Larry G. Adams, DVM, PhD, DACVIM (SAIM)
Common causes of urethral obstruction include uroliths, urethral plugs from feline idiopathic cystitis (FIC), urethral masses (transitional cell carcinoma or proliferative urethritis), urethral strictures, and functional urinary retention. Before concluding that a patient has functional urinary retention, thoroughly evaluate the patient for mechanical urinary obstruction.
Obstruction to urine flow limited to one ureter or kidney will not cause postrenal azotemia/uremia, provided the other kidney and ureter are functional. The degree of renal damage from chronic obstruction depends on the degree, duration, and site of obstruction. Complete ureteral obstruction (without UTI) can lead to irreversible renal damage within 2–4 weeks. Chronic, partial obstruction will lead to hydroureter, hydronephrosis and potential for severe renal damage of the obstructed kidney. In animals with unilateral ureteral obstruction, reduction in renal blood flow during obstructive uropathy may result in a small, irregular kidney rather than hydronephrosis. Damage from urinary obstruction is accelerated if UTI is also present. Urinary obstruction with UTI may result in sepsis (urosepsis). An obstructed, infected kidney may be irreversibly damaged within a few days. The degree of reversibility of renal damage is variable and difficult to predict in clinical patients.
Urethral obstruction may cause excessive bladder distension resulting in detrusor atony or weakness, which disrupts tight junctions between muscle cells. This is common in cats with prolonged obstructive FIC from urethral plugs, and usually resolves over several days if the bladder is decompressed.
The cause of death with complete lower urinary tract obstruction is hyperkalemia and severe metabolic acidosis rather than postrenal azotemia. Findings on ECG from hyperkalemia include tall T waves, prolonged P-R, QRS, and Q-T intervals, bradycardia, and terminally ventricular asystole. Hypothermia and dehydration are also common with severe postrenal uremia. Urinary obstruction causes increased tubular pressure, which impairs glomerular filtration, renal blood flow, and tubular function. Tubular function is often impaired for several days after relief of the obstruction. Urine specific gravity is variable in animals with postrenal azotemia from obstruction. During acute urethral obstruction, urine-concentrating ability is preserved and concentrated urine is stored in the obstructed urinary bladder. Therefore, most male cats with obstructive FIC have highly concentrated urine. With prolonged, complete or partial obstruction, the impaired tubular flow disrupts the urine-concentrating ability, resulting in inappropriately dilute urine specific gravity along with postrenal azotemia. Postobstructive diuresis may result in massive polyuria for hours to days following relief of urinary obstruction.1 Fluid requirements to maintain hydration with postobstructive diuresis are substantially higher than normal maintenance needs.
Treatment of Urinary Obstruction
The goals in treating urethral obstruction are to reestablish urine flow via low-pressure excretory pathway, treat metabolic consequences of obstruction, treat/prevent UTI, and preserve renal function. In the initial treatment of patients with complete urethral obstruction, the bladder should be decompressed by careful cystocentesis with samples saved for urinalysis and culture. This reduces intravesical pressure, allows the kidneys to resume urine production (allowing for renal excretion of potassium and hydrogen), and makes relief of the obstruction easier. Intravenous fluid therapy is initiated to correct azotemia, hyperkalemia, acidosis, and dehydration. The estimated deficit should be replaced IV with Plasmalyte or Lactated Ringer's solution over 6–12 hours unless cardiac or pulmonary disease prevents rapid replacement. Although traditional fluid therapy has been to administer 0.9% saline, saline is an acidifying solution and does not correct the concurrent metabolic acidosis.2 Alkalinizing IV fluids such as Plasmalyte or Lactated Ringer's are equally effective for treating hyperkalemia and more effective for correction of acidosis.2 Animals with hypovolemic shock require an immediate bolus of ¼ to ½ shock dose of IV fluids to effect to restore arterial blood pressure. Intravenous bicarbonate was previously recommended to correct the acidosis and to decrease serum potassium levels; however, this may also decrease serum ionized calcium concentrations, which are commonly decreased with obstruction.3 Therefore, IV bicarbonate is not the safest or most effective means to treat hyperkalemia. A more effective approach is intravenous glucose and insulin therapy. Intravenous calcium gluconate may be necessary to counteract the cardiac effects of hyperkalemia in patients with profound bradycardia.
