Urogenital Concerns

Urogenital Concerns

Carrie A. Davis

Animal Imaging, Irving, TX, 75039, USA


Minimally invasive procedures and surgeries may be indicated for evaluation or treatment of congenital, acquired, and neoplastic conditions involving the urogenital tract. Patients may present in a critically ill state encompassing an array of shock states with fluid, acid–base, electrolyte, and renal disturbances, in addition to anemia or other metabolic derangements. Thus, the anesthetist should not only be familiar with the pathophysiology and expected clinicopathologic abnormalities of the various conditions in order to appropriately stabilize patients prior to anesthesia, but also be cognizant of the pharmacologic agents and procedural risks while preparing to manage complications. Discussion of anesthetic concerns involving acute and chronic renal disease is described elsewhere (see Chapter 6).

Urogenital Emergencies

Urinary‐tract‐associated emergencies are broadly classified as (i) obstructive to urine flow, or (ii) resulting in accumulation of urine within the peritoneal cavity or retroperitoneal space. Discussion of emergencies involving the genital tract will center on pyometra, while cesarean sections are discussed in Chapter 18.

Urogenital emergencies are commonly encountered in small‐animal practice and present with, or have the potential of progressing to, a life‐threatening crisis if not rapidly managed [1]. Although reestablishing urine flow, surgical repair of the urinary tract, or ovariohysterectomy may be required for resolution, patients that are metabolically and hemodynamically unstable are regarded as urgent medical emergencies. Subjecting such patients to immediate anesthesia or surgery would likely compromise the outcome [2, 3]; however, pain management is essential. Additionally, sedation is commonly necessary to obtain diagnostics or perform minor procedures that are paramount to patient survival and stabilization prior to anesthesia. Emergency procedures of the urinary tract may be required in the recently traumatized patient, and to appropriately prioritize patient care, a thorough examination is required for identification of concomitant injuries or conditions.

Urethral Obstruction

Feline urethral obstruction is a common urinary tract emergency with an incidence rate between 2% and 13% at veterinary teaching hospitals across North America [4]. The condition is most common in male cats that are predisposed to obstruction due to their long, narrow urethra (compared to females). Various causes have been identified and can be categorized as anatomical or physical (urethral plugs, obstructive idiopathic urethritis, urolithiasis, urethral stricture, and neoplasia) or functional (urethral spasm). Canine urethral obstruction is less common, and occurs most frequently in males due to urolithiasis, but can also result from urethral strictures or neoplasia. Calculi commonly lodge just behind the caudal aspect of the os penis, but also lodge at the ischiatic arch and prostatic urethra [5].

Although most patients with urethral obstruction present in stable condition permitting rapid restoration of urethral patency using techniques such as retropulsion, urethrotomy, or urethrostomy, prolonged urethral obstruction results in severe cardiovascular compromise and collapse due to life‐threatening electrolyte and acid–base abnormalities. Therefore, patients presenting with urethral obstruction should be treated as a medical emergency with evaluation of clinical signs being performed simultaneously with diagnostic evaluations, patient stabilization, and treatment.

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 (VE), 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.

Table 7.1 Immediate evaluation and stabilization options in urinary tract obstruction/uroabdomen.

Abnormality Immediate stabilization/comments
Bradycardia or arrhythmia

  • Immediate ECG evaluation (Table 7.3)
  • Measure serum potassium
  • Obtain IV access
  • Immediately stabilize myocardium with calcium gluconate, followed by other treatments for hyperkalemia (Table 7.4)
  • Oxygen support, if tolerated

  • Examine for bradycardia or arrythmia
  • ECG evaluation (Table 7.3)
  • Obtain IV access
  • IV fluid support, based on individual, consider 10–20 ml kg−1 h−1 balanced crystalloid
  • Treat hyperkalemia (Table 7.4)
  • Reestablish urine flow. Consider urine diversion when appropriate:

