Urinary System Disorders PDF

Urinary System Disorders 28 CHA P TE R Dennis J. Chew...

Urinary System Disorders 28 CHA P TE R Dennis J. Chew a. Urine cannot be highly concentrated. USG GENERAL INFORMATION less than 1.030 in dogs and less than 1.040 I. Upper urinary tract: Renal parenchyma, renal pelves, in cats is expected at the same time as the and ureters. Lower urinary tract: Bladder and ure- azotemia thra. Useful for diagnosis, prognosis, and treatment b. Urine sediment may show casts, WBCs, and to decide how much of a urinary tract disease in- proteinuria volves the upper urinary tract, lower urinary tract, B. Magnitude of azotemia does not distinguish or both prerenal, primary renal, or postrenal causes. USG II. Upper urinary tract disorders: Chronic renal failure is the most important factor to evaluate. Imaging (CRF), acute renal failure (ARF), upper urinary tract is also usually necessary infection (UTI), renal neoplasia, renal pelvic or ure- II. Chronic renal failure (CRF) teral obstructions, and renal bleeding A. CRF occurs with permanent loss of at least 75% III. Lower urinary tract disorders: Bacterial UTIs, of functional nephron mass as a result of idiopathic cystitis of cats, urethral obstruction, chronic lesions (nephron dropout, fibrosis, tubu- urinary incontinence, and neoplasia of the bladder lointerstitial nephritis [TIN]). Increased serum and urethra phosphorus is observed after 85% of nephron IV. In general, animals are more likely to be sick from mass has become nonfunctional upper urinary tract disorders compared with those B. Cause is usually idiopathic. Probably due to of the lower urinary tract unassociated with urinary glomerular injury obstruction C. Any age, breed, or sexual status can be affected. Risk is low for younger animals and higher for older animals. Incidence increases in those UPPER URINARY TRACT DISORDERS older than 10 years I. Renal failure (general) D. CRF in young animals: Usually familial nephropa- A. Excretory renal failure exists when blood urea thy or renal injury from infection or toxins. Cats nitrogen (BUN) and serum creatinine are above rarely have familial nephropathy except for renal the upper normal range (azotemia). Decide amyloidosis in Abyssinians and Oriental short- whether azotemia is prerenal, primary renal, hairs or postrenal E. Causes of CRF: Dogs and cats 1. Prerenal azotemia occurs when perfusion is 1. Chronic TIN of unknown cause (most com- reduced and nitrogenous waste accumulates mon pathologic diagnosis) in blood 2. Chronic pyelonephritis (can be difficult to a. Causes include dehydration, shock, distinguish histologically from TIN) congestive heart failure (CHF) 3. Chronic glomerulonephritis (can be difficult b. Urine should be highly concentrated. to distinguish histologically from TIN) Urinary specific gravity (USG) is expected 4. Amyloidosis (familial in shar-pei dogs and to be greater than 1.030 in dogs and 1.040 Abyssinian cats) in cats 5. Polycystic kidney disease (familial in c. Urine sediment is normal; kidney size normal Persians) 2. Postrenal azotemia 6. Hypercalcemic nephropathy a. Causes are leakage of urine into retroperito- 7. Chronic obstructive uropathy neal or peritoneal cavities or from obstruc- (hydronephrosis) tion to outflow from both kidneys 8. Familial renal disease b. USG is variable. Urinary sediment may be 9. Progression after ARF active with red blood cells (RBCs) or white 10. Chronic toxicity (e.g., food-associated, drugs, blood cells (WBCs) environmental toxins) c. Imaging is necessary for diagnosis 11. Neoplasia (e.g., renal lymphoma) 3. Primary renal azotemia is due to renal paren- 12. Pyogranulomatous nephritis from feline chymal lesions, either acute or chronic infectious peritonitis (cats) 384  CHAPTER 28 Urinary System Disorders 385 13. Hypokalemic (kaliopenic) nephropathy (cats) I. Treatment 14. Chronic toxicity (e.g., food-associated, drugs, 1. Very little evidence exists to make decisions environmental toxins) about treatment of CKD cases that are not 15. Primary systemic hypertension yet azotemic. Nearly all of our data about F. Familial renal diseases of dogs and cats treatment come from dogs and cats that are 1. Amyloidosis: Abyssinian, Siamese, Oriental obviously azotemic shorthair cat, beagle, English foxhound, 2. Dietary therapy shar-pei a. Feed a renal diet; not been determined 2. Unilateral renal agenesis: Beagle whether this is helpful if not azotemic. 3. Glomerulopathy (basement membrane May increase survival and extend the time disorder): Beagle between uremic crises 4. Tubular dysfunction (Fanconi syndrome): b. The two major factors of benefit: Basenji Phosphorus restriction and omega-3 5. Tubular dysfunction (renal glucosuria): supplementation Norwegian elkhound c. Protein restriction as the sole change does 6. Periglomerular fibrosis: Norwegian elkhound not protect the kidney from progression or 7. Basement membrane disorder: Bull terrier, extend the life of the dog or cat with CRF; dalmatian, Doberman pinscher, English does not reduce the workload of the kidney. cocker spaniel, Samoyed, Texas NAV dogs, Dietary protein restriction with adequate rottweiler caloric intake reduces BUN, which may 8. Polycystic kidney disease: Bull terrier, Cairn parallel clinical signs of uremia in some terrier, West Highland white terrier, Persian patients cat d. Dietary phosphate restriction may be 9. Membranoproliferative glomerulonephritis: adequate treatment to control serum Bernese mountain dog, soft-coated Wheaten phosphorous and (PTH) concentrations Terrier, Brittany spaniel in those with early CRF 10. Renal dysplasia: Soft-coated wheaten terrier, 3. Intestinal phosphate binders Alaskan malamute, chow chow, golden re- a. Often needed to gain optimal control of triever, Lhasa apso, shih-tzu, miniature serum phosphorus and serum PTH. Goal: schnauzer, standard poodle To provide a compound that binds to 11. Multiple renal cystadenocarcinomas: German intestinal phosphate, prevents its absorp- shepherd dog tion, and increases its fecal excretion 12. Renal telangiectasia: Pembroke Welsh corgi b. Aluminum salts (hydroxide, carbonate): G. Diagnosis Mainstay treatment 1. Azotemia, submaximally concentrated urine; c. Calcium salts (carbonate, acetate): reduction in kidney size, irregular kidneys, Developed in human medicine to avoid nephrocalcinosis, nonregenerative anemia, toxicity from aluminum accumulation; chronic failure to thrive (loss of body condi- sometimes used tion, muscle mass, hair coat quality), anorexia, d. Newer-generation medications: Sevelamer vomiting, depression, weight loss HCl and lanthanum carbonate have not yet 2. Renal biopsy findings: Not specific achieved mainstream use 3. Renal biopsy: Not indicated in those with small e. Epakatin: Veterinary product marketed for kidneys use in cats with CRF. Decreases serum H. Progressive chronic kidney disease (CKD) phosphorus in normal cats. Reported to eventually results in CRF decrease digestibility of phosphorus in 1. CKD can be discovered before CRF in those in the diet which kidney size progressively decreases, f. Phosphate binders work best when given renal mineralization progressively increases, with food or within 1 to 2 hours of food urine concentration declines from maximal ingestions values, and proteinuria increases 4. Antacids 2. Once a certain nephron mass has been lost a. Gastric hyperacidity: Presumed to cont- from CKD, a progressive self-destructive ribute to gastric erosions, nausea, and cascade of events happens in the remaining vomiting during CRF. Increased circulating healthier kidney that eventually results in gastrin has been documented to occur further nephron damage (glomerulosclerosis in dogs and cats with CRF as a result and TIN) of decreased renal degradation of 3. Progressive self-propagating destruction of gastrin the chronically damaged kidney involves b. Histamine (H2) receptor blockade (e.g., glomerular hypertension and glomerular famotidine, ranitidine): Usually helpful hyperfiltration first-line treatments 4. Other mechanisms for progressive destruction: c. Proton pump blockade (omeprazole) pro- Renal mineralization and damage from uncon- vides an option either instead of or when H2 trolled renal secondary hyperparathyroidism blockade is not effective 386 SECTION II SMALL ANIMAL 5. Angiotensin-converting enzyme (ACE) inhibition b. BUN and serum creatinine decreased in a a. Proven beneficial in treatment of protein- study of a small number of cats receiving losing nephropathy; will likely achieve stan- this treatment; long-term effects on dard of care status for all progressive CKD progression of CRF have not been reported b. Renoprotective