Urinary obstruction or functional urinary retention (Proceedings)

One of the common clinical scenarios that may present a diagnostic challenge is dogs or cats with urine retention without an obvious cause. The fundamental question in these cases is: "Does this patient have functional urinary retention or mechanical urinary obstruction?" Partial urethral obstruction is common and can easily be confused with functional urinary retention. Before concluding that a patient has functional urinary retention, one should always thoroughly diagnostically evaluate the patient for mechanical urinary obstruction. Animals with severe post-renal azotemia rarely have functional urinary retention and should be thoroughly evaluated for mechanical urinary obstruction.

Urinary obstruction

Urinary obstruction (UO) is obstruction that prevents low-pressure urine flow located anywhere in the excretory pathway. The obstruction may be acute or chronic, partial or complete. Mechanical obstructions can be intraluminal such as uroliths, urethral plugs, and blood clots. They can also be intramural, including neoplasia (TCC) or strictures. Extramural mechanical obstructions can be caused by prostatic neoplasia or bladder herniation into a perineal hernia.

There are several causes of functional urinary retention. One of the most commonly encountered causes of functional urinary retention is neurogenic disruption of normal innervation of the micturition reflex by spinal cord disease. Depending on the location of spinal cord disease, there may be several different clinical presentations. Other less common causes of functional urinary retention include reflex dyssenergia, bladder atony from prolonged overdistention, and side effects of medications.

Consequences of urinary obstruction

Complete lower urinary tract obstruction causes death due to acid base and electrolyte abnormalities associated with postrenal uremia within 3 to 5 days. Obstruction to urine flow limited to one ureter or kidney will not cause postrenal azotemia/uremia provided the other kidney and ureter are functional. Chronic, partial obstruction will lead to hydroureter, hydronephrosis and severe renal damage of the obstructed kidney. Damage is accelerated if a UTI is also present. Total urinary obstruction in a patient with UTI frequently results in sepsis. UO may cause excessive distension of the urinary bladder resulting in detrusor atony or weakness, which disrupts tight junctions between muscle cells. This is common in cats obstructed by urethral plugs, and usually resolves over several days if the bladder is kept decompressed.

Diagnosis of urinary obstruction is by demonstration of obstruction to urine flow by physical exam, radiographically or cystoscopy. Physical exam of dogs with urethral obstruction should include a rectal exam to rule out urethral uroliths or masses. Although urethral catheterization may indicate obstruction in some animals, the ability to pass a urinary catheter does NOT rule out urethral obstruction. Urethral obstructions are frequently missed if the sole means of ruling out urethral obstruction is based on ability to pass urinary catheters. This is one of the most common errors in veterinary urology. Another potential complication of passing urinary catheters to rule out uroliths is that rarely the catheter and urolith may become lodged together in the urethra.

Diagnostic imaging is the most common means of confirming urinary obstruction. Ultrasonography an excellent screening tool for detecting upper tract obstruction. A positive contrast urethrocystogram is useful for confirmation of lower urinary tract obstruction. For upper urinary tract obstruction an intravenous urogram will often document ureteral obstruction. Antegrade pyelography using ultrasonographic guidance also may be used to document ureteroliths. The most sensitive imaging technique of detecting ureteral obstruction is to perform a CT scan before and after intravenous contrast.

Cystoscopy may also be used to document urethral obstruction. Urethral masses, strictures or urethroliths can easily be detected during cystoscopy. If a urethral mass or urethral stricture causes the lumen to be too narrow to allow passage of the cystoscope, a flexible tipped urologic guide wire may be passed through the strictured area under fluoroscopic guidance. In some animals, the cystoscope may then be advanced over the guidewire. Alternatively, an open ended catheter or vascular access sheath may be passed over the guide wire and retrograde contrast studies may be performed to delineate the extent and severity of urethral obstruction.

Consequences of urinary obstruction

Complete lower urinary tract obstruction causes death due to acid-base and electrolyte abnormalities associated with postrenal uremia. 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 infection) can lead to irreversible renal damage within 2 to 4 weeks. Chronic, partial obstruction will lead to hydroureter, hydronephrosis and severe renal damage of the obstructed kidney. In some animals with unilateral ureteral obstruction, reductions in renal blood flow to the kidney during obstructive uropathy results in a small, irregular kidney rather than hydronephrosis. Damage from urinary obstruction is accelerated if UTI is also present. Urinary obstruction in a patient with UTI may result in sepsis (urosepsis). An obstructed, infected kidney may be irreversibly damaged within a few days. The degree of reversibility of decreased renal function 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 obstructed by urethral plugs, and usually resolves over several days if the bladder is kept decompressed.

Severe hyperkalemia is the usual cause of death from urethral obstruction. An ECG will reveal tall T waves, prolonged P-R, QRS, and Q-T intervals, bradycardia, and ventricular asystole. Severe metabolic acidosis also occurs due to lack of excretion of metabolic acids. 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 the relief of obstruction. Post-obstructive diuresis may result in massive polyuria for several days. The mechanism of post-obstructive diureses may be tubular dysfunction, solute diuresis, volume expansion, or humoral factors such as atrial natruretic factor.

