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Ovid: Oxford Handbook of Urology

Authors: Reynard, John; Brewster, Simon; Biers, Suzanne Title: Oxford Handbook of Urology, 1st Edition Copyright ©2006 Oxford University Press > Table of Contents > Chapter 9 – Stone disease Chapter 9 Stone disease P.350
Kidney stones: epidemiology ~10% of Caucasian men will develop a kidney stone by the age of 70. Within 1 year of a calcium oxalate stone, 10% of men will form another calcium oxalate stone, and 50% will have formed another stone within 10 years. The prevalence of renal tract stone disease is determined by factors intrinsic to the individual and by extrinsic (environmental) factors. A combination of factors often contribute to risk of stone formation. Intrinsic factors

  • Age. The peak incidence of stones occurs between the ages of 20–50 years.
  • Sex. Males are affected 3 times as frequently as females. Testosterone may cause increased oxalate production in the liver (predisposing to calcium oxalate stones) and women have higher urinary citrate concentrations (citrate inhibits calcium oxalate stone formation).
  • Genetic. Kidney stones are relatively uncommon in Native Americans, Black Africans, and US Blacks, and more common in Caucasians and Asians. ~25% of patients with kidney stones report a family history of stone disease (the relative risk of stone formation remaining high after adjusting for dietary calcium intake). Familial renal tubular acidosis (predisposing to calcium phosphate stones) and cystinuria (predisposing to cystine stones) are inherited.1

Extrinsic (environmental) factors

  • Geographical location, climate, and season. The relationship between these factors and stone risk is complex. While renal stone disease is more common in hot climates, some endogenous populations of hot climates have a low incidence of stones (e.g. Black Africans, Aborigines) and many temperate areas have a high incidence of stones (e.g. Northern Europe and Scandanavia). This may relate to Western lifestyle—excess food, inadequate fluid intake, limited exercise—combined with a genetic predisposition to stone formation.
  • Ureteric stones become more prevalent during the summer, the highest incidence occurring a month or so after peak summertime temperatures, presumably because of higher urinary concentration in the summer (encourages crystallization). Concentrated urine has a lower pH, encouraging cystine and uric acid stone formation. Exposure to sunlight may also increase endogenous vitamin D production, leading to hypercalciuria.
  • Water intake. Low fluid intake (<1200ml/day) predisposes to stone formation.2 Increasing water ‘hardness’ (high calcium content) may reduce risk of stone formation, by decreasing urinary oxalate.
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  • Diet. High animal protein intake increases risk of stone disease (high urinary oxalate, low pH, low urinary citrate).3,4 High salt intake causes hypercalciuria. Contrary to conventional teaching, low calcium diets predispose to calcium stone disease, and high calcium intake is protective.5
  • Occupation. Sedentary occupations predispose to stones compared with manual workers.

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Kidney stones: types and predisposing factors Stones may be classified according to composition, X-ray appearance, or size and shape. Composition

Stone composition % of all renal calculi1
Calcium oxalate 85%
Uric acid2 5–10%
Calcium phosphate + calcium oxalate 10% Pure calcium phosphate Rare
Struvite (infection stones) 2–20%
Cystine 1%
1 The precise distribution of stone types will vary depending on the characteristics of the study population (geographical location, racial distribution, etc.). Hence, the quoted figures do not equate to 100.
2 ~80% of uric acid stones are pure uric acid, and 20% contain some calcium oxalate as well.

