Nonneurogenic Causes of Abnormal Micturition in the Dog and Cat

Nonneurogenic Causes of Abnormal Micturition in the Dog and Cat

Symposium on Neurology of Visceral Function Nonneurogenic Causes of Abnormal Micturition in the Dog and Cat Delmar R. Finco, D.V.M., Ph.D.,* Carl A. ...

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Symposium on Neurology of Visceral Function

Nonneurogenic Causes of Abnormal Micturition in the Dog and Cat Delmar R. Finco, D.V.M., Ph.D.,* Carl A. Osborne, D.V.M., Ph.D.,t and Robert E. Lewis, D.V.M., M.S.f_

The nervous system plays a vital role in normal micturition. It may be involved in abnormal micturition either because of a primary neurologic defect, or because of altered stimulus to a normal nervous system. This discussion is restricted to micturition abnormalities that are caused by primary defects in structures other than the nervous system. However, in some instances, insufficient knowledge exists to establish the role of the nervous system in micturition disorders of the dog and cat. Some disorders now believed to be neurogenic in origin may not be, and vice versa. This discussion will undoubtedly require alteration as more knowledge is acquired concerning micturition defects of the dog and cat. Y.. Signs commonly associated with abnormal micturition are: polyuria-frequent voiding of large quantities of urine, oliguria-infrequent voiding of small quantities of urine, anuria- absence of micturition, dysuria- frequent attempts to urinate associated with straining and pain, and urinary incontinence-involuntary passage of urine. When trying to establish the cause of abnormal micturition, it is of utmost importance that the patient be carefully evaluated so that erroneous conclusions are not made concerning the type of defect that is present. Casual attention to owners' complaints concerning their pets may lead to errors in interpretation, inasmuch as incontinence, polyuria, and dysuria may be confused with one another. If the history is questionable and the defect cannot be detected by physical examination, the *Professor, Department of Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens tAssociate Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul tProfessor and Head, Department of Anatomy and Radiology, College of Veterinary Medicine, University of Georgia, Athens Veterinary Clinics of North America- Vol. 4, No.3, August 1974

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patient should be hospitalized so that the act of micturition can be observed by the clinician. The anatomic site of the abnormality can sometimes be deduced from the type of abnormal micturition that is present. ~ is an abnormality that is related to renal or extrarenal disorders. It is never due to diseases of the bladder or urethra unless diseases of the lower tract cause secondary renal failure. Primary or secondary generalized renal dysfunction may result in polyuria when at least 2/3 of the nephrons of both kidneys are nonfunctional. Adrenocortical excess, diabetes mellitus, and diabetes insipidus are examples of extrarenal diseases causing polyuria. Polyuria may be physiologic if large quantities of water are consumed. Causes of anuria and oliguria are more difficult to localize anatomically since prerenal, renal, and postrenal diseases may cause these types of abnormal micturition. For example, physiologic oliguria may occur as a result of dehydration, inasmuch as renal tubular reabsorption of water is increased and small quantities of concentrated urine are produced. Severe dehydration, shock, or cardiovascular disease may cause prerenal oliguria or anuria as a result of impaired renal perfusion. Renal oliguria or anuria may be due to generalized renal disease. In the dog and cat, oliguria or anuria due to renal disease is uncommon, but may be observed with sudden, massive parenchymal destruction or as a terminal feature of polyuric renal failure. Postrenal oliguria or anuria is associated with obstruction, rupture, displacement, or neuromuscular dysfunction of the outflow tract. Anuria that follows neuromuscular dysfunction is usually transient since overflow incontinence develops as soon as the urinary bladder becomes markedly distended. Causes of obstructive anuria and oliguria include cellular debris and crystals, calculi, neoplastic and nonneoplastic masses, and trauma with soft tissue swelling. Urethral valves have been described as a cause of obstruction in man. Rupture of the bladder and proximal urethra may also result in anuria. Urination through a fustula may occur following distal urethral obstruction. In instances in which these signs are associated with cessation of or decrease in rate of deposition of urine in the bladder, stimulus for micturition is absent or delayed but micturition is normal when it occurs. In contrast, dysuria and incontinence may be associated with oliguria or anuria caused by impairment of urine outflow. Texts on nephrology and urology should be consulted for additional information on causes of anuria and oliguria. Whereas polyuria, oliguria, and anuria represent instances in which the act of micturition is normal but altered in frequency, dysuria and urinary incontinence represent signs that are frequently associated with abnormal micturition. Because of the scope of this discussion, attention will be focused on the latter causes of abnormal micturition.

