Kelly St. Denis
MSc, DVM, DABVP (Feline Practice)
Dr. St. Denis is a practicing feline medicine specialist, board certified with the American Board of Veterinary Practitioners in the specialty of feline practice. In her early career she trained in molecular biology and immunology, working in the field of cancer research. In 1999 she graduated from the Ontario Veterinary College, going on to own and operate the Charing Cross Cat Clinic from 2007 to 2020. Dr. St. Denis is the 2020-2021 president for the American Association of Feline Practitioners and an active volunteer in the organization, participating in many committees and task forces. Dr. St. Denis is a consultant on the Veterinary Information Network in feline internal medicine.Read Articles Written by Kelly St. Denis
Feline urethral obstruction (UO) is a common presenting emergency in veterinary medicine. Prognosis for survival with proper, timely treatment is 90% to 95%, and recurrence rates are estimated to be 15% to 40%.1 UO is secondary to feline lower urinary tract disease (FLUTD), a clinical entity with a variety of etiologies. Feline idiopathic cystitis (FIC) accounts for 53% of FLUTD cases, followed by urolithiasis (29%) and urethral plugs (18%).2 Urethral plugs may consist of crystals (e.g., magnesium phosphate, calcium oxalate), cellular matter, mucus/mucoid matter, or other accumulations. Urinary tract infection (UTI) is an uncommon cause of FLUTD. Predisposing factors for feline UO are listed in BOX 1.1,3
Cats are masters at hiding illness. As a result, the early signs of UO may go unnoticed and the problem may not be recognized until hours or days after it begins. Clinical signs of UO include periuria, pollakiuria, stranguria, dysuria, and oliguria. Microscopic or macroscopic hematuria may be noted. As UO advances, clinical signs include vomiting, lethargy, and collapse. The hallmark clinical sign of UO is a painful, firm, full to overdistended urinary bladder with little to no urine passing from the urethra. Clinical parameters may include normo- to hyperthermia and bradycardia or tachycardia with or without arrhythmias.
Diagnostic testing in UO patients is critical to identifying complications. TABLE 1 lists diagnostic tests for UO patients in order of priority. Urgent tests include blood gas and serum electrolyte measurements and electrocardiography (ECG). Results of these tests allow targeted stabilization of possible life-threatening metabolic and electrolyte disturbances. Radiographic imaging to detect the presence of obstructing urethroliths guides the approach to urinary catheter placement and bladder decompression (FIGURE 1). Determining the renal status of the patient is a priority, as severe kidney injury may affect prognosis and client decisions. Other diagnostic tests provide valuable information for ongoing patient care but are not critical to early stabilization.
The approach to stabilization varies with each case. The establishment of a tailored list of priorities is essential, with the goal being to achieve all in a timely fashion.
A necessity for UO patients, analgesia is often neglected in the rush to treat the obstruction and related complications. Provision of analgesia should be an immediate and ongoing priority. The PLATTER algorithm can guide the use of analgesic care (BOX 2).4 Validated pain scales such as the Glasgow Composite Measure Pain Scale–Feline (aprvt.com) and the Feline Grimace Scale (felinegrimacescale.com) minimize subjectivity and provide consistency in evaluation.
A multimodal approach to analgesia is essential, using analgesics from several drug classes. Analgesic options are presented in TABLE 2. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be used with caution. Use in patients that are dehydrated, have confirmed kidney disease, or have unknown kidney function should be avoided until the patient is rehydrated and/or resolution of azotemia is confirmed. While NSAIDs may not show a direct benefit in preventing recurrence of UO in FIC patients,5,6 they should be considered as a beneficial component of multimodal analgesia.