Other rare stone types (all of which are radiolucent): indinavir (a protease inhibitor used for treatment of HIV); triamterene (a relatively insoluble potassium sparing diuretic, most of which is excreted in urine); xanthine. Radiodensity on X-ray Three broad categories of stones are described, based on their X-ray appearance. This gives some indication of the likely stone composition and helps, to some extent, to determine treatment options. However, in only 40% of cases is stone composition correctly identified from visual estimation of radiodensity on plain X-ray.6 Radio-opaque Opacity implies the presence of substantial amounts of calcium within the stone. Calcium phosphate stones are the most radiodense stones, being almost as dense as bone. Calcium oxalate stones are slightly less radiodense. Relatively radiolucent Cystine stones are relatively radiodense because they contain sulphur (Fig. 9.1). Magnesium ammonium phosphate (struvite) stones are less radiodense than calcium containing stones. Completely radiolucent Uric acid, triamterene, xanthine, indinavir (cannot be seen even on CTU). Size and shape Stones can be characterized by their size, in centimetres. Stones which grow to occupy the renal collecting system (the pelvis and one or more renal calyx) are known as staghorn calculi, since they resemble the horns of a stag (Fig. 9.2). They are most commonly composed of struvite—magnesium ammonium phosphate—(being caused by infection and forming under the alkaline conditions induced by urea-splitting bacteria), but may be composed of uric acid, cystine, or calcium oxalate monohydrate.

Fig. 9.1 A left cystine stone, barely visible just below the midpoint of the 12th rib
Fig. 9.2 A large, right staghorn calculus

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Kidney stones: mechanisms of formation Urine is said to be saturated with, for example, calcium and oxalate, when the product of the concentrations of calcium and oxalate exceeds the solubility product (Ksp). Below the solubility product, crystals of calcium and oxalate will not form and the urine is said to be undersaturated. Above the solubility product, crystals of calcium and oxalate should form, but they do not because of the presence of inhibitors of crystal formation. However, above a certain concentration of calcium and oxalate, inhibitors of crystallization become ineffective, and crystals of calcium oxalate start to form. The concentration of calcium and oxalate at which this is reached (i.e. at which crystallization starts) is known as the formation product (Kf) and the urine is said to be supersaturated with the substance or substances in question at concentrations above this level. Urine is described as being metastable for calcium and oxalate at concentrations between the solubility product of calcium and oxalate and the formation product. (See box) The ability of urine to hold more solute in solution than can pure water is due partly to the presence of various inhibitors of crystallization (e.g. citrate forms a soluble complex with calcium, preventing it from combining with oxalate or phosphate to form calcium oxalate or calcium phosphate stones). Other inhibitors of crystallization include magnesium, glycosaminoglycans, and Tamm–Horsfall protein. Periods of intermittent supersaturation of urine with various substances can occur as a consequence of dehydration and following meals. The earliest phase of crystal formation is known as nucleation. Crystal nuclei usually form on the surfaces of epithelial cells or on other crystals. Crystal nuclei form into clumps—a process known as aggregation. Citrate and magnesium not only inhibit crystallization but also inhibit aggregation. P.355
Steps leading to stone formation

  • Calcium and oxalate concentration < solubility product → NO STONE FORMATION
  • Metastable calcium and oxalate concentrations → NO STONE FORMATION
  • Calcium and oxalate concentrations > formation product → STONE FORMATION

In the urine of subjects who do not form stones, the concentrations of most stone components are between Ksp and Kf. P.356
Factors predisposing to specific stone types Calcium oxalate (~85% of stones) Hypercalciuria Excretion of >7mmol of calcium per day in men and >6mmol per day in women. A major risk factor for calcium oxalate stone formation: it increases the relative supersaturation of urine. About 50% of patients with calcium stone disease have hypercalciuria. 3 types:

  • Absorptive—increased intestinal absorption of calcium
  • Renal—renal leak of calcium
  • Resorptive—increased demineralization of bone (due to hyperparathyroidism)

Hypercalcaemia Almost all patients with hypercalcaemia who form stones have primary hyperparathyroidism. Of hyperparathyroid patients, about 1% form stones (the other 99% do not because of early detection of hyperparathyroidism by screening serum calcium). Hyperoxaluria Due to:

  • Altered membrane transport of oxalate leading to increased renal leak of oxalate
  • Primary hyperoxaluria—increased hepatic oxalate production; rare
  • Increased oxalate absorption in short bowel syndrome or malabsorption (enteric hyperoxaluria)—the colon is exposed to more bile salts and this increases its permeability to oxalate.