    • Urethral obstruction: catheterize urinary bladder, cystocentesis

    • Uroabdomen: catheterize urinary bladder (if possible), peritoneal urine drainage

  • Manage concurrent metabolic acidosis and hypocalcemia

  • Obtain IV access
  • IV fluid support targeting endpoints of resuscitation based on individual, options:

    • Balanced crystalloid: ¼ shock dose increments (approximately 20 ml kg−1 dog, approximately 12 ml kg−1 cat); reassess before repeating

    • Hypertonic saline (7.5%) over 10 min (4–7 ml kg−1 dog, 3–4 ml kg−1 cat)
Metabolic acidosis

  • Obtain IV access
  • IV fluid support FIRST

    • Balanced crystalloid

  • Sodium bicarbonate, consider in severe case not responding to fluid support and pH <7.0 (Table 7.4)
Ionized hypocalcemia

  • Obtain IV access
  • IV fluid support
  • IV calcium gluconate (Table 7.4)

  • Based on individual patient, opioid ± benzodiazepine (Table 7.2) and avoid drugs listed in Table 7.5

ECG, electrocardiogram; IV, intravenous.

Table 7.2 Common analgesics, sedatives, and anesthetics for urogenital anesthesia.

Drug a Agent/dose Comment
Premedicant, sedative, analgesic
Analgesia, always titrate to effect, possible bradycardia, minimal effects on cardiovascular system, reversible with naloxone
Hydromorphone (full mu‐agonist) 0.05–0.2 mg kg−1 SC, IM, IV

  • May induce vomiting or pant
  • Repeat every 2–6 h
Morphine (full mu‐agonist) Cat: 0.1–0.5 mg kg−1 SC, IM, slowly IV
Dog: 0.2–1.0 mg kg−1 SC, IM, slowly IV

  • Repeat every 2–4 h
  • Histamine release when administered rapidly IV
  • Caution: active metabolites in dogs may have delayed elimination in renal insufficiency, prolonging effects. Clearance may be slower in affected cats. Consider low‐dose or other opioids in significant renal disease
Fentanyl (full mu‐agonist) 1–5 μg kg−1 IV bolus or loading dose

  • One dose duration approximately 15–30 min, requires CRI for continued effect (see below)
Methadone (mu‐agonist, N‐methyl‐D‐aspartate (NMDA) antagonist) Dog: 0.05–0.6 mg kg−1 SC, IM, IV
Cat: 0.05–0.5 mg kg−1 SC, IM, IV

  • Repeat every 2–6 h
Butorphanol (kappa‐agonist/mu‐antagonist) 0.1–0.5 mg kg−1 SC, IM, IV

  • Mild analgesia, favorable for sedation and antiemetic effects
  • Repeat every 1–4 h
Buprenorphine (partial mu‐agonist) 0.005–0.03 mg kg−1 SC, IV, IM or 0.01–0.03 mg kg−1 OTM in cats

  • Moderate analgesia, difficult to reverse
  • 30 min to full effect
  • Repeat every 6–12 h
Sedation and muscle relaxation, no analgesia, antagonized with flumazenil, alone may induce excitement
Midazolam 0.2–0.5 mg kg−1 IV, IM

  • Water‐soluble
Diazepam 0.2–0.5 mg kg−1 IV

  • Contains propylene glycol
  • Metabolized to active metabolites, may cause prolonged sedation
Combine opioid and benzodiazepine Benzodiazepine 0.1–0.5 mg kg−1 and opioid of choice, such as butorphanol 0.1–0.4 mg kg−1, etc.

  • Maintain cardiovascular stability
  • May permit minor procedures ± sacrococcygeal epidural to remove urethral obstruction
Sedation option for relief of urethral obstruction
Benzodiazepine, ketamine, and opioid Ketamine 0.5–4.0 mg kg−1 and benzodiazepine 0.1–0.5 mg kg−1 and opioid of choice such as butorphanol 0.1–0.4 mg kg−1, etc.