The goals of fluid therapy for UO patients include support of intravascular volume, dilution of serum potassium, and correction of metabolic derangements. Patients presented with cardiovascular collapse should receive shock doses of crystalloid solutions (50 to 55 mL/kg IV)7 in bolus fractions to restore vascular volume.1 The first bolus of 25% of the calculated shock dose should be administered over 15 to 20 minutes, followed by reassessment of the patient’s perfusion parameters. Additional boluses of fluids can be administered in 25% increments. If the patient is not responding after 50% of the calculated shock dose has been administered, colloids may be required.7
Once intravascular fluid volume is stabilized, fluid rates should be based on replacement of interstitial dehydration amounts plus maintenance fluid at 2 to 3 mL/kg/h.1 Anecdotally, higher rates of 10 to 20 mL/kg may be chosen in an effort to “flush out” the urinary tract and reduce hyperkalemia and/or in anticipation of postobstructive diuresis (POD).8,9
Balanced electrolyte solutions such as lactated Ringer’s solution and Plasma-Lyte (Baxter, baxter.com) contain low levels of potassium (4 to 5 mEq/L) and are safe for use in hyperkalemic UO patients.7,8 They do not negatively affect the rate of normalization of serum potassium, and, as most UO cats have metabolic acidosis, their alkalinizing effect can be beneficial in restoring pH in the first 12 hours of fluid therapy.1,8,9 In contrast, 0.9% NaCl is acidifying and may compromise attempts to restore acid-base balance.8
POD with urine production in excess of 2 mL/kg/h occurs within 4 to 6 hours after relief of obstruction in as many as 46% to 74% of patients.10,11 It is a result of the accumulation of osmotically active substances in the blood. Pressure necrosis, medullary washout, and antidiuretic hormone resistance may also contribute to POD. Monitoring of fluid input/output and changes in body weight assists in early identification of POD. Fluid therapy is tailored to ongoing fluid losses. Since POD can lead to kaliuresis, monitoring of serum potassium is recommended, and potassium should be supplemented if required.
Hyperkalemia is a potentially life-threatening complication of UO. It may be evident early in patient assessment, based on the presence of arrhythmias, bradycardia, or tachycardia.
ECG patterns alter with worsening hyperkalemia. With mild potassium elevations (5.5 to 6.5 mEq/L), classic early changes include tall T waves with a prolonged QRS complex. Mild elevations in potassium usually resolve in response to dilutional fluid therapy (10 to 20 mL/kg/h).1
Moderate hyperkalemia of 6 to 8 mmol/L requires immediate fluid therapy and treatment. Regular insulin administered at 0.1 to 0.25 IU/kg IV will drive an intracellular shift of potassium within 1 hour.12 To reduce the risk of hypoglycemia, 10% to 20% dextrose should be given as a bolus of 0.5 g/kg. Intravenous fluids can be supplemented with 1% to 2% dextrose to maintain blood glucose levels.12
Serum potassium elevations in excess of 8 mmol/L are severe and require additional treatment to protect cardiac function. Calcium gluconate is administered slowly at 50 to 100 mg/kg IV, with continuous ECG monitoring. Calcium gluconate has a myocardial protective effect for 20 to 30 minutes.12
Hypocalcemia may occur as a complication of UO related to reduced renal clearance of phosphorus.12 Decreases in ionized calcium to below 1.6 mEq/L can lead to impaired cardiac electrical and mechanical function. Intravenous calcium gluconate may be indicated as described above.
Bladder Decompression and Relief of UO
Once the patient has been stabilized, bladder decompression and relief of the urinary obstruction are necessary. Decompressive cystocentesis is a valid approach to relieve bladder pressure and associated pain in the initial phases of treatment and has been evaluated as a safe alternative treatment for UO when finances do not permit urinary catheterization.13 In cases of UO where decompressive cystocentesis was used, the risk of bladder tear or rupture and/or clinically significant abdominal effusion was determined to be low.13,14
Relief of the UO and placement of a urinary catheter should not be attempted without heavy sedation or full general anesthesia.1 Use of a coccygeal epidural can reduce sedative and anesthetic requirements and improve comfort levels during the recovery phase.15
Urinary catheters are available in a variety of materials, sizes, and configurations (TABLE 3). For initial unblocking, more rigid catheters such as olive tip catheters or polypropylene catheters are often selected, although the rigidity of these catheters may increase the risk of urethral trauma. As rigid catheters are not ideal as indwelling catheters, placement of a second, softer catheter is necessary after unblocking, which increases the risk of urethral trauma and irritation. Catheters made of polytetrafluoroethylene and polyurethane are more rigid at room temperatures and soften at body temperature. They are ideal for both unblocking and placement as an indwelling catheter.
In cats with a UO, urinary catheter sizes should be no larger than 3.5 to 5 Fr. Smaller urethral catheters (3.5 Fr) may be associated with decreased risk of recurrent obstruction 24 hours after catheter removal.16 Indwelling urinary catheters are generally left in place for 1 to 3 days, although no conclusive data exist to specify duration.1 Factors to consider include patient stability, resolution of biochemical abnormalities, POD, and gross and microscopic character of urine.
