RVT, VTS (Anesthesia and Analgesia) | The Ohio State University Veterinary Medical Center
Courtney works at The Ohio State University Veterinary Medical Center in the Small Animal Emergency and Critical Care department. She graduated from Columbus State Community College in 2006 and obtained her VTS in Anesthesia and Analgesia in 2005. Courtney has several publications to her credit. She enjoys spending her free time with her husband and two daughters.Read Articles Written by Courtney Beiter
Urethral obstruction is a potentially life-threatening emergency. Male cats are more prone to obstruction than female cats.1 When the urethra becomes partially or completely blocked, urine is unable to drain from the bladder, resulting in fluid, electrolyte, and acid–base abnormalities.2 Feline urethral obstruction is a relatively common condition, accounting for up to 10% of feline cases presented to small animal referral and emergency clinics.3,4
Editor’s Note: This article was originally published in May 2016. Please use this content for reference or educational purposes, but note that it is not being actively vetted after publication. For the most recent peer-reviewed content, see our issue archive.
The urethra—the tubular passage through which urine is discharged from the bladder to outside the body—can become obstructed for several reasons. The urethra is longer and narrower in male cats than in female cats; therefore, male cats are more likely to develop an obstruction. The most common cause of obstruction is a urethral plug, which consists of mineral crystals (e.g., struvite, calcium oxalate), white blood cells, red blood cells, protein (mucus), and epithelial cells.5 The underlying cause of urethral plugs is unknown; however, plugs have been linked to struvite crystalluria — suggesting that diet may play a role — and idiopathic cystitis.6 Other causes of urethral obstruction include urethral edema and spasm associated with lower urinary tract inflammation and pain.7 Uroliths, neoplasms, and urethral strictures can also lead to urethral obstruction; however, they are reported less frequently than other causes.5
History and Clinical Signs
Cats with a history of lower urinary tract disease—particularly interstitial cystitis—are at an increased risk for developing urethral obstruction.8 Some patients may have a history of obstruction.9 Clinical signs of urethral obstruction can vary depending on the severity and duration of the obstruction. Initially, the most common clinical sign is stranguria, which is sometimes mistaken by the owner as constipation.8 Affected cats may urinate frequently, strain to urinate, urinate inappropriately, and pass small volumes of blood-stained urine (hematuria).10 Lethargy, anorexia, vomiting, and other signs of systemic illness are also common.1 Signs of discomfort or pain caused by an inflamed urethra and increased bladder size include vocalization, inappetence, and hiding. Affected cats can be observed frequently licking their genital region.10 Vomiting and lethargy may also be noted.1 In addition, the patient’s mucous membranes will be pale, and capillary refill time is prolonged.4
On abdominal palpation, the urinary bladder is often large and firm and cannot be expressed easily. Caution should be used when attempting to express a possibly obstructed bladder. If too much pressure is applied to the distended bladder, it can rupture. If bladder rupture is suspected, the goal is to immediately stabilize the patient so that the clinician can perform emergency surgery. If the urethral obstruction goes untreated for more than 24 to 48 hours, the resulting uremia can lead to hypothermia, bradycardia, tachypnea, altered levels of consciousness (including coma), and death.4
A common finding associated with urethral obstruction is a large, firm bladder on abdominal palpation. Urine should be collected for urinalysis, culture, and sensitivity testing.10 Blood work (i.e., complete blood count and serum chemistry profile, including serum potassium levels) should also be obtained. Serum potassium levels can be used to assess cardiotoxicity associated with hyperkalemia.10 An electrocardiogram (ECG) should be obtained to evaluate cardiac function and identify abnormalities consistent with hyperkalemia. Signs of hyperkalemia include diminished to absent P waves, widened QRS complexes, prolonged PR intervals, and tall, “tented” T waves.11 These abnormalities, which most often appear on lead II tracings when serum potassium concentration is >7 mEq/L, are the result of a raised (more positive) resting membrane potential that slows depolarization and exaggerates repolarization.12
