerability of treating primary nocturnal enuresis with Solifenacin Plus Desmopressin, Tolterodine Plus Desmopressin, and Desmopressin alone: a randomized controlled clinical trial _______________________________________________ Parvin Mousavi Ghanavati 1, Dinyar Khazaeli 2, Mohammadreza Amjadzadeh 2 1 Golestan Hospital, Iran, Tehran, Republic of Islamic; 2 Ahvaz Jundishapur University, Ahvaz, Khuzestan, Iran, Tehran, Republic of Islamic ABSTRACT ARTICLE INFO Introduction: Nocturnal enuresis (enuresis) is one of the most common developmental Parvin Mousavi Ghanavati problems of childhood, which has often a familial basis, causes mental and psychological https://orcid.org/0000-0001-9255-6468 damage to the child and disrupts family solace. Objectives: In this study, we compared therapeutic effi cacy and tolerability of treating Keywords: primary nocturnal enuresis (PNE) with solifenacin plus desmopressin, tolterodine plus Nocturnal Enuresis; Solifenacin desmopressin, and desmopressin alone. Because we don’t have enough information Succinate; desmopressin, about this comparison especially about solifenacin plus desmopressin. valyl(4)-glutaminyl(5)- [Supplementary Concept] Patients and Methods: This clinical trial study was performed on 62 patients with enuresis aged 5-15 years who referred to the urology clinic of Imam Khomeini Int Braz J Urol. 2021; 47: 73-81 Hospital in Ahwaz in 2017-2018. Patients were randomly assigned to one of the three different therapeutic protocols and any participants were given a specifi c code. After that, we compared the therapeutic response and the level of satisfaction of each _____________________ therapeutic group in different months. Data were analyzed using SPSS 22 software Submitted for publication: and descriptive and analytical statistics.
    [Show full text]
  • Urinary System Diseases and Disorders
    URINARY SYSTEM DISEASES AND DISORDERS BERRYHILL & CASHION HS1 2017-2018 - CYSTITIS INFLAMMATION OF THE BLADDER CAUSE=PATHOGENS ENTERING THE URINARY MEATUS CYSTITIS • MORE COMMON IN FEMALES DUE TO SHORT URETHRA • SYMPTOMS=FREQUENT URINATION, HEMATURIA, LOWER BACK PAIN, BLADDER SPASM, FEVER • TREATMENT=ANTIBIOTICS, INCREASE FLUID INTAKE GLOMERULONEPHRITIS • AKA NEPHRITIS • INFLAMMATION OF THE GLOMERULUS • CAN BE ACUTE OR CHRONIC ACUTE GLOMERULONEPHRITIS • USUALLY FOLLOWS A STREPTOCOCCAL INFECTION LIKE STREP THROAT, SCARLET FEVER, RHEUMATIC FEVER • SYMPTOMS=CHILLS, FEVER, FATIGUE, EDEMA, OLIGURIA, HEMATURIA, ALBUMINURIA ACUTE GLOMERULONEPHRITIS • TREATMENT=REST, SALT RESTRICTION, MAINTAIN FLUID & ELECTROLYTE BALANCE, ANTIPYRETICS, DIURETICS, ANTIBIOTICS • WITH TREATMENT, KIDNEY FUNCTION IS USUALLY RESTORED, & PROGNOSIS IS GOOD CHRONIC GLOMERULONEPHRITIS • REPEATED CASES OF ACUTE NEPHRITIS CAN CAUSE CHRONIC NEPHRITIS • PROGRESSIVE, CAUSES SCARRING & SCLEROSING OF GLOMERULI • EARLY SYMPTOMS=HEMATURIA, ALBUMINURIA, HTN • WITH DISEASE PROGRESSION MORE GLOMERULI ARE DESTROYED CHRONIC GLOMERULONEPHRITIS • LATER SYMPTOMS=EDEMA, FATIGUE, ANEMIA, HTN, ANOREXIA, WEIGHT LOSS, CHF, PYURIA, RENAL FAILURE, DEATH • TREATMENT=LOW NA DIET, ANTIHYPERTENSIVE MEDS, MAINTAIN FLUIDS & ELECTROLYTES, HEMODIALYSIS, KIDNEY TRANSPLANT WHEN BOTH KIDNEYS ARE SEVERELY DAMAGED PYELONEPHRITIS • INFLAMMATION OF THE KIDNEY & RENAL PELVIS • CAUSE=PYOGENIC (PUS-FORMING) BACTERIA • SYMPTOMS=CHILLS, FEVER, BACK PAIN, FATIGUE, DYSURIA, HEMATURIA, PYURIA • TREATMENT=ANTIBIOTICS,
    [Show full text]
  • THE MODERN TREATMENT of ANURIA and OLIGURIA by DAVID K
    583 Postgrad Med J: first published as 10.1136/pgmj.34.397.583 on 1 November 1958. Downloaded from THE MODERN TREATMENT OF ANURIA AND OLIGURIA By DAVID K. BROOKS, M.B., B.S. Research Fellow Surgical Unit, St. Mary's Hospital, London, W.z2 There are few conditions which offer a greater operative procedures; bilateral renal calculi; challenge to the medical and nursing staff than carcinoma of the prostate and cervix; procidentia, that of acute renal failure. There are also few etc. conditions where the application of modern tech- (b) Dehydration and electrolyte depletion, e.g. niques and careful clinical biochemical assess- low salt syndrome. ment are more essential to the achievement of (c) Tubular necrosis such as follows: gross success. dehydration; prolonged hypertension; separation True or complete anuria rarely occurs except of placenta; abortion; crush syndrome; miss- where there is mechanical obstruction and, as matched blood transfusion; nephrotoxins, e.g. early recognition of oliguria is essential in acute mercuric chlorides, bismuth, sulphonamides. renal failure, it is important to define it in a (d) Acute nephritis. Protected by copyright. recognizable form. The history of a successfully treated case of The normal output of urine varies between one acute suppression of urine normally falls into four and two litres per day. On a mixed diet it is phases: obligatory to pass a minimum volume of approxi- (a) The precipitating condition or cause. mately 500 ml. in 24 hours (Gamble, I947). This (b) The anuric phase. entails good renal function and the ability to con- (c) The diuretic or pre-recovery phase.
