How to Treat Feline Urethral Obsructions

In the Diagnote appearing in the August issue of DVM Newsmagazine, decompressive cystocentesis and a five-step plan to re-establish urethral patency was described. The primary purpose of this Diagnote is to answer the question, "What should be considered immediately following restoration of urethral patency?"

Table 1

Managing uremia

How should post renal uremia be managed?

An in-depth discussion of post-renal uremia caused by urethral obstruction is beyond the scope of this discussion. Briefly, obsructive urethropathy that persists longer than about 24 hours usually results in post-renal azotemia. This occurs because back-pressure induced by obstruction of outflow impairs glomerular filtration, renal blood flow and tubular function. After obstruction of the urethra of otherwise normal cats, death will occur within three to six days. Damage to the mucosal surface of the urinary bladder may shorten survival time. Despite the potentially catastrophic outcome of urethral obstruction, the biochemical consequences of this disorder are potentially reversible provided appropriate supportive and symptomatic parenteral therapy is given. In severe cases, supportive therapy to minimize hyperkalemia, metabolic acidosis, hypocalcemia and extracellular fluid depletion should be given a very high priority.

Following restoration

What should be considered immediately following restoration of urethral patency?

After urine flow has been reestablished by nonsurgical techniques, most of the urine should be removed from the bladder lumen. However, removing all the urine from the bladder lumen is unnecessary and inadvisable since trauma associated with such efforts may aggravate the severity of bladder lesions. Manual compression may be used provided it does not require substantial pressure to induce voiding. Manual compression of the bladder is not necessarily the procedure of choice if an overdistended bladder has been recently decompressed by cystocentesis, since it may result in extravasation of urine into the bladder wall or peritoneal cavity. Alternative methods include use of a catheter and syringe or cystocentesis. Each of these procedures has benefits and risks that must be considered in light of the status of the urinary bladder and urethra of each patient.

If the gross appearance of voided or aspirated urine suggests that reobstruction due to intraluminal debris is likely, removal of this material with saline or lactated Ringer's solution flushes of the bladder lumen may be of value in minimizing re-obstruction. Particulate material located in the dependent portion of the bladder may be dispersed throughout the bladder lumen by digitally moving the bladder in and up-and-down fashion, which may, in turn, facilitate aspiration of crystals, inflammatory reactants and blood clots into the catheter and syringe.

Use of antimicrobials

Local instillation of antimicrobial agents into the bladder lumen in attempt to prevent or treat urinary tract infection is of unproved value. Unless the bladder wall is hypotonic or atonic, the antimicrobial agent is likely to be voided soon after instillation. If circumstances warrant use of antimicrobial agents, they should be given orally or parenterally to maximize their effectiveness (Table 1).

Table 2

Evaluate the bladder

The urinary bladder should be periodically evaluated following restoration of adequate urethral patency to ensure that urethral obstruction has not recurred and/or that the detrusor muscle is not hypotonic. Micturition induced by gentle digital compression of the bladder may facilitate evaluation of urethral patency.

Although glucocorticoid therapy has been advocated to minimize inflammatory swelling of the urethra, we do not recommend glucocorticoids in this situation. Why not? Because, they may aggravate the severity of uremia by inducing protein catabolism (via gluconeogenesis), and because they may predispose the patient to nosocomial bacterial UTI.

Following relief of urethral obstruction, a transitory obligatory post-obstructive diuresis may develop. Even though cats with post-obstructive polyuria may consume some water, it is often insufficient to maintain proper fluid balance. Therefore, supplementing water intake by parenteral administration of rehydrating or maintenance fluids is often advisable.

Risks

What risks are associated with indwelling transurethral catheters?

We do not recommend routine use of indwelling urinary catheters in cats following relief of urethral obstruction because they may induce further damage to the urinary tract. Disruption of the glycosaminoglycan (GAG) coating of the urothelium as a result of indwelling urethral catheters may promote adherence of microbes and urinary tract infection. Disruption of the GAG coating may also facilitate adherence of crystals to the urothelium, facilitating their growth and/or aggregation.

Catheter-induced nosocomial urinary tract infections are common, especially in cats with pre-existing disease of the lower tract. Why? Because catheters interfere with host defenses that normally prevent ascending migration of bacteria through the urethral lumen. Even when closed catheter systems are used, catheters allow bacteria to ascend the urethral lumen via the interface between the catheter and the mucosal surface.

Bacteria may also adhere to the surface of urinary catheters and initiate growth of biofilms composed of bacteria, bacterial glycocalicies, Tamm-Horsfall protein and struvite crystals. These biofilms may shield the bacteria they contain from antimicrobial drugs, resulting in treatment failures. They are especially prevalent in cats with LUTD, and have the potential to cause significant morbidity including pyelonephritis, renal failure and septicemia. Therefore, unnecessary use of urinary catheters should be avoided! Factors to consider in the prevention and treatment of catheter-induced infections are summarized in Table 1.