Hypocitraturia Low urinary citrate excretion. Citrate forms a soluble complex with calcium, so preventing complexing of calcium with oxalate to form calcium oxalate stones. Hyperuricosuria High urinary uric acid levels lead to formation of uric acid crystals, on the surface of which calcium oxalate crystals form. Uric acid (~5–10% of stones) Humans are unable to convert uric acid (which is relatively insoluble) into allantoin (which is very soluble). Human urine is supersaturated with insoluble uric acid. Uric acid exists in 2 forms in urine—uric acid and sodium urate. Sodium urate is 20 times more soluble than uric acid. At a urine pH of 5, <20% of uric acid is present as soluble sodium urate. At urine pH 5.5, half the uric acid is ionized as sodium urate (soluble) and half is non-ionized as free uric acid (insoluble). At a urine pH of 6.5, >90% of uric acid is present as soluble sodium urate. Thus, uric acid is essentially insoluble in acid urine and soluble in alkaline urine. Human urine is acidic (because the end products of metabolism are acid) and this low pH, combined with supersaturation of urine with uric acid, predisposes to uric acid stone formation. ~20% of patients with gout have uric acid stones. Patients with uric acid stones may have:

  • Gout. 50% of patients with uric acid stones have gout. The chance of forming a uric acid stone if you have gout is in the order of 1% per year from the time of the first attack of gout.
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  • Myeloproliferative disorders. Particularly following treatment with cytotoxic drugs, cell necrosis results in release of large quantities of nucleic acids which are converted to uric acid. A large plug of uric acid crystals may form in the collecting system of the kidney, in the absence of ureteric colic, causing oliguria or anuria.
  • Idiopathic uric acid stones (no associated condition).

Calcium phosphate (calcium phosphate + calcium oxalate = 10% of stones) Occur in patients with renal tubular acidosis (RTA)—a defect of renal tubular H+ secretion resulting in impaired ability of the kidney to acidify urine. The urine is therefore of high pH, and the patient has a metabolic acidosis. The high urine pH increases supersaturation of the urine with calcium and phosphate, leading to their precipitation as stones. Types of renal tubular acidosis

  • Type 1 or distal RTA. The distal tubule is unable to maintain a proton gradient between the blood and the tubular fluid. 70% of such patients have stones. Urine pH is >5.5, the patient has a metabolic acidosis and hypokalaemia, urinary citrate is low, and hypercalciuria is present.
  • Type 2 or proximal RTA. Due to failure of bicarbonate resorption in the proximal tubule. There is associated increased urinary citrate excretion, which protects against stone formation.
  • Type 3. A variant of type 1 RTA.
  • Type 4. Seen in diabetic nephropathy and interstital renal disease. These patients do not make stones.

If urine pH is >5.5, use the ammonium chloride loading test. Urine pH that remains above 5.5 after an oral dose of ammonium chloride = incomplete distal RTA. Struvite (infection or triple phosphate stones) (2–20% of stones) These stones are composed of magnesium, ammonium, and phosphate. They form as a consequence of urease-producing bacteria which produce ammonia from breakdown of urea (urease hydrolyses urea to carbon dioxide and ammonium), and in so doing alkalinize urine as in the following equation: NH2–O–NH2 + H2O → 2NH3 + CO2 Under alkaline conditions, crystals of magnesium, ammonium, and phosphate precipitate. Cystine (1% of all stones) Occur only in patients with cystinuria—an inherited (autosomal-recessive) disorder of transmembrane cystine transport, resulting in decreased absorption of cystine from the intestine and in the proximal tubule of the kidney. Cystine is very insoluble, so reduced absorption of cystine from the proximal tubule results in supersaturation with cystine and cystine crystal formation. Cystine is poorly soluble in acid urine (300mg/l at pH 5, 400mg/l at pH 7). P.358
Evaluation of the stone former Determination of stone type and a metabolic evaluation allows identification of the factors that led to stone formation, so advice can be given to prevent future stone formation. Metabolic evaluation depends, to an extent, on the stone type (see Table 9.1). In many cases a stone is retrieved. Stone type is analysed by polarizing microscopy, X-ray diffraction, and infrared spectroscopy, rather than by chemical analysis. Where no stone is retrieved, its nature must be inferred from its radiological appearance (e.g. a completely radiolucent stone is likely to be composed of uric acid) or from more detailed metabolic evaluation. In most patients, multiple factors are involved in the genesis of kidney stones and, as a general guide, the following evaluation is appropriate in most patients. Risk factors for stone disease