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DYSURIA pATHOPHYSIOLOGY "'- Information concerning the pathophysiology of dysuria is sparse. Sensory fibers in the pelvic nerves apparently transmit impulses signaling the desire to void, sensations of pain, and impulses of proprioception. Pain reception appears to occur in instances of bladder distention or in instances of trauma to the mucosa of the bladder and urethra. In the latter instance, the desire to void exists even when bladder volume is nil. ~ Several diseases may result in dysuria in the dog and cat. Cystitis and bladder calculi may cause dysuria because of trauma to the epithelium. Dysuria associated with calculi may be caused primarily by concomitant ,infecti9B. Dysuria may be due to partial occlusion of the urethra caused by calculi, inflammation, or neoplastic tissue. In these instances, bladder distention or urethral distention is thought to initiate micturition which is painful and prolonged because of impingement on the outflow tract. INFECTION

Predisposing Factors

K In the normal dog, bladder urine is usually sterile, but organisms are detected in progressively greater numbers from the proximal to the distal urethra. Mechanisms that provide protection against ascent of infectious agents include the physical flushing of bacteria from the urinary tract by micturition, the protective effect of intact bladder epithelium, bacteriostatic or bacteriocidal components in urine, and immunologic mechanisms. ( Conversely, factors which predispose a dog or cat to urinary tract infection include retention of urine within the tract, damage to the epithelial barrier, glucosuria, and factors enhancing exposure of the urinary tract to pathogens (Fig. 1). In the human, females have a higher incidence of cystitis and urethritis than do males. This is apparently due to the shorter length of the urethra through which bacteria ascend to the bladder. Infectious Agents A variety of bacteria have been isolated from the urinary tract of the dog and cat. Generally, _gram-negative organisms as Escherichia coli, Proteus spp., and Pseudomonas spp. are most common, but gram-positive organisms as Streptococcus spp. and Staphylococcus spp. are not uncommon.

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Figure I . Intravenous urogram on a 5-month-old dog presenting with repeated episodes of cystitis. A, 15-minute, ventrodorsal radiograph. There is good visua lization of the right kidney but no ,·isualization o f the le ft kidney. R, Lateral a nd C, ventrodorsal radiographs made at 30 minutes. T here is a tortuous ureter on the left side of the urinary bladder. This animal had agenesis of the left kidney and the short, tortuous ureter on the left is a remnant of that developmental abnormality. The blind ureter held residua l urine predisposing to cystitis. Surgical re moval resulted in relief of the problem.

Dysuria and he maturia occurs in cats in which bacteria h ave n ot been isola ted from the urine. Evidence suggests that viral infection may be involved in the etiology of the cystitis, urethritis, urethral obstruction complex of the cat. Mycotic agents and Candida albicans may occasion ally be isolated from urine. However , these agents ar e uncommonly isolated compared to bacter ia. A bladder nematode, Capillaria plica, may be detected by finding characteristic bioperculate ova in the urine. The parasite rarely causes clinical signs. Clinical Signs. Dysuria is a common sign of ure thral or bladder in-