When to use

When should indwelling transurethral catheters be used?

The likelihood of whether or not a cat will voluntarily resume adequate voiding following restoration of urethral patency may be assessed by evaluation of:

• the caliber of the urine stream during the voiding phase of micturition.

• the abundance of material in urine with the potential to occlude the urethral lumen.

• and the adequacy of detrusor tone immediately following relief of urethral obstruction.

• facilitate measurement of the rate of urine formation during intensive care of critically uemic cats,

• promote recovery of detrusor atony by maintaining an empty bladder.

• And prevent recurrence of urethral obstruction caused by urine precipitates or mural abnormalities in high risk patients (Table 2, page 27).

• the cat has a good urine stream during the voiding phase of micturiton.

• a functional detrusor muscle

• and urine does not contain particulate matter that could reobstruct the urethral lumen.

Dysfunctional urinary bladders

Severe and/or prolonged distension of the urinary bladder caused by obstruction to urine outflow may cause impaired capacity of the detrusor muscle to contract during the voiding phase of micturition. The underlying cause is thought to be related to disruption of specialized portions of bladder smooth muscle cells (so-called tight junctions) that normally transmit neurogenic impulses from smooth muscle pace-maker cells.

In this situation, the cat has impaired ability to completely empty the bladder. However, voiding can usually be induced by manual compression applied through the abdominal wall.

Therapy

Once urethral patency has been reestablished, therapy designed to maintain relatively low pressure within the bladder lumen often results in restoration of adequate detrusor function. One therapeutic option consists of trial therapy with bethanachol, a parasympathomimetic (muscarinic) agent. This drug may enhance detrusor contractility. The recommended oral dosage for cats is 1.25 to 2.5 mg given every eight hours. If the desired effect does not occur within a few days, the dose may be increased incrementally up to 5 to 7.5 mg every eight hours, provided harmful side effects do not occur (e.g. excessive salivation, abdominal cramping, vomiting and/or diarrhea).

Since bethanachol can also increase urethral resistance by its nicotinic effects on smooth muscle in the proximal urethra, it may be given with phenoxybenzamine. Phenoxybenzamine is an alpha adrenergic antagonist which facilitates relaxation of smooth muscle in the proximal urethral (oral dose = 0.25 mg/kg every 12 hours. Alternatively, an indwelling catheter whose tip is located within the bladder lumen may be used. Periodic attempts to induce voiding by manual compression of the urinary bladder may also be considered, provided they do not result in a marked increase in intraluminal pressure.

If an indwelling urinary catheter is used to minimize accumulation of urine within the bladder, the previously described precautions designed to prevent catheter-induced injury should be considered.

In addition to orally administered antimicrobial agents, irrigation of the bladder lumen with antimicrobial solutions may be considered, provided a sufficient quantity of the agent will remain in the bladder long enough to have a beneficial effect. Only sterilized solutions should be injected in volume sufficient to allow contact with all portions of the bladder mucosa.

Persistent urethral outflow resistance

Following restoration of urethral patency (as confirmed by transurethral catheterization, induced voiding or contrast radiography), impaired flow of urine through the urethra may persist. This may be related to one or more primary, predisposing or perpetuating causes (Table 2). One cause is inflammatory swelling induced by trauma during attempts to remove plugs or stones from the urethra. This problem can be expected to resolve within a few days provided there is not persistent periurethral extravasation of urine.

Another possibility is spasm of smooth or skeletal muscles surrounding the urethra. However, the frequency with which this type of abnormality occurs, and its responsiveness to smooth and skeletal relaxants have not been extensively characterized.

In a pilot study of six cats with urethral obstruction of undetermined cause, urodynamic studies indicated that urethral muscle spasm was not a significant problem following restoration of urethral patency. On the basis of logic, one would predict that striated muscle relaxants would be helpful for cats with obstructions localized to the post-prostatic urethra. However, at this time, this hypothesis has not been evaluated. On the basis of current evidence, routine use of smooth and skeletal relaxants in cats following urethal obstruction is not warranted.

Other potential causes of impaired voiding through the urethra include reflex dyssynergia, intraluminal accumulations of sloughed tissue, inflammatory cells, or red blood cells and reformation of matrix-crystalline urethral plugs. Urethral strictures may cause persistent outflow resistance in patients with recurrent urethral obstruction. Urethral strictures usually occur as a sequela to: 1) catheter trauma induced at the time of treatment of urethral plugs or urethroliths, 2) use of indwelling transurethral catheters, especially those constructed of material that stimulates a foreign body response and 3) self-trauma.

Formation of urethral strictures may be minimized by proper patient restraint during urethral catheterization, avoiding use of indwelling urethral catheters when possible, and use of restraint devices to minimize self-trauma. If urethral strictures predispose to clinical signs, corrective surgery should be considered, but not before the lower urinary tract has been evaluated by antegrade cystourethrography or retrograde urethrocystography.