Ureterolithiasis and Ureteral Obstruction

Ureterolithiasis and ureteral obstruction refer to the presence of uroliths (calculi) within the ureter, leading to partial or complete obstruction of urine flow from the kidney to the urinary bladder. This condition is a significant cause of acute kidney injury (AKI) and chronic kidney disease (CKD) in dogs and cats. Ureteral obstruction can be unilateral or bilateral, and may be partial or complete. The obstruction leads to increased intrapelvic pressure, hydronephrosis, and progressive renal parenchymal damage. Surgical intervention is often required to relieve the obstruction and preserve renal function. The condition is classified based on the location of the stone (proximal, mid, or distal ureter), the degree of obstruction (partial vs. complete), and the presence of concurrent urolithiasis in the kidney or bladder. In veterinary medicine, ureterolithiasis is most commonly seen in cats, particularly those with calcium oxalate uroliths, and in dogs with struvite or calcium oxalate stones. The surgical management includes ureterotomy, ureteral stenting, ureteroneocystostomy (reimplantation), or nephroureterectomy in severe cases. The choice of procedure depends on the stone location, size, number, and the condition of the kidney.

The primary etiology of ureterolithiasis is the formation of uroliths in the kidney or ureter, which then migrate into the ureter. The most common stone types in dogs and cats are calcium oxalate and struvite. Calcium oxalate stones form due to hypercalciuria, hyperoxaluria, and hypocitraturia, often associated with metabolic disorders, dietary factors, or genetic predisposition. Struvite stones typically form in the presence of urease-producing bacterial infections (e.g., Staphylococcus, Proteus) that alkalinize the urine and increase ammonia and phosphate concentrations. Other less common stone types include urate, cystine, and silica. Ureteral obstruction can also result from strictures, neoplasia (e.g., transitional cell carcinoma), trauma, or iatrogenic causes such as ligation during surgery. In cats, ureterolithiasis is often idiopathic, but risk factors include obesity, indoor confinement, and dry food diets. In dogs, breed predispositions exist for certain stone types (e.g., Dalmatians for urate stones, Miniature Schnauzers for struvite). The anatomical vulnerability of the ureter, particularly at the ureteropelvic junction and ureterovesicular junction, predisposes to stone impaction due to physiological narrowing. The cellular mechanisms involve crystal aggregation, tubular cell injury, and stone growth, leading to obstruction and subsequent hydronephrosis.

Ureterolithiasis is more common in cats than in dogs. In cats, the prevalence has increased significantly over the past few decades, with calcium oxalate being the most common stone type. Cats of any age can be affected, but the median age is around 7 years. Breeds such as Persians, Himalayans, and British Shorthairs are overrepresented. In dogs, ureterolithiasis is less common but can occur in any breed; however, small breeds like Miniature Schnauzers, Yorkshire Terriers, and Shih Tzus are predisposed to calcium oxalate stones, while Dalmatians and English Bulldogs are prone to urate stones. There is no strong sex predilection, but some studies suggest a slight male predominance in dogs. The condition is often unilateral, but bilateral involvement occurs in up to 20% of cases. The incidence of ureterolithiasis is higher in animals with a history of urolithiasis, and recurrence rates are significant if underlying metabolic abnormalities are not addressed. In working dogs, ureterolithiasis is not specifically related to activity, but dehydration and urinary stasis during work may contribute to stone formation.

The pathophysiology of ureteral obstruction begins with the presence of a urolith within the ureter, causing mechanical blockage. This leads to increased intraluminal pressure proximal to the obstruction, which is transmitted to the renal pelvis and calyces. The elevated pressure compresses the renal vasculature, reducing renal blood flow and glomerular filtration rate (GFR). Within hours, there is a decrease in GFR and an increase in tubular pressure, leading to tubular cell injury and necrosis. If the obstruction is complete and prolonged, irreversible renal damage occurs within 24 to 48 hours. The kidney undergoes hydronephrosis, characterized by progressive dilation of the renal pelvis and atrophy of the renal parenchyma. In partial obstruction, the kidney may undergo chronic changes, including interstitial fibrosis and tubular atrophy, leading to progressive CKD. The obstruction also predisposes to urinary tract infection, which can exacerbate renal damage. In bilateral obstruction, acute kidney injury can rapidly progress to uremia and death if not treated emergently. The systemic inflammatory response to renal injury includes activation of the renin-angiotensin-aldosterone system, leading to hypertension and further renal damage. Additionally, the release of inflammatory cytokines and reactive oxygen species contributes to tubular injury and fibrosis.