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fection or both. Hematuria may or may not be present. When present, blood is more frequently voided at the end of urination. The patient is usually alert, active, and does not have anorexia or fever unless the infection is not confined to the lower urinary tract. The urinary bladder may feel normal or thickened and it is usually empty. The patient may exhibit discomfort when the bladder is palpated, and occasionally palpation induces contraction of the detrusor (bladder) muscle. Diagnosis. The history is indicative of induction of the micturition reflex without bladder distention as the stimulus. Careful physical examination should be performed to rule out other causes of dysuria (calculi, bladder masses). Urinalyses should be evaluated, particularly in cases that do not respond to antibacterial therapy. Urinalysis reveals signs of inflammation and or hemorrhage in the urinary tract. Proteinuria is present ~ecause of the inflammatory process and because capillary rupture liberates not only red blood cells but also plasma protein into the urine. It is usually not possible to localize the site of infection in the genitourinary tract solely on the basis of urinalysis, since the same abnormalities (WBC, RBC, protein) are present regardless of the site. Involvement of the genital tract may be ruled out by careful collection of midstream urine or by obtaining urine by catheterization or cystocentesis. The presence of large numbers of casts are indicative of renal involvement but their absence does not eliminate the kidney as the source of the inflammatory process. Visualization of bacteria by microscopic examination of urinary sediment usually suggests that sufficient numbers are present to cause infection. If nonsterile containers are used or if urine is allowed to stand for several hours prior to analysis, significant numbers of bacteria may occur as a result of contamination of the sample. Bacterial culture and antibiotic sensitivity testing aid in diagnosis and therapy. When organisms are not isolated from urine with the use of conventional media, all but unusual bacterial pathogens of urine may be eliminated as the cause of disease. Positive urine cultures are more difficult to interpret, because of the potential for contamination of urine with organisms that are invariably present in the urethra and genital tract. Quantitative urine culture has been used to aid in interpreting the significance of bacterial growth on the assumption that high bacterial counts indicate infection and low bacteria counts represent contamination. One study in dogs suggested that a bacterial count greater than 104 organisms per ml in a carefully collected early morning sample obtained by catheterization was significant. Commercial kits* are available for estimating numbers of organisms without elaborate laboratory techmques. In chronic cases of urinary tract infection, identification of the organism is helpful inasmuch as isolation of the same organism in serial cui*Culturia Clinical Convenience Products, Inc., P.O. Box 1493, Madison, Wisconsin.

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tures suggests failure to eradicate the organism. Isolation of different microorganisms suggests eradication with subsequent reinfection. Sensitivity testing is used to guide in formulating therapy. However, apparent in vivo sensitivity as evaluated by clinical signs and in vitro sensitivity as determined by laboratory procedures are not invariably in agreement. Treatment. Antibiotics, sulfonamides, and nitrofurantoin compounds provide the best solution for dysuria due to bacterial infection. Methenamine, a urinary antiseptic, has antibacterial properties only when urine pH is below 5.5. l.lrinary acidifiers are inferior tp other products and should be used as an adjuvant to therapy if at all&"eomycin, streptomycin, gentamicin, kanamycin, erythromycin, and chloramphenicol have optimal activity in alkaline urine. Penicillin, nitro(ilrantoin, and methenamine have optimal activity in acid urineJ For tetracycline and sulfonamjdes urine pH is not a significant factor in activity. The useof~nary acidifiers to alter urine pH to an optimum value for the antibiotic being used is more rational than their use for bacteriostatic or bacteriocidal activity, since acidifiers are weak in antibacterial effect. Dysuria in the cat presumed to be of viral etiology is not responsive to antibacterial therapy, although antibacterial drugs may be used to prevent or treat secondary bacterial infection. Parasympatholytic drugs may be utilized to decrease detrusor spasm but results have not been consistently good. Dysuria due to acute bacterial cystitis should be treated for a minimum of 10 d~s. Chronic cystitis may require weeks to months of ~i-ttibacterial therapy for eradication of the organism. If factors predisposing to bacterial cystitis cannot be removed, reinfection may occur following eradication of bacteria. In these cases, lifelong therapy may be required. UROLITHIASIS

Etiology The etiology of urolithiasis is obscure. Several predisposing factors have been identified and have a direct relationship to the mineral composition of calculi. Triple phosphate uroliths are commonly associated with infection. ~ystine uroliths are observed in dogs with an impaired renal tubular absorption of cystine. This abnormality (cystinuria) is apparently inherited in 16 breeds of dogs and mongrels but rarely occurs in female dogs. lJrate uroliths occur in dogs that excrete large quantities of urates rather than exclusively allantoin as an endproduct of purine metabolism. The Dalmatian is most commonly affected with urate uroliths, but other breeds may also be affected. q_xalate stones have been reported in the dog but predisposing factors have not been identified.