    [Show full text]
  • Anuria Ascribed to Acute Tubular Necrosis in Infkncy and Early Childhood by I
    Arch Dis Child: first published as 10.1136/adc.31.160.512 on 1 December 1956. Downloaded from ANURIA ASCRIBED TO ACUTE TUBULAR NECROSIS IN INFKNCY AND EARLY CHILDHOOD BY I. J. C-ARRE and J. R. SQUIRE From the Children's Hospital, Birmingham, and the Department of Evperimnental Pathology. University of Birmingham (RECEIVED FOR PUBLICATION JUNE 29, 1956) The improved prognosis of acute renal failure has vomiting and dehydration. Varying proportions of the largely resulted from the use of conservative dietary following three solutions were given: normal saline, regimes of treatment as suggested by Borst (1948), 500 dextrose in 1/5 isotonic saline, and 500 dextrose Pratt (1948) and Bull, Joekes and Lowe (1949, 1950). solution. No urne was passed. Antibiotic therapy Few publications refer to children with acute tubular was confined to penicillin. Next day she appeared improved and the fever had necrosis treated in this manner. In 1948 Pratt subsided. Abdominal distension and absent bowel reported seven children with acute anuria of over sounds were noted. The blood pressure was 115 80 mm. '4 hours' duration treated conservatively with a Hg. Vomiting persisted and intravenous fluids were limited fluid and liberal glucose diet: five recovered. continued. By evening the sacral region and ankles Children with acute tubular necrosis successfully were slightly oedematous. No calculus or renal Protected by copyright. treated on similar lines have also been reported by calcification was demonstrated radiologically. One Riddell (1951, two patients), Kaplan and Fomon millilitre of urine was obtained on catheterization: this (1953, one patient) and Wagner (1954, one patient). contained numerous red and white blood cells but no Other recent reports of acute tubular necrosis in casts or crystals.
    [Show full text]
  • Voidingdysfunction Inside Pages
    Getting Ready For Certification: Voiding Dysfunction Jeffrey Guse 1. The definition of dysuria is: Dorland’s, 2007). Anuria, also called anuresis, is a. a lack of the ability to urinate. defined as the lack of urination or urine produc- b. failure of urinary excretion. tion of less than 100 ml per day (Dorland’s, 2007). c. accumulation of urine within the bladder. 2. C – Anuria, also called anuresis, is defined as the d. painful urination. lack of urination or urine production of less than 100 ml per day secondary to pre-renal, renal or 2. All of the following are true of anuria except: post-renal causes (Dorland’s, 2007; Tanagho & a. is often caused by renal failure. McAninch, 2008; Van Arsdalen, 2007, p. 41). b. may occur due to severe obstruction. Oliguria, a less extreme reduction in urine pro- c. defined as urinary output of less than 500 mL duction defined as urinary output of less than per day. 500 mL per day (Mosby's, 2009). d. may occur with end stage renal disease. 3. B – Polyuria is defined as an excessive produc- tion of urine or the excretion of an abnormally 3. All of the following are true of polyuria except: large quantity of urine on a daily basis (Mosby's, a. characterized by large volumes of urine. 2009; Van Arsdalen, 2007, p. 41). Polydipsia, b. always appears in conjunction with polydip- defined as excessive or abnormal thirst, can sia. appear in conjunction with polyuria, but not c. is physiologically normal in some circum- always. stances. 4. C – Inability to completely empty the bladder and d.
