Uroliths can be found in the renal pelvis, the ureter, the bladder, or the urethra. The most common locations are the bladder
and the urethra. A higher incidence of calcium oxalate has been reported in the ureter and kidney in cats. This higher incidence
seems to parallel the diet changes instituted several years ago to prevent stones in the lower urinary tract. Different types
of uroliths have been identified in veterinary medicine such as struvite or magnesium ammonium phosphate, calcium oxalate,
ammonium urate, silicate and cystine. Pathophysiology behind each type of urolith needs to be well understood in order to
accomplish a successful surgical treatment.
Hematuria, stranguria, and pollakiuria are the most common clinical signs associated with uroliths. Blood work, urinalysis,
radiographic evaluation of the urinary system and ultrasounds are required to diagnosed urolithiasis in dogs and cats.
Detection of uroliths is not in itself an indication for surgery. Along with medical management, surgical intervention has
an important role in the therapy for urolithiasis. Surgical candidates include:
• Patients with urolith induced obstruction to urine outflow that cannot be corrected by non-surgical techniques
• Patients with uroliths that are refractory to current methods of medical dissolution: silica, calcium oxalate, and
calcium phosphate uroliths
• Patients with uroliths that are increasing in size while under medical therapy
• Patients with nephroliths and renal dysfunction
• Patients with anatomical defects that predispose to UTI
• Patients not responding to therapy because of poor owner compliance.
Evaluation of patients before surgery
If an obstruction is present several metabolic changes can occur that will compromise the patient. First a post-renal azotemia
will develop. This azotemia should be reversible as soon as the urine can flow freely. This azotemia may not develop if the
obstruction is only compromising one ureter or one kidney. Electrolyte imbalance will develop very quickly with urinary obstruction
or uroabdomen. Uroabdomen can appear if an obstruction has been sustained for a long period of time. Hyperkalemia will induce
serious bradycardia with tall T wave (K >5.5 mEq/L), prolongation of QRS complex (K>6.5 mEq/L), decrease amplitude of P wave
and prolongation of P wave (K>7.5 mEq/L), and disappearance of P wave when K>8.5 mEq/L. High potassium concentration will
induce a temporary atrial standstill. It is important to recognize those changes because induction of anesthesia in such a
patient is not indicated. To lower the potassium concentration induction of diuresis is the best option. Either a small urinary
catheter can be placed in the urethra to bypass the obstruction or a cystocenthesis can be performed to empty the bladder
as much as possible. If a uroabdomen is present an abdominal drain can be placed under local anesthesia. If diuresis does
not lower the level of potassium a combination of insulin glucose and bicarbonate can be used. Potassium concentration will
decrease for a period of time allowing a safe induction of anesthesia to perform surgery. Finally if insulin is not helping
injection of calcium gluconate will help protect the heart against the effect of potassium.