  • Diet. Enquire about volume of fluid intake, meat consumption (causes hypercalciuria, high uric acid levels, low urine pH, low urinary citrate), multivitamins (vitamin D increases intestinal calcium absorption), high doses of vitamin C (ascorbic acid causes hyperoxaluria).
  • Drugs. Corticosteroids (increase enteric absorption of calcium, leading to hypercalciuria); chemotherapeutic agents (breakdown products of malignant cells leads to hyperuricaemia).
  • Urinary tract infection. Urease-producing bacteria (Proteus, Klebsiella, Serratia, Enterobacter) predispose to struvite stones.
  • Mobility. Low activity levels predispose to bone demineralization and hypercalciuria.
  • Systemic disease. Gout, primary hyperparathyroidism, sarcoidosis.
  • Family history. Cystinuria, RTA.
  • Renal anatomy. PUJO, horseshoe kidney, medullary sponge kidney (up to 2% of patients with calcium-containing stones have MSK).
  • Previous bowel resection or inflammatory bowel disease. Causes intestinal hyperoxaluria.

Metabolic evaluation of the stone former Patients can be categorized as low risk and high risk for subsequent stone formation. High risk: previous history of a stone, family history of stones, GI disease, gout, chronic UTI, nephrocalcinosis. Low-risk patient evaluation Urea and electrolytes, FBC (to detect undiagnosed haematological malignancy), serum calcium (corrected for serum albumin), and uric acid, urine culture, urine dipstick for pH (see below). High-risk patient evaluation As for low-risk patients plus 24-h urine for calcium, oxalate, uric acid, cystine; evaluation for RTA.

Table 9.1 Characteristics of stone types
Stone type Urine acidity Mean urine pH (SEM)
Calcium oxalate Variable 6 (±0.4)
Calcium phosphate Tendency towards alkaline urine >5.5
Uric acid Acid 5.5 (±0.4)
Struvite Alkaline* —
Cystine Normal (5–7) —
* Urine pH must be above 7.2 for deposition of struvite crystals.

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Urine pH Urine pH in normal individuals shows variation, from pH 5–7. After a meal, pH is initially acid because of acid production from metabolism of purines (nucleic acids in, for example, meat). This is followed by an ‘alkaline tide’, pH rising to >6.5. Urine pH can help establish what type of stone the patient may have (if a stone is not available for analysis), and can help the urologist and patient in determining whether preventative measures are likely to be effective or not.

  • pH <6 in a patient with radiolucent stones suggests the presence of uric acid stones.
  • pH consistently >5.5 suggests type 1 (distal) RTA (~70% of such patients will form calcium phosphate stones).

Evaluation for RTA Evaluate for RTA if: calcium phosphate stones, bilateral stones, nephrocalcinosis, MSK, hypocitraturia.

  • If fasting morning urine pH (i.e. first urine of the day) is >5.5, the patient has complete distal RTA.
  • First and second morning urine pH is a useful screening test for detection of incomplete distal RTA, over 90% of cases of RTA having a pH >6 on both specimens. The ammonium chloride loading test involves an oral dose of ammonium chloride (0.1g per kg; an acid load). If serum pH falls <7.3 or serum bicarbonate falls <16mmol/l, but urine pH remains >5.5, the patient has incomplete distal RTA.

