Managing urethral obstruction in male cats (Proceedings)

According to conventional wisdom, UO in cats usually is associated with urethral plugs. Recent studies however found that only 18% of UO episodes were associated with urethral plugs. This is consistent with findings from an unpublished pilot study at Ohio State University using urethroscopy at the time of initial evaluation. Urethral plugs have minimal intrinsic cohesive structure, but often are cylinder-shaped after extrusion from the urethra. Urethral plugs are fundamentally different from calculi that lodge within the urethra (i.e., urethroliths). Uroliths have an organized internal structure with much less matrix, and are not easily compressed or distorted. Urethral plugs consist largely of matrix mucoprotein with embedded minerals. The predominant mineral composition in most plugs is magnesium ammonium phosphate hexahydrate (i.e., struvite).

This is true despite the fact the cats form calcium oxalate and struvite uroliths with nearly equal frequency. Most plugs are assumed to lodge within the penile urethra, but obstructions also can occur at more proximal sites. Definitive diagnosis of a urethral plug requires retrieval of the plug. Supportive evidence for the presence of a urethral plug can be seen on radiographs in some cats with UO. Previously, the crystalline-matrix hypothesis proposed that plugs formed secondary to precipitation of struvite crystals in the urine that then became embedded in a matrix. According to this hypothesis, plugs created UO and urethritis. It is now hypothesized that plugs form as a consequence of underlying idiopathic urethritis and cystitis (i.e., inflammation occurs first, followed by plug formation).

Most male cats with urethral obstruction have no identifiable cause (i.e., idiopathic), which may be an extension of idiopathic/interstitial cystitis (FIC). Some cats have signs of non-obstructive idiopathic/interstitial cystitis before UO. Many cats have signs of idiopathic/interstitial cystitis after relief of UO. Obstruction is secondary to urethral spasm in addition to swelling of the urethra due to edema and hemorrhage. Pathologic or neurogenic processes cause contraction of the circular smooth or skeletal muscle of the urethra or both. Stimulation of adrenoreceptors (particularly α-1) within the urethra increases urethral tone in normal cats. Pain and stress after UO increase sympathetic outflow from the central nervous system, leading to additional urethral spasm.

Signalment, history, physical examination

Approximately 75% of cats presented with UO are experiencing their first episode. The median age is 4 to 5 years old, but any age can be affected (0.5 to 16 years). Most affected cats in the United States are neutered males.  Intact males comprise 10% of cats with UO. In the United States, over 80% of affected cats are housed exclusively indoors. Median duration of clinical signs before initial presentation was 3 days in a study of 223 cats. Signs include those of cystitis and partial obstruction before development of complete obstruction. The majority of cats with UO are relatively stable; approximately 10% are critically ill.

Severe bradycardia (< 100 bpm) from the effects of hyperkalemia  (Lee and Drobatz 2003) has been reported in 5% of cases, moderate bradycardia (100-140 bpm) in 6% of cases and mild bradycardia (140-160 bpm) in 12% of cases; arrhythmias were detected in 11% of cases. 50% of cats can be expected to have normal body temperature, hypothermia in about 40% and hyperthermia in 10%.  Rectal temperature < 95-96.6°F or heart rate < 120 bpm was most the accurate predictor of severe hyperkalemia. A combination of hypothermia and bradycardia was 98 to 100% predictive for severe hyperkalemia (> 8.0 mEq/L).  Twitching or seizures is very uncommon (0.5%) and related to ionized hypocalcemia. 

Diagnostics

Initial magnitude of BUN, serum creatinine, and serum phosphorus concentrations do not predict survival or failure to regain normal renal function. In one study (Lee and Drobatz 2003) the BUN was above the reference range in 33% of cats with UO, serum creatinine concentration was above the reference range in 29%, and serum phosphorus concentration was above the reference range in 25%. Hyperkalemia does not occur in isolation and often is accompanied by acidosis and low serum ionized calcium concentration.

Serum potassium concentrations ranged from 3.4 to 10.5 mEq/L in 199 cats. 6% were below the reference range; 41% were above the reference range, and 53% in the reference range. Serum potassium concentration was < 6.0 mEq/L in 66% of cases, > 6.0 but < 8.0 mEq/L in 12% of cases, > 8.0 but < 10.0 mEq/L in 12% of cases, and > 10.0 mEq/L in < 1% of cases. Hyperkalemia most often was encountered with acidosis (pH < 7.2 in 74% of cases) and low serum ionized calcium concentration (< 1.0 mmol/L in 75% of cases).