Intrinsic risk factors for ureterolithiasis include breed and genetic predisposition to certain stone types, such as calcium oxalate in Miniature Schnauzers and urate in Dalmatians. Age is a factor, with middle-aged to older animals more commonly affected. Obesity and a sedentary lifestyle increase the risk of stone formation. Metabolic abnormalities such as hypercalcemia, hyperparathyroidism, and hypercortisolism can predispose to calcium oxalate stones. Extrinsic factors include diet, particularly high-protein, high-sodium, or low-moisture diets that increase urine concentration and stone-forming constituents. Inadequate water intake and infrequent urination lead to urinary stasis, promoting crystal aggregation. Prior urinary tract infections with urease-producing bacteria increase the risk of struvite stones. Iatrogenic factors include previous urinary tract surgery, which may cause strictures or foreign body nidus for stone formation. Environmental factors such as indoor confinement and litter box use in cats may contribute to urine retention. Additionally, certain medications, such as corticosteroids and furosemide, can alter calcium metabolism and increase the risk of calcium oxalate stones.

Clinical signs of ureterolithiasis and ureteral obstruction vary depending on the degree and duration of obstruction. In acute complete obstruction, animals may present with severe abdominal pain, vomiting, anorexia, and lethargy. Palpation of the abdomen may reveal a painful, enlarged kidney (hydronephrosis). In partial obstruction, signs may be more subtle, including intermittent vomiting, decreased appetite, and polyuria/polydipsia. Hematuria may be present, especially if there is concurrent urinary tract infection. As renal function deteriorates, signs of uremia develop, including oral ulceration, uremic breath, and depression. In bilateral obstruction, acute anuria or oliguria may be observed. Cats may exhibit vocalization, restlessness, and hiding behavior due to pain. On physical examination, the affected kidney may be palpably enlarged and painful. Dehydration and poor body condition may be noted. In chronic cases, signs of CKD, such as weight loss and poor hair coat, are common. Neurological signs such as weakness and seizures can occur in severe uremia. It is important to note that some animals with unilateral obstruction may be asymptomatic, and the condition is often discovered incidentally during imaging for other reasons.

Differential diagnoses for ureterolithiasis and ureteral obstruction include: 1) Renal calculi (nephrolithiasis) without ureteral obstruction, which may be asymptomatic or cause hematuria and pain, but imaging shows stones confined to the renal pelvis. 2) Ureteral neoplasia (e.g., transitional cell carcinoma) can cause obstruction and hematuria; imaging may show a mass rather than a stone, and cytology/histopathology is definitive. 3) Ureteral stricture, which can be congenital or acquired, presents with hydronephrosis but no visible stone on imaging; contrast studies or ureteroscopy may be needed. 4) Acute kidney injury from other causes (e.g., toxins, ischemia) may present with similar clinical signs but no evidence of obstruction on imaging. 5) Pyelonephritis can cause renal pain and hematuria, but imaging typically shows no hydronephrosis or stones. 6) Renal neoplasia (e.g., renal cell carcinoma) may cause renomegaly and hematuria, but imaging shows a mass lesion. 7) Urinary bladder stones (cystolithiasis) can cause similar lower urinary tract signs, but imaging shows stones in the bladder. 8) Peritonitis or pancreatitis can cause abdominal pain and vomiting, but imaging and laboratory tests differentiate. 9) Ureteral trauma (e.g., from vehicular trauma) can cause obstruction due to swelling or rupture; history and imaging are key. 10) Retroperitoneal fibrosis or abscess can cause ureteral compression; advanced imaging and cytology are helpful.