Diagnostic tests for suspected cystinuria Cyanide-nitroprusside colorimetric test (‘cystine spot test’): if positive, a 24-h urine collection is done. A 24-h cystine >250mg is diagnostic of cystinuria. P.361
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Kidney stones: presentation and diagnosis Kidney stones may present with symptoms or be found incidentally during investigation of other problems. Presenting symptoms include pain or haematuria (microscopic or occasionally macroscopic). Struvite staghorn calculi classically present with recurrent UTIs. Malaise, weakness, and loss of appetite can also occur. Less commonly, struvite stones present with infective complications (pyonephrosis, perinephric abscess, septicaemia, xanthogranulomatous pyelonephritis). Diagnostic tests

  • Plain abdominal radiography: calculi that contain calcium are radiodense. Sulphur-containing stones (cystine) are relatively radiolucent on plain radiography.
  • Radiodensity of stones in decreasing order: calcium phosphate > calcium oxalate > struvite (magnesium ammonium phosphate) >> cystine.
  • Completely radiolucent stones (e.g. uric acid, triamterene, indinavir) are usually suspected on the basis of the patient’s history and/or urine pH (pH <6—gout; drug history—triamterene, indinavir), and the diagnosis may be confirmed by ultrasound, CTU, or MRU.
  • Renal ultrasound: its sensitivity for detecting renal calculi is ~95%.8 A combination of plain abdominal radiography and renal ultrasonography is a useful screeing test for renal calculi.
  • IVU: increasingly being replaced by CTU. Useful for patients with suspected indinavir stones (which are not visible on CT).
  • CTU: a very accurate method of diagnosing all but indinavir stones. Allows accurate determination of stone size and location and good definition of pelvicalyceal anatomy.
  • MRU: cannot visualize stones, but is able to demonstrate the presence of hydronephrosis.

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Kidney stone treatment options: watchful waiting The traditional indications for intervention are pain, infection, and obstruction. Haematuria caused by a stone is only very rarely severe or frequent enough to be the only reason to warrant treatment. Before embarking on treatment of a stone which you think is the cause of the patient’s pain or infections, warn them that though you may be able to remove the stone successfully, their pain or infections may persist (i.e. the stone may be coincidental to their pain or infections, which may be due to something else). Remember, UTIs are common in women, as are stones, and it is not therefore suprising that the two may coexist in the same patient, but be otherwise unrelated. Options for stone treatment are watchful waiting, ESWL, flexible ureteroscopy, PCNL, open surgery, and medical ‘dissolution’ therapy. When to watch and wait—and when not to It is not necessary to treat every kidney stone. As a rule of thumb, the younger the patient, the larger the stone, and the more symptoms it is causing, the more inclined are we to recommend treatment. Thus, one would be inclined to do nothing about a 1cm symptomless stone in the kidney of a 95-year-old patient. On the other hand, a 1cm stone in a symptomless 20-year-old runs the risk over the remaining (many) years of the patient’s life of causing problems. It could drop into the ureter causing ureteric colic, or it could increase in size and affect kidney function or cause pain. Asymptomatic stones which are followed over a 3-year period are more likely to require intervention (surgery or ESWL) or to increase in size or cause pain if they are >4mm in diameter and if they are located in a middle or lower pole calyx.10 The approximate risks, over 3 years of follow-up, of requiring intervention, of developing pain, or of increase in stone size, relative to stone size, is shown in Table 9.2. Another factor determining the need for treatment is the patient’s job. Airline pilots are not allowed to fly if they have kidney stones, for fear that the stones could drop into the ureter at 30,000ft, with disastrous consequences! Some stones are definitely not suitable for watchful waiting. Untreated struvite (i.e. infection related) staghorn calculi will eventually destroy the kidney if untreated and are a significant risk to the patient’s life. Watchful waiting is therefore NOT recommended for staghorn calculi unless patient comorbidity is such that surgery would be a higher risk than watchful waiting. Historical series suggest that ~30% of patients with staghorn calculi who did not undergo surgical removal died of renal related causes—renal failure, urosepsis (septicaemia, pyonephrosis, perinephric abscess).10,11 Combination of a neurogenic bladder and staghorn calculus seems to be particularly associated with a poor outcome.12