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Clinical Signs

Clinical signs associated with uroliths are dependent on th e anatomic site of the urolith. Cystoliths may cause signs identical to those described for bacterial cystitis. In some insta n ces, signs may be due to bacterial cystitis associated with cystoliths since treatment with an tibiotics may result in transient remission of signs. U rinary incontinence may occasionally be observed in female dogs with cystoliths. Urethral calculi may cause d ysuria or incontine nce if obstruction is nearly complete (see Urinary Incontinence). Renoliths do not cause signs of abnormal micturition unless bilateral renal disease results in p olyuria or oliguria. Diagnosis. Cystoliths can frequentl y be detected by abdominal palpation. Radiography is usually confirmatory if abdominal palpation is not diagnostic (Figs. 2 and 3). Visualization of small cystoliths or those with less radiodensity m ay be enhanced by pneumocystography or double contrast r adiography. Urethral obstruction is presumptive evidence but not confirmatory for urethral calculi. Treatment. Surgical r e moval of u roliths is indicated unless diseases of other body systems are sufficientlY severe to contraindicate general anesthesia. Prior to treatment, radiographs should be made to determine if uroliths are present in multiple locations in the urinary tract. Surgical removal of cystoliths should be followed by postoperative treatm ent of the patient to prevent recu rrence of stones. Recurrence occu rs in 11 to 20 per cent of dogs. Postoperative prophylactic therapy is guided by a knowledge of the predominant mineral component of the urolith. Commercial kits* are *Oxford Stone Analysis Kit, Oxford Co., San Mateo, California.

Figure 2. Lateral radiograph of p repuce ma de by pulling the prepuce away from the body wall and the rear legs caudally. T here are multiple calculi in th e ureth ra of the caudal o s penis.

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Figure 3. 11, Lateral and B, ventrodorsal pneumocystogram of a female dog with dysuria a nd he m aturia. On latera l view a calculus a ppears to be within the urinary bladder, but the ventrodorsal view shows the d ense mass to be outside of the urinary bladder. This emphasizes the importance of two views to substa ntiate the location of lesions by radiograph y.

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available for qualitative chemical analysis of calculi. The central portion of the calculus should be used for analysis since peripheral portions may contain minerals not related to the etiology of the calculus. The following guidelines are used to prevent calculi: 1. Regardless of chemical composition, induce polyuria by oral administration of sodium chloride. This reduces the concentration of solute and decreases the chance of precipitation of salts. Depending on body size, a dose of 0.5 to 10 gm of salt is administered daily in order to double urine volume or keep urine specific gravity below 1.025. 2. Phosphate uroliths a. Eradicate bacterial infection. This entails treatment as for chronic cystitis- at least 1 month of suitable antibacterial therapy with antibiotics or sulfonamides. Subsequently, urine is cultured and urinalysis is performed to determine if infection has been eradicated. The most common cause of recurrence of phosphate uroliths is inadequate followup to determine if infection has been eradicated. b. Maintain a urine pH below 6.5. This generally occurs spontaneously if infection is eradicated, unless the dog is fed a diet high in cereal content. 3. Urate uroliths ,~ bttf,wl f,o·il a. Administer sodium bicarbonate in sufficient quantity to keep urine pH above 6.5. Generally, 0.25 to 1.0 gm daily is sufficient but urine pH should be monitored by the owner to assure correct dosage. b. Feed a diet low in purines. Avoid glandular organs as sources of protein. c. Administer allopurinolt to decrease the quantity of purine excreted as urates. Initially 30 mg per kg is given in 3 divided doses daily. After 1 month the dosage may be decreased to 10 mg per kg per day. This drug appears to be quite valuable in prophylaxis of urate uroliths when utilized with sodium chloride and sodium bicarbonate. d. Therapy should be continued for the life of the patient since the metabolic trait cannot be permanently altered. 4. Cystine uroliths a. Administer sodium bicarbonate to keep the urine alkaline. Unfortunately, urine pH must be maintained above 7.5 to increase solubility of cystine. This may be difficult to achieve; urine pH should be monitored by the owner and the dose adjusted accordingly. Urinary acidification is of no value in cystine calculi. Methionine is contraindicated because it increases cystine excretion. b. Consider the use of D-penicillamine.:j: This compound facilitates excretion of cystine as a soluble D-penicillamine-cysteine complex. Unfortunately, the drug is expensive and vomiting may occur with its use. A dose of 10 mg per kg is administered in 2 divided daily doses with food. c. Feed a diet in sulfur-containing amino acids. Generally, animal proteins are high in sulfur-containing amino acids and vegetable proteins are low in these amino acids. d. Therapy should be continued for the life of the patient inasmuch as the basic defect is irreversible. tZyloprim, Burroughs Wellcome Co., Research Triangle Park, North Carolina. :j:Cuprimine, Merck, Sharp and Dohme, West Point, Pa.