Abdominal radiographs can help determine the presence of cystic or urethral calculi. Identification of calculi (stones) affects how an obstruction is treated. The presence of calculi can make it much more difficult to use a urinary catheter to remove the obstruction and can result in additional urethral trauma. If bladder stones are present, a cystotomy should be performed after the urethral obstruction has been removed and the patient is stable enough to undergo anesthesia. Voiding urohydropulsion is another method that can be used to remove bladder stones.13
Address Metabolic Abnormalities
When treating a cat with a urethral obstruction, it is important to quickly stabilize the patient’s vital signs and address metabolic abnormalities so that urethral catheterization can be performed to remove the obstruction. Administering IV fluids is the initial step in therapeutic management. Traditionally, 0.9% NaCl has been the fluid of choice because it does not contain potassium and has the greatest dilutional effect on hyperkalemia; however, a balanced electrolyte solution, such as Normosol-R, Plasmalyte 148, or lactated Ringer’s solution, can be administered as an alternative. Although these solutions contain some potassium, the concentrations are 5 mEq/L or less,14 which may also make the solutions effective in treating concurrent metabolic acidosis. Fluid rate and quantity should be determined based on the patient’s clinical signs and physical examination findings. Aggressive fluid therapy is indicated in patients that are markedly depressed or unresponsive. A shock dose of 60 mL/kg should be administered to these patients and titrated to effect.15 Hydration and cardiovascular status must be reevaluated after each bolus is administered. In patients with stable vital signs, the percentage of dehydration should be used to calculate the fluid rate and quantity required to correct hydration status (BOX 1).
If results of the serum biochemistry profile indicate a potassium concentration that is life threatening (>6 mEq/L),12 and/or if ECG findings suggest hyperkalemia, 10% calcium chloride at 0.1 mg/kg IV should be administered immediately to protect the heart from the effects of hyperkalemia.12 This dose should be given slowly over 5 to 10 minutes while monitoring the patient’s cardiac status on an ECG for conversion to a normal sinus rhythm.
To decrease serum potassium concentration, a combination of regular insulin and dextrose can be administered. Insulin drives potassium into the intracellular space, and dextrose helps prevent hypoglycemia that may result from insulin administration. Regular insulin should be given at a dose of 1 U/cat.a Blood glucose concentration should be monitored every 4 hours after administration of insulin and dextrose. If the glucose concentration decreases to 60 to 70 mg/dL or less, a dextrose constant-rate infusion should be initiated at the fluid rate already being administered. Dextrose 50% can also be administered without insulin to stimulate the release of endogenous insulin. The dose is 0.5 g/kg diluted 1:1 with NaCl or sterile water.5 The dextrose should be diluted 1:1 to decrease the osmolarity and should be administered with caution to avoid extravasation, since it can cause skin sloughing.
Alternatively, sodium bicarbonate (1 mEq/kg given slowly over 10 minutes) can be used to drive potassium into the intracellular space. Administration of sodium bicarbonate may result in ionized hypocalcemia, hypernatremia, alkalosis, and seizures; therefore, its use should be restricted only to patients with severe hyperkalemia (potassium concentration >10 mEq/L) or acidemia (pH <7.1).
Remove the Obstruction
Urethral catheterization is the method most commonly used to remove a urethral obstruction.1 If urethral catheterization cannot be performed immediately, or if the patient is too unstable or in too much pain, the urinary bladder can be emptied through cystocentesis to help stabilize vital signs and to relieve discomfort (BOX 2). Cystocentesis should be performed with caution because the bladder wall is friable and prone to tearing.
A caudal epidural (BOX 3) can facilitate the deobstruction, help decrease the amount of inhalation anesthesia required, and provide analgesia during the recovery period. Various medications can be used for the epidural injection. Lidocaine 2% without epinephrine at a dose of 0.1 to 0.2 mL/kg can be used (approximately 0.5 mL/cat).17 Bupivicaine 0.75% can also be used at the same dose18; its duration of action is approximately 2 hours. Astramorph (Fresenius Kabi, USA; preservative-free morphine) can also be used at a dose of 0.1 mg/kg, with a duration of action of 10 to 24 hours.18
Administration of a sedative before the collection procedure may be required in fractious patients or patients with severe pain. Detailed information on the catheterization procedure as well as sedation is provided in BOX 4.