The diagnostic algorithm for suspected ureterolithiasis begins with a thorough history and physical examination, focusing on abdominal palpation and assessment of renal size and pain. Initial laboratory tests include a complete blood count (CBC), serum biochemistry profile, and urinalysis. The biochemistry profile may reveal elevated blood urea nitrogen (BUN) and creatinine, hyperkalemia, and hyperphosphatemia in cases of renal dysfunction. Urinalysis may show hematuria, pyuria, crystalluria, and a urine pH that is acidic (calcium oxalate) or alkaline (struvite). Urine culture and sensitivity should be performed if infection is suspected. Abdominal radiography is the next step; many ureteral stones are radiopaque (calcium oxalate, struvite) and can be visualized. However, small stones or radiolucent stones (urate, cystine) may not be visible. Abdominal ultrasonography is highly sensitive for detecting hydronephrosis and proximal ureteral dilation, and can often identify the stone as a hyperechoic focus with acoustic shadowing. If the stone is not visualized, contrast studies such as excretory urography (intravenous pyelogram) or antegrade pyelography can be performed. Computed tomography (CT) with or without contrast is the most sensitive imaging modality for detecting ureteral stones and assessing renal function. In cases where surgical intervention is planned, a CT scan provides detailed anatomical information. If the diagnosis remains uncertain, ureteroscopy or exploratory surgery may be indicated. The algorithm should also include assessment of renal function via serum creatinine and symmetric dimethylarginine (SDMA) levels, and possibly renal scintigraphy to evaluate differential renal function.

Laboratory findings in ureterolithiasis and ureteral obstruction reflect the degree of renal dysfunction and the underlying cause. Complete blood count may show leukocytosis with a left shift if there is concurrent infection, or stress leukogram. Serum biochemistry typically reveals elevated BUN and creatinine, with the magnitude correlating with the severity of obstruction. Hyperkalemia, hyperphosphatemia, and metabolic acidosis are common in acute obstruction due to decreased GFR. Hypercalcemia may be present if the stone is calcium oxalate and there is an underlying metabolic disorder. Urinalysis often shows hematuria (microscopic or macroscopic), pyuria, and crystalluria. The urine pH can provide a clue to stone type: acidic urine (pH < 6.5) is associated with calcium oxalate, urate, and cystine stones, while alkaline urine (pH > 7.0) is associated with struvite stones. Urine specific gravity may be low if renal concentrating ability is impaired. Urine culture and sensitivity should be performed to rule out bacterial infection. In chronic cases, proteinuria may be present due to glomerular damage. Additional tests include serum ionized calcium, parathyroid hormone (PTH) levels, and bile acids if portosystemic shunt is suspected (urate stones). Coagulation panel (PT/aPTT) is recommended if surgery is planned, as uremic animals may have platelet dysfunction. Inflammatory biomarkers such as C-reactive protein (CRP) may be elevated in cases of pyelonephritis.

Imaging plays a crucial role in the diagnosis and surgical planning of ureterolithiasis. Survey radiography: Many ureteral stones are radiopaque and can be visualized on abdominal radiographs. However, small stones, radiolucent stones (urate, cystine), and stones overlying bony structures may be missed. The sensitivity of radiography for ureteral stones is low, especially in cats. Ultrasonography: This is the most commonly used imaging modality. It can detect hydronephrosis (dilation of the renal pelvis) and hydroureter (dilation of the ureter proximal to the obstruction). The stone itself appears as a hyperechoic focus with distal acoustic shadowing. Ultrasonography is also useful to assess renal parenchymal thickness and echogenicity, and to guide antegrade pyelography. Excretory urography (intravenous pyelogram): This involves intravenous administration of iodinated contrast medium, followed by serial radiographs or fluoroscopy. It can delineate the level of obstruction and the degree of hydronephrosis. However, it is less commonly used now due to the risk of contrast-induced nephropathy, especially in animals with compromised renal function. Computed tomography (CT): CT is the most sensitive imaging modality for detecting ureteral stones, including small and radiolucent ones. It provides excellent anatomical detail and can be used to plan surgical approaches. CT urography (with contrast) can assess renal perfusion and excretion. Magnetic resonance imaging (MRI) is rarely used for ureteral stones but may be helpful in cases of suspected neoplasia. Antegrade pyelography: This is performed under ultrasound guidance by percutaneously injecting contrast into the renal pelvis. It is useful when excretory urography is contraindicated or when the stone is not visible on other imaging. It can also be used therapeutically to flush small stones. Fluoroscopy is used during interventional procedures such as ureteral stenting.