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5. Oxalate uroliths a. At present, no specific measures are known to be beneficial in prophylaxis of oxalate calculi in the dog. b. In man, oxalate calculi comprise the majority of stones. Many prophylactic procedures have been used, but no unanimity of opinion exists on the value of the various procedures. c. Diuresis should be maintained with sodium chloride.

Methylene blue has been used to prevent urolith formation and to dissolve existing uroliths in man. It has appeared to be effective in some instances in both phosphate and nonphosphate uroliths. Unfortunately, methylene blue causes hemolytic anemia in both the dog and cat. Although the dog may be less sensitive to methylene blue than the cat, toxicity data are not presently available. Until such data are available, methylene blue should not be used for calculi prophylaxis in the dog or cat.

SOFT TISSUE BLADDER MASSES

Etiology On clinical examination, mild, diffuse increase in thickness of the bladder wall is usually interpreted as inflammation or muscle hypertrophy until proved otherwise. Severe diffuse thickening of the bladder wall or discrete masses well delineated from surrounding bladder tissue are likely to increase the clinician's suspicion of a neoplasm. However, available data suggest that both neoplastic and nonneoplastic masses may be diffuse or discrete. Therefore, other criteria should be used to differentiate these general classes of disease. An outline for a clinical approach to diagnosis of bladder masses is subsequently discussed. Primary malignant neoplasms are relatively uncommon in the dog and rare in the cat. Carcinomas and, occasionally, sarcomas occur. Malignant metastatic neoplasms are very uncommon. Benign neoplasms of the bladder occur with less frequency than malignant neoplasms. Papillomas, fibromas, and leiomyomas are the most frequent types of benign neoplasms. Response of the bladder to irritation may result in diffuse increase in bladder wall thickness or polypoid lesions of the epithelium that are grossly indistinguishable from neoplasms. The reason for this focal reaction of the bladder is not apparent.

Clinical Signs Clinical signs associated with bladder masses are variable. Dysuria and hematuria are common signs. Urinary incontinence may occur, and appears to be related to the anatomic site of the mass. Masses involving the trigone and bladder neck are more likely to result in urinary incon-

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tinence than masses elsewhere. Diffuse masses that prevent dilatation of the bladder may cause incontinence or frequent voiding of small quantities as a result of marked reduction in bladder volume.

Diagnosis and Clinical Management In the cooperative patient, abnormal bladder anatomy is frequently palpable. Patients that are difficult to palpate or that have persistent dysuria or hematuria should be subjected to further diagnostic procedures to establish if anatomic bladder defects are present. Pne umocystography and positive contrast cystography are helpful in establishing the presence and location of masses (Figs. 4 and 5). Cystoscopy may be utilized to detect and biopsy bladder masses in medium-sized and large bitches. Urine sediment should be examined by a competent cytologist to determine if neoplastic cells are present. Positive results indicate neoplasia but negative results do not exclude it. Urine culture and sensitivity testing may be a valuable aid in therapy, but is not helpful diagnostically since infection may be present in both neoplastic and nonneoplastic conditions. Diagnosis may not be possible without laparotomy and biopsy. At laparotomy, adjacent organs and lymph nodes should be carefully examined for signs suggestive of neoplasia. Biopsy of the lesion, preferably by complete excision, may be indicated for definitive diagnosis. Depending on the location of the lesion, ureterocystopexy may be required . Partial cystectomy may result in decreased vesicular volume temporarily, but

Figure 4. Lateral pneumocystogram of a cat with persistent d ysuria and he maturia. A thick, irregular bladder wall is present, particularly on th e cranioventral surface. Histopathologic diagnosis: chronic cystitis.