Acepromazine (0.03 to 0.1 mg/kg IV q6-8h)14 can be administered following urethral catheterization to provide sedation and decrease urethral spasms. It can be administered with buprenorphine (0.006 to 0.01 mg/kg IV q6-8h).20 (In the author’s clinic, doses of 0.01 to 0.03 mg/kg IV have been used q6-8h.) Buprenorphine should be administered to provide analgesia. Buprenorphine solution can be administered orally and should be placed on the oral mucosa, where it has been shown to have excellent bioavailability. Following urethral catheterization, urine output should be measured every 4 hours to ensure that output equals 1 to 2 mL/kg/hr. IV fluids should be recalculated every 4 hours to match urine output plus the maintenance fluid rate for that individual patient. Packed cell volume and serum concentrations of total protein, electrolytes, blood urea nitrogen, and creatinine should be measured once or twice a day to assess hydration status and resolution of metabolic abnormalities.
In some patients with significant azotemia, postobstructive diuresis occurs as a result of medullary washout, osmotic diuresis, pressure necrosis, or antidiuretic hormone resistance. Diuresis should be suspected if urine output exceeds 2 mL/kg/hr. Diuresis can cause rapid dehydration and electrolyte depletion. Urine output of these patients should be monitored closely. Serum potassium concentration should also be measured regularly and potassium supplementation provided as needed.
The urinary catheter should be left in place for 24 to 48 hours after urethral catheterization. Once urine output and results of blood and serum studies are normal, the catheter can be removed. A sterile urine sample for culture should be obtained from the urinary catheter just before removal. After the urinary catheter has been removed, the patient should be monitored closely during the next 24 hours to ensure that urination is normal.
Following discharge to the owner, a patient treated for urethral obstruction should continue to receive treatment with acepromazine at 0.5 mg/kg PO and buprenorphine at 0.01 mg/kg PO for 5 to 7 days to provide continued sedation and analgesia as well as to decrease urethral spasms. Antibiotics should be administered based on the results of culture and susceptibility testing of the urine sample obtained immediately before urinary catheter removal.
Other medications can be used in the hospital or at home after discharge to help to decrease urethral spasms. Phenoxybenzamine, for example, is used mainly to decrease internal urethral sphincter tone, at a dose of 0.5 mg/kg PO q24h. The dose can be increased by 2.5 mg/kg to a maximum of 10 mg. The initial dose should be used for 5 days before reevaluation and then increased, if needed.14 Prazosin can also be used at a dose of 0.5 mg/cat PO q12h.24 Recently, Cosequin for Cats (Nutramax Laboratories, Lancaster, SC) has been used as a symptomatic treatment in cats with FLUTD (feline lower urinary tract disease). This medication, which contains glucosamine and chondroitin sulfate, is a nutritional supplement indicated for cats with arthritis. In cats with FLUTD, it helps to create a water barrier that protects the cells of the urinary tract, which in turn helps prevent bacteria and crystals from adhering to their surface. Some studies show no significant effect compared with placebo; however, some cats in the treatment group showed dramatic improvement when given the medication. The capsule can be opened and the contents sprinkled over the cat’s food.25
Long-Term Dietary and Environmental Management
Long-term management should be geared toward decreasing the recurrence of interstitial cystitis, which may lead to another obstruction. Patients with a history of bladder or urethral stones should be placed on a urinary care prescription diet that keeps pH neutral to help prevent the crystals from returning. These patients can also benefit from increased water intake, with access to fresh running water. Although not ideal, water can be added to their canned food.
Cats that are prone to cystitis need environmental enrichment. Scratching posts and toys can help increase their activity. They also need to be in an environment that has reduced levels of stress, and they need a quiet place for their food and litterbox.
The short-term prognosis for cats treated for urethral obstruction is good when appropriate treatment and supportive care are provided as soon as an obstruction is suspected. Cats that have had one urethral obstruction are at increased risk for reobstruction. In addition, cats that develop urethral obstructions multiple times may require perineal urethrostomy to widen and shorten the urethra. This procedure should drastically reduce the chances of another obstruction from occurring; however, stones or calculi could possibly cause another obstruction.
a. Cooper E, VMD, MS, DACVECC. Personal communication. The Ohio State University Teaching Hospital, 2008.
The author thanks Edward Cooper, VMD, MS, DACVECC, who is affiliated with The Ohio State University Veterinary Medical Center, for his help in reviewing the original article.
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