Urolithiasis

Urinary stones affect about 10 % of the population, more in men. The incidence is increasing due to rise in incidence of obesity. One half has family history of urinary stones. Children with stones have usually an undelying (familiar) metabolic abnormality or congenital uropoetic anomalies. Most frequent composition of urinary stones is calcium oxalate, uric acid, struvite (magnesium ammonium calcium phosphate) and cystine. These chemicals are usually soluble in the urine, but supersaturation with absence of stone inhibitors or present urinary tract obstruction or urinary infection can result in precipitation and aggregation of crystalline concretions on renal papillas (Randall´s plaques). These depositions continue in growth until the stones is big enough to pass in the collecting system. Here it may continue to grow and can cause obstruction and pain.

Etiology
Hyperuricaemia, gout or chemotherapy can lead to hyperuricosuria and creation of uric acid stones. Struvite are considered an infectious stones, developed due to urease producing microorganisms (proteus mirabilis, klebsiella, enterobacter or pseudomonas). Urease cleaves urea into ammonium, which makes urine alkaline and phosphate precipitate with ammonium, magnesium and calcium as the struvite stones. Developement of these stones is very rapid and large staghorn-shaped stones may fill the entire renal pelvis and calyces. Hyperparathyreoidism leads to hypercalcemia and hypercalciuria with subsequent development of calcium oxalate or calcium phosphate stones. Cystine stones develope in patients with hereditary disease cystinuria. Urinary stones may produce obstruction and subsequent pain from ureteral dilation and renal capsule distension. In the initial phase (1-2 hours) there is increased intrarenal pelvic pressure and increased blood flow, but decreased glomerular filtration. In the next phase (6-24 hours) blood flow decreases, but renal pelvis pressure remain elevated. Later renal ischemia leads to renal impairement, which can be after 2-4 weeks irreversible.

Clinical presentation
The classic presentation of a renal stone is acute renal colic – flank pain (often very severe) radiating to the groin or scrotum, associated with nausea and vomiting. Stone in the distal ureter close to the bladder can manifest with lower quadrant pain, urinary frequency, urgency and dysuria. Physical exam shows a constantly moving distressed patient. Costovetebral angle or lower quadrant tenderness may be present. Gross or microscopic hematuria is present in 80-90 % of patients (in case with complete obstruction there is absence of hematuria). Nausea and vomiting are often present. Acute renal colic may mimic other acute abdominal conditions.

Diagnostic evaluation
The current gold standard for confirming urinary stones in patients with acute flank pain is non-contrast (low dose) computed tomography (CT). Ultrasound (US) is used to estimate the degree of urinary obstruction (dilation-hydronephrosis), also kidney stones are visible. Plain abdominal radiograph (KUB) can distinguish radiopaque stones (calcium) from non-radiopaque stones (uric acid). The most important is to determine whether or not urgent intervention is needed. Urgent intervention is needed in: 1. obstruction with urinary tract infection (urinalysis, microscopy, urine culture, C-reactive protein, leukocytosis) 2. obstruction with renal deterioration (serum creatinin level) 3. bilateral obstruction 4. obstruction in immunosuppresive patients 5. obstruction with refractory pain Completelly obstructed or infected dilated upper urinary tract should be invasive decompressed either by uretheral stent placement or percutaneous nephrostomy. Delay in surgical intervention can be potentially dangerous. Definitive treatment of the obstructive stone should be delayed until infection is cleared. Pharmacological treatment of renal colic include analgetic treatment - nonsteroidal anti-inflammatory drugs (NSAIDs) e.g. ketoprofen and medical expulsive therapy (MET) – which includes calcium channel blockers (e.g. e.g. nifedipim) or alpha blockers (e.g. tamsulosin). Ureteral stones smaller than 6 mm have more than 50-90 % chance of passing. Generally asymptomatic patients with stones less than 10 mm, may be observed up to 4 weeks, unless symptoms, infection and renal deterioration warrant intervention. It is important to encourage patients to strain their urine for stone passage, collect and submit the stone for chemical analysis. Risk factors for stone formation include low fluid intake, high sodium intake, low fiber diet, low fruit and vegetable intake and high intake of animal proteins. Medical conditions with increased risk of stone formation include hyperparathyroidism, inflammatory bowel disease, malabsorption disorders, chronic diarrhea, renal tubular acidosis type I and diabetes mellitus. Treatment of these conditions and excluding of risk factors are the cornerstone of metaphylaxis of urinary stones. Treatment 1.Oral stone dissolution with potassium citrate (alkalisation therapy) in uric acid stones 2. Extracorporeal shock wave lithotripsy - focuses shock ultrasound waves on the stone to desintegrate it into small fragments. 3. Ureteroscopy - insertion of flexible or semirigid ureteroscope through bladder into the ureter and renal collecting system and desintegration of the stone with laser lithotripsy or removing with endocopic baskets. 4. Percutaneous nephrolithotomy (PCNL) is method prefered for renal stones 2 cm and more in maximal diameter. Puncture of renal collecting system under radiographic guidance is performed, tract into the kidney is dilated and rigid or flexible nephroscope is inserted. Lasers, ultrasonic probe or pneumatic device is then inserted and stone is fragmented and fragments are evacuated. 5. Open or laparoscopic lithotomy are surgical procedures, when stones are removed in toto. Stone prevention requires metabolic evaluation (stone composition analysis, 24-hour urine collection - volume, pH, calcium, oxalate, sodium, uric acid, citrate, phosphate, magnesium, sulfate, creatinine, cystine and serum studies - uric acid, calcium, phosphorus, creatinine, alkaline phosphatase, parathormon, D-vitamin). Oral fluid intake should generate a 24 hour urine volume of at least 2,5 l. Hypercalciuria is managed by normal amount of dietary calcium ( < 2000 mg/day), limit sodium intake (< 2 g/day) and thiazide diuretics. Hyperparathyroidism should be managed by endocrinologist – in parathyroid adenoma with it´s surgical removing. Hyperoxaluria can be caused by increased dietary intake of oxalate (high intake of spinach, chocolate, nuts, tea, vitamin C) or in fat malabsorption (Crohn´s disease, intestinal bypass surgery). Effective treatment is Vitamin B6, calcium citrate and dietary oxalate reduction. Hypocitraturia is risk factor for calcium oxalate and uric acid stone disease. Citrate inhibits the stone formation. Hypocitraturia occurs in patients with chronic acidosis, hypokalemia, distal renal tubular acidosis, enteric hyperoxaluria, chronic diarrhea, use of acetazolamid. Treatment is potassium citrate. Hyperuricosuria can lead to calcium oxalate and uric acid stones. Treatment is increasing fluid intake, decreasing sodium intake and decreased intake of animal proteins (including fish) and allopurinol. Treatment of cystinuria requires high fluid intake (diuresis more than 3 l), potassium citrate or sodium bicarbonate (the goal is urinary pH 7,5) and thiopronin. Patient motivation and physician-patient collaboration are critical for long-term compliance of patients (usually < 80 %).

Courses

• Surgery 4 (Trauma Surgery, Urology) [ChK/CH-V4/09]