Treatment of Urinary Obstruction

Patient Stabilization: The goals in treating urethral obstruction are to re-establish urine flow via low pressure excretory pathway, treat metabolic consequences of obstruction, treat/prevent UTI, and preserve renal function. In the treatment of complete urethral obstruction, the bladder should be decompressed by careful cystocentesis with samples saved for urinalysis and culture. This relieves intravesical pressure and allows the kidneys resume urine production, and relieves intravesical pressure, which makes relieve of obstruction easier. Intravenous fluid therapy is needed to correct the azotemia, hyperkalemia, acidosis, and dehydration. The estimated deficit is replaced IV with normosol-R or LRS over 6-12 hours unless cardiac or pulmonary disease prevents rapid replacement. Intravenous bicarbonate was previously recommended to correct the acidosis and to decrease serum potassium levels; however this will also decrease serum ionized calcium concentrations, which are commonly decreased with obstruction. A more effective means to correct hyperkalemia by transcelluar shifts is intravenous glucose and insulin therapy. Intravenous calcium gluconate may be necessary to treat the ionized hypocalcemia and to counteract the cardiac affects of hyperkalemia in patients at risk for dying from cardiac arrhythmias. Hypothermic animals should be placed on a warm water blanket until the temperature is normal.

Relief of urethral obstruction: Urethroliths should NOT be pushed back to the urinary bladder using a urinary catheter. This is an extremely common error made by many experienced 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 re-obstructs with the urethrolith. Urethroliths should be retropulsed back into bladder for medical dissolution or surgical removal. If the urethrolith cannot be retropulsed into bladder, laser lithotripsy is a highly effective for removal of urethroliths.4-6

Retrograde urohydropropulsion of uroliths: General anesthesia is usually required for retropulsion. 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. 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 5 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, because the urethra is well lubricated. 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: Urethral plugs should be dislodged manually or flushed back into bladder. After flushing urethral plugs back into the urinary bladder, thoroughly lavage the bladder with warmed sterile saline if needed to remove debris (matrix and crystals) to reduce risk of recurrent obstruction. Perineal urethrostomy is rarely required for acute urethral obstruction by urethral plugs. If necessary, an indwelling urinary catheter should be maintained connected to a closed collection system. Indwelling urethral catheters predispose to UTI, and may promote urethral inflammation, edema, and potentially, urethral stricture formation. Indications for an indwelling urethral catheter in cats are: inability to produce adequate size and force of urine stream by bladder compression following urethral flushing, repeated episodes of obstruction occurring over a period of hours, severely azotemia cats with severe electrolyte abnormalities, and cats with large amounts of urine sediment and/or blood clots in the urine. After urethral catheter removal, cats should be monitored closely for recurrent obstruction for 24-48 hours.

Recent observations of cats with urethral plugs indicate that urethral obstructions by plugs are due at least in part from urethral spasms which prevent passage of the plug. Empirical observations and unpublished studies indicate that sedation may facilitate passage of urethral plugs in some cats. Therefore, an alternative approach may be attempted for cats without severe dehydrations, azotemia or acid-base and electrolyte abnormalities. The urinary bladder is decompressed by cystocentesis, and the cat is sedated with a combination of narcotics and low-dose acepromazine. The cat is placed in a quiet environment and monitored for passage of urine. Decompressive cystocentesis is repeated once if needed. If passage of the urethral plug does not occur, then traditional relief of obstruction is indicated.

Urethral Strictures: Treatment options for urethral strictures are dependent on the location of the stricture. Distal urethral strictures my require urethrostomy; however, the location and extent of the stricture must be determined to be certain that the urethrostomy opening will be proximal to the stricture. Alternatively, urethral strictures may be dilated over the guide wire using serially enlarging dilators (e.g., ureteral dilation catheters) or appropriately sized balloon dilation catheters. Urethral strictures may re-stricture after dilation and may require re-dilation or placement of urethral stents. We have successfully dilated urethral strictures in dogs and cats.

Urethral Stents: Urethral stents are most commonly indicated to relieve urethral obstruction by neoplasia such as transitional cell carcinoma (TCC).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. In one report of 12 dogs with malignant urethral obstruction, all 12 dogs were able to urinate immediately after stent placemen. In this report, 9 of 12 dogs were continent or mildly incontinent following urethral stent placement and 2 dogs were severely incontinent. The remaining dog had an atonic urinary bladder. These reported results are similar to our clinical experience for urethral stent placement for correction of urethral obstruction by TCC.

Functional urinary retention

Urethral obstruction may occur due to mechanical or functional causes. Functional obstruction results from failure of coordination of urethral relaxation with detrusor contraction (reflex dyssynergia). Functional urinary retention is an uncommon condition that is most often caused by neurologic conditions that disrupt innervation to the spinal cord and micturition reflex. Animals with urethral obstruction resulting in urinary retention should be thoroughly evaluated for mechanical causes on urethral obstruction before concluding that the condition is caused by functional obstruction.

Neurogenic causes of urinary retention most often are due to spinal cord diseases that disrupt communication of the brain stem with the lubosacracal spinal segments. Therefore, careful neurologic examination should be performed in dogs with suspected functional urinary retention. Some dogs with apparent reflex dyssynergia have subtle disease in the lumbosacral spine. Urethral spasms during urethral pressure profilometry are supportive evidence of reflex dyssynergia. Treatment of suspected reflex dyssynergia should begin with the a-adrenergic antagonists phenoxybenzamine or prazocin. If these drugs do not resolve the urinary retention, then bethancol is added to facilitate detrusor contraction. Then, benzodiazepine may be added as a skeletal muscle relaxant, although response is often poor. In some patients, these therapies are not effective and urinary retention continues. Advanced imaging (MRI) of the caudal spinal cord may reveal an underlying cause in some refractory patients. In refractory patients, salvage procedures may include tube cystotomy or potentially urethral stent placement.

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