Obstructive uropathy is mechanical or functional obstruction to normal outflow of urine. Clinical signs depend on the location of the obstruction; common signs include stranguria, lethargy, and vomiting. Diagnosis is based on identification of a distended bladder on examination or hydronephrotic kidney(s) on advanced abdominal imaging with corresponding clinicopathological abnormalities consistent with postrenal azotemia. Treatment involves first addressing life-threatening electrolyte and fluid derangements and ultimately relieving the obstruction to urine flow.
Obstructive uropathy is mechanical or functional obstruction to normal outflow of urine. Even though the kidneys would otherwise be able to function normally, obstruction of urine flow at any point distal to the kidneys leads to accumulation of metabolic wastes and postrenal azotemia/uremia.
Obstruction frequently occurs at the level of the urethra and is often caused by matrix-crystalline plugs in young male cats and uroliths in dogs. In both species, however, urethral obstruction can be caused by numerous other factors, including tumors, strictures, and extramural compression from any space-occupying lesions that affect the pelvis.
Obstructive uropathy can also be caused by any other mechanical obstruction that prohibits normal urine flow, including through the ureterovesicular junctions, ureters, and renal pelvises. The ureters can be obstructed by uroliths (particularly in cats), blood clots, tumors, strictures, and iatrogenic ligation, among other etiologies.
Hydronephrosis is characterized by dilatation of the renal pelvis resulting from partial or complete obstruction of urine outflow from one or both kidneys (see renal pelvic dilation images). When the obstruction is acute, complete, and bilateral, morphological changes in the kidneys are less extensive because the survival time is short. In unilateral or partial obstruction, the animal often survives long enough for severe pressure atrophy of the renal parenchyma and cystic enlargement of the affected kidney to develop.
Courtesy of Dr. Erin McQuinn.
Hydroureter commonly develops when the obstruction is located lower in the tract (see hydroureter image). Increased hydrostatic pressure results in atrophy of functional renal parenchyma. The pseudodiverticula of the renal pelvis disappear first; later even the cortex can atrophy. The affected kidneys eventually become grossly enlarged, functionless sacs, filled with urine or serous fluid that can harbor bacteria.
Courtesy of Dr. Erin McQuinn.
Clinical Findings of Obstructive Uropathy in Dogs and Cats
Animals with urethral obstruction frequently exhibit lower urinary tract signs, such as pollakiuria, stranguria, and hematuria. Occasionally, efforts to urinate are mistaken by owners as constipation.
Pearls & Pitfalls
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On examination, the bladder is distended and painful on palpation.
Rectal examination in dogs might reveal a palpable pelvic urethral obstruction from a stone or mass. In male dogs and cats, the penis should be extruded; it may be erythematous or purple in color, show signs of trauma, or have obstructive material in the lumen.
With complete urethral obstruction, signs of uremia develop rapidly and include vomiting, dehydration, hypothermia, and severe depression. Bradycardia or cardiac arrhythmias due to hyperkalemia can be present, particularly if plasma potassium concentration is > 7 mEq/L.
Because compensatory hypertrophy of the nonaffected kidney results in a nonazotemic state, unilateral ureteral obstruction often goes undiagnosed. When the contralateral kidney is already diseased or when obstruction is bilateral, clinical signs attributed to uremia (vomiting, dehydration, anorexia, lethargy) occur. Hyperkalemia and associated clinical signs can also develop as in cases of urethral obstruction.
On examination, affected kidneys are often palpably enlarged and painful.
Diagnosis of Obstructive Uropathy in Dogs and Cats
Imaging
Laboratory analysis
Urethral obstruction is usually a straightforward diagnosis based on history, clinical signs, and physical examination findings.
Ureteral obstruction can be more challenging to diagnose because lower urinary tract signs are often not present, and the bladder is not distended on palpation. Ureteral obstruction should be considered in any acutely uremic animal—especially cats, including those with a history of chronic kidney disease (CKD).
Imaging (most commonly abdominal ultrasonography, but also potentially excretory urography and/or abdominal CT) is necessary to establish a diagnosis in animals with bilateral or unilateral ureteral obstruction.
Laboratory analysis for obstructive uropathies show azotemia—often severe and progressive—unless the obstruction developed recently or there is adequate function of the contralateral kidney in unilateral ureteral obstructions. Serum potassium concentrations should be determined in all cases, even in the absence of cardiac arrhythmias, because dangerous hyperkalemia can develop.
