Emergency Management of Urethral Obstruction in Male Cats

Catherine V. Sabino, DVM, DACVECC, Red Bank Veterinary Hospital, Tinton Falls, New Jersey

Ainsley Boudreau, DVM, DACVECC, Toronto Veterinary Emergency Hospital

Karol A. Mathews, DVM, DVSc (Surgery), DACVECC, University of Guelph

ArticleLast Updated September 202514 min readPeer Reviewed
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Ask the Expert: How can urethral obstruction be diagnosed, stabilized, and treated in feline patients?

Urethral obstruction in cats usually occurs in males 2 to 10 years of age and is less common in female cats because of the wider, shorter formation of the female urethra.

Causes of urethral obstruction are physical (urethral plugs, obstructive idiopathic urethritis, urolithiasis [with or without bacterial infection], urethral stricture, neoplasia [less frequently]) or functional (urethral spasm).

Diagnosis & Assessment

Clinical Signs

Classic signs of obstruction are vocalization and straining while posturing to urinate. Less specific signs can vary from vomiting and mild lethargy to profound lethargy and weakness or collapse.

Physical Examination

Diagnosis is based on the presence of a nonexpressible urinary bladder, which is usually large and firm on palpation; however, a patient obstructed for a shorter period may have a smaller urinary bladder at the time of physical examination. Care should be taken to gently palpate the urinary bladder because mucosal injury from distention can weaken the bladder wall and make it susceptible to leakage and tearing. A partially obstructed bladder may be managed with analgesia and antispasmodic therapy, and the patient can be evaluated for ability to urinate. Catheterization will be required if the bladder remains nonexpressible.

Initial Diagnostics

Blood for baseline electrolytes should be collected to evaluate for life-threatening electrolyte derangements, particularly hyperkalemia. If possible, pretreatment BUN and creatinine should be obtained. Alternatively, CBC and serum chemistry profile (for evaluation of renal parameters) can be collected and performed at this time.

Additional Diagnostics

Other patient-dependent diagnostic testing may be done after urethral catheterization and fluid therapy have been initiated, including urine sediment examination, urinalysis, urine culture, abdominal radiography, and abdominal ultrasonography.

Urinary sediment may reveal pyuria, crystalluria, hemorrhage (cystitis), or atypical cells (neoplasia). Crystal identification is recommended to guide future treatment and prevention. Samples should be collected during urethral catheter placement. If possible, a urine sediment examination should be prepared for slide evaluation within 30 minutes to prevent development of artefactual crystalluria.

Stabilization & Monitoring

Stabilization

All cats presented with urethral obstruction should be treated as emergency cases. Analgesia and a short period of general anesthesia or heavy sedation (depending on patient stability) are necessary for the process of relieving the obstruction. Cardiovascular stability should be ensured as soon as possible (see Hyperkalemia), and, if required, the patient should be prepared for general anesthesia.

Intravenous fluid administration depends on the individual patient. For shock or poor perfusion, small boluses (5 mL/kg) of a buffered, balanced electrolyte solution (eg, lactated Ringer’s solution) should be administered until the patient improves. Otherwise, hydration should be assessed (mild signs, 5% dehydration; moderate signs, 8% dehydration; severe signs, 12% dehydration) and the fluid requirement calculated using the following formula: Percentage dehydration × body weight (kg) = L. For example, the formula for 5% dehydration in a 3-kg (6.6-lb) cat would be: 5/100 × 3 kg = 0.15 L = 150 mL. This deficit should be replaced over 12 to 24 hours and should be administered in addition to the maintenance IV fluid daily rate.

Biochemical & Electrolyte Abnormalities

Many clinicopathologic abnormalities occur in cats with urethral obstruction.

Hyperkalemia

Clinical signs of hyperkalemia are generally nonspecific (eg, muscle weakness, profound lethargy). Bradyarrhythmias can indicate hyperkalemia, but there is no threshold potassium level that can predict development of an arrhythmia. Monitoring the electrocardiogram (ECG) is the quickest way to document that a life-threatening hyperkalemia may affect myocardial function (Figure 1). Wide-complex tachycardia, as well as ventricular tachycardia, may also be present. ECG abnormalities resolve with appropriate treatment of hyperkalemia.