Many abnormal results from urinalysis are typical for cats with urethral obstruction. Urine specific gravity (USG) is unpredictable. USG can be > 1.040 when evaluated early during UO. In more advanced cases, submaximal urine concentration can occur due to the effects of obstruction on renal tubular function. Hematuria is almost always observed due to the presence of underlying idiopathic urethritis/cystitis and due to the effects of overdistension of the bladder wall with resultant hemorrhage.

Struvite crystals may be observed, especially if urine pH is alkaline, likely secondary to urine stasis or alkaline urine pH than a primary cause of obstruction. Nearly all cats with UO have sterile urine on original presentation for obstruction. Bacterial culture at the time of urinary catheter removal is more likely to identify pathogenic bacteria. Isolation of bacteria from cats with a previous history of UO is more likely than isolation from cats suffering an initial episode.  

Conventional management of uo

The degree of uremia, electrocardiographic stability, and the magnitude of bladder distension dictate how quickly and in what order treatment must be performed. The causes of collapse and hypotension are multifactorial, including the effects from hyperkalemia, bradycardia, metabolic acidosis, ionized hypocalcemia, acute uremia, and hypothermia. Stabilize the patient and treat the adverse effects of uremia if present before administering any anesthesic agents. Hypovolemia, hyperkalemia, metabolic acidosis, and hypocalcemia must be treated first. Intravenous (IV) administration of fluids is needed for seriously ill cats with UO.

IV fluid therapy at 10 – 20 mL/kg/hr is started and the rate adjusted as the animal becomes more stable. 0.9% NaCl often is recommended as the fluid of choice because it contains no potassium, but no difference in the rate of decline in serum potassium concentration was seen in a randomized study of 68 cats with UO treated with 0.9% NaCl compared to a more balanced polyelectrolyte solution containing 5 mEq/L of potassium as well as the base precursors acetate and gluoconate (i.e., Normosol-R).   More rapid correction of acidosis was accomplished within 12 hours of treatment with the more balanced polyelectrolyte solution compared to 0.9% NaCl.

Serum potassium concentration decreases soon after relief of urethral obstruction and often is normal by the time substantial decreases in BUN and serum creatinine concentrations are observed.  Management of hyperkalemia will be needed in the approximately 12% of cats that have severe hyperkalemia and may be warranted in another 12% that have moderate hyperkalemia. No specific treatment is needed for cats with mild hyperkalemia. Calcium gluconate is the treatment of choice for cats with severe hyperkalemia (> 8.0 mEq/L), heart rate < 140 bpm, and especially in cats with ECG instability.

Conversion to a more normal ECG tracing is very rapid (minutes). This treatment stabilizes the heart, but does nothing to change the severity of the hyperkalemia. These beneficial effects are short-lived (about 20 to 30 minutes), and other methods to lower serum potassium concentration are needed. IV dextrose alone or with insulin, and sodium bicarbonate are additional considerations for treatment.

Relief of obstruction due to plugs or idiopathic causes

An IV catheter is placed before sedation, analgesia, and anesthesia in unstable cats. An IV catheter can be placed after sedation and analgesia in stable cats. Nearly all cats benefit from pre-anesthetic analgesics to decrease pain and anxiety; these usually are given before decompressive cystocentesis and before anesthesia to pass a urinary catheter. Little or no sedation is indicated for cats with severe uremia. Many different sedation protocols are available depending on the cat's condition and the clinician's comfort and familiarity with their use (buprenorphine, acepromazine, hydromorphone or oxymorphone, fentanyl, diazepam or midazolam).

Decompressive (therapeutic) cystocentesis is the next step to perform after sedation and IV catheter placement. The benefits of decompressive cystocentesis outweigh potential adverse effects. Cystocentesis to empty the bladder should be performed as soon as possible in cats with very large bladders to prevent rupture of the bladder and to allow renal excretory function to resume. We have performed decompressive cystocentesis before passage of a urinary catheter in cats with UO for over 15 years and have found the procedure to be safe. The use of a 22-gauge needle on an extension set or  a 22-gauge butterfly needle can minimize trauma and urine leakage during the procedure.

Do not immediately anesthetize severely affected cats; they should be stabilized with IV fluids and decompressive cystocentesis first. The goal is to administer sufficient anesthesia to provide immobilization and urethral relaxation because less urethral trauma occurs under these conditions.  Ketamine and diazepam or ketamine and acepromazine generally are very safe protocols having been used for many years by primary care veterinarians. Ketamine plus diazepam may be better in cats that are very sick because diazepam is less likely to cause hypotension than is acepromazine.