effects: Independent of ef- 10. Kremezin: Japanese product for treatment of fects to control systemic blood pressure; cats with CRF. Contains granules of activated lowers intraglomerular hypertension caused charcoal that provide nonselective adsorption by lowering the tone of the efferent glomer- of uremic toxins from the GI tract ular arteriole (analogous to afterload reduc- J. Prognosis tion for the heart). Also reduces angiotensin 1. Progression of CKD and CRF: Variable; slower II and aldosterone (which increase adverse in cats than in dogs. Many cats with CRF tissue healing in damaged kidneys) live for months to years. Dogs with CRF on c. Enalapril, benazepril, lisinopril, and imi- occasion live years, but up to a year is more dapril have similar effects. Enalapril and common with first-line treatments of diet benazepril are most commonly used 2. Serial analysis of serum creatinine, phospho- d. Excess lowering of efferent arteriolar tone rus, PTH, albumin, body weight, systemic results in emergence of azotemia or worsen- blood pressure, and patient history: Necessary ing of azotemia in those with CRF. Systemic to determine success of treatment and disease blood pressure and renal function testing progression should be performed before and periodi- III. Acute primary (intrinsic) renal failure (AIRF) cally following ACE inhibitor treatments A. AIRF: Syndrome when there has been loss of more 6. Calcitriol therapy than 75% of nephron mass, at least temporarily. a. Proven benefit for survival in dogs Differs from CRF; possibility for healing of lesions b. Main effect of calcitriol for patients with of AIRF with recovery of renal function in some CRF: Decreased synthesis of PTH through instances genomic effects in the parathyroid gland. 1. Increased serum phosphorus often occurs Excess PTH is toxic to a variety of tissues, early in the development of AIRF, unlike that of including the kidneys CRF, in which increases in PTH provide a pro- c. Calcitriol: Dosed to the effect on ionized tective lowering of serum phosphorus as neph- calcium and PTH status. Doses from 2.5 to ron mass gradually proceeds 3.5 ng/kg once daily are usually sufficient to 2. Progressive azotemia with or without oliguria lower PTH without increasing serum ionized develops as the result of some combination of calcium; can do intermittent dosing with vasoconstriction of the afferent arteriole, 9 ng/kg twice weekly (every 3.5 days) increased tubular pressure from intratubular d. Serum phosphorus should be controlled obtruction or extraluminal compression, tubu- to less than 6.0 mg/dL before calcitriol lar backleak, or failure to filter due to changes treatment can be safely started in the character of the glomerular filter 7. Control of systemic hypertension B. Renal lesions of AIRF a. Important to prevent end-organ damage 1. Classically acute tubular necrosis (ATN); (eyes, brain, kidney) spectrum of necrosis to subtle degeneration. b. Uncontrolled hypertension transmits exces- ATN is secondary to either ischemic or sive pressure to the glomerular capillary nephrotoxic causes beds. Increased pressure contributes to 2. Acute interstitial nephritis also can create glomerular hypertension and hyperfiltra- AIRF secondary to infectious causes (allergic tion, which further damages nephrons reaction rarely). Acute interstitial nephritis c. ACE inhibitor: Choice for dogs, although in dogs is classically associated with monotherapy at the usual dose is often not leptospirosis effective (0.5 to 1.0 mg/kg twice daily). In- C. Ischemic causes of ATN and AIRF creasing doses of ACE inhibitor or addition 1. Systemic hypotension is not necessary for the of amlodopine are provided to effect as development of tubular lesions. Renal blood monitored by serial measurement of blood supply determines if lesions develop pressure 2. Causes include dehydration, trauma, anesthe- d. Amlodopine: Drug of choice for control of sia, sepsis, heat stroke, pigment nephropathy systemic hypertension in cats. Most often, (hemolysis from immune-mediated hemolytic 0.625 mg/cat/day is safe and effective anemia, coral snake envenomation, bee sting, 8. Potassium salt treatment: Assess potassium myoglobinuria), ACE inhibitors, shock, hemor- status periodically (especially cats). Give po- rhage, surgery, burns, hypothermia, nonstero- tassium salts if there is persisting hypokalemia dal antiinflammatory drugs (NSAIDs), acute 9. Azodyl: Recently launched in the veterinary papillary necrosis (medullary renal amyloido- market sis, Fanconi syndrome) a. Probiotic (oral) given daily to maintain D. Nephrotoxins a population of colonic bacteria that 1. True nephrotoxin: Compound capable of creat- metabolize nitrogenous waste ing renal tubular cell membrane injury directly  CHAPTER 28 Urinary System Disorders 387 2. Nephrotoxicant: Describes acute renal injury or F. Treatment AIRF following the effects of a chemical com- 1. Most important aspect of treatment: Optimal pound, whether the injury is direct or indirect IV fluid therapy. With inadequate fluid therapy, from the agent. For example, NSAIDs are neph- the kidneys do not receive enough perfusion, rotoxicants and not nephrotoxins because they allowing the development of further lesions require systemic hypotension to create AIRF of ATN from ischemia. Excess fluid therapy re- 3. Nephrotoxic causes of ATN sults in development of overhydration, CHF, a. Ethylene glycol (EG) pulmonary edema, and death b. Antimicrobials: Aminoglycosides, a. Measurement of urine output is imperative amphotericin-B, sulfonamides adminis- during the first 24 to 48 hours tered to a dehydrated patient, Tetracy- b. Normal urine output is 0.5 to 1.0 mL/kg/h; if clines administered intravenously (IV), on IV fluids, 2.0 to 5.0 mL/kg/h is expected. Nafcillin administered intraoperatively Less than 2 mL/kg/h defines oliguria in c. Easter Lily ingestion (cats) patients on IV fluids d. Grape or raisin toxicity (dogs) 2. If oliguria or anuria persists after correction e. Hypercalcemia and hypercalciuria of dehydration, increase urine flow using some f. Cholecalciferol rodenticide (Quintox, combination of mannitol, furosemide, or Rampage) dopamine g. Calcipotriene (Dovonex) 3. If urine flow is not increased after diuretic h. Anticancer drugs: Cisplatin, high-dose doxo- treatments, stop diuretics and decrease IV rubicin (Adriamycin), radiocontrast agents fluids to avoid the development of overhydra- administered IV, heavy metals (e.g., zinc, tion and allow time for natural healing and arsenic, lead), hydrocarbons resolution of AIRF if possible i. Fluorinated inhalation anesthetics 4. Dialysis improves prognosis for survival and j. Calcium edetate renal recovery; early rather than late dialysis k. Mycotoxins (e.g., ochratoxin, citrinin) treatments are more effective in providing a E. AIRF: Three classic phases—latent or incipient beneficial outcome. Hemodialysis is available phase, maintenance, and recovery at a few regional centers in the United States; 1. Latent phase: Time from initial exposure to the peritoneal dialysis is more widely available and nephrotoxin or ischemic event until there is less expensive evidence for renal injury (cylindruria, renal G. Prognosis varies with the specific cause of the epithelial cyturia, renal tubular enzymuria, sub- AIRF. In general, the higher the level of the azote- maximal urine concentration, decreased glo- mia during the maintenance phase, the poorer merular filtration rate [GFR] before azotemia) the prognosis. Overall, leptospirosis has the best a. Animals in this phase are usually asymp- prognosis for survival and recovery of normal re- tomatic and will be discovered only if there nal function; EG cases with azotemia and oligo- is suspicion for the development of AIRF anuria have the worst prognosis. while in the hospital and being treated with H. EG intoxication drugs with known nephrotoxic potential 1. Occurs following ingestion of 4 to 13 mL/kg in b. Removal of the inciting cause stops further dogs and 1.5 mL/kg in cats; can be lethal. EG is renal injury transformed to cytotoxic metabolites in the 2. Maintenance phase: Develops after a critical liver by alcohol dehydrogenase. The half-life mass of lethal renal cell injury has occurred of EG is less than 12 hours in dogs and consid- a. Azotemia has developed by this time and erably shorter in cats does not immediately respond to correction 2. Diagnosis is based on observation of ingestion, of dehydration or volume expansion finding a source for possible ingestion, and b. Removal of the inciting phase does not acute onset of alcohol-like inebriation. Painful result in correction of azotemia kidneys and