Cytology and histopathology are not typically required for the diagnosis of ureterolithiasis, but they are important in cases of suspected neoplasia or to analyze the stone composition. Stone analysis: Retrieved stones should be sent for quantitative analysis (e.g., X-ray diffraction or infrared spectroscopy) to determine the mineral composition. This is essential for formulating preventive strategies. Urine cytology: If a mass is suspected, fine-needle aspiration of the mass or urine sediment cytology may reveal neoplastic cells (e.g., transitional cell carcinoma). Histopathology: If a ureteral mass is found during surgery, a biopsy should be taken for histopathological examination. In cases of chronic obstruction, renal biopsy may be performed to assess the degree of interstitial fibrosis and tubular atrophy. Histopathological findings in the kidney may include tubular necrosis, interstitial nephritis, and glomerulosclerosis. Special stains, such as von Kossa stain for calcium, may be used to identify mineral deposits. In cases of pyelonephritis, bacterial culture and sensitivity of renal tissue or urine are important.

Treatment of ureterolithiasis and ureteral obstruction depends on the severity of obstruction, renal function, and the presence of concurrent disease. Medical management: In cases of partial obstruction with small stones (<3 mm in cats, <5 mm in dogs) and no evidence of progressive renal damage, medical management may be attempted. This includes aggressive fluid therapy to increase urine flow, administration of diuretics (e.g., mannitol) to promote diuresis, and pain management. However, medical management is often unsuccessful, and surgical intervention is usually required. Surgical options: 1) Ureterotomy: This involves a longitudinal incision into the ureter over the stone, removal of the stone, and primary closure of the ureter. It is indicated for stones in the mid-ureter. The ureter is approached via a ventral midline celiotomy. The incision is made with a #11 blade, and the stone is removed with forceps or a stone basket. The ureter is closed with 5-0 or 6-0 monofilament absorbable suture (e.g., polydioxanone) in a simple interrupted pattern. A ureteral stent or nephrostomy tube may be placed to protect the repair. 2) Ureteroneocystostomy (reimplantation): This is indicated for stones in the distal ureter, near the bladder. The distal ureter is transected and reimplanted into the bladder using a submucosal tunnel technique (modified Leadbetter-Politano) or a simple end-to-side anastomosis. The bladder is mobilized to reduce tension. 3) Ureteral stenting: This is a minimally invasive option where a double-pigtail stent is placed cystoscopically or surgically. The stent bypasses the obstruction and allows urine flow. Stents can be placed in dogs and cats, but are more challenging in cats due to the small ureteral diameter. Complications include stent migration, encrustation, and infection. 4) Nephroureterectomy: This is indicated if the kidney is non-functional (e.g., severe hydronephrosis with <10% function) or if there is a concurrent renal tumor. The entire kidney and ureter are removed. 5) Subcutaneous ureteral bypass (SUB) device: This is a novel technique where a catheter is placed from the renal pelvis to the bladder, bypassing the ureter. It is particularly useful in cats with ureteral obstruction. Postoperative care includes fluid therapy, pain management, and monitoring of urine output and renal function. Antibiotics are indicated if infection is present. Dietary modification and medical management of underlying metabolic disorders are essential to prevent recurrence.