Some cats are not relaxed enough with these ketamine combination protocols, and adding inhalational anesthesia may be necessary. Inhalation of isoflurane via endotracheal tube can be used after pre-medication and induction provides the most complete relaxation and affords time that may be needed by less experienced personnel. Standard epidural techniques require special expertise and training but a new simplified method using sacro-coccygeal placement of local anesthetic to allow urethral catheterization and pain management appears promising (O'Hearn, 2011).

Aseptic and gentle technique should be used when placing a urethral catheter. Urethral irrigation with sterile physiologic solutions (Lactated Ringer's solution or 0.9% saline) may dilate the urethra and flush the obstructing plug distally out the external urethral opening around the catheter. Sterile irrigating solution is injected rapidly through the urinary catheter so as to advance plugs into the bladder or fatigue the urethra (referred to as reverse flushing or hydropulsion). Irrigating with a 50:50 mixture of water-soluble lubricant and sterile 0.9% NaCl through the catheter can facilitate catheter advancement and decrease urethral trauma by providing lubrication along the entire length of the urethra as the catheter advances.

Do not attempt to force the catheter through the site of obstruction. It should advance easily after adequate irrigation. The bladder is flushed and drained several times. Replace the shorter, stiffer (polypropylene) open end  urinary catheter used to relieve the obstruction with a longer, softer (polyvinyl or silastic) catheter to leave in place as an indwelling urinary catheter to maintain bladder drainage. A sterile collection system should be attached to the urinary catheter and secured to the cat's tail - It is not acceptable to leave an indwelling urinary catheter exposed to the environment due to the high risk of bacterial contamination.

Remove the catheter as soon as possible to minimize complications associated with indwelling catheters (e.g. ascending UTI). Leave the catheter in place until the urine has become clear, azotemia has resolved, and diuresis has subsided. Studies in cats have shown that indwelling polyvinyl catheters create less urethral trauma and inflammation than do indwelling polypropylene catheters. Do not administer glucocorticoids to a cat while an indwelling urinary catheter is in place. The risk for bacterial pyelonephritis is great in this setting and glucocorticoids are unlikely to control urethritis in this setting (i.e. continuous trauma from an indwelling catheter). The use of antibiotics does not prevent the development of UTI in patients with indwelling urinary catheters.

Post-obstructive diuresis of variable magnitude is expected in cats with substantial azotemia at the time of relief of UO. The magnitude of diuresis often is proportional to the magnitude of azotemia at presentation though this was not found in a recent study (Francis, 2010). In this study, diuresis occurred in 46% of cats within the first 6 hours and was predicted most by cats with a venous pH of < 7.35 at admission. Marked post-obstructive diuresis can lead to hypovolemia and hypokalemia. Some cats produce up to 20 mL/kg/hr of urine initially. Post-obstructive diuresis usually lasts 2 to 5 days in cats with substantial azotemia at presentation. A poor prognosis may be warranted in cats with initially severe azotemia that do not undergo post-obstructive diuresis after relief of obstruction and rehydration.

Continue analgesics and antispasmodics while the cat is in the hospital and for 5 to 7 days after release. We treat most UO cats with a combination of acepromazine and buprenorphine. Try to transition the cat's diet to one that has more water (e.g., canned food) as would be done in management of idiopathic cystitis Stress reduction and environmental enrichment is warranted because cats with UO likely have underlying idiopathic cystitis. Owners should be advised about the normal volume of urination to be expected for their cat, which is….. Most cats will have stranguria and pollakiuria for several days after the urinary catheter has been removed. Some hematuria may persist and potentially will be visible to the owner.

An excellent acute prognosis with high survival rate is expected when treatment is started soon enough. In a recent study, almost 94% of affected cats survived initial treatment and were discharged from the hospital (Drobatz 2003). Mortality of 16% was reported in an older study (Bovee 1979). There is a good prognosis for being able to urinate voluntarily after removal of the urinary catheter. Approximately 14% of affected cats re-obstructed soon after removal of the urinary catheter in one study (Drobatz, 2003). Depending on severity of the episode of UO, hospitalization may last 1 to 6 days.  Urinary catheters were in place a median of 2 days (and up to 6 days) in one study (Gerber 2007) and for a median of 1 day (and up to 7 days) in another study (Lee, 2003).

