Stone disease of the urinary tract

Published on 11/04/2015 by admin

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37

Stone disease of the urinary tract

Introduction

Stone disease is second only to prostatic disease in the overall urological workload. Stones may occur in all parts of the urinary tract, including the pelvicalyceal system of the kidney, the ureter, the bladder and even sometimes the urethra. Stones most commonly provoke symptoms due to obstruction or by predisposing to urinary tract infections.

The pattern of stone disease has changed markedly over the last 150 years. Bladder stones were once common and were one of the few conditions successfully treated by surgery. ‘Cutting for stone’, or lithotomy (lithos = stone), was often performed by itinerant surgeons. They used a perineal approach, placing the patient in the manner still described as the lithotomy position.

Upper tract calculi are much more common than bladder calculi and the incidence is rising. Stones range from the uncommon staghorn calculus which fills the pelvicalyceal system, to small stones developing in the pelvicalyceal system that can migrate and obstruct the ureter. Acute ureteric obstruction causes severe pain and presents as the surgical emergency ureteric colic. Most stone disease is, however, asymptomatic or else presents non-urgently to the outpatient clinic.

In developed countries stone disease in childhood is now rare. It peaks in the 20s and 30s and declines slowly thereafter (Fig. 37.1). Males are affected two and a half times more often than females. There is also a high incidence of recurrent stones.

Pathophysiology of stone disease

Chemical composition

Stones are often formed from a mixture of chemical substances and minerals (e.g. calcium and oxalate) when their concentration exceeds their solubility in urine. Intermittent periods of super-saturation due to dehydration, following meals or medical conditions, can lead to the earliest phase of crystal formation. Lack of crystallisation inhibitors in the urine may also play a role in stone formation. Table 37.1 provides a simple chemical classification showing the relative frequency of stone types and their important clinical characteristics and aetiology. Calcium is present in approximately 80%, as oxalate or phosphate compounds or both. The aetiology of stone disease is multifactorial in most cases.

Mechanisms of stone formation

Other predisposing factors

A specific predisposing factor can be detected in a further minority of cases. These include chronic infection, urinary stasis and foreign bodies, and are summarised in Box 37.1.

Clinical features of stone disease

The clinical problem of discrete urinary stones should not be confused with calcification of the renal parenchyma, which can be a feature of tuberculosis and medullary sponge kidney. These and similar diseases can usually be diagnosed by their characteristic X-ray appearance.

The clinical presentation of stones depends on the size, morphology and site of the stone(s). Many cause no symptoms but represent a potentially serious problem. Other stones produce marked pathological effects which present with acute or chronic symptoms or are discovered incidentally on investigation of unrelated symptoms. The presentation of urinary tract stones is summarised in Box 37.2.

Obstruction of urinary flow

Passage of stones into the ureter

If small renal stones pass into the ureter, there are several possible outcomes:

• Stones may pass to the bladder and exit via the urethra causing minor symptoms. The patient may intermittently pass ‘gravel’ or ‘sand’ (see Fig. 37.2) and experience dysuria and sometimes haematuria

• Stones may pass into the bladder and act as a nidus for a larger bladder stone. Bladder stones occasionally cause bladder outlet obstruction and urinary retention

• A stone may impact in the ureter causing chronic partial obstruction and eventually hydroureter. This presents typically as loin pain but, surprisingly, may be asymptomatic

• A stone may impact in the ureter, causing sudden obstruction. The patient experiences extremely severe, unilateral colicky pain (ureteric colic) radiating from loin to the groin or tip of the penis. There is often loin tenderness due to renal distension. The pain is due to waves of ureteric peristalsis and at the peak of the pain, the patient writhes in agony

Investigation and management of suspected urinary tract stones

Methods of investigation

In general, the objectives can be met by performing the following investigations. For convenience, they are conducted concurrently:

• Urine dipstick testing, microscopy, culture and sensitivities

• Tests of renal function, i.e. plasma urea, electrolytes and creatinine levels

• A ‘KUB’ (kidney, ureter, bladder) plain abdominal X-ray. Around 90% of stones are radiopaque because they contain calcium. Urate stones are radiolucent

• CT imaging of the abdomen and pelvis. In developed countries, this has become the standard modality for diagnosing loin pain and renal tract stones (Fig. 37.4)

• Intravenous urography (IVU). This consists of a pre-injection KUB and further films at 5–20 minutes after injection of radiopaque contrast and after micturition. Figure 37.2 shows an IVU with the effects of stone obstruction

• Renal ultrasonography. This demonstrates hydronephrosis as well as the stones

• Special contrast techniques. These are occasionally required when other techniques do not give the required information, e.g. percutaneous (antegrade) pyelography or ascending (retrograde) ureterography

• Biochemical analysis of any recovered stones

• Tests for metabolic disorders (for recurrent stones), i.e. serum calcium, phosphate, oxalate, uric acid and alkaline phosphatase; 24-hour urinary excretion of calcium, uric acid and cysteine

Indications for stone removal (Box 37.3)

The finding of a urinary tract stone is not an automatic indication for its removal or destruction. The exception is in airline or military pilots in whom ureteric colic could prove disastrous. The usual indications for stone removal are summarised in Box 37.3. Small stones in the pelvicalyceal system often remain unchanged and asymptomatic for many years and can safely be monitored by annual radiography. Stones of 5 mm or less in diameter often pass right through the tract, although in doing so they may produce severe but short-lived symptoms of ureteric colic, haematuria or dysuria.