muscles may be detected on physi- c. This is a fixed phase of excretory renal cal examination. Finding some combination of failure that can last 1 to 3 weeks, or it may metabolic acidosis that may be severe, hyper- last forever (when no healing occurs) phosphatemia out of proportion to the azote- d. Some will be oliguric or anuric (e.g., EG mia observed, high anion gap, and very high intoxication); others may have polyuria osmole gap are highly supportive for the early (e.g., aminoglycoside intoxication) diagnosis of EG toxicity. A positive colorimetric 3. End of maintenance phase: When the patient reaction on the EG test kit (in-house method) dies or is euthanized, returns to normal renal provides convincing evidence for this diagno- function based on BUN and creatinine, or heals sis. Chromatographic techniques are available as a renal cripple with CRF of varying magnitude for definitive diagnosis using blood and urine a. Some patients return to a normal BUN samples, but it usually takes days to get results and creatinine. GFR may still be lower than 3. Polyuria and polydipsia can be intense shortly normal if measured after ingestion of EG and are often followed by b. Maximal ability to concentrate urine may or development of oliguria and then anuria that may not be restored persists despite all treatments 388 SECTION II SMALL ANIMAL 4. Azotemia may take greater than 24 hours to 6. Treatment develop from renal lesions; prerenal azotemia a. Penicillin: Drug of choice to eliminate may be apparent earlier (vomiting, obligatory leptospiral organisms from most of the polyuria from EG excretion) body; doxycycline is the treatment of 5. Treatment choice to rid dogs of the renal carrier state. a. In dogs, 4-methylpyrazole (4-MP) is the b. Supportive treatment with IV fluids for 1 to definitive antidote for treatment before EG 2 weeks in addition to penicillins. Short- has been completely metabolized. 4-MP an- term dialysis may be needed in those with tagonizes the activity of alcohol dehydroge- oligoanuria and high-level azotemia nase, which lessens biotransformation of EG 7. Prognosis is generally good for AIRF secondary to toxic metabolites. Effective after inges- to leptospiral infection when penicillins are tion of a lethal dose up to at least 5 hours in started early enough most dogs and up to 8 hours in many. After J. Parenteral antibiotics 8 hours following ingestion, most EG has 1. Occasionally cause AIRF from ATN. All IV been transformed to its toxic compounds antibiotics can at times cause AIRF, especially b. Cats require much higher doses of 4-MP when given rapidly at high doses. Aminoglyco- than dogs; sedation is a side effect at these side toxicity is most common; most reports are high doses from gentamicin in dogs or cats, but all c. Ethyl alcohol: Antidote of choice before aminoglycosides are nephrotoxic and capable 4-MP was developed in both dogs and cats; of inducing AIRF competes with EG for metabolism by alco- 2. Aminoglycoside nephrotoxicity has become hol dehydrogenase. Severe depression from less common because of the development of ethyl alcohol is a major side effect; it also the fluoroquinolones for treatment of serious adds to dehydration. Respiratory depres- bacterial infections sion can cause death 3. Aminoglycosides are prescribed in compli- d. Hemodialysis of dogs for 6 to 9 months has cated medical conditions, often those that are been effective for recovery of renal function life-threatening in some dogs that were anuric. Prognosis 4. Giving the total daily dose of aminoglycoside for survival in anuric patients without once daily rather than in divided doses reduces access to dialysis is near zero renal exposure to this nephrotoxin. This method I. Leptospirosis of dosing may contribute to the decreased inci- 1. Leptospirosis is a systemic disease of dogs dence of aminoglycoside nephrotoxicity that can cause AIRF from acute to subacute 5. A “cast watch” can be useful to detect renal interstitial nephritis. Infection usually follows damage before BUN and creatinine increase; mucosal penetration of organisms from drink- reduction in USG and increases in excretion ing water that has been contaminated with of urinary enzymes also precede increases in urine from infected carriers BUN and serum creatinine 2. Vaccination against serovars canicola and ic- K. Lily intoxication terohemorrhagiae has greatly lessened clinical 1. Creates a specific syndrome of AIRF in cats, disease with these serovars. Clinical syn- but not in dogs. Indoor cats are particularly dromes are usually due to “atypical” serovars, attracted to this plant in which vaccines have not been administered 2. All parts of the lily are toxic, and only a small to most dogs (pomona, grippotyphosa, part need be eaten for the nephrotoxic effects Bratislava in the United States) to be seen. Detection of plant pieces in vomitus 3. Encroachment of wildlife into suburban living or feces should increase the suspicion for lily spaces accounts for infections with atypical toxicity serovars; exposure to farm animals also 3. Severe azotemia and oligoanuria can be seen accounts for infection with some serovars in this form of AIRF. Despite massive azotemia, 4. Infections with serovars canicola and some cats have recovered with medical icterohemorrhagiae classically have changes treatment for several weeks in liver enzymes at the same time renal failure 4. There is no antidote; the specific toxin has yet is discovered. Atypical serovars do not to be isolated typically increase liver enzymes; if elevated, L. Raisin or grape ingestion liver enzymes may not be increased at 1. Cause AIRF in dogs with or without the same time as increased BUN or hypercalcemia; toxicity not reported in cats creatinine 2. Gastric decontamination is recommended, 5. Oliguria initially is prerenal as a result of sys- even for small amounts if there are GI signs temic effects of the infection; as renal lesions 3. Dehydration from GI signs is common: IV fluid accrue, oliguria from primary renal mecha- support may be needed for up to 1 week, longer nisms predominate. Urinary concentration is if already in renal failure. Prognosis is fair to initially high and becomes progressively less good when supportive treatment instituted early concentrated. USG is often in the isosthenuric 4. No antidote available; the toxic principle is not range when AIRF is diagnosed known  CHAPTER 28 Urinary System Disorders 389 M. NSAID ingestion 2. Ureteral urolithiasis is occasional, especially in 1. Overdose or accidental ingestion can create cats AIRF but only if vasoconstrictor signals have 3. Blood clots in ureter from a bleeding renal been activated by the body’s perception of lesion are uncommon volume contraction. Volume contraction from 4. Neoplasia of the renal pelvis can rarely create whatever cause increases release of norepi- urinary outflow obstruction nephrine and angiotensin II as well as activa- 5. Iatrogenic obstruction from a ligature around tion of the sympathetic nervous system to ureter is rare cause vasoconstriction, which increases core C. Acute obstruction of one kidney does not result blood pressure. This same vasoconstrictive in azotemia if the kidneys were healthy before the response happens in the kidneys, but this ef- obstructing process fect is normally blunted by the kidney’s syn- D. Acute obstruction of both kidneys does result thesis of vasodilatory prostaglandins. NSAIDs in azotemia if the obstruction is complete. block the ability of the kidney to protect it- Not compatible with life for more than 3 to self by producing vasodilatory prostaglan- 5 days dins; the net effect favors vasoconstriction E. Partial obstruction to one or both kidneys results that can be severe enough to create ATN and in hydroureter and hydronephrosis AIRF VI. Renal neoplasia 2. Ingestion of NSAIDs can create hypotension A. Primary tumors of the kidney are more common following GI bleeding from ulcers in some in- than metastases to kidneys. Malignant tumors are stances. Absorption of NSAID blocks synthe- far more common than benign ones sis of renal vasodilatory prostaglandins at 1. Adenocarcinoma of the renal tubule is the the time vasoconstrictor signals have been most common renal neoplasm in dogs activated 2. Renal lymphosarcoma (LSA) is most common 3. AIRF can be prevented following toxic NSAID in cat, usually bilateral ingestion by ensuring euvolemia until the 3. Transitional cell carcinoma can arise from the NSAID is cleared and renal effects abate. This renal pelvis and cause obstruction or renal usually means 2 to 3 days of IV fluids to ensure bleeding renal perfusion 4. Renal lymphoma is usually