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Figure 5 . Lateral pneumocystogram of a dog with long-term dysuria a nd hematuria. There is one large mass with its base in the trigone and numero us smaller masses associated with the wall of the urinary bladder. Histopathologic diagnosis: transitional cell carcinoma.

bladder volume usually increases with time. In man , generalized neoplasia of the bladder is often treated by total cystectomy and transplantation of ureters into an ilia! conduit which drains urine to a cutaneous abdominal site.

URINARY INCONTINENCE Estrogen-Responsive Incontinence Estrogen responsive incontinence may occur in the aged bitch that was ovariohysterectomized as a young dog. The incidence of this abnormality is not documented. Considering the number of dogs spayed and the number of diagnoses of this abnormality , it appears to be an uncommon complication of ovariohysterectomy . The pathophysiology of the incontinence is unknown . One theory is that the uterine stump becomes adherent to the bladder neck following ovariohysterectomy, and that subsequent retraction of the stump associated with senescence results in mechanical interference with physiologic sphincter activity. Clinical diagnosis is based on history and lack of abnormalities found on physical examination. Affected dogs appear to urinate normally. Urinalysis should be performed to evaluate whether inflammation is present, and to establish if urine specific gravity is indicative of renal concentrating ability. With uncomplicated estrogen-responsive in-

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continence, urinalysis should be normal and concentrating ability should be present. Oral or parenteral therapy with estrogens or diethylstilbestrol causes remission of signs in a few days. If available, diethylstilbestrol may be administered orally at a dose of 0.1 to 1.0 mg per day for 3 to 5 days, followed by a maintenence dose of 0.2 to 3.0 mg per week. Alternatively, estrogens such as estradiol cypionate (ECP*) may be administered at a dose of 0.1 to 1.0 mg parenterally at intervals of weeks to months. Excessive quantities of estradiol cypionate should not be administered since this drug may cause severe aplastic anemia. Ectopic Ureter(s) Termination of one or both ureters into structures other than the urinary bladder is a congenital anomaly associated with faulty differentiation of the mesonephric and metanephric ducts. Incontinence due to ectopic ureters is apparent in the female dog, but rarely occurs in the male. In the male, the ectopic ureter usually empties into the prostatic urethra, and urine refluxes into the bladder. Entrance of an ectopic ureter into either the urethra or vagina of the female is likely to result in incontinence. Urinary incontinence associated with ectopic ureters has not been reported in cats. Urinary incontinence is usually first noticed after weaning, when the pup is no longer cleaned by the bitch. Urine may drip from the vulva constantly, or pool in the vagina and gravitate out the vulva when body position changes. Diagnosis of ectopic ureters may be established by vaginoscopy and demonstration of abnormal orifice(s) confluent with the kidney. Excretory urography may be utilized in diagnosis, but may be limited by difficulty in determining the course of the distal ureter. However, the ectopic ureters are usually dilated throughout their entire length so that abnormal vaginal orifices and hydroureter provide some evidence of ectopic ureters even though the exact termination of the ureter cannot be visualized radiographically (Fig. 6). Definitive radiologic diagnosis may be obtained by retrograde ureteropyelography. A sterile catheter is introduced into the abnormal vaginal orifice, intravenous organic iodide contrast media is injected, and radiographs are made. Others have recommended that a vaginogram may be used in small dogs that are difficult to examine by vaginoscopy but we have not had experience with this technique. The vagina is distended with contrast material as the head is tilted down. Insertion of a catheter with an inflatable tip into the vagina and inflation of the catheter may aid in keeping contrast media in the vaginal lumen. Reflux of radiopaque media into ectopic ureters may occur. Exploratory laparotomy may also be utilized for direct visualization of ectopic ureters. Saline injected into an ectopic ureter should immediately be voided through the vulva. *Upjohn Co., Kalamazoo, Mich.