Relief of Urethral Obstruction
Urethroliths (or urethral plugs) should not be pushed back to the urinary bladder using a urinary catheter. Instead, they should be flushed back into the urinary bladder. Attempting to push uroliths using a urinary catheter is an extremely common error by veterinarians. Successful passage of a urinary catheter often occurs without displacing the urethroliths from the urethra by the catheter passing to the side of the urolith(s). Then, when the urinary catheter is removed, the patient often reobstructs with the urethrolith. Urethroliths should be retropulsed back into the bladder for medical dissolution or surgical removal. If the urethrolith cannot be retropulsed into the bladder, laser lithotripsy is highly effective for fragmentation and removal of urethroliths.4
General anesthesia is usually required for retrograde urohydropropulsion of urethroliths. If the bladder is overdistended, decompressive cystocentesis (using a 22-gauge needle connected to a 60-ml syringe by extension tubing and a three-way valve) is performed and fluid therapy should be administered to correct acid-base and electrolyte imbalances before anesthesia to perform retrograde urohydropropulsion. The largest urinary catheter possible is gently passed into the distal urethra and the urethral orifice is compressed gently around the catheter with sterile gauze sponges. An assistant compresses the urethra against the pubis via digital rectal palpation. A 2:1 mixture of sterile saline and sterile aqueous lubricant is rapidly flushed into the urethra while compressing the urethral orifice around the catheter to prevent fluid leakage from the penis. An estimate of the total volume of flush required is 6 ml/kg of body weight or 60 ml, whichever is less. Once the urethra begins to dilate, the rectal compression is released while flushing continues. If the urethroliths pass retrograde, the catheter is gently advanced to the trigone. If the calculus does not move retrograde, the degree of bladder distention should be assessed prior to repeating the procedure. Subsequent retrograde flushes are done with sterile saline alone using a smaller syringe, because the urethra is well lubricated and smaller syringes generate greater flush pressures. Successful retrograde movement of the urethroliths should be confirmed by cystoscopy or radiography. The aim of retrograde urohydropropulsion is to flush the uroliths into the bladder, not to push them with the urinary catheter. Pushing against urethroliths with rigid polyethylene catheters may result in mucosal trauma, urethral perforation, or the catheter being passed round the urolith. Catheter-induced trauma predisposes to future urethral stricture formation.
Urethral plugs should be dislodged manually or flushed back into the bladder. Placement of stay sutures in the prepuce may be used to maintain sterility and straighten the urethra of male cats to facilitate urethral flushing. The urethral catheter should be slowly advanced while continuously flushing sterile IV fluids up the urethra. After flushing urethral plugs retrograde, the bladder should be thoroughly lavaged with warmed sterile 0.9% saline to remove the debris, protein matrix and crystals to reduce the risk of recurrent obstruction. Solutions that are more acidic than 0.9% saline should not be used for lavage of the urinary bladder. Perineal urethrostomy is rarely required for acute urethral obstruction by urethral plugs. If necessary, an indwelling urinary catheter should be maintained, connected to a sterile, closed-collection system. Indwelling urethral catheters predispose to UTI, and may promote urethral inflammation, edema, and potentially, urethral stricture formation. Silicone or soft rubber feeding tubes are preferred over polyethylene catheters for indwelling urinary catheters. Indications for an indwelling urethral catheter in cats are inability to produce adequate size and force of urine stream following urethral flushing, repeated episodes of obstruction, severely azotemic cats with severe electrolyte abnormalities, and cats with large amounts of urine sediment or blood clots in the urine.
Recent observations of cats with urethral plugs indicate that urethral obstructions by plugs are at least partially due to urethral spasms, which prevent passage of plugs.5 One recent study documented that sedation may facilitate passage of urethral plugs in most cats without urinary catheterization.5 Therefore, an alternative approach may be attempted for cats without severe dehydration, azotemia or electrolyte abnormalities. The urinary bladder is decompressed by cystocentesis, and the cat is sedated with a combination of narcotics and high-dose acepromazine. The cat is placed in a quiet environment and monitored for passage of urine. Decompressive cystocentesis is repeated every 4–8 hours as needed. If spontaneous voiding does not occur, then urethral catheterization is indicated.
Urethral stents are most commonly utilized to relieve urethral obstruction by urethral neoplasia, such as transitional cell carcinoma (TCC) in dogs.6,7 Urethral stents may also be useful for management of severe, refractory urethral obstruction from proliferative urethritis, but this has not been reported. Self-expanding nitinol urethral stents are preferred for palliative stenting of malignant urethral obstructions, because they have more outward expansile strength than balloon expandable stents.6 In 19 dogs with urethral obstruction from TCC, 17 dogs were successfully stented allowing the dogs to urinate and be discharged from the hospital.7 Median survival was 78 days, and 59% of the dogs had metastasis at the time of death.7
1. Francis BJ, et al. Retrospective study to characterize postobstructive diuresis in cats with urethral obstruction. J Feline Med Surg. 2010;12:606–608.
2. Cunha MG, 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;71:840–846.
3. Drobatz KJ, et al. Concentration of ionized calcium in plasma from cats with urethral obstruction. Am J Vet Res. 1997;211:1392–1395.
4. Adams LG, et al. Use of laser lithotripsy for fragmentation of uroliths in dogs: 73 cases (2005–2006). J Am Vet Med Assoc. 2008;232:1680–1687.
5. Cooper ES, et al. A protocol for managing urethral obstruction in male cats without urethral catheterization. J Am Vet Med Assoc. 2010;237:1261–1266.
6. Weisse C, et al. Evaluation of palliative stenting for management of malignant urethral obstructions in dogs. J Am Vet Med Assoc. 2006;229:226–234.
7. McMillian SK, et al. Outcome of urethral stenting for management of obstruction secondary to transitional cell carcinoma in 19 dogs. J Am Vet Med Assoc. (In press).