bilateral in cats N. Hypercalcemia and often the only organ identified with the 1. Hypercalcemia that is severe and rapid in tumor initially. Often lymphoma is in the GI development can create AIRF; usually occurs tract and bone marrow. Half of cats have following exposure to vitamin D or its been noted to be feline leukemia virus posi- metabolites tive. Can be in excretory renal failure, de- 2. Ingestion of rat-bait poison containing chole- pending on how much of both kidneys are calciferol or antipsoriasis creams containing infiltrated with neoplastic cells. Fine-needle the potent calcitriol analogue calcipotriene can aspirate and cytology of affected kidney(s) cause hypercalcemia is often diagnostic 3. Cholecalciferol toxicity can be confirmed 5. Bilateral renal cystadenoma occurs in by finding very high concentrations of German shepherds, usually in association 25-hydroxyvitamin D with generalized nodular dermatofibrosis 4. Calcipotriene toxicity is diagnosed on history; and uterine leiomyoma. It is an autosomal there is no vitamin D metabolite test available dominant trait. Prognosis is poor and death to test for its presence is usually due to renal failure or metastatic IV. Upper UTI disease A. Pyelonephritis occurs with the same bacterial 6. Other less common primary tumors organisms that create lower UTI (see section include adenoma, fibrosarcoma, and below). Escherichia coli is the most common and hemangiosarcoma important organism B. Painless hematuria is a common clinical sign B. Pyelonephritis is much more commonly a chronic C. Renal adenocarcinoma often presents with a rather than acute condition polar mass lesion detected on palpation or renal C. Fever, renal pain, leukocytosis, leukocyturia, posi- imaging. Polycythemia is sometimes detected tive urine culture, dilatation of the renal pelvis, or as a paraneoplastic syndrome. Metastases are diverticulae in some combination will support the common to the other kidney and to other sites. diagnosis May present for hematuria, discovered fortu- D. Infections without predisposing conditions of itously, or discovered during workup of metasta- anatomy, function, or metabolism are unusual ses to other sites. Not azotemic, as only one V. Obstructive nephropathy kidney is obviously involved at time of A. Refers to anatomic and functional effects on the diagnosis kidneys D. Nephrectomy is the treatment of choice for B. Causes unilateral renal neoplasia 1. Obstruction of ureter and kidney from lesion in E. LSA can respond favorably to standard chemo- bladder trigone is common therapy protocols 390 SECTION II SMALL ANIMAL exist in cystocentesis samples when growth LOWER URINARY TRACT is more than 1000 CFU, especially if antibac- DISORDERS (LUTD) terial medications have been given recently I. Bacterial UTIs b. Catheterized samples reveal more than A. Introduction 1000 CFU/mL in male dogs and cats in 1. Bacteria: E. coli accounts for more than half those with a true UTI. Contamination of UTIs in dogs and cats. Staphylococcus and with urethral and genital flora can be very Proteus spp. are common in dogs; Enterococci, high (i.e., more than 1,000,000 CFU) from Enterobacter, Klebsiella, and Pseudomonas spp. catheterized samples from female dogs, so are less common this method can be misleading and is not 2. Cats younger than 10 years of age rarely recommended develop UTI unless they have an underlying c. Voided samples are not recommended for urinary concentrating defect from renal or culture as these are often positive for bacte- endocrine disease, have undergone urethral rial growth and can reveal very large growth catheterization, or have a perineal urethros- of organisms in those that do not have a UTI tomy. Dogs can develop a UTI without underly- D. Treatment ing anatomic, functional, or metabolic risk 1. Urinary antibacterial treatment should be factors, depending on exposure to a virulent based on susceptibility testing results uropathogen 2. First-line choices for urinary antimicrobials: 3. Metabolic conditions predisposing for UTI: Amoxicillin, potentiated sulfa (trimethoprim or Diabetes mellitus, hyperthyroidism, ometoprim), and first-generation cephalosporins hyperadrenocorticism; exogenous steroids 3. For more resistant organisms: Fluoroquinolones and immunosuppressive medications also (enrofloxacin, marbofloxacin, difloxacin, create increased risk orbifloxacin) and clavulanate-potentiated 4. Anatomic defects should be excluded: Ectopic amoxicillins ureters, loss of urethral tone due to sphincter 4. For highly resistant organisms: Fluoroquino- mechanism incompetence, urachal diverticu- lones, ticarcillin, piperacillin, aminoglycosides, lum, urethral stricture, and excessive hooding imipenem, and meropenem of the vulva with overlying skin 5. Urinary antimicrobial treatment is usually pre- 5. Functional defects in the emptying capacity scribed for 2 to 3 weeks for uncomplicated UTI of the bladder should be excluded. Urinary 6. Treatment success: Based on sterile quantita- retention after voiding can make it impossible tive urine culture results 3 to 5 days after stop- to permanently sterilize the urine ping urinary antimicrobial treatment and again B. Clinical signs: Various combinations of urinating in 1 and 3 months. Do not rely on resolution of in unusual locations in the house, hematuria, clinical signs stranguria, pollakiuria, dysuria, excessive E. Recurrent UTI attention to the genitalia (licking); rarely 1. Recurrent UTI: Positive quantitative urine urinary incontinence unless due to urge culture following a course of treatment in a C. Diagnosis patient with or without clinical signs 1. Urinalysis usually suggests UTI when there is 2. Possibility for reinfection with a different pyuria and bacteriuria in urinary sediment. organism than originally isolated (old infection Hematuria and proteinuria are often present, was eradicated and a new one took place). but not specific for UTI. In the presence of Faulty host defenses against ascending bacte- urease bacterial UTI, persistent alkaline urine rial organisms account for multiple new infec- (pH 7) may be observed tions; routine short courses of antibacterials 2. Quantitative urine culture is the gold standard achieve sterile urine until the next infection to prove UTI exists. Large bacterial growth is ascends. Prophylactic treatment protocols expected from infected urine in dogs and cats. may be necessary Bacterial growth is reported as colony-forming 3. Infection may be from same organism as origi- units (CFU)/mL (how many organisms would nally isolated and was never eradicated; organ- have grown from 1 mL of urine, extrapolated ism is deeply seated in a location that is difficult from a 0.01 or 0.001 mL sample) for antibacterials to achieve eradication (polyps, a. Cystocentesis samples avoid genital and extensive bladder wall changes from chronic distal urethral contamination and are ideal cystitis, urachal diverticulum, pyelonephritis, for documentation of UTI. Urine from the prostatitis) or the organism is resistant to com- bladder should normally reveal no bacterial monly prescribed urinary antimicrobial drugs. growth, but sometimes a small number of Treatment for 6 to 8 weeks may be curative; a organisms do grow from skin contamina- different class of antimicrobial with greater tion; by convention, for a UTI to exist, more tissue penetration may be required than 1000 CFU/mL is required. Large quanti- II. Feline idiopathic cystitis (FIC): Nonobstructive tative growth more than 100,000 CFU/mL oc- A. Introduction curs in many dogs with UTI; most with UTI 1. Cats with signs of LUTD (hematuria, dysuria, have more than 10,000 CFU/mL. UTI can pollakiuria, stranguria) frequently do not have  CHAPTER 28 Urinary System Disorders 391 a readily identifiable cause. These clinical signs based on urinary tract imaging, quantitative traditionally were referred to as feline urologic urine culture is negative, and anatomic defects syndrome or feline lower urinary tract disease, are absent based on imaging studies but these terms have been abandoned in favor a. RBCs and protein in the urine are frequently of referring to the specific diagnosis such as positive; this can wax and wane so not al- idiopathic or urolithiasis ways present despite the presence of disease 2. Idiopathic cystitis: Most common condition b. A mild increase in WBC in the urinary sedi- associated with signs of irritative voiding in ment can be observed, but often the WBC cats, followed by struvite and calcium oxalate count is normal and is dwarfed by the num- urolithiasis, anatomic defects such as urethral bers of RBCs. Typical urinary sediment is stricture and urachal