Table 9.2 Approximate 3-year risk of intervention, pain, or increase in stone size
  Stone size
<5mm 5–10mm 11–15mm >15mm
% requiring intervention 20% 25% 40% 30%
% causing pain 40% 40% 40% 60%
% increasing in size 50% 55% 60% 70%

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Stone fragmentation techniques: extracorporeal lithotripsy (ESWL) The technique of focusing externally generated shock waves at a target (the stone). First used in humans in 1980. The first commercial lithotriptor, the Dornier HM3, became available in 1983.13 ESWL revolutionized kidney and ureteric stone treatment. Three methods of shock wave generation are commercially available—electrohydraulic, electromagnetic, and piezoelectric. Electrohydraulic Application of a high voltage electrical current between 2 electrodes about 1mm apart under water causes discharge of a spark. Water around the tip of the electrode is vaporized by the high temperature resulting in a rapidly expanding gas bubble. The rapid expansion and then the rapid collapse of this bubble generates a shock wave which is focused by a metal reflector shaped as a hemi-ellipsoid. Used in the original Dornier HM3 lithotriptor. Electromagnetic Two electrically conducting cylindrical plates are separated by a thin membrane of insulating material. Passage of an electrical current through the plates generates a strong magnetic field between them, the subsequent movement of which generates a shock wave. An ‘acoustic’ lens is used to focus the shock wave. Piezoelectric A spherical dish is covered with about 3000 small ceramic elements, each of which expands rapidly when a high voltage is applied across them. This rapid expansion generates a shock wave. X-ray, ultrasound, or a combination of both are used to locate the stone on which the shock waves are focused. Older machines required general or regional anaesthesia because the shock waves were powerful and caused severe pain. Newer lithotriptors generate less powerful shock waves, allowing ESWL with oral or parenteral analgesia in many cases, but they are less efficient at stone fragmentation. Efficacy of ESWL Likelihood of fragmention with ESWL depends on stone size and location, anatomy of renal collecting system, degree of obesity, and stone composition. Most effective for stones <2cm in diameter, in favourable anatomical locations. Less effective for stones >2cm diameter, in lower pole stones in a calyceal diverticulum (poor drainage), and those composed of cystine or calcium oxalate monohydrate (very hard). Stone free rates for solitary kidney stones are 80% for stones <1cm in diameter, 60% for those between 1–2cm, and 50% for those >2cm in diameter. Lower stone free rates as compared with open surgery or PCNL are accepted because of the minimal morbidity of ESWL. There have been no randomized studies comparing stone free rates between different lithotriptors. In non-randomized studies, rather surprisingly, when it comes to efficacy of stone fragmentation, older (the original Dornier HM3 machine) is better (but higher requirement for analgesia and sedation or general anaesthesia). Less powerful (modern) lithotriptors have lower stone free rates and higher retreatment rates. P.367
Side-effects of ESWL ESWL causes a certain amount of structural and functional renal damage (found more frequently the harder you look). Haematuria (microscopic, macroscopic) and oedema are common, perirenal haematomas less so (0.5% detected on ultrasound with modern machines, although reported in as many as 30% with the Dornier HM3). Effective renal plasma flow (measured by renography) has been reported to fall in ~30% of treated kidneys. There is data suggesting that ESWL may increase the likelihood of development of hypertension. Acute renal injury may be more likely to occur in patients with pre-existing hypertension, prolonged coagulation time, coexisting coronary heart disease, diabetes, and in those with solitary kidneys. Contraindications to ESWL Absolute contraindications: pregnancy, uncorrected blood clotting disorders (including anticoagulation). BAUS procedure-specific consent form: potential complications after ESWL Common

  • Bleeding on passing urine for short period after procedure
  • Pain in the kidney as small fragments of stone pass after fragmentation
  • UTI from bacteria released from the stone, needing antibiotic treatment.