The prognosis for ureterolithiasis and ureteral obstruction depends on the duration and severity of obstruction, the degree of renal damage, and the success of surgical intervention. In animals with acute unilateral obstruction and early intervention, the prognosis is good, with recovery of renal function expected. However, if the obstruction is complete and lasts more than 48 hours, irreversible renal damage may occur, leading to chronic kidney disease. In cats, the prognosis is guarded, as they often have concurrent CKD. Studies have shown that cats with ureteral obstruction have a median survival time of about 1 to 2 years after surgical treatment, with many requiring ongoing management of CKD. Dogs generally have a better prognosis, especially if the underlying cause is addressed. Complications such as ureteral stricture, urine leakage, and recurrent stone formation can negatively affect the outcome. Negative prognostic indicators include bilateral obstruction, severe azotemia at presentation, and poor body condition. With appropriate surgical and medical management, many animals can have a good quality of life, but long-term monitoring is essential.

Postoperative follow-up is crucial for monitoring renal function and detecting complications. Immediately after surgery, urine output should be monitored closely, and serum creatinine and electrolytes should be checked daily for the first 2 to 3 days. An indwelling urinary catheter may be placed to monitor urine output. Suture removal: Skin sutures are typically removed 10 to 14 days after surgery. If a ureteral stent or nephrostomy tube is placed, it may be removed after 2 to 4 weeks, depending on the case. Serial imaging: Abdominal ultrasound or radiography should be performed at 2, 4, and 8 weeks postoperatively to assess renal pelvis size, ureteral patency, and the presence of any residual stones. A recheck at 3 to 6 months is recommended to evaluate for recurrence. Restricted activity: Animals should be strictly rested for 2 to 4 weeks after surgery to allow healing. Leash walks only, no jumping or running. Physical therapy: Gentle massage and passive range of motion exercises may be beneficial, but are not typically required for ureteral surgery. Long-term monitoring: Blood work (BUN, creatinine, SDMA) should be checked every 3 to 6 months to monitor renal function. Urinalysis and urine culture should be performed if there are signs of urinary tract infection. Dietary management and medications (e.g., potassium citrate for calcium oxalate stones) should be continued as directed. Owners should be educated on the signs of recurrence, such as vomiting, decreased appetite, and changes in urination.

Clinical pearls: 1) Always assess renal function before surgery; if the animal is azotemic, stabilize with fluid therapy and consider temporary nephrostomy tube placement. 2) In cats, the ureter is very small (1-2 mm), so delicate handling and magnification (loupes or operating microscope) are essential. 3) When performing a ureterotomy, make the incision directly over the stone, and use stay sutures to manipulate the ureter. 4) Place a ureteral stent or nephrostomy tube to protect the repair and ensure urine flow. 5) For distal ureteral stones, ureteroneocystostomy is preferred over ureterotomy due to the risk of stricture. 6) Consider a subcutaneous ureteral bypass (SUB) device in cats with severe ureteral disease, as it has a high success rate. 7) Always submit stones for analysis to guide preventive therapy. Pitfalls: 1) Failure to identify a second stone or bilateral obstruction can lead to persistent azotemia. 2) Incomplete stone removal can lead to recurrence. 3) Ureteral closure with excessive tension or improper suture technique can cause leakage or stricture. 4) Inadequate postoperative pain management can lead to decreased urine output. 5) Not addressing underlying metabolic abnormalities (e.g., hypercalcemia) can result in rapid stone recurrence. 6) Overlooking concurrent urinary tract infection can lead to pyelonephritis and further renal damage. 7) In cats, excessive manipulation of the ureter can cause spasm and postoperative obstruction.