  • Consider sacrococcygeal epidural
  • Selection based on patient stability
  • Avoid if underlying cardiac disease
  • Urethral obstruction removal may require inhalant general anesthesia
Anesthetic induction agents
Propofol 2–6 mg kg−1 IV titrated slowly to effect

  • Rapid‐acting, short duration
  • Respiratory depression
  • Peripheral vasodilation
  • Myocardial depression
Alfaxalone 0.5–5 mg kg−1 IV titrated slowly to effect, reduced doses advised in critically ill

  • Add sedative to improve recovery
  • Respiratory depression
  • Off‐label IM use in combination with opioid ± benzodiazepine to aid in fractious patient sedation to permit IV catheterization
Etomidate 1–2 mg kg−1 IV titrated to effect

  • Cardiovascular stability
  • Caution: induces adrenocortical suppression which may be contraindicated in septic patients who have adrenal insufficiency (possible in severe pyometra)
Ketamine 2–5 mg kg−1 IV
Use in combination with propofol, alfaxalone, or benzodiazepine

  • Prolonged effects in patients with renal insufficiency or inability to excrete urine
  • Reduce dose by adding coinduction agents
  • May be contraindicated with some underlying cardiovascular diseases, dysrhythmias, or tachycardia
  • Caution in critically ill patients with catecholamine depletion, since direct myocardial depressant effects may induce hypotension
Inhalant anesthetics Isoflurane 1–2% or sevoflurane 2–3% to effect

  • Dose‐dependent cardiovascular and respiratory depression
Opioid CRI Fentanyl 2–20 μg kg−1 h−1
after loading dose IV
30–50% MAC reduction
Ketamine CRI 0.1–1.2 mg kg−1 h−1 after loading dose of 0.5 mg kg−1 IV 10–30% MAC reduction
Lidocaine CRI (dog only) 1–6 mg kg−1 h−1 after loading dose of 1–2 mg kg−1 IV 15–30% MAC reduction
Epidural anesthesia:
2% lidocaine 0.1–0.2 mg kg−1 See Table 7.6
Epidural anesthesia:
Lumbosacral (LS)
Morphine 0.1 mg kg−1
Bupivacaine 0.5 mg kg−1
(each may be used alone or together)

  • If morphine is used alone, dilute with 0.9% saline to make 0.1 ml kg−1 volume
  • LS epidural total volume should not exceed 0.25 ml kg−1 or a maximum volume 8 ml (use 0.9% sterile saline to make up to 0.25 ml kg−1 volume)
Postoperative analgesics
Opioids As mentioned above, intermittent dosing or CRI
Ketamine CRI As mentioned above
Lidocaine CRI in dogs only As mentioned above

a Other agents and doses are possible. SC, subcutaneous; IM, intramuscular; IV, intravascular; OTM, oral transmucosal; CRI, constant rate infusion; MAC, minimum alveolar concentration.

Table 7.3 Hyperkalemia‐induced electrocardiographic (ECG) changes.

Serum potassium concentration (mEq l−1) Expected ECG abnormalities
>5.5 T wave: tall and tented
>6.5 P‐R interval: prolonged
Q‐R‐S complex: duration prolonged
R wave: amplitude decreased
S‐T segment: depressed
>7.0 P wave: amplitude decreased; duration increased
Q‐T segment: prolonged
>8.5 P wave: may disappear (atrial standstill)
Abnormal rhythm: sinoventricular
>10.0 Q‐R‐S complex: widened and biphasic
Abnormal rhythms: ventricular flutter, fibrillation, or asystole

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 [2022]. 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.

Table 7.4 Hyperkalemia treatment.