diverticulum referred to as hemorrhagic inflammation, em- 3. Bacterial UTI: Exceedingly uncommon as the phasizing the paucity of the WBC response cause for signs of LUTD in young cats that c. Sometimes transitional epithelial cells are have not had a perineal urethrostomy or seen in excess during FIC because of the undergone urethral catheterization exfoliation of cells from the bladder during 4. Bladder or urethral neoplasia: Much less the inflammatory response common in cats than dogs d. Urine should be concentrated to at least B. Risk factors USG of 1.035. Many cats with FIC have USG 1. Male and female cats at equal risk. Male cats in excess of 1.050 and some are above 1.070 with FIC can progress to urethral obstruction e. Bladder imaging with contrast cystography (urethral plugs or spasm) or ultrasonography can reveal focal or dif- 2. Risk factors include neutering (but not time fuse thickening of the bladder wall in of neutering), obesity, amount of dry food chronic cases. Normal bladder imaging does consumed, and time spent indoors. Highly not exclude the diagnosis of FIC sensitive cats are at more risk for FIC than f. Cystoscopy often reveals signs of cystitis less sensitive cats such as increased vascularity, vascular C. Physical examination: Thickened and or painful tortuousity, and edema of the bladder wall; bladder; bladder is small or normal size “glomerulations” (submucosal petecchia- D. Pathophysiology tion) may be visible 1. A highly permeable bladder with activation F. Treatment includes special attention to reduction of sensory nerve endings is important in of stress in the environment, dietary change, wa- initiation and maintenance of FIC; excessive ter dynamics, litter box hygiene, and pain relief stimulation of uroepithelial cells by 1. Antibiotics are useless in most cases because catecholamines may be important. Decreased this is not a bacterial disease glycosaminoglycan (GAG) excretion is part of 2. Glucocorticosteroids provide no known benefit FIC pathophysiology; decreased GAG excretion 3. NSAIDs have not been studied as to their utility could contribute to increased bladder 4. Analgesia is given for 3 to 5 days. Oral bu- permeability if there is a GAG layer on top prenorphine or butorphanol is usual first of the uroepithelial cells. Access of the choices. Opioids can be chosen for severe constituents of urine to the bladder wall pain following increased permeability activates the 5. Increasing water intake appears to be useful in sensory neurons to bombard the brainstem prevention of recurrences with pain signals a. This is most readily accomplished by the 2. Excessive activation of neuradrenergic outflow feeding of canned foods if the cat can be from the brainstem is central to the patho- successfully transitioned to these foods. physiology of FIC in cats; may be secondary to Adding water to both canned and dry food activation from pain sensation in the brainstem can be attempted. The goal is to decrease or from activation of the brainstem from the USG to less than 1.030 or at least less higher centers (as from stress recognized in than it was initially the cerebral cortex). Excess adrenergic outflow b. Fresh water can be used to increase water can upregulate the inflammatory response intake. Many cats will consume more water within the bladder. The process is called when water bowls are filled to the top sev- neurogenic inflammation eral times throughout the day. The use of E. Diagnosis distilled water has not been studied, but 1. More than 80% of cats with FIC resolve their some cats may drink more water if their clinical signs within 1 week of an acute usual source of water is heavy with chlorine episode; more than 50% of cats will have or minerals from the tap recurrence within 1 year. Outcome can be a c. The goal of diluting the USG is that more di- one-time episode, occasional acute episodes, lute urine may be less noxious when it gains multiple acute episodes, or chronic smoldering access to the bladder wall (see permeability episodes that never go completely away pathophysiology above). Presumably, a 2. Diagnosis is mostly one of exclusion. Diagnos- larger urine volume will result in more tic evaluation is negative for urinary stones frequent emptying of the bladder 392 SECTION II SMALL ANIMAL 6. There is no specific veterinary food that has precipitation of minerals to promote growth been developed to specifically manage FIC; of the urolith such products are usually marketed to in- C. Pathophysiology clude management of urinary stones that 1. Urethral obstruction occurs if stones are small have an inherently different pathophysiology. enough to move out of the bladder but too big Urinary acidification and magnesium restric- to move through the urethra tion have no useful role in the treatment 2. Calculi can cause irritation to the bladder of FIC mucosa, leading to inflammation and cystitis 7. Neither GAG replacement nor feline facial 3. Calculi can also serve as substrate for pheromones have been shown to be more bacteria, leading to difficulty resolving effective than placebo in treatment of FIC bacterial UTI in cats D. History and clinical signs 8. Tricyclic reuptake inhibitors such as amitrip- 1. Clinical signs: Hematuria, stranguria, dysuria, tyline and clomipramine: Useful in the man- and pollakiuria; signs are similar regardless agement of some cats with chronic FIC. Pro- of the type of urolith present. Some exhibit no zac (fluoxetine) has had a benefit for some clinical signs. Bacterial infections worsen the cats. Not used to manage acute FIC; reserved signs for those with multiple recurrences or those 2. Some uroliths may be passed in the urine. with smoldering FIC unresponsive to more If obstruction occurs, there will be difficulty conservative treatments. There are many voiding possible mechanisms for the benefits of E. Diagnosis these drugs including antiinflammatory and 1. Uroliths are considered in animals that have analgesic effects, and reduced activation of predisposing factors (e.g., systemic disease, the adrenergic nervous system that can history of stone formation) be helpful to reduce the inflammatory 2. Physical examination: Stones may be palpable response in the bladder or the urethra 9. Environmental modification or enrichment: 3. Urinalysis may reveal hematuria, bacteriuria, Single most powerful treatment for cats with and changes in pH typical of the type of stone FIC. Increasing the opportunities for explora- present tion and for excitement while living indoors 4. Crystalluria may be present without stones, can be pivotal in helping some cats. Environ- and stones may be present without crystallu- mental modification and enrichment include ria. Therefore, crystalluria is not helpful in the excellent litter box management (one litter box diagnosis of calculi for each cat plus one additional box, good 5. Urine culture is indicated to identify any UTI cleaning habits), provision of vertical climbing (primary or secondary) spaces, enhanced interaction with people, 6. Complete blood cell count (CBC)/biochemistry: good water management, increased access to Usually normal; hypercalcemia in 4% of dogs the outdoors and 35% of cats with calcium oxalate uroliths III. Urolithiasis (bladder calculi) 7. Radiographs: Radiopaque uroliths include A. Introduction. struvite, calcium oxalate, and calcium phos- 1. Definition: Uroliths or calculi are concretions phate. Stones must be 3 mm or greater in of minerals with a small portion of matrix diameter to be seen. Radiograph the entire proteins that form in the urinary tract. Uroliths urethra to look for calculi. Double-contrast form when urine is oversaturated with miner- radiography may be needed to demonstrate als in susceptible individuals. Supersaturation urate and cysteine uroliths, which are occurs when the concentration of calculogenic radiolucent minerals is increased 8. Ultrasonography is helpful in identifying 2. Location: Urinary bladder is the most common calculi in the bladder and proximal urethra site. Uroliths may be present without crystals, regardless of their radiodensity but cannot and crystals may be present without forming examine the distal urethra uroliths (Figure 28-1) 9. All retrieved uroliths should be submitted for B. Risk factors quantitative analysis 1. Urine pH and promoters or inhibitors of F. Differential diagnosis crystal formation: May affect the solubility 1. Any form of cystitis of the calculogenic minerals 2. Bladder neoplasia 2. Metabolic disease such as urate-containing G. Treatment (general) calculi in dalmatians and calcium-containing 1. Remove surgically if there is repeated urethral uroliths in animals with hypercalcemia obstruction or the owners do not wish to 3. Additional risk factors for urolith formation: attempt medical dissolution Breed, gender, age, and diet. Once initiation 2. If the urolith is smaller than the diameter of of urolith formation has occurred, the nidus the urethra, it may be retrieved using voiding must be retained within the urinary tract, urohydropropulsion or catheter-assisted and conditions must favor continued retrieval technique  CHAPTER 28 Urinary System Disorders 393 Leucine Tyrosine Cystine Amorphous urates Uric acid Dihydrate Monohydrate Sodium urate Calcium oxalate Dicalcium phosphate Triple phosphate Calcium carbonate Amorphous phosphate Ammonium biurate Figure 28-1 Casts commonly found in urine sediment smears. (From Cowell RL et al. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed. St Louis, 2007, Mosby.) 3. If using medical dissolution, continue therapy H. Prevention of uroliths (general) for 1 month after radiographic resolution of 1. Most uroliths can recur; therefore, preventive the uroliths. If there has been no improvement measures should be instituted after 4 to 6 weeks of therapy, surgery should 2. Increase water intake: Feed canned food or add be considered water to dry food. Provide additional water 4. After initial therapy, prevention and follow-up bowls, good water bowl hygiene, and different evaluations should occur sources of water 394 SECTION II SMALL ANIMAL I. Types of uroliths apso, Yorkshire terrier, miniature poodle, 1. Struvite uroliths Persian, Himalayan, ragdoll, British short- a. Struvite (triple phosphate) is the most com- hair, foreign shorthair, exotic shorthair, mon urolith in dogs Havana brown, and Scottish fold. Birman, b. In both dogs and cats, struvite uroliths are Abyssinian, and Siamese cats are at more likely to form in alkaline and infected decreased risk urine d. Treatment: Remove surgically or by c. A urine culture positive for urease- urohydropropulsion producing organism (usually Staphylococcus e. Recurrence is common. Evaluate for spp. or Proteus spp., occasionally Strepto- hypercalcemia, metabolic acidosis, coccus spp., Klebsiella spp., or Ureaplasma hyperadrenocorticism, or UTI. Avoid spp.) is necessary for infection-induced glucocorticoids; increase water intake. struvite uroliths to develop. In cats, 95% Avoid acidifying diets, diets restricted in of struvite uroliths are sterile phosphorus or magnesium; avoid vitamins d. Increased risk: Miniature schnauzer, shih- C and D and calcium supplements. Fasting tzu, bichon frise, Lhasa apso, miniature urine pH should be maintained between poodle, cocker spaniels (sterile type), 6.5 and 7.0 ragdoll, foreign shorthair, domestic short- 3. Ammonium urate uroliths hair, Oriental shorthair, Chartreux, and a. Cause: Increased urates in urine, usually Himalayan. Decreased risk: Rex, Burmese, from increased dietary intake of purines Abyssinian, Russian blue, Siamese, and (precursors of uric acid); more likely in Birman cats acidic urine. Occurs secondary to impaired e. Risk factors: Diets high in protein, magne- ability to convert uric acid to allantoin (espe- sium, and phosphorus, with increased cially in dalmatians, English Bulldogs); for- urine excretion of magnesium and mation is also associated with portosystemic phosphorous shunts or hepatic microvascular dysplasia f. Treatment b. Treatment with portosystemic shunt: Surgi- (1) Infection-induced: Use appropriate cal removal. Feed low protein, alkalinizing antimicrobial therapy based on culture diet if shunt is not correctable. Canned for- and sensitivity and a diet designed for mulations are more effective than dry struvite dissolution (protein and magne- c. Treatment for other causes: Feed low-protein sium restricted; acidic urine). Average diet without fish or glandular organs, main- time for dissolution of canine uroliths is tain urine pH at 7.0 to 7.5, increase water in- 12 weeks take; treat with allopurinol if diet alone is not (2) Sterile: Same as infection-induced stru- effective. Average dissolution time is 4 weeks, vite uroliths except that antimicrobial and medical dissolution is successful in therapy is not necessary. Average disso- about 50% of cases. Animals treated with lution time for dogs and cats is 4 to allopurinol are at increased risk of developing 6 weeks xanthine uroliths (Figure 28-2) g. Prevention of infection-induced uroliths: 4. Calcium phosphate uroliths Prevent recurrence of infection, treat causes a. Pure calcium phosphate (hydroxyapatite) of recurrent UTI (hyperadrenocorticism, uroliths occur infrequently in dogs and diabetes mellitus); correct structural cats. Calcium phosphate is more commonly abnormalities (perivulvar dermatitis, re- found as a component of other stones cessed vulva) that can predispose to (such as struvite uroliths) UTI, use low-dose antibiotic therapy as b. Increased risk: Miniature schnauzer, bichon prophylaxis if necessary. Increase water frise, shih-tzu and Yorkshire terrier intake; encourage frequent voiding c. Alkaline urine causes increased precipita- h. Prevention of sterile uroliths: Modify diet; tion; hyperparathyroidism is associated acidify diet, but avoid excess acidification with calcium phosphate urolithiasis of urine (pH less than 6.0). Magnesium d. Calcium phosphate uroliths should be restriction may be beneficial surgically removed 2. Calcium oxalate uroliths 5. Cystine uroliths a. Calcium oxalate crystalluria: More likely to a. Result of a congenital metabolic defect. occur in acidic urine because of systemic Stone formation is uncommon but is more acid-base effects and not the effects of urine common in acidic urine pH favoring precipitation b. Increased risk: Mastiff, Newfoundland, b. Risk factors: Hypercalcemia, administration English bulldog, dachshund, Tibetan of calciuretic substances (e.g., saline spaniel, basset hound, and Siamese cats. diuresis, furosemide, glucocorticoids), Males are more likely to develop cystine hyperadrenocorticism uroliths than females c. Increased risk: Male dogs; miniature c. Medical treatment includes increasing water schnauzer, shih-tzu, bichon frise, Lhasa intake, maintaining a urine pH of 7.0 to 7.5  CHAPTER 28 Urinary System Disorders 395 Purines Hypoxanthine Allopurinol Xanthine Xanthine oxidase Oxypurinol Uric acid Uricase Allantoin Inhibition Figure 28-2 Metabolic pathway of purine degradation to allantoin showing site of action of allopurinol. (From Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine, 6th ed. St Louis, 2005, Saunders.) with diet or potassium citrate, avoiding high- females. There is no reported feline protein diets, and using a thiol-containing predisposition drug such as n-(2-mercaptopropionyl)- d. Treatment: Surgery; no medical therapy glycine (2-MPG) or penicillamine. Regenera- IV. Urinary incontinence tive anemia, myopathy, and aggression have A. Introduction been noted with the use of 2-MPG. Time for 1. Urinary incontinence is defined as the stone dissolution is 4 to 12 weeks involuntary passage of urine; differentiate d. Any secondary UTI should be treated, and from polyuria and polydipsia and increased recurrence is common voiding from lower UTI 6. Xanthine uroliths 2. More common in dogs than cats. In cats, urge a. Primary xanthine urolithiasis: Uncommon; incontinence secondary to lower urinary tract due to an inborn error of metabolism inflammation is most common (xanthine oxidase deficiency) 3. Causes: Anatomic and functional defects of the b. Occur secondary to allopurinol administra- bladder and urethra; bladder pressure is greater tion, especially if on a high-purine diet than urethral pressure (low urethral tone is most c. Increased risk: Cavalier King Charles common). Differentials include the following: spaniels and dachshunds. More frequent a. Neurogenic: Lower or upper motor neuron in breeds most likely to be treated with disorders, an inability to voluntarily initiate allopurinol (dalmatians) a detrussor contraction, associated with d. Treatment: Low-purine diet; diets are low in urine retention in the bladder protein with mostly plant-based protein b. Anatomic: Ectopic ureter, patent urachus, sources vesicourethral fistula, urethral-vaginal 7. Silica uroliths fistula, urethral-rectal fistula, pelvic bladder a. Silica uroliths occur rarely in dogs and (some have no clinical signs) cats c. Functional: Urge, primary urethral sphincter b. Cause: Diets high in corn gluten or soybean mechanism incompetence, overactive hulls bladder (detrussor hyperreflexia), c. German Shepherd dogs and Old English detrussor-urethral-dyssynergia (DUD), sheepdogs have an increased incidence. paradoxical overflow (outflow