Methods of stone removal

Stones can be removed by endoscopic methods, percutaneously or very rarely by open surgery. The choice of technique depends on the size, nature and site of the stone, the availability of expertise and special equipment, and whether there is a need to correct congenital or acquired structural abnormalities.

Cystoscopic techniques

Cystoscopic methods (Fig. 37.5) are suitable for most bladder stones and for impacted stones in the lower third of the ureter. Bladder stones can be broken into small fragments (litholapaxy) using a stone punch or lithotrite, a cystoscope incorporating stone-crushing jaws. The fragments are then washed out by irrigation. Stones can also be fragmented by directly applied pulsed ultrasound, laser or other energy sources via a cystoscope.

A rigid ureteroscope can be used to examine the entire length of the ureter and assist with stone removal (see Fig. 37.6a), as well as to apply energy via laser fibre, ultrasonic, electrohydraulic, or lithoclast probes directly onto the surface of a stone to destroy it. It can also help capture elusive stones via a Dormia basket (declining in popularity). Flexible ureteroscopes allow access to the renal pelvis and calyces so stone fragmentation can be achieved using holmium laser probes.

A ureteric stent may be placed after repeated instrumentation of the ureter to assist drainage. If an impacted stone is causing complete ureteric obstruction and leading to marked proximal dilatation, or if there is infection, a percutaneous nephrostomy tube should be inserted above the stone without delay (see Fig. 37.7, p. 470) to preserve renal function.

Management of acute ureteric colic

Most patients with ureteric colic are seen urgently by a GP or brought straight to the accident and emergency department. Non-steroidal anti-inflammatory drugs given as suppositories or injection have largely replaced intramuscular opiate analgesia to settle the pain. NSAIDs (usually diclofenac) are more effective, longer-lasting and without risk of addiction or legal compromise. Morphine should be avoided as it tends to provoke or prolong ureteric spasm and pain. The patient may have become pain-free by the time of first examination, but the pain history is usually diagnostic. Occasionally, ureteric colic is less severe but more persistent, in which case it may mimic other acute abdominal conditions.

Many patients settle with a single analgesic dose but two or three doses may be required. In most cases, the stone gradually passes down the ureter and into the bladder. Each stage of movement may be accompanied by an attack of colic. If a stone is retrieved, it should be chemically analysed. If there is complete obstruction of the ureter, or infection above an obstructing stone, urgent intervention is usually required to prevent renal damage. Immediate treatment may involve placing a percutaneous nephrostomy tube to drain the renal pelvis (see Fig. 37.7), placing a stent beside the stone to allow drainage, or removing the stone endoscopically. After nephrostomy or stent placement, the stone sometimes passes spontaneously but more often further treatment is required. In cases with persistent pain not needing immediate intervention, plain abdominal X-rays usually record changes in the stone’s position. Very large stones may have to be surgically removed. If a stone appears to be small enough to pass spontaneously, yet fails to progress, the patient can safely be allowed home provided criteria for urgent intervention are not fulfilled. The patient can be reviewed after a week or two with a plain abdominal X-ray and a decision taken then about any need for intervention.

Investigation of ureteric colic

Ureteric colic almost always causes microscopic haematuria, so the first investigation is ‘dipstick’ testing of urine for blood; if positive it should be confirmed on microscopic examination. A positive result reinforces the diagnosis. A CT scan or an IVU should then be performed urgently to confirm or refute the diagnosis (see Fig. 37.4, p. 467).

Characteristic radiological features of acute ureteric obstruction on IVU are:

Long-term management of urological stone disease

Management of metabolic abnormalities

Hyperparathyroidism is the only stone-forming metabolic abnormality that can be corrected by surgical treatment (parathyroidectomy). It is diagnosed by elevated plasma calcium, lowered plasma phosphate and elevated plasma parathormone levels. Most patients are also hypercalciuric.

Dietary hypercalciuria should be treated by reducing the intake of milk, cheese, butter, bread and pastry. Local tap water and bottled water imbibed by the patient should have its calcium level checked. Idiopathic hypercalciuria can be treated with thiazides. Urate stones dissolve in alkaline urine and treatment may involve alkalinising the urine with potassium citrate. Primary oxaluria is very rare; secondary oxaluria only occurs with huge intakes of tea, coffee, chocolate, strawberries or rhubarb.

The drug allopurinol may be given for hyperuricaemia (gout) and is routinely used during chemotherapy for leukaemia. Allopurinol inhibits xanthine oxidase, an enzyme involved in synthesis of uric acid. Allopurinol can be used in hyperuricaemia (see below) and may also prevent nidus formation in urine around which calcium crystals deposit during stone formation.