    [Show full text]
  • Post-Graduate Medical Journal Vol
    THE Postgrad Med J: first published as 10.1136/pgmj.2.21.129 on 1 June 1927. Downloaded from POST-GRADUATE MEDICAL JOURNAL VOL. II. JUNE, 1927. NO. 21. CONTENTS SUPPRESSION AND RETENTION OF URINE. REVIEWS. By R. H. JOCELYN SWAN, M.S., F.R.C.S. 129 PRACTICAL METHODS IN THE DIAGNOSIS AND TREAT- MENT OF VENEREAL DISEASES. H2EMOPTYSIS. By DAVID LEES, D.S.O., M.A., M.B., F.R.C.S. 144 By L. S. T. BURRELL, M.D., F.R.C.P. 133 CAVERNOUS SINUS THROMBOPHLEBITIS. WELLS P. M.D.. 144 FUNCTIONAL NERVOUS DISORDERS OF THE HEART. By EAGLETON, By R. TRAVERS SMITH, M.D., F.R.C.P. 136 EDITORIAL NOTES.-OFFICIAL INTIMATIONS . 142 FELLOWSHIP OF MEDICINE AND POST-GRADUATE THE CARE AND FEEDING OF THE PREMATURE INFANT. MEDICAL ASSOCIATION.-OFFICERS, 1927 . 5 By DONALD PATERSON, M.B., M.R.C.P. 139 SPECIAL COURSES . 5 care anuria remained complete for 17 days before SUPPRESSION AND death occurred without the onset of headache or vomiting until the twelfth day, and the mental RETENTION OF URINE.* condition remained clear almost until the end. BY Causes of Anuria. R. H. JOCELYN SWAN, M.S. Loxi., F.R.C.S., Anuria may occur from a variety of causes, which SURGEON TO THE CANCER HOSPITAL; CONSULTING SURGEON TO for convenience may be divided into (a) obstructive ST. PAUL'S HOSPITAL FOR GEN-TO-URINARY DISEASES. and (b) non-obstructive. In the former group obstruction may be due to calculous disease, to IT is necessary in the first place to define vesical growths involving both ureteric orifices, exactly what we mean when we speak of suppression to the spread of uterine carcinoma into the broad and of retention of urine-suppression or anuria ligaments causing pressure on the lower ends of are synonymous terms used when there is a failure, the ureters, or to large pelvic or abdominal tumours.
    [Show full text]
  • Renal and Urological Disorders Barbara Rideout, MSN, APRN-BC
    509 509 10 Renal and Urological Disorders Barbara Rideout, MSN, APRN-BC GENERAL APPROACH • Kidney pain is commonly located in the area of the costovertebral angle (CVA). Radiation to the umbilicus or the testicle or labia is possible. • Pain associated with infection is typically constant. • The normal urinary tract is sterile, and the immunocompetent patient is resistant to bacterial colonization. Urinary tract infection (UTI) is, however, the most common bacterial infection in all age groups. • Urinary tract infection is also the most common nosocomial infection. • UTI should be part of differential diagnoses in any febrile infant or child. • UTI is a marker in young children for abnormalities of the urinary tract. Imaging tests should be conducted in all boys of any age with first UTI, in girls younger than 5 years with first UTI, older girls with recurrent UTI, and any child with pyelonephritis to identify abnormalities that may lead to renal damage (e.g., vesicoureteral reflux [VUR]). • Limit antibiotics to category B if patient is pregnant or lactating; most antibiotics enter breast milk. • Refer unusual presentations of disease as well as those that do not respond to standard treatment. 510 510 496 FAMILY NURSE PRACTITIONER REVIEW anD RESOURCE ManUal Red Flags • Wilms’ tumor: Embryonal malignant tumor of the kidney in children <5 years can be asymptomatic and present with abdominal mass felt in flank over to midline. Consult with a physician for prompt work-up and appropriate referral. Do not be aggressive with abdominal exam in
    [Show full text]
  • CASE REPORTA Case of Reflex Anuria and Uremia Related to a Unilateral Ureteral Stone
    CASE REPORTA case of reflex anuria and uremia related to a unilateral ureteral stone Kayo HAYASHI, Satoshi HORIKOSHI, Kiyoshi HIRANO, Isao SHIRATO, and Yasuhiko TOMINO Division of Nephrology, Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan A 63-year-old man had anuria associated with a unilateral ureteral stone for 24 hours. Laboratory data indicated marked azotemia with the serum creatinine concentration of 7.2 mg/dL and urea nitrogen of 48 mg/dL. The radiological findings revealed contralateral hydronephrosis. Spontaneous discharge of the ureteral stone reversed the anuria and uremia. Both ureteral and vascular spasms were attributed to the anuria in this patient. Jpn J Nephrol 38:460-462, 1996 Key words: reflex anuria, unilateral ureteral stone, acute renal failure Case report tended with tenderness, but there was no rebound tenderness or palpable organomegaly. A 63-year-old man presented to his physician with Urethral catheterization produced no urine. The serum right flank pain and macroscopic hematuria over the creatinine concentration was 7.2 mg/dl, urea nitrogen preceding 2 days. He voided hematuria shortly after 48 mg/dl, serum sodium concentration 127 mEq/l, visiting the physician. Although 20 mg of scopolamine potassium 4.7 mEq/l, chloride 94 mEq/l, calcium and 250 mg of mefenamic acid were administered, he 4.3 mEq/l, phosphorus 5.0 mg/dl, and uric acid 12.8 mg/ noted increased right flank pain. An abdominal plain dl. The white blood cell count was 8.3 •~ 1031mm3 and film revealed a small calcified shadow in the right abdo hematocrit was 35.7%.
    [Show full text]