Drug Dose Mechanism Comments
IV fluid therapy: crystalloid Based on individual patient, consider 10–20 ml kg−1 Dilutional: IV volume expansion
Elimination: increasing GFR
Effective within minutes, relief of urinary obstruction or peritoneal drainage must coincide, not advised as sole method for severe or life‐threatening hyperkalemia
Insulin and 50% dextrose 0.5 U kg−1 IV regular insulin and 2 g U−1 (4 ml U−1) IV 50% dextrose diluted 1:3 with saline Redistribution: stimulates Na+‐K+‐ATPase activity, glucose and potassium move into cells Onset 30 min, serial blood glucose measurements and supplement dextrose to prevent continued hypoglycemia
50% dextrose alone 0.5–1 g kg−1 (1–2 ml kg−1) IV diluted 1:3 with saline, slowly over 3–5 min Redistribution: induces endogenous insulin release, see above Onset within 1 h, not advised as sole treatment in severe or life‐threatening hyperkalemia
Terbutaline 0.01 mg kg−1 IV slowly Redistribution: stimulation of Na+‐K+‐ATPase activity, moving potassium intracellularly Onset 20–40 min, not advised as sole agent therapy,
option to use inhaled β2‐adrenergic agonists
Sodium bicarbonate 0.3 × base deficit × body weight (in kg) and give 1/3–1/2 dose IV slowly over 15–30 min
OR 1–2 mEq kg−1 IV slowly over 15 min
Redistribution: improves extracellular acidosis, indirectly stimulates activity of Na+‐K+‐ATPase resulting in exchange of potassium for hydrogen ions Onset 15 min, other treatments are advised first, can result in CSF acidosis and cerebral edema if given overzealously, caution in ionized hypocalcemia
10% calcium gluconate 50–150 mg kg−1 (0.5–1.5 ml kg−1) IV slowly over 5–10 min with ECG monitoring during infusion to recognize bradycardia or worsening of arrhythmia Antagonism: decreases cardiac excitability via reestablishing a more normal gradient between resting membrane and threshold potentials Effective immediately (3–5 min) with short‐ lived duration, but a life‐saving measure, antagonizes the effect of hyperkalemia on myocardium, does NOT alter serum potassium, other treatments should be instituted simultaneously
Urinary diversion Uroabdomen: urethral catheterization and peritoneal drainage
Urethral obstruction: urethral catheterization, alternatively perform cystocentesis
Elimination: uroabdomen, potassium‐containing urine exits the body, no longer being reabsorbed.
Urethral obstruction, relief permits elimination
Recommended stabilization procedures in uroabdomen.
Cystocentesis stabilization option when relief of urethral obstruction is not immediately possible

IV, intravenous; GFR, glomerular filtration rate; CSF, cerebrospinal fluid.

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.

Sedation and Anesthesia

The treatment goal is to rapidly relieve the obstruction without traumatizing the urethra [3]. Therefore, once cardiovascular stability is ensured, analgesia with sedation or general anesthesia is necessary for reestablishing urethral patency. Appropriate fluid replacement and correction of acid–base and electrolyte abnormalities are likely more important to success versus the recommendation of a specific anesthetic protocol. Drug selection should be individualized according to the procedure and specific needs of the patient; however, short‐acting, reversible agents that provide adequate sedation and analgesia are ideal (Table 7.2). Injectable or inhalational anesthetic agents added to produce neuroleptanalgesia (opioid and a sedative such as a benzodiazepine) may be indicated. Severely debilitated patients may require only minimal sedation for diagnostics and the unblocking procedure.

Mask or box induction with volatile anesthetics should be avoided whenever possible, since inhalant anesthetic drugs cause dose‐dependent depression of the central nervous system (CNS), cardiovascular, and respiratory systems. Compromised animals may not tolerate the high concentrations (possibly an overdose) of volatile anesthetics required to induce anesthesia when no concurrent drugs are administered. Additionally, masking/boxing is dangerous to the staff secondary to environmental contamination.