Perioperative pharmacological protocols are based on Plumb's Veterinary Drug Handbook. Preoperative: If the animal is azotemic, administer intravenous fluids (e.g., Lactated Ringer's solution) at a rate to correct dehydration and maintain diuresis (e.g., 60-100 ml/kg/day in dogs, 40-60 ml/kg/day in cats). Prophylactic antibiotics: Cefazolin (22 mg/kg IV) or cefoxitin (30 mg/kg IV) administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperative antibiotics: Continue cefazolin (22 mg/kg IV q8h) or amoxicillin-clavulanate (13.75 mg/kg PO q12h) for 24 hours postoperatively, or longer if infection is present. Analgesics: Opioids: Hydromorphone (0.05-0.1 mg/kg IV or IM q4-6h) or buprenorphine (0.01-0.02 mg/kg IV or IM q6-8h) for moderate to severe pain. NSAIDs: Carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) for mild to moderate pain, but use with caution in animals with renal disease. Local anesthesia: Epidural analgesia with morphine (0.1 mg/kg) and bupivacaine (0.5-1 mg/kg) can provide excellent pain relief. Constant rate infusion (CRI) of fentanyl (2-5 mcg/kg/hr IV) or lidocaine (25-50 mcg/kg/min IV) may be used for severe pain. Muscle relaxants: Not typically required, but diazepam (0.2-0.5 mg/kg IV) may be used for ureteral spasm. Chondroprotectants: Not applicable. Additional medications: If hypercalcemia is present, treat with saline diuresis and furosemide (1-2 mg/kg IV q8h). For calcium oxalate stones, potassium citrate (40-75 mg/kg PO q12h) may be used to alkalinize urine. For struvite stones, antibiotics based on culture and sensitivity, and urinary acidifiers such as ammonium chloride (100-200 mg/kg PO q12h) may be used. Antiemetics: Maropitant (1 mg/kg SC q24h) or ondansetron (0.1-0.2 mg/kg IV q8h) for vomiting. Gastroprotectants: Omeprazole (0.7-1 mg/kg PO q24h) or famotidine (0.5 mg/kg IV q12h) to prevent stress ulcers.

Key literature on ureterolithiasis and ureteral obstruction includes: 1) A study by Kyles et al. (2005) in cats with ureteral obstruction reported that surgical intervention (ureterotomy, ureteroneocystostomy, or nephroureterectomy) resulted in a 91% survival rate, with 66% of cats having improved renal function. 2) A study by Berent et al. (2014) evaluated the use of subcutaneous ureteral bypass (SUB) devices in cats and found a 95% success rate in relieving obstruction, with a median survival time of 498 days. 3) A retrospective study by Snyder et al. (2004) in dogs with ureterolithiasis found that ureterotomy and ureteroneocystostomy had similar success rates, but complications such as urine leakage and stricture were more common with ureterotomy. 4) A consensus statement from the American College of Veterinary Internal Medicine (ACVIM) on urolithiasis recommends that surgical intervention be considered for ureteral stones that are >3 mm in cats and >5 mm in dogs, or if there is progressive hydronephrosis or azotemia. 5) A study by Lulich et al. (2016) on medical management of ureteral stones in dogs reported that 50% of stones passed spontaneously, but this was associated with a high risk of renal damage. 6) A meta-analysis by Palm et al. (2015) found that ureteral stenting had a lower complication rate compared to surgery, but stent migration and encrustation were common. 7) Guidelines from the American College of Veterinary Surgeons (ACVS) recommend that animals with ureteral obstruction and azotemia should be stabilized with fluid therapy and dialysis if necessary before surgery. 8) A study by Ross et al. (2011) on the use of ureteral stents in cats reported a 70% success rate in relieving obstruction, with a median survival time of 1.5 years. 9) A study by Greenwell et al. (2013) evaluated the long-term outcome of cats with ureteral obstruction and found that 50% developed chronic kidney disease, but many had a good quality of life. 10) A study by Defarges et al. (2013) compared surgical and interventional treatments for ureteral obstruction in cats and found that interventional procedures (stenting, SUB) had shorter hospital stays and lower complication rates, but were more expensive. These studies support the use of surgical and interventional techniques for the management of ureterolithiasis, with the choice of procedure based on individual patient factors and owner preferences.