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Figure 6. Ventrodorsal radiograph of a 5-month-old male dog made 50 minutes after injection fo r intrave nous urography. There is a normal right kidney and ureter. The left kidney appears to be excr eting contrast media, but there is enlargement of the pelvis of the kidney as well as a hydroureter. There are air bubbles in the terminal left ureter introduced by previous catheterization of ectopic left ureter.

Treatment of ectopic ureter is surgical. Transplantation of the ureter to the urinary bladder is the preferable method of treatment. Although incontinence due to unilateral ectopic ureter may be cured by unilateral nephrectomy, this procedure must be condemned because renal tissue is needlessly sacrificed. Nephrectomy is justified only if severe disease of the ipsilateral kidney is present, and if it is established that adequate renal function exists in the opposite kidney. Determining the specific gravity of urine from the bladde r or evaluation of PSP excretion into the bladder following intrave nous injection of dye allows evaluation of the kidney whose ureter inserts into the bladder. If urinary tract infection accompanies an ectopic ureter, it should be treated prior to surgery. Evaluation of the entire urinary tract and the micturition reflex should be performed prior to surger y inasmuch as other abnormalities may accompany ectopic ureter. Some abnormalities may result in persistence in urinary incontine nce subsequent to cystoureteropexy. Patent Urachus

The urachus provides a route of exit of wastes from the fetal bladder to the allantoic sac. At birth, it normally becomes fibrotic and nonfunctional. Rarely, proper closure of the urachus fails to occur. As a result, urine may be voided through the umbilicus in addition to the urethra. Infection of the umbilicus and the urachal stalk may occur sec-

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Figure 7. Late ra l pne umocystogram of a 10-month-o ld female pe ka poo with urinary incontinence. The bladder is located within the pelvic canal rather tha n cranial to the brim o f the pelvis. T he animal had an extre mely sho rt u rethra.

ondarily. Urach al cysts may be found between the the umbilicus and the urinary bladder, but these are generally of no consequence. Diverticula of the urinary bladder may represent a remnant of the urachus. Secondary infection and dysuria may occur in these instances. Treatment of patent urachus is d irected toward eradication of infection and surgical extirpation of the urachal stalk. Abnormal micturition ceases following surgical correction. Developmental Anomalies of the Urethra Rarely, developme ntal urethral anomalies may result in urinar y incontinence. H ypospadias, in which the ure thra may open be tween the anus and the tip of the penis, may be accompanied by urinar y incontinence. However, it is likely that oth er abnormalities are present in these patients inasmuch as the integrity of the urethra proximal to the prostate is sufficient to attain urine continence in the normal dog. Intensive study of incontinen ce associated with h ypospadias has not been conducted. An abnormally short urethra, probably of congenital origin, was associated with urinary incontinence in a 10-month-old fe male p e ka poo (Fig. 7). Loss of Bladder Wall Elasticity Loss of bladder wall elasticity may be found in some cases of urinary incontinen ce in the dog. Neoplastic, infla mmatory, and fibrotic ch a nges may be found in the bladde r in these instances.

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At present, it is not apparent whether incontinence is related to alteration in detrusor muscle or in the nerve endings within the bladder wall. It is also possible that nonneoplastic alterations in the bladder wall are a consequence of incontinence rather than a cause of it. Treatment is directed toward the primary cause when it can be identified. In instances where the etiology cannot be established, symptomatic treatment has been unrewarding.

GENERAL REFERENCES 1. Finco, D. R.: Current status of canine urolithiasis. J.A.V.M.A., 158:327, 1971. 2. Kirk, R. W.: Treatment of Urinary Tract Infections. Proc. 37th Annual Meeting of the American Animal Hospital Association, Elkhart, Indiana, p. 260, 1970. 3. Osborne, C. A., Low, D. G., and Finco, D. R.: Canine and Feline Urology. Philadelphia, W. B. Saunders Company, 1972. 4. Osborne, C. A., Rhodes, J. D., and Hanlon, G. F.: Patent urachus in the dog. Anim. Hosp., 2:245, 1966. 5. Owen, R.: Canine ureteral ectopia-a review. J. Small Anim. Pract., 14:407, 1973. College of Veterinary Medicine University of Georiga Athens, Georgia 30602