obstruction), Males are affected more frequently than overflow associated with atonic bladder 396 SECTION II SMALL ANIMAL B. Primary sphincter mechanism incompetence drugs or estrogens, and some dogs with (PSMI) congenital urinary incontinence due to 1. PSMI (idiopathic incontinence, hormone- sphincter mechanism incompetence. responsive incontinence) is the most common Collagen is implanted in the submucosal and important acquired cause of incontinence layer of the proximal urethra; success rate in dogs 68%, lasting about 17 months 2. Cause e. Colposuspension is a surgical option. Ure- a. Typically in spayed female dogs; in thral pressure is increased as the uterine some breeds incontinence may precede remnant is stretched cranially and sutured ovariohysterectomy (OHE) to the prepubic tendon. This is an invasive b. Decreases in maximal urethral closure pres- procedure and has largely been replaced by sure and functional urethral length predict- urethral bulking procedures ably occur during the first 12 to 18 months C. Ureteral ectopia after spaying, with a deterioration of ure- 1. Introduction thral closure function; the decline continues a. Ectopic ureters (EUs) are the most common with age. About 20% develop PSMI a mean congenital cause for urinary incontinence of 2.9 years after OHE. Increased risk: Dogs in female dogs. Much higher incidence in weighing more than 20 kg (31%); boxers females. Males may not show signs of (Europe), Dobermans, and giant schnauzers incontinence (United States). Incontinence is about half b. Breeds: Most common in golden retrievers, as frequent in bitches that undergo OHE Labrador retrievers, Siberian husky, before their first heat, but episodes of in- soft-coated wheaten terrier, poodles, and continence are worse Newfoundlands 3. Diagnosis 2. Clinical signs a. Diagnosis is by exclusion in most cases a. The degree of urinary incontinence is variable b. Confirmation with urethral pressure studies: b. Dogs with EU typically demonstrate normal Low maximal urethral closure pressure and voiding behavior in addition to constant decreased functional profile length or intermittent leakage of urine; up to 40% c. Typical cases of PSMI have episodes of have intermittent incontinence incontinence while resting or recumbent, c. The history of urinary incontinence usually without signs of urgency at other times can be traced to the time of weaning and d. UTI is usually absent; some have ascending is often mistaken as a behavioral problem infection associated with housebreaking e. Should be able to concentrate urine d. Diagnosis of EU occurs most often by f. Urinary tract imaging: Usually normal; may 7 months of age, although many can be see pelvic positioning of bladder. diagnosed earlier 4. Treatment e. UTI is encountered with EU in about two a. Phenylpropanolamine (PPA): PPA orally two thirds of the cases to three times daily effectively controls in- f. Decreased urethral pressure is associated continence in about 74% to 92% of dogs by with EU in some dogs and may influence stimulating -adrenoreceptors in the ure- the prognosis for continence after surgical thra and increasing urethral tone. May lose correction effectiveness over time; side effects include g. Hydroureter occurs in some dogs with restlessness and mild behavioral changes intramural ectopic ureter (rare). Contraindicated in hypertension, 3. Diagnosis cardiac disease, or renal disease a. Intravenous pyelography (IVP) can confirm b. Estrogens: Increases the sensitivity of the presence of ectopic ureter and is -adrenoreceptors in the urethra and enhanced when performed using computed increases urethral tone; effective in 65% to tomography (CT) or fluoroscopy. IVP is 83%. Diethylstilbestrol is used at the lowest typically done in private practice dose that will maintain continence. Adverse b. Positive contrast vaginography or effect: Bone marrow toxicity but safe at low ultrasound can also be used doses. Do not use estradiol cypionate (ECP)! c. Urethrocystoscopy is the method of choice c. Treat with gonadotropin-releasing hormone to confirm EU analogues (leuprolide); results in complete d. Helical CT is superior to cystoscopy in males continence in more than half 4. Location of those that failed traditional medical a. Most have bilateral EU (more han 90%) therapy; most of the remaining dogs were b. Nearly half of the ectopic ureteral openings improved but not completely continent are found in the distal urethra, with other d. Urethral bulking agents: Periurethral openings in abnormal locations of the submucosal injections are administered trigone, vesicourethral junction, proximal through an operating cystoscope. Also used urethra, midurethra (rarely in the vesti- in dogs that cannot tolerate -adrenergic bule). Most are intramural  CHAPTER 28 Urinary System Disorders 397 5. Treatment B. Clinical signs a. Surgical correction is based on location of 1. Partial obstruction: Stranguria, pollakiuria, the ectopic ureter and associated pathology dysuria, hematuria, inappropriate urinations, b. Ureteral reimplantation: Reimplantation of and urine dribbling the distal segment of the ureter into the 2. Complete urethral obstruction: Frequent at- bladder may restore continence tempts to urinate with no production of urine. c. Neoureterostomy and urethral/trigonal A small amount of urine may pass as a result reconstruction: Intramural ectopic ureters of paradoxical incontinence. Uremia develops that attach to the bladder in a normal ana- within a few days tomic position and fail to terminate and 3. Functional urethral obstruction results in open into the bladder lumen at the tip of normal initiation of voiding, followed by a the trigone should be considered for decrease in urine flow with typical signs of neoureterostomy partial urinary obstruction d. Nephroureterectomy: Removal of a nonfunc- C. Physical examination tional or poorly functioning kidney and 1. The urinary bladder is distended, turgid, and associated ureter as a salvage procedure painful. By definition, there is urethral obstruc- (if contralateral kidney is normal). Severe tion if the bladder is full at a time of urinary dilation of the ureter and renal pelvis may urgency be an indication for removal 2. It is usually not possible to express the blad- e. Complications: Persistent urinary inconti- der; do not apply great pressure on an already nence in over half of patients after surgery. enlarged bladder -Adrenergic drugs (phenylpropanolamine, 3. Rectal palpation and inspection of the tip ephedrine sulfate) may help of the penis may disclose a cause for the D. Detrussor-urethral dyssynergia (DUD) obstruction 1. Urethra fails to relax while the detrussor is D. Diagnosis contracting; usually due to excessive smooth 1. Hyperkalemia, metabolic acidosis, and muscle tone but excessive somatic tone can azotemia; severity is dependent on duration also occur. Often idiopathic of obstruction 2. DUD occurs in large male dogs (weighing more 2. Urinalysis: Hematuria, proteinuria, pyuria, and than 25 kg); occurs in castrated and intact bacteriuria, depending on the underlying cause males of the obstruction 3. A urine stream is initiated but is small and 3. Electrocardiogram: Cardiac arrhythmias result- weak with premature termination; spasms may ing from hyperkalemia and metabolic acidosis be observed. Urine dribbling may occur; distin- 4. Radiography, contrast radiography (urethro- guish from partial obstruction gram, cystogram), or ultrasonography is 4. Treatment: Decrease sympathetic tone with useful to define the location and extent of -adrenergic blocking agents (phenoxybenza- the obstruction mine, prazosin, terazosin). A third of dogs E. Treatment respond with immediate and complete conti- 1. Place indwelling IV catheter for crisis manage- nence. Diazepam, antibiotics, and bethanecol ment may help. Skeletal muscle relaxation may be 2. Give potassium-free IV fluids (0.9% NaCl) to provided with diazepam or dantrolene correct dehydration and replace urinary losses E. Patent urachus during postobstructive diuresis 1. If the urachus fails to close by birth, urine 3. With cardiac arrhythmias, assume hyperkale- leaks from near the umbilicus mia and metabolic acidosis. Dilution with IV 2. Diagnosis: Physical examination, imaging fluids, IV dextrose (alone or in combination 3. Surgically remove; prognosis is excellent for with insulin), calcium salts, and sodium bicar- continence bonate infusions can be given V. Urethral obstruction 4. Decompress the bladder by cystocentesis be- A. Causes fore passing a urinary catheter. This takes pres- 1. Structural urethral obstruction is caused by sure off the bladder and allows