ECG results of a cat.
FIGURE 1

ECG changes seen with urethral obstruction. Early changes include peaked T waves (pink boxes), a shortened QT interval, and an ST segment depression. Progressive changes include bundle-branch blocks, an increase in the PR interval, and decreased amplitude of the P wave. Late changes include disappearance of the P wave (yellow boxes), widened QRS (to resemble a sine wave), and ventricular fibrillation or asystole that follows. Image adapted with permission from Drs. Michael O’Grady and Lynne O’Sullivan; Veterinary Cardiology Online (vetgo.com)

For patients with ECG abnormalities and potassium levels ≥8 mEq/L, emergent treatment consisting of 10% calcium gluconate (0.5 mL/kg slowly IV over 5-10 minutes) should be administered while ECG is continuously evaluated to allow stabilization of the heart until definitive treatment (see below) takes effect. Calcium gluconate will not reduce potassium level.

For definitive treatment of patients with arrhythmias due to hyperkalemia, a beta-blocker (eg, albuterol sulfate, 1 measured dose via a metered dose inhaler; terbutaline, 0.01 mg/kg IM or IV) can be administered to cause intracellular shifting of potassium. Regular IV insulin (0.25-0.5 IU/kg) followed by an IV bolus of 50% dextrose (0.5 mL/kg, diluted 1:4 in 0.9% sodium chloride) and IV CRI dextrose (2.5%-5%) in a buffered balanced electrolyte solution can be given for the next 6 to 12 hours as needed to prevent hypoglycemia caused by insulin administration to a nondiabetic patient. Insulin causes a faster decrease in serum potassium than dextrose alone and is preferred if available. If regular insulin is not available or the potassium level is 6.5 to <8 mEq/L, 50% dextrose (0.5 mL/kg IV, diluted 1:4 in 0.9% sodium chloride) alone can stimulate release of endogenous insulin to drive potassium intracellularly and may be adequate for mild-to-moderate hyperkalemia when no other alternatives are available.

For patients with mild hyperkalemia (potassium level <6.5 mEq/L), resolution is possible with IV volume expansion with a buffered balanced electrolyte solution.

Refractory hyperkalemia is possible in patients that develop acute kidney injury secondary to urethral obstruction. If available, dialysis (peritoneal or hemodialysis) can be considered, particularly if hyperkalemia persists once the obstruction has been relieved

Hypocalcemia

If hypocalcemia is documented, supplementation with 10% calcium gluconate (0.5 mL/kg IV) may be needed over 5 to 10 minutes, along with evaluation of a continuous ECG.

Acidosis

Most cases of metabolic acidosis can be corrected with IV administration of a buffered balanced electrolyte solution. Severe metabolic acidosis (total carbon dioxide or bicarbonate [HCO3¯] level <12 mEq/L [<12 mmol/L], or pH ≤7.2) or acidosis associated with bradyarrhythmia that is not resolved with fluid therapy may necessitate administration of sodium bicarbonate. If metabolic acidosis does not improve after bolus fluid therapy, sodium bicarbonate administration should be continued. The aim is to bring pH out of the critical zone (ie, pH <7.2 or HCO3¯ <12 mmol/L), not to correct to normal.

The bicarbonate requirement should be calculated according to the following formula: Bicarbonate deficit (mEq) = (normal HCO3¯ − actual HCO3¯) × 0.3 × body weight (kg). Typically, a value of 20 to 24 is used as the normal HCO3¯ in this calculation. Half of this bicarbonate deficit should be administered (diluted; administered via syringe pump, dilution into IV fluids in a burette, or slow IV push) over 30 minutes, with ECG monitored.

Azotemia

Patients with urethral obstruction may have postrenal azotemia. Those with prolonged urethral obstruction may also be severely dehydrated and have significant prerenal azotemia in addition to renal and postrenal azotemia. This is usually corrected with relief of the obstruction and IV administration of a balanced electrolyte solution.

Monitoring

When an arrhythmia has been documented, the patient should be closely monitored with continuous ECG and indirect blood pressure measurement at frequent, regular intervals. In patients with initial electrolyte abnormalities, electrolytes should be reassessed 30 to 60 minutes after treatment to correct hyperkalemia; depending on the patient’s condition, reassessment should be repeated at variable intervals. Physical examination and urine output monitoring should also be performed.

Treatment

Relief of Urethral Obstruction

Step 1. Induce anesthesia with short-acting agents (Table). Ensure adequate sedation and analgesia to reduce the risk for movement or struggling during catheterization and to improve the chance for successful catheterization. Severely debilitated patients may require only minimal sedation (eg, low dose of a benzodiazepine or a short-acting opioid).