Occasional

  • Stone will not break as too hard, requiring an alternative treatment
  • Repeated ESWL treatments may be required
  • Recurrence of stones.

Rare

  • Kidney damage (bruising) or infection, needing further treatment
  • Stone fragments occasionally get stuck in the tube between the kidney and the bladder requiring hospital attendance and sometimes surgery to remove the stone fragment
  • Severe infection requiring intravenous antibiotics and sometimes drainage of the kidney by a small drain placed through the back into the kidney.

Alternative therapy Telescopic surgery, open surgery, or observation to allow spontaneous passage. P.368
Intracorporeal techniques of stone fragmentation (fragmentation within the body) Electrohydraulic lithotripsy (EHL) The first technique developed for intracorporeal lithotripsy. A high voltage applied across a concentric electrode under water generates a spark. This vaporizes water, and the subsequent expansion and collapse of the gas bubble generates a shock wave. An effective form of stone fragmentation. The shock wave is not focused, so the EHL probe must be applied within 1mm of the stone to optimize stone fragmentation. EHL has a narrower safety margin than pneumatic, ultrasonic, or laser lithotripsy, and should be kept as far away as possible from the wall of the ureter, renal pelvis, or bladder to limit damage to these structures, and at least 2mm away from the cystoscope, ureteroscope, or nephroscope to prevent lens fracture. Principal uses Bladder stones (wider safety margin than in the narrower ureter). Pneumatic (ballistic) lithotripsy A metal projectile contained within the handpiece is propelled backwards and forwards at great speed by bursts of compressed air (see Fig. 9.3). It strikes a long, thin, metal probe at one end of the handpiece at 12Hz (12 strikes per second) transmitting shock waves to the probe, which when in contact with a rigid structure such as a stone, fragments the stone. Used for stone fragmentation in the ureter (using a thin probe to allow insertion down a ureteroscope) or kidney (a thicker probe may be used, with an inbuilt suction device—‘Lithovac’—to remove stone fragments). Pneumatic lithotripsy is very safe since the excursion of the end of probe is about a millimetre, and it bounces off the pliable wall of the ureter. Ureteric perforation is therefore rare. Also low cost and low maintenance. However, its ballistic effect has a tendency to cause stone migration into the proximal ureter or renal pelvis, where the stone may be inaccessible to further treatment. The metal probe cannot bend around corners, so it cannot be used for ureteroscopic treatment of stones within the kidney. Principal uses Ureteric stones. Ultrasonic lithotripsy An electrical current applied across a piezoceramic plate located in the ultrasound transducer generates ultrasound waves of a specific frequency (23,000–25,000Hz). The ultrasound energy is transmitted to a hollow metal probe, which in turn is applied to the stone (see Fig. 9.4). The stone resonates at high frequency and this causes it to break into small fragments (the opera singer breaking a glass) which are then sucked out through the centre of the hollow probe. Soft tissues do not resonate when the probe is applied to them, and therefore are not damaged. Can only be used down straight instruments. Principal uses Fragmentation of renal calculi during PCNL.

Fig. 9.3 The Lithoclast: a pneumatic lithotripsy device. (Reproduced with permission from Walsh et al. 2002)15
Fig. 9.4 The Calcuson: an ultrasonic lithotripsy device. (Reproduced with permission from Walsh et al. 200213)

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Laser lithotripsy The holmium: YAG laser. Principally, a photothermal mechanism of action, causing stone vaporization. Minimal shock-wave generation, and therefore less risk of causing stone migration. The laser energy is delivered down fibres which vary in diameter from 200 to 360 microns. The 200 micron fibre is very flexible and can be used to gain access to stones even within the lower pole of the kidney (see Figs. 9.5 and 9.6). Zone of thermal injury is limited from 0.5 to 1mm from the laser tip. No stone can withstand the heat generated by the Ho:YAG laser. Laser lithotripsy takes time, however, since the thin laser fibre must be ‘painted’ over the surface of the stone to vaporize it. Principal uses Ureteric stones, small intrarenal stones.