renal function anything that physically blocks the urethral to resume. Give adequate pain relief, sedation, lumen or compresses the urethral lumen from and anesthesia to pass catheter without trauma outside the urethra. Examples include intralu- 5. May be able to pass a urinary catheter minal lesions (urethral calculi, neoplasia, mu- around a urethral stone; if so, drain bladder cous and crystal plugs, blood clots, strictures), and then use retropulsion to push stone back and, less commonly, compression from external into the bladder. May be able to use retropul- trauma to the pelvis area or lymphadenopathy sion even if urinary catheter will not pass 2. Functional urethral obstruction can be second- the stone ary to neurologic suprasacral spinal lesions, 6. Maintain an indwelling urinary catheter until termed reflex dyssynergia, may be idiopathic, azotemia and postobstructive diuresis or secondary to pain and inflammation in the have resolved and urethral swelling has area (swelling and compression) diminished 398 SECTION II SMALL ANIMAL 7. Urethrospasmomytic therapy with aceproma- b. Early on, BUN, creatinine, and phosphorus zine and analgesics (buprenorphine) may are normal, but they increase as uroabdomen facilitate a more patent urethra develops (postrenal azotemia). Azotemia 8. Cystotomy for removal of stones retropulsed develops by 24 hours postrupture; it may into the bladder occur sooner if there is shock or dehydration F. Postobstructive diuresis occurs following the (prerenal factors) relief of complete urethral obstruction c. BUN and potassium elevate earlier than do 1. The magnitude of urine output usually paral- phosphorus and creatinine lels the degree of azotemia and spontaneously d. Sodium and chlorine decrease, and decreases as the azotemia decreases potassium increases as urine in the 2. Monitor urine output; with large urine output, abdomen equilibrates with extracellular potassium supplementation to IV fluids is fluid needed to prevent hypokalemia 4. Survey abdominal radiographs in urinary tract VI. Uroabdomen rupture: “Ground-glass” appearance with loss A. Causes of abdominal detail 1. Urine can enter the peritoneal cavity from a. Use positive contrast cystography to tears in the bladder, urethra, or kidneys. Urine document urine leakage from the can enter the retroperitoneal space from the bladder kidney and ureter b. Rupture of upper urinary tract: Loss of 2. Bladder tears are most common, most retroperitoneal detail, failure to observe the following blunt trauma kidneys, and streaking of the retroperitoneal 3. Penetrating wounds occasionally are the cause space for urine leakage c. IVP is needed to document the site of urine 4. Tears can occur during overzealous expression leakage from the kidney or ureter of the bladder, passage of a urinary catheter, 5. Analysis of abdominal fluid: If urine, BUN, and cystocentesis, abdominocentesis, surgical injury, creatinine in the fluid should be higher than in breakdown of cystotomy closure, overdistension serum during contrast radiography and cystoscopy, E. Treatment and secondary to prolonged urethral obstruc- 1. If a bladder tear is small, place indwelling tion. Transient leakage of sterile urine into the urinary catheter for a few days. With larger abdomen following cystocentesis is usually tears, surgical closure is needed self-limiting and resolves quickly on its own 2. Rupture of the urethra usually requires B. Clinical signs primary surgical closure. Rupture of the 1. Hematuria, dysuria, and stranguria kidney often requires nephrectomy 2. There may be no urine output; in others, some 3. Ureteral rupture can sometimes be managed urine is voided and some accumulates in the by reimplantation of the ureter into the abdomen bladder; ureteral rupture can be surgically 3. Systemic signs progressively develop over closed, but stricture is common time 4. Short-term peritoneal dialysis or peritoneal 4. Progressive abdominal enlargement after drainage may be needed if urine flow cannot administration of IV fluids be established adequately with urethral C. Physical examination catheterization 1. Abdominal or inguinal bruising or a penetrating VII. Urinary bladder neoplasia wound may be observed A. Introduction 2. Pain during abdominal or rectal palpation 1. Most frequently identified urinary tract 3. The presence of pelvic fracture increases the tumor in dogs, accounting for 1% of all risk of bladder rupture canine neoplasms. They tend to occur in 4. The urinary bladder may not be palpable or older animals. Rare in cats small if there is a bladder tear 2. Transitional cell carcinoma (TCC) is most D. Diagnosis common in dogs. Lymphoma, fibroma, 1. If there is a urethral tear, it might not be possi- rhabdomyosarcoma, papilloma, squamous ble to pass a urinary catheter. With a bladder cell carcinoma, and adenocarcinoma tear, the catheter may retrieve urine or urine occasionally occur. Rhabdomyosarcomas plus fluid from the abdominal cavity are rare but are seen in dogs younger 2. Urinalysis results vary depending on the than 2 years of age duration of the tear. Early after a tear, urine is B. Transitional cell carcinoma (TCC) diluted in the peritoneal cavity. Urinalysis may 1. TCC is more frequent in female than male show hematuria, proteinuria, and pyuria from dogs; more common in male cats trauma or chemical peritonitis 2. Malignant and highly invasive by time of 3. Serum biochemistry diagnosis a. Creatine kinase, alanine aminotransferase, 3. Differential diagnoses: Cystitis (especially and aspartate aminotransferase may proliferative cystitis), tumors of vagina, increase from trauma prostate, or urethra  CHAPTER 28 Urinary System Disorders 399 4. Risk factors 3. Piroxicam (dosage for dogs is 0.3 mg/kg orally a. Breeds: Scottish terriers (nearly 18 times the every 48 hours; undetermined dosage for cats) risk compared with mongrel dogs), Shetland is recommended in all cases both for its sheepdogs, collies, airedales, and beagles. analgesic and anti-tumor properties. Side German shepherd dogs are at reduced risk effects include anorexia, vomiting, diarrhea, b. Exposure to herbicide lawn treatment or and GI ulceration cyclophosphamide, flea or tick dips, 4. Tube cystotomy can be performed if urinary overweight or obese, living near marshes obstruction is present sprayed for mosquito control 5. Treat secondary UTI, and monitor for c. Reduced risk if consuming green leafy development vegetables at least three times weekly G. Long-term prognosis is poor 5. Location: In dogs, about two thirds of TCCs VIII. Urethral diseases occur in the trigone; about 30% of males have A. Clinical signs: Lower urinary tract urgency from prostatic invasion. In cats, about 50% occur in inflammation and obstruction. Diagnosis by exam- the trigone. Masses can obstruct outflow into ination, urinalysis, imaging (urethrography). urethra or obstruct both ureters Ultrasound is not very useful except to evaluate C. Clinical signs prostate 1. Clinical signs: Hemorrhage, sterile cystitis, B. Congenital urethral disease secondary UTI, and outflow obstruction 1. Ectopic ureters terminating in the urethra is (hematuria, pollakiuria, stranguria, dysuria). most common Systemic signs (and azotemia) if there is total 2. Urethral hypospadia: Urethra opens on ventral obstruction. May see cancer cachexia, penis or prepuce; from incomplete fusion of lameness, or bone pain from paraneoplastic the urethral groove. Urinary scalding, recur- hypertrophic osteopathy or bone metastasis rent UTI, and pyoderma may result 2. Many dogs with TCC have secondary C. Urethral obstruction bacterial UTI 1. The most common urethral disorder 3. Large bladder tumors may be detected by 2. Urolithiasis is most common in dogs; urethral abdominal palpation. A rectal examination plugs and idiopathic causes are common in cats. can reveal extension of a bladder mass into Neoplasia of the urethra or prostate or extralu- the urethra. Bladder is large with urethral minal tumors or swelling can cause obstruction obstruction; kidney is enlarged if the ureter 3. Clinical signs include urinary urgency; sys- is obstructed temic signs if obstruction is long-standing D. Urinalysis D. Urethritis 1. Urine sediment: Hematuria, pyuria, neoplastic 1. Proliferative urethritis (formerly called granu- cells (often in clumps) lomatous urethritis) 2. Cystocentesis is not recommended (can seed a. Secondary to chronic UTI; possibly immune- the abdomen and skin with neoplastic cells). mediated. Occurs in middle-aged to older Use catheterization or a voided sample female dogs E. Diagnosis b. Urethra feels abnormally thickened on 1. Imaging: Enlarged kidneys or bladder with