Author Insight. Sacrococcygeal epidural under sedation can be used for placement of a urinary catheter in cats and may alleviate the need for further anesthesia or sedation to relieve an obstruction. This method can be considered in patients for which alternative anesthesia is not possible because of unavailability of medications or contraindications to general anesthesia. Lidocaine is preferred for its rapid onset, can result in anesthesia after injection, and can last up to 60 minutes. Epidural anesthesia (2% preservative-free lidocaine, 0.1-0.2 mL/kg) is appropriate for all patients without a contraindication to epidural anesthesia and should be performed by clinicians with experience. The patient should be sedated prior to epidural anesthesia. Efficacy should be visible within minutes and includes relaxation of the tail and rectum, with no response to pinching of the tail. Additional analgesia can be considered on an ongoing basis.

Step 2. Attempt to induce voiding with gentle bladder palpation to confirm urethral obstruction. Patients with functional obstruction (eg, urethral dyssynergia, urethritis) may pass urine with gentle palpation of the bladder.

Step 3. Apply sterile lidocaine gel (or sterile 2% lidocaine, 0.25 mL) in the urethral orifice. Lubricate the catheter with sterile gel (with or without lidocaine) to aid in placement. Some lidocaine in the gel will be absorbed systemically through the urethral mucosa; however, a period of local analgesia is beneficial.

Author Insight. The toxic dose of lidocaine is 2 mg/kg in cats; this should be calculated and considered prior to use of topical lidocaine.

Step 4. Perform extrusion of the penis, and examine the distal urethra. A small plug or calculus may be removed at this time using gentle massage. To extrude the penis, use one hand to stabilize and retract the prepuce and the other to pass the catheter. Always start with the least rigid type of catheter available to prevent trauma. A second person can retract the prepuce with one hand and stabilize the tip of the penis with the other hand, leaving the first person with both hands to pass the catheter. Once the catheter has been advanced a few millimeters, the second person can straighten the urethra as much as possible by releasing the hold on the penis and allowing for easier passage of the catheter.

Author Insight. Several catheter types are designed for management of urethral obstruction, including polypropylene tomcat catheters, polyurethane tomcat catheters with and without a stylet, polytetrafluroethylene urinary catheters, and red rubber urinary catheters. Other catheters that can be considered for more persistent obstruction include olive-tipped catheters and peripheral IV catheters with the stylet removed.

Step 5. If the obstruction is not immediately relieved by catheter passage, try retrograde urohydropulsion using an open-ended tomcat catheter. Fill a 12-mL syringe with sterile saline, and add a small amount of sterile lubricant jelly (shake into an emulsion) to lubricate the urethra during hydropulsion. If initial attempts at hydropulsion are unsuccessful, use a smaller syringe (eg, 3 mL) for added pressure. Hold the prepuce, extend the penis dorsocaudally (straighten the urethra as much as possible), and flush the penile urethra while advancing the catheter. Rectal compression of the urethra with concurrent hydropulsion may help relieve the obstruction.

Step 6. If the obstruction cannot be resolved, cystocentesis may be needed to decompress an overly distended bladder. Place a 22-gauge butterfly catheter or a needle with an extension and a 3-way stopcock in the midpoint of the bladder to allow a single penetration through the bladder wall. If available, use ultrasound guidance to visualize the bladder to ensure proper positioning. Insert the needle at an angle (not perpendicular) to ensure the bladder wall is not traumatized as the bladder empties. Remove as much urine as possible, and submit for urinalysis and urine culture. At this time, another attempt at urethral catheterization can be performed and is frequently successful with reduced back-pressure in the bladder.

Author Insight. Not all obstructions can be relieved via urethral catheterization. In these cases, patients can be stabilized and the bladder emptied via intermittent cystocentesis, placement of a cystostomy tube, or cystotomy with antegrade catheterization while waiting for definitive diagnosis and treatment. Treatment should be performed as soon as possible to avoid complications associated with intermittent cystocentesis.

Step 7. Following placement of the urinary catheter, use imaging to confirm correct catheter placement prior to suturing in place and to evaluate for the presence of uroliths. Abdominal radiography (minimally, lateral radiography) or ultrasonography can be performed. If straightforward diagnosis of obstructive uropathy (eg, urethroliths) is not apparent on radiographs, ultrasonographic or contrast urography is required to evaluate for nonradiographically apparent causes (eg, stricture). Evaluation of the upper and lower urinary tract (via ultrasonography or cystoscopy) may be required in some patients.

Inpatient/Outpatient Care

Patients stable on presentation may not require hospitalization or an indwelling catheter once the inciting cause (eg, urethral plug) has been removed. These patients can be managed on an outpatient basis; however, for patients with metabolic abnormalities or a difficult obstruction, a urinary catheter should remain in place for 24 to 48 hours or until urine appears normal. These patients may be discharged from the hospital when normal, consistent voiding behavior is witnessed. If the cat cannot urinate, re-obstruction, bladder atony, urethral damage, urethral spasm, or reflex dyssynergia due to inflammation can be considered.