A closed collection system facilitates monitoring of catheter patency, measurement of urine output, and early identification of POD. It may reduce urine soiling and scalding. Anecdotally, clinicians may prefer open systems based on concerns about the comfort level of the patient and obstruction of urine flow with a closed system. Closed urinary catheter systems are recommended as the standard of care.17
UTI is uncommon in UO patients.18 The use of an indwelling urinary catheter presents a low risk for acquired UTI.18 Empiric use of antibiotics is not warranted at the time of presentation or during treatment.17 Urine culture after 24 hours of catheterization or at the time of catheter removal has been recommended.1,18 However, in the absence of clinical signs associated with cystitis, the identification of pyuria in urine sediment or bacteriuria by urine culture does not necessarily warrant treatment.17
Detrusor atony can occur as a result of bladder overstretch during a prolonged, untreated UO. Recovery of normal detrusor function is promoted by keeping the bladder small during the days after relief of the obstruction. Indwelling urinary catheters or manual bladder expression may suffice. Parasympathomimetic drugs such as bethanechol increase smooth muscle contractility and may further support detrusor recovery.12 Side effects of bethanechol include vomiting and diarrhea; this drug should not be used in patients with active UO or high risk of recurrent UO.
Postobstruction Supportive Care
Multimodal analgesia (TABLE 2) should be continued based on patient reassessment (BOX 2) in the clinic and after discharge of the patient from the hospital.
Muscle Relaxant/Antispasmodic Medications
The feline urethra is composed of smooth muscle along the proximal quarter to third of its length and skeletal muscle distally. Only proximal portions of the feline urethra are responsive to smooth muscle relaxants. Prazosin (alpha-1 adrenergic antagonist) can cause urethral smooth muscle relaxation, has a rapid onset of action, and is the antispasmodic of choice. Potential side effects include hypotension, lethargy, ptyalism, diarrhea, anorexia, and malodorous stool.19 Phenoxybenzamine is a less effective alpha-1 adrenergic antagonist sometimes used for UO. It requires up to a week to take effect.1 Acepromazine may be used to reduce proximal urethral pressures, acting also as a sedative; however, the risks of hypotension are significantly higher than with prazosin or phenoxybenzamine.
Given the limited effect of antispasmodics on the feline urethra, their need as a treatment for UO has been called into question. Controlled studies have failed to demonstrate a benefit of their use.1 Although a 2013 study failed to find a difference in the incidence of recurrent UO and severity of lower urinary tract signs among cats receiving prazosin and those receiving placebo,19 larger studies are still needed.
During the postobstruction recovery phase and following discharge, antianxiety medications may be indicated. Patients diagnosed with FIC sometimes benefit from short- or long-term use of antianxiety medications such as alprazolam or amitriptyline. The use of these medications should not replace appropriate dietary and/or environmental modifications.
Urinary prescription diets play a role in the management of UO secondary to urolithiasis. Some of these diets promote elimination of crystalluria, dissolution of struvite uroliths, and/or the prevention of subsequent urolith formation. At least one of these diets has also been shown to reduce recurrence of several clinical signs associated with FIC.20
In the case of life-threatening urolith UO, surgical removal of the uroliths may be indicated. However, if patients can be safely unobstructed and stabilized, dietary dissolution of existing sterile struvite stones is a less invasive and less costly treatment option.21,22 Urolith size should be reassessed 2 weeks after diet initiation to determine if dietary dissolution is possible. A 50% or greater reduction in the stone size indicates likely success for dietary dissolution.22
Meeting the environmental needs of cats and providing the appropriate number and distribution of resources is key to reducing anxiety and often appropriate in the treatment of FLUTD.23,24 The American Association of Feline Practitioners/International Society of Feline Medicine guidelines on environmental needs in cats23 and guidelines to diagnosing and resolving house-soiling behavior in cats24 are excellent resources for advising clients. In cases of FIC, multimodal environmental modification has been demonstrated to reduce lower urinary tract signs and signs of anxiety in potentially reducing the risk of FIC-related UO.25
Feline UO is a common emergency. Diagnosis of UO in cats is straightforward, but the difficulty lies in recognition of the problem at home. Client education is key to prevention as well as prompt treatment. Diagnostic testing facilitates identification of complicating metabolic and electrolyte disturbances, and treatment is aimed at providing analgesia and stabilization of the patient prior to attempts at UO relief. Lifelong care in the form of diet and environmental modification is likely necessary.
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2. Gerber B, Eichenberger S, Reusch CE. Guarded long-term prognosis in male cats with urethral obstruction. J Feline Med Surg
3. Jukes A, Lui M, Morton JM, et al. Associations between increased body condition score, bodyweight, age and breed with urethral obstruction in male castrated cats. Vet J 2019;244:7-12.
4. Epstein ME, Rodan I, Griffenhagen G, et al. 2015 AAHA/AAFP pain management guidelines for dogs and cats. J Feline Med Surg 2015;17(3):251-272.