The anesthetist should inquire about current medications used for long‐term management of lower urinary tract conditions, including alpha‐adrenergic receptor antagonists such as phenoxybenzamine and prazosin. These may result in vasodilation and hypotension, which may be exacerbated in anesthetized patients. To this end, drugs known to induce hypotension, cardiovascular compromise, or nephrotoxicity should be avoided if possible (Table 7.5). Animals with decreased renal perfusion of any cause, such as shock, hypovolemia, dehydration, or hypotension, may be susceptible to nonsteroidal anti‐inflammatory drug (NSAID)‐induced renal damage; therefore, use of NSAIDs is not advised until appropriate renal function has been confirmed and cardiovascular status is stabilized [24]. Although the sedative effects of acepromazine and promotion of urethral smooth muscle relaxation seem desirable, simultaneous vasodilation may lead to hypotension, even with low IV doses. Therefore, acepromazine use in patients with preexisting hypovolemia, dehydration, or hypotension is discouraged, and, if selected, close monitoring and maintenance of normotension are advised. Alpha‐2‐adrenergic receptor agonists such as dexmedetomidine should be used with caution or avoided in patients with unresolved urinary obstruction, considering their diuretic effect secondary to inhibition of arginine vasopressin (AVP) or a hyperglycemic osmotic diuresis due to insulin inhibition [25]. Additionally, the bradycardia, peripheral vasoconstriction, decreased cardiac output (CO), and potential arrhythmias [26] may exacerbate the cardiotoxic effects of hyperkalemia [13].

Premedication using neuroleptanalgesia is an ideal choice (Table 7.2). Opioids have minimal direct effects on the cardiovascular system and provide analgesia, sedation, and reversibility. Potential negative opioid effects include bradycardia, emesis (hydromorphone, etc.), and possibly histamine release (e.g., morphine administered rapidly IV). In the face of severe hyperkalemic bradycardia, anticholinergics may not be effective [27, 28]; therefore, the clinician should consider treatment with immediate cardioprotective mechanisms (i.e., calcium administration) and reduction of potassium (Table 7.4) prior to administration of opioids, which may worsen bradycardia. Benzodiazepines in combination with an opioid cause minimal depression of the cardiovascular system and provide reversibility and sedation, permitting minor treatments or diagnostics and may aid in urethral relaxation through their effects on striated muscle. However, benzodiazepines may induce excitation and dysphoria, particularly when used alone; fortunately, more reliable sedation is likely to occur in geriatric or sick patients, and when coadministered with opioids.

Table 7.5 Drugs to avoid or use with caution.

Drug or drug class Comments

  • Ill‐advised in presence of decreased renal perfusion such as shock, hypovolemia, dehydration, hypotension, or presence of azotemia
  • Consider only after renal function has been confirmed and cardiovascular status is stabilized
Alpha‐2‐adrenergic receptor agonists (dexmedetomidine)

  • Reduced cardiac output, increased SVR, bradycardia, and potential to induce dysrhythmias, may exacerbate the cardiotoxic effects of concurrent hyperkalemia
  • Promotes diuresis in face of inability to void urine
  • May consider in a patient with a stable cardiovascular system with timely establishment of urine flow
Phenothiazines (acepromazine)

  • Vasodilation‐induced hypotension possible at any dose, use is discouraged in cases with preexisting hypovolemia, dehydration, or hypotension
  • Negative effects may be exacerbated when used with other drugs, inducing cardiovascular depression
  • Consider only after cardiovascular status is stabilized, 0.005–0.03 mg kg−1 IV

  • While etomidate exerts minimal cardiovascular effects, it induces adrenocortical suppression which may be contraindicated in septic patients who have adrenal insufficiency (possible in severe pyometra)

  • May be contraindicated with some underlying cardiovascular diseases, dysrhythmias, or tachycardia
  • Caution in critically ill patients with catecholamine depletion in which ketamine’s direct myocardial depressant effects may induce hypotension
  • Liver metabolism to varying degrees based on species; metabolites depend on renal excretion. Prolonged drug effects possible in cats with renal insufficiency, inability to eliminate urine and uroabdomen (continuously resorbed from urine in abdomen)
  • When ketamine is used, consider reduced dose and avoidance of repeat doses or a CRI until urine elimination is restored (cats)

  • Systemic lidocaine infusions are not advised for balanced anesthesia in cats due to severe cardiovascular depression and lack of effect on thermal pain
  • Systemic lidocaine is contraindicated in patients with escape rhythms, absence of P waves/atrial standstill, and should be used cautiously in bradycardia

NSAIDs, nonsteroidal anti‐inflammatory drugs; SVR, systemic vascular resistance; IV, intravenous; CRI, constant rate infusion.

