Clinical Signs and Physical Examination

Clinical signs of urethral obstruction depend on the severity and duration of the occlusion, but can include stranguria or dysuria, vocalization, frequent licking of the perineal area in cats or the penis in dogs, hematuria, pollakiuria, oliguria or anuria, vomiting, mild lethargy, profound weakness, obtundation, or collapse [1, 6].

The presence of a firm, nonexpressible urinary bladder, which usually elicits a painful response on palpation, often reveals the diagnosis [1]; radiographs or ultrasound may also be helpful. Bladder size varies based on duration of obstruction and gentle palpation is encouraged due to the likelihood of mucosal injury weakening the bladder wall. Nevertheless, the presence of urine flow does not rule out partial urethral obstruction, particularly if the rate or pressure of the stream is reduced compared to normal. Additionally, absence of a palpable bladder does not rule out urethral obstruction, as the bladder may have ruptured.

In canines, an examination per rectum to assess the prostate and intrapelvic urethra may reveal abnormalities such as urethral enlargement, a mass or a palpable urolithiasis. Discoloration of the penis tip in a cat or visualization of a urethral plug is possible. The patient may be hypothermic or hyperthermic, tachycardic or bradycardic, tachypneic, and may have poor pulse quality. The critical patient has clinical signs associated with systemic acid–base and electrolyte abnormalities including dehydration (prolonged skin turgor and tacky mucous membranes [MMs]), hypovolemia, bradycardia, arrhythmias, hypothermia, weak pulses, and possibly obtundation and collapse [1, 7, 8].

Bradycardia and other arrhythmias should alarm the clinician into immediate action, as hyperkalemia is typically the cause. Furthermore, a low normal heart rate (HR) that inappropriately matches the clinical situation should urge the clinician to investigate hyperkalemia. A retrospective study of cats with urethral obstruction reported moderate bradycardia (100–140 beats min⁻¹) in 6% of cats and severe bradycardia (<100 beats min⁻¹) in 5% [7]. Additionally, bradycardia (<120 beats min⁻¹) in combination with hypothermia (<95.0–96.6 F) was 98% specific for severe hyperkalemia (8 mEq l⁻¹) [7].

Initial Database and Clinicopathology

The urgent database includes electrocardiogram (ECG), electrolytes, venous blood gas, packed cell volume (PCV), total solids (TSs), blood urea nitrogen (BUN), creatinine, blood glucose (BG), lactate, and ionized calcium (iCa), followed by a complete blood count (CBC) and biochemical panel. Dehydration, hypovolemia, decreased tissue perfusion, azotemia, metabolic acidosis, hyperkalemia, hyperphosphatemia, and hypocalcemia are possible sequelae to urethral obstruction [6, 7].

Dehydration results from a lack of oral fluid intake and losses by nonrenal routes such as vomiting [7]. Therefore, severe dehydration and significant prerenal azotemia in addition to renal and postrenal azotemia may be present. Urine outflow obstruction induces pressure back on the kidneys which decreases glomerular filtration rate (GFR), resulting in azotemia and decreased phosphorus, potassium, and hydrogen ion secretion [7]. Phosphorus retention may cause chelation of calcium [7, 9]; thus, iCa concentrations may be decreased. Ionized hypocalcemia (<1.0 mmol l⁻¹) occurred in 20% of cats in one study [7], and up to 75% in another [10]. The mechanical and electrical dysfunction induced by such ionized hypocalcemia amplifies the cardiac effects of hyperkalemia [7, 11].

Metabolic acidosis may induce respiratory compensation including increased minute ventilation (V_E), clinically recognized as larger tidal volume (TV) and occasionally tachypnea [12]. However, patients with life‐threatening hyperkalemia often have poor compensatory responses, and the resulting respiratory acidosis will exacerbate the existing metabolic acidosis. Additionally, a concurrent metabolic acidosis may amplify the hyperkalemia‐induced cardiotoxicity [7, 13]. However, these effects usually do not occur unless severe acidemia (pH <7.1) occurs [11].

Hyperkalemia may result from several mechanisms including shifting of potassium from the intracellular space in exchange with hydrogen ions in response to acidemia, impaired GFR with resultant inability to excrete potassium, and reabsorption from the damaged bladder mucosa [7]. Hyperkalemia increases the resting membrane potential of cells, resulting in a reduced gradient between the resting membrane and threshold potential, causing an increase in cell membrane excitability [13]. Additionally, potassium ion concentration is altered, resulting in cells that are slower in reaching threshold potential with prolonged recovery and prolonged cardiac action potential duration [14]. Eventually, the resting membrane potential may become less negative than the threshold potential, making the cell unable to repolarize after depolarization [6]. Life‐threatening cardiac arrhythmias can result, progressing from bradycardia to ventricular fibrillation or asystole. The ECG may reveal bradycardia, prolonged P‐R interval, decreased or absent P waves, widened Q‐R‐S complexes, and/or spiked T waves, to even wide complex tachycardia or ventricular tachycardia. Establishing cardiovascular stability is imperative, particularly in the face of severe hyperkalemia. Therefore, after the baseline HR, pulse palpation, and rhythm evaluation, an ECG and arterial blood pressure (ABP) should be obtained, especially in patients with bradycardia, tachycardia, arrhythmias, obtundation, or collapse.