5. Dorsch R, Zellner F, Schulz B, et al. Evaluation of meloxicam for the treatment of obstructive feline idiopathic cystitis. J Feline Med Surg 2016;18(11):925-933.
6. Nivy R, Segev G, Rimer D, et al. A prospective randomized study of efficacy of 2 treatment protocols in preventing recurrence of clinical signs in 51 male cats with obstructive idiopathic cystitis. J Vet Intern Med 2019;33(5):2117-2123.
7. Davis H, Jensen T, Johnson A, et al. 2013 AAHA/AAFP fluid therapy guidelines for dogs and cats. JAAHA 2013;49(3):149-159.
8. Drobatz KJ, Cole SG. The influence of crystalloid type on acid–base and electrolyte status of cats with urethral obstruction. J Vet Emerg Crit Care 2008;18(4):355-361.
9. Cunha MG, Freitas GC, Carregaro AB, et al. Renal and cardiorespiratory effects of treatment with lactated Ringer’s solution or physiologic saline (0.9% NaCl) solution in cats with experimentally induced urethral obstruction. Am J Vet Res 2010;71(7):840-846.
10. Francis BJ, Wells RJ, Rao S, Hackett TB. Retrospective study to characterize post-obstructive diuresis in cats with urethral obstruction. J Feline Med Surg 2010;12(8):606-608.
11. Fröhlich L, Hartmann K, Sautter-Louis C, Dorsch R. Postobstructive diuresis in cats with naturally occurring lower urinary tract obstruction: incidence, severity and association with laboratory parameters on admission. J Feline Med Surg 2016;18(1):809-817.
12. Little S. The Cat: Clinical Medicine and Management. St. Louis, MO: Elsevier Saunders; 2011.
13. Cooper ES, Owens TJ, Chew DJ, Buffington CAT. A protocol for managing urethral obstruction in male cats without urethral catheterization. JAVMA 2010;237(11):1261-1266.
14. Gerken KK, Cooper ES, Butler AL, Chew DJ. Association of abdominal effusion with a single decompressive cystocentesis prior to catheterization in male cats with urethral obstruction. J Vet Emerg Crit Care 2020;30(1):11-17.
15. O’Hearn AK, Wright BD. Coccygeal epidural with local anesthetic for catheterization and pain management in the treatment of feline urethral obstruction. J Vet Emerg Crit Care 2011;21(1):50-52.
16. Hetrick PF, Davidow EB. Initial treatment factors associated with feline urethral obstruction recurrence rate: 192 cases (2004-2010). JAVMA 2013;243(4):512-519.
17. Weese JS, Blondeau J, Boothe D, et al. International Society for Companion Animal Infectious Diseases (ISCAID) guidelines for the diagnosis and management of bacterial urinary tract infections in dogs and cats. Vet J 2019;247:8-25.
18. Cooper ES, Lasley E, Daniels JB, Chew DJ. Incidence of bacteriuria at presentation and resulting from urinary catheterization in feline urethral obstruction. J Vet Emerg Crit Care 2019;29(5):472-477.
19. Reineke EL, Thomas EK, Syring RS, et al. The effect of prazosin on outcome in feline urethral obstruction. J Vet Emerg Crit Care 2017;27(4):387-396.
20. Kruger JM, Lulich JP, MacLeay J. Comparison of foods with differing nutritional profiles for long-term management of acute nonobstructive idiopathic cystitis in cats. JAVMA 2015;247(5):508-517.
21. Lulich JP, Kruger JM, Macleay JM, et al. Efficacy of two commercially available, low-magnesium, urine-acidifying dry foods for the dissolution of struvite uroliths in cats. JAVMA 2013;243(8):1147-1153.
22. Lulich JP, Berent AC, Adams LG, et al. ACVIM small animal consensus recommendations on the treatment and prevention of uroliths in dogs and cats. J Vet Intern Med 2016;30(5):1564-1574.
23. Ellis SLH, Rodan I, Carney HC, et al. AAFP and ISFM feline environmental needs guidelines. J Feline Med Surg 2013;15(3):219-230.
24. Carney HC, Sadek TP, Curtis TM, et al. AAFP and ISFM guidelines for diagnosing and solving house-soiling behavior in cats. J Feline Med Surg 2014;16(7):579-598.
25. Buffington CAT, Westropp JL, Chew DJ, Bolus RR. Clinical evaluation of multimodal environmental modification (MEMO) in the management of cats with idiopathic cystitis. J Feline Med Surg 2006;8(4):261-268.