Continuing Medical Therapy

Opioids (eg, buprenorphine, hydromorphone, methadone, fentanyl) at the lowest dose needed to attain comfort can be used for analgesia and to help relax the urethral sphincter.

Anti-inflammatory therapy may reduce inflammation and discomfort in cats straining because of inflammation. In the author’s experience, these drugs can bebeneficial in reducing inflammation and dyssynergia postobstruction.

NSAIDs are appropriate only in patients without a contraindication to NSAIDs but can be useful in cases in which other analgesic options are unavailable or contraindicated. To decrease the risk for adverse effects, these medications should be used following sedation, administered only in stable patients with normal hydration and without hypotension, and administered based on ideal body weight (which may lead to a dose reduction in obese patients).

Labeled dosage schedule (ie, duration of therapy, dose frequency) may vary by country.

  • Meloxicam (initial dose, 0.1-0.2 mg/kg PO once; after 24 hours, maintenance dose, 0.01-0.05 mg/kg PO every 24 hours)

  • Robenacoxib (2 mg/kg SC every 24 hours up to 3 days, or 6 mg/cat PO every 24 hours in cats weighing 5.5-13.2 lb [2.5-6 kg] or 12 mg/cat PO every 24 hours in cats weighing 13.5-26.6 lb [6.1-12 kg])

Corticosteroids

  • Dexamethasone (0.06-0.16 mg/kg IV or IM every 24 hours) until clinical signs resolve

  • Prednisolone (0.5-1 mg/kg PO every 24 hours; dose can be divided) until clinical signs resolve

  • Acepromazine (0.01-0.05 mg/kg IV) can also be used to promote relaxation of the urethral sphincter.

Parasympathomimetics (eg, bethanechol) should be used only in patients with bladder atony secondary to severe prolonged distention of the bladder and only after urethral patency is confirmed and there is no evidence of remaining calculi.

Follow-Up

After successful medical management, pet owners should be counseled about long-term management of the underlying cause. More information about treatment for bacterial cystitis, feline idiopathic cystitis, crystalluria, and urolithiasis is available in the literature. If medical management fails repeatedly or all medical options have been exhausted, surgical treatment (perineal urethrostomy) may be indicated.

Complications

Torn Urethra

During placement of a urinary catheter, the urethra can be torn, especially if the patient is moving. This is determined by feeling a pop through a band of tissue and an absence of urine flow into the catheter and can be confirmed on radiographs (visualization of the urinary catheter outside of the urethra) or via contrast cystography. Treatment involves leaving an indwelling urinary catheter in place for 72 hours to 7 days and allowing the tear to heal via second intention. Healing can be evaluated by clinical signs or confirmed with contrast cystography. To decrease the risk for urethral damage, the softest catheter possible should be used; more rigid types should only be used if passing the soft catheter is unsuccessful.

Uroperitoneum

Uroperitoneum can result from bladder rupture (iatrogenic or noniatrogenic). Treatment may involve exploratory laparotomy and surgical correction if conservative management (ie, urinary catheterization and abdominal drain placement to allow continuous evacuation and lavage) does not allow healing of tissues. Small defects in the urinary bladder (eg, caused by cystocentesis) may heal with conservative management. In cases of septic peritonitis secondary to leakage of infected urine, surgical management should be performed. An abdominal drain (eg, Jackson-Pratt drain) can be placed in addition to a urethral catheter before definitive surgical correction is performed.

Diuresis & Azotemia

Postobstructive diuresis frequently occurs with prolonged obstruction. High rates of IV balanced electrolyte solution are initially required to compensate for losses; therefore, careful balancing of the patient’s ins (fluid administration) and outs (quantification of urine production) is necessary. BUN and/or creatinine levels should be monitored daily, and fluid therapy can be tapered after azotemia resolves, as urine production should return to normal levels. Urine production can be measured via a closed urinary catheter collection system, calculated as mL/kg per hour, and compared with normal urinary production (1-2 mL/kg/hour) during receipt of IV fluids. If definitive urine output is unknown (eg, catheter malfunction or removal), changes in hydration status and body weight can be used as a crude assessment of fluid balance. (The patient should be weighed 2-6 times daily; change in body weight of 0.1 kg is equal to a fluid loss or gain of 100 mL). If a urinary catheter cannot be maintained, urine can be collected using nonabsorbing litter and then measured.