Treatment of Obstructive Uropathy in Dogs and Cats
Treatment of Urethral Obstruction
Patient stabilization
Relief of obstruction (eg, urethral catheterization)
Ultimately, urethral obstructions should be relieved (see Urolithiasis in Small Animals); however, stabilization before anesthesia or heavy sedation required to safely relieve the obstruction is essential.
Dehydration and hypovolemia, if present, should be addressed with IV crystalloid therapy.
The choice of pain management should take into consideration patient stability and the future sedation/anesthetic protocol to be used for relieving the obstruction.
If hyperkalemia is life-threatening (potassium concentration > 7.5 mEq/dL), 10% calcium gluconate can be administered over 20 minutes (0.5–1.5 mL/kg, IV) with concurrent ECG monitoring. This will temporarily counteract cardiotoxic effects but will not lower plasma potassium concentrations.
Additional treatments to facilitate intracellular translocation of potassium should also be administered: dextrose (1 mL/kg 50% dextrose diluted 1:4, IV); regular insulin (0.25 U/kg, IV) in combination with dextrose to avoid hypoglycemia (approximately 1 mL 50% dextrose per 0.5 U insulin given, diluted, IV; 2.5–5% dextrose should be added to fluids with monitoring of blood glucose until the effects of the insulin have passed).
Beta-2-adrenergic receptor agonists such as albuterol (1–2 puffs via metered dose inhaler, to effect) also promote intracellular translocation of potassium and can be given alongside insulin/dextrose to further decrease potassium concentration.
Administration of bicarbonate can also promote intracellular translocation of potassium but is often avoided in favor of aforementioned potassium-lowering methods because of the potential to cause paradoxical cerebral acidosis.
Decompressive cystocentesis can be considered for animals as part of the stabilization process. Although controversial, this procedure has been shown to have minimal risk for complications. It can temporarily relieve back pressure on the kidneys and relieve the pain of a full bladder while efforts are made to stabilize the patient before urethral catheter placement.
Treatment of Ureteral Obstruction
Patient stabilization
Surgical and medical management
Postobstruction management
Uremia, dehydration/hypovolemia, and life-threatening hyperkalemia can occur in some cases of ureteral obstruction and can be addressed similarly to the way they are addressed for urethral obstruction.
Advanced surgery or interventional procedures are typically needed for ureteral obstructions. The type of procedure depends on the nature of the obstruction, financial capacity of the owner, and resources available. Placement of ureteral stent(s), subcutaneous ureteral bypass systems, or ureteral surgery (ureteroneocystostomy, ureterotomy, etc) could be indicated.
In cats, there is an appreciable complication rate with surgery involving the ureter. Furthermore, some cases of feline ureteral obstruction resolve with medical management alone. It is therefore reasonable to attempt medical management before surgical intervention.
Treatment can include a combination of IV fluid therapy, diuretics, and medications (eg, prazosin in cats [0.25–0.5 mg/kg, PO, every 12–24 hours as needed], tamsulosin in cats [0.004–0.006 mg/kg, PO, every 12–24 hours as needed]) that relax ureteral smooth muscle. Obstructions that do not respond to medical management within 24–72 hours should be relieved with ureteral surgery (eg, ureterotomy, ureteroneocystostomy) or surgical placement of a subcutaneous ureteral bypass or ureteral stent to prevent ongoing kidney damage.
Postobstructive diuresis, requiring longer and more intensive management, can develop after correction of urethral or ureteral obstructions. After relief of obstruction, animals can produce urine volumes well above normal, requiring careful monitoring and adjustment of fluid and electrolyte therapy to prevent dehydration and hypokalemia. Patients with more severe azotemia before relief of obstruction are more likely to experience more severe and prolonged postobstructive diuresis.
Key Points
Obstructive uropathy occurs when there is a mechanical or functional obstruction to urine outflow anywhere in the urinary tract from the level of the kidneys down to the urethra. Complete obstruction can lead to life-threatening electrolyte derangements and severe postrenal azotemia.
Management of obstructive uropathy depends on effective patient stabilization, followed by relief of the obstruction.
For More Information
George CM, Grauer GF. Feline urethral obstruction: diagnosis & management. Today’s Vet Pract. July/August 2016:36-44.
Wuillemin F, Vachon C, Beauchamp G, Dunn M. Subcutaneous ureteral bypass device placement in 81 cats with benign ureteral obstruction (2013–2018). J Vet Intern Med. 2021;35(6):2778-2786.
Also see pet owner content regarding noninfectious diseases of the urinary system in dogs and cats.