It is important to consider anemia in patients with chronic renal dysfunction, urinary bladder hemorrhage associated with urethral obstruction [15], and cases of recent repeat urethral obstruction, during which anemia may develop secondary to dilutional fluid therapy required to manage postobstructive diuresis. Additionally, cats and patients with underlying cardiac disease may be subject to fluid overload during this diuresis phase, and this should be considered prior to and during anesthesia. Anemia induces impaired oxygen‐carrying capacity, and oxygen supplementation is imperative throughout stabilization. In some cases, a blood transfusion may be necessary to address this complication.

Additional patient‐dependent diagnostics may occur once the patient is stabilized and may include urinalysis with sediment evaluation, urine culture, and abdominal radiographs and/or ultrasound. Radiographs may be obtained in the conscious or sedated patient to localize and identify a cause of obstruction prior to passing a urethral catheter. Contrast urethrography, if required, should be attempted only after stabilization, as it generally requires deep sedation or general anesthesia to prevent the animal from responding to manipulation, which may result in iatrogenic trauma. Details of anesthetic‐related concerns during imaging are described in the following text (see the section titled “Urinary Tract Diagnostic Imaging”), and the sedation protocol should be based on the procedure and individual patient.

Preanesthetic Management and Initial Stabilization

While prompt return of urethral patency is a priority, patients with metabolic abnormalities have an increased risk of complications if anesthetized, including cardiopulmonary arrest [3]. Therefore, rapid preanesthetic stabilization is imperative and includes restoring circulating volume and correction of electrolyte and acid–base abnormalities (Table 7.1). The degree of hyperkalemia, ECG alterations, and bladder distention dictate treatment priority, and how promptly relief of urethral obstruction should occur.

Throughout the stabilization process, supplemental oxygen and serial hands‐on monitoring are advised, particularly when an arrhythmia or bradycardia has been documented. Monitoring parameters should include HR and rhythm with continuous ECG monitoring, pulse quality, and ABP. Intravenous (IV) access is a priority in all patients; to facilitate catheter placement, consider the patient’s temperament, stability, and discomfort, and provide sedation when necessary, to avoid distress. Additionally, because urethral obstruction is classified as being moderately painful [16], appropriate analgesics are required (Table 7.2).

Crystalloids, as balanced electrolyte solutions, are preferred for correcting acid–base imbalances and remedy hypovolemia and dehydration. There was no difference in the rate of decline of serum potassium, but there was a more rapid correction of acidemia in cats treated with lactated ringer’s solution (LRS) or Normosol‐R than those treated with 0.9% sodium chloride [17, 18]. Fluid rates depend on the individual patient; however, for shock or poor perfusion conditions, fluid rates should be tailored to reach endpoints of resuscitation. Increments of approximately 25% of a shock dose (approximately 20 ml kg⁻¹ in dogs, approximately 12 ml kg⁻¹ in cats) over 15–20 min with reevaluation of endpoints such as mentation, HR, capillary refill time (CRT), and ABP are advised prior to continuing with fluid boluses. Once volume expansion is deemed adequate, or if resuscitation is not necessary, the fluid rate is based on patient hydration status, adding the calculated replacement of dehydration to normal maintenance fluid requirements. In patients with cardiac disease or predisposed breeds, more cautious fluid therapy and closer monitoring are advised.

Although most cats with urethral obstruction are relatively stable without serious metabolic abnormalities, severe hyperkalemia is the most common life‐threatening problem (approximately 12% of cats, serum potassium >8 mEq l⁻¹) [7, 19]. Interestingly, the severity of clinical signs does not necessarily correlate with serum potassium concentrations; therefore, monitoring the ECG is the quickest way to document a life‐threatening hyperkalemia. ECG issues will resolve with appropriate stabilization of the cardiac membrane and treatment of hyperkalemia. While cardiac conduction disturbances vary based on potassium concentrations, there is no threshold potassium concentration that can predict arrhythmia development, but generalizations can be made (Table 7.3). Although ultimate resolution of hyperkalemia involves reestablishing urethral patency, concentrations of potassium greater than 7.0 mEq l⁻¹ may induce irregular idioventricular rhythms. Therefore, if the serum potassium concentration is greater than 7.0 mEq l⁻¹, regardless of ECG findings, correction is advised to reduce the risk of cardiopulmonary arrest. In a perfect situation, potassium concentrations should be near normal (<5.5–6.0 mEq l⁻¹) before anesthesia. Management of hyperkalemia is ultimately focused on antagonizing the cardiotoxic effects on the myocardial cells, reducing serum potassium through dilution, and increasing its elimination and redistribution. Therapy options for hyperkalemia management are listed in Table 7.4 and discussed in the following text.