Depending on the patient, analgesia and injectable or inhalational maintenance anesthesia may be necessary to reestablish urethral patency using catheterization and retropulsion. Some patients may respond to neuroleptanalgesia with the addition of subanesthetic doses of propofol (0.25–1.0 mg kg−1), possibly in combination with a sacrococcygeal epidural (Table 7.6). Propofol is desirable for its short duration of action and is advisable in stable patients, but caution is advised in debilitated patients due to potential dose‐dependent vasodilation and hypotension. However, methods to reduce the dose of propofol including adequate sedation and use of a coinduction agent (e.g., benzodiazepines, opioids, or ketamine) may attenuate these effects. Alfaxalone, when used at recommended doses, maintains cardiovascular parameters within normal limits in healthy animals, and doses of 1–2 mg kg−1 IV over 60 s provide acceptable induction in dogs considered to be a poor anesthetic risk [29]. However, it should be administered to an appropriately sedated patient to prevent muscle twitching or poor recovery. Additionally, similar to propofol, respiratory depression and apnea can occur with alfaxalone; therefore, its use requires supplemental oxygenation and the ability to intubate the airway. Intramuscular (IM) use of alfaxalone in combination with other drugs (opioids, benzodiazepines, ketamine) is an option for sedation in patients in which it is not initially possible to obtain IV access, avoiding mask or box induction with inhalational anesthetics.

Table 7.6 Sacrococcygeal epidural procedure.

  1. Patient should be adequately sedated or under general anesthesia with appropriate monitoring
  2. Place the patient in sternal recumbency
  3. Locate the sacrococcygeal space while mobilizing the tail, or the space between the first two coccygeal vertebrae, either is acceptable
  4. Clip and aseptically prepare the area
  5. Use sterile techniques for the procedure
  6. Relocate the sacrococcygeal space, or space between the first two coccygeal vertebrae
  7. Use a 25‐gauge 1‐in. needle with the index finger near the insertion site on midline to guide placement
  8. Direct the needle at a 45° angle and slowly advance. A palpable “pop” may occur when passing through the ligament.
  9. The needle should enter the epidural space without resistance. If the needle is superficial to the spinal canal or advanced beyond the epidural space to the floor of the vertebral canal, bone will be encountered. If superficial, redirect, walking along the bone until the space is entered. If the needle placement is deep, back out slightly.
  10. Once the needle is placed, attach a syringe, aspirate, ensuring no blood is encountered, followed by infusion of 0.1–0.2 ml kg−1 (average 0.5 ml per cat) of 2% lidocaine. Injection should encounter minimal resistance.
  11. Successful block reveals tail and rectal relaxation, producing anesthesia to the perineum, penis, urethra, colon, and anus

A ketamine coinduction with a benzodiazepine after premedication with an opioid is also an option, with or without the addition of inhalational anesthesia. However, caution is advised in patients with underlying cardiovascular disease [30], arrhythmias, tachycardia, or hemodynamic instability. Additionally, ketamine is metabolized by the liver in most species and its metabolites depend on renal excretion. Cats rely more extensively on renal elimination [31, 32], which may result in accumulation and prolonged anesthesia in cases of urinary obstruction. However, ketamine can be used in obstructed patients, being cognizant that no antagonist is available and repeat doses are discouraged until patency is established.

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Oct 18, 2022 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Urogenital Concerns
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