The chronic prognosis for recurrence of lower urinary tract signs following relief of UO is guarded. 8 of 22 (36%) cats with idiopathic UO re-obstructed after a median of 17 days in one study whereas 3 of 7 (43%) cats with UO associated with urethral plugs re-obstructed within 7 months  Recurrent obstruction was the cause for euthanasia in 21% of cats in this study (Gerber, 2007). In an older study, the recurrence rate was 35% within 6 months (Bovee, 1979). No studies on recurrence rates for UO have been reported prospectively after implementation of environmental modification. Urethral stricture occurred in 11% of affected cats in one study (Barsanti, 1996).

Non-conventional treatment for urethral obstruction in male cats

A report describing a method for relief of urethral obstruction in male cats without the use of urethral catheterization was recently described (Cooper, 2010). This treatment is proposed only as an alternative to euthanasia due to financial constraints of owners. Conventional treatment with passage of a urinary catheter and IV fluid infusion in the hospital was offered as the first choice. This approach is not meant for cats with urethral calculi or those with severe metabolic derangements. The severity of azotemia does not determine use of this protocol. A plain lateral abdominal radiograph is taken to exclude calculi. Decompressive cystocentesis is performed initially and then as needed up to every 8 hours  The urethra was not irrigated or catheterized. No IV catheter was placed and IV fluids were not administered.

Drug treatments included: acepromazine (0.25 mg IM or 2.5 mg PO q8h), buprenorphine (0.075 mg PO q8h), medetomidine (0.1mg IM q24h if no urinations are noted in the first 24 hours). The cats were placed in a dark, quiet, low stress environment.  Some fluids may be given subcutaneously as needed, but the goal is to avoid excessive urine production from full hydration. Treatment success was defined as spontaneous urination within 72 hours and subsequent discharge from the hospital - this occurred in 11/15 cats (73%). Treatment failure occurred in 4/15 (27%) cats due to uroabdomen (3) or hemoabdomen (1). Cats that experienced treatment failure had significantly higher serum creatinine concentrations. At necropsy, severe bladder inflammation was found, but there was no evidence of bladder rupture.

Selected reading

Cooper ES, Owens TJ, Chew DJ, Buffington CA. A protocol for managing urethral obstruction in male cats without urethral catheterization. J Am Vet Med Assoc 2010;237:1261-6.

Cunha MG, Freitas GC, Carregaro AB, et al. Renal and cardiorespiratory effects of treatment with lactated Ringer's solution or physiologic saline (0.9% NaCl) solution in cats with experimentally induced urethral obstruction. Am J Vet Res 2010;71:840-6.

Drobatz KJ, Hughes D. Concentration of ionized calcium in plasma from cats with urethral obstruction. J Am Vet Med Assoc. 1997; 211(11):1392-5.

Francis BJ, Wells RJ, Rao S, Hackett TB. Retrospective study to characterize post-obstructive diuresis in cats with urethral obstruction. J Feline Med Surg 2010;12:606-8.

Gerber B, Boretti FS, Kley S, Laluha P, Muller C, Sieber N, Unterer S, Wenger M, Fluckiger M, Glaus T, Reusch CE: Evaluation of clinical signs and causes of lower urinary tract disease in European cats. J Small Anim Pract 46(12): 571-577, 2005.

Gerber B, Eichenberger S, Reusch CE. Guarded long-term prognosis in male cats with urethral obstruction. J Feline Med Surg 2008;10:16-23.

Lee JA, Drobatz KJ : Characterization of the clinical characteristics, electrolytes, acid-base, and renal parameters in male cats with urethral obstruction. J Vet Emerg Critical Care 13(4):227-233, 2003.

Lee JA, Drobatz KJ: Historical and physical parameters as predictors of severe hyperkalemia in male cats with urethral obstruction. Journal of veterinary emergency and critical care 16: 104-111, 2006.

O'Hearn AK, Wright BD. Coccygeal epidural with local anesthetic for catheterization and pain management in the treatment of feline urethral obstruction. J Vet Emerg Crit Care (San Antonio) 2011;21:50-2.

Saevik BK, Trangerud C, Ottesen N, Sorum H, Eggertsdottir AV. Causes of lower urinary tract disease in Norwegian cats. J Feline Med Surg 2011;13:410-7.

Segev G, Livne H, Ranen E, Lavy E. Urethral obstruction in cats: predisposing factors, clinical, clinicopathological characteristics and prognosis. J Feline Med Surg 2011;13:101-8.