Mild increases in serum potassium in the stable patient may be corrected with dilutional fluid therapy and relief of the obstruction. Rapid intravascular volume expansion results in dilution of plasma potassium within minutes, and elimination via increased GFR simultaneously occurs. However, cystocentesis or reestablishment of urethral patency is imperative to permit elimination of potassium and prevent exacerbation of urine volume. Therefore, consider the patient’s bladder size when administering necessary fluid support in correlation with how rapid the restoration of urine flow will occur. Therapeutic cystocentesis should be considered, particularly in cases with maximally expanded bladders in the presence of hyperkalemia‐induced ECG abnormalities that do not permit rapid relief of urethral obstruction. Decompressive cystocentesis aids in rapid stabilization, allowing improved GFR and reduction of bladder pressure, which may facilitate urethral catheterization and retrograde urohydropropulsion [20]. Additionally, cystocentesis appears to be safe, as the overall risk of bladder rupture is low [20–22]. An injectable opioid ± benzodiazepine combination (Table 7.2) may be administered prior to cystocentesis not only to prevent patient movement leading to iatrogenic trauma but also to ease the discomfort secondary to the obstruction and procedure.

Additional therapies are indicated in patients with moderate potassium increases. Potassium redistribution via dextrose and insulin administration is effective within 20–40 min. Regular insulin (0.5 U kg⁻¹ IV) promotes cellular uptake of glucose with simultaneous cotransport of potassium. Dextrose prevents hypoglycemia following insulin administration and is provided as a bolus (50% dextrose solution: 1 ml kg⁻¹, diluted 1:3 due to hyperosmolarity), followed by an infusion (1.25–2.5% dextrose: cats 2–3 ml kg⁻¹ h⁻¹, dogs 2–6 ml kg⁻¹ h⁻¹, expected 4–6 h duration), adjusted based on frequent BG monitoring. Another approach is to administer only IV dextrose as a bolus to induce the endogenous secretion of insulin.

In the presence of moderate to severe hyperkalemia, life‐threatening bradycardia, or arrhythmias, calcium administration is indicated for immediate stabilization of the myocardium. Calcium gluconate (10% solution: 0.5–1.5 ml kg⁻¹) should be administered slowly IV over 5–10 min while continuously monitoring the ECG. If bradycardia worsens or shortening of the Q‐T interval occurs, the infusion should be stopped. The effects of calcium administration only last 20–30 min, but it may be a life‐saving measure [13]. Calcium therapy does not reduce serum potassium concentrations; therefore, its administration should be promptly followed with therapies including insulin and dextrose administration.

Beta‐2‐adrenergic receptor agonists can be used to redistribute potassium intracellularly. These agents reduce the potassium concentration by activating the sodium–potassium‐ATPase pump. However, beta‐2‐adrenergic receptor agonists are not recommended as the sole therapy for management of hyperkalemia.

Concurrent abnormalities such as metabolic acidosis and ionized hypocalcemia can exacerbate hyperkalemic effects on cardiac conduction [13]. IV fluid therapy is the initial treatment in the management of metabolic acidosis; sodium bicarbonate therapy should be reserved for use only when fluid therapy is not effective and in the face of severe acidemia (pH <7.0). Sodium bicarbonate raises the pH, driving potassium intracellularly in exchange for hydrogen ions. This therapy may be less effective than dextrose and insulin at reducing potassium and should be used with caution due to resultant cerebrospinal fluid (CSF) acidosis and cerebral edema with overzealous administration. Therefore, incremental dosing is advised to avoid oversupplementation and a resulting alkalosis [23]. Additionally, acid–base management with alkalization in the face of ionized hypocalcemia should be considered with caution. As the pH increases, calcium binds to negatively charged proteins in addition to intracellular movement, potentially exacerbating ionized hypocalcemia and cardiac dysfunction [7]. While hypocalcemia resolves rapidly after reestablishing urine flow as serum phosphorus concentrations decrease, associated cardiac disturbances or muscle twitching or seizures (less common) should be managed with an IV infusion of calcium gluconate.

Electrolyte and acid–base abnormalities should be reassessed every 30–60 min after the initial treatment to correct derangements. The results should be used to guide continued therapy until the patient is stable and laboratory parameters are deemed acceptable for anesthesia.