Fig. 9.5 A laser fibre
Fig. 9.6 Access to the lower pole of the kidney with a flexible ureteroscope

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Kidney stone treatment: flexible ureteroscopy and laser treatment The development of small-calibre ureteroscopes with active deflecting mechanisms and instrument channels, in combination with the development of laser technology, small-diameter laser fibres, and stone baskets and graspers, has opened the way for intracorporeal, endoscopic treatment of kidney stones. Access to virtually the entire collecting system is possible with modern instruments. The holmium: YAG laser has a minimal effect on tissues at distances of 2–3mm from the laser tip and so ‘colateral’ tissue damage is minimal with this laser type. Flexible ureteroscopy and laser fragmentation offers a more effective treatment option compared with ESWL, with a lower morbidity than PCNL, but usually requires a general anaesthetic (some patients will tolerate it with sedation alone). It can also allow access to areas of the kidney where ESWL is less efficient or where PCNL cannot reach. It is most suited to stones <2cm in diameter. Indications for flexible ureteroscopic kidney stone treatment

  • ESWL failure.
  • Lower pole stone (reduces likelihood of stone passage post ESWL—fragments have to pass ‘uphill’).
  • Cystine stones.
  • Obesity such that PCNL access is technically difficult or impossible (nephroscopes may not be long enough to reach stone).
  • Obesity such that ESWL is technically difficult or impossible. BMI >28 is associated with lower ESWL success rates. Treatment distance may exceed focal length of lithotriptor.
  • Musculoskeletal deformities such that stone access by PCNL or ESWL is difficult or impossible (e.g. kyphoscoliosis).
  • Stone in a calyceal diverticulum (accessing stones in small diverticulae in upper and anterior calyces is difficult and carries significant risks).
  • Stenosis of a calcyceal infundibulum or ‘tight’ angle between renal pelvis and infundibulum. The flexible ureteroscope can negotiate acute angles and the laser can be used to divide obstructions.
  • Bleeding diathesis where reversal of this diathesis is potentially dangerous or difficult.
  • Horseshoe or pelvic kidney. ESWL fragmentation rates are only 50% in such cases15 due to difficulties of shock-wave transmission through overlying organs (bowel). PCNL for such kidneys is difficult because of bowel proximity and variable blood supply (blood supply derived from multiple sources).
  • Patient preference.

Disadvantages Efficacy diminishes as stone burden increases—it simply takes a long time to ‘paint’ the surface of the stone with laser energy, so destroying it. A dust-cloud is produced as the stone fragments and this temporarily P.373
obscures the view, until it has been washed away by irrigation. Stone fragmentation rates for those expert in flexible ureteroscopy are ~70–80% for stones <2cm in diameter and 50% for those >2cm in diameter16 and ~10% of patients will require 2 or more treatment sessions. P.374
Kidney stone treatment: percutaneous nephrolithotomy (PCNL) Technique PCNL is the removal of a kidney stone via a ‘track’ developed between the surface of the skin and the collecting system of the kidney. The first step requires ‘inflation’ of the renal collecting system (pelvis and calyces) with fluid or air instilled via a ureteric catheter inserted cystoscopically (Fig. 9.7). This makes subsequent percutaneous puncture of a renal calyx with a nephrostomy needle easier (Fig. 9.8). Once the nephrostomy needle is in the calyx, a guidewire is inserted into the renal pelvis to act as a guide over which the ‘track’ is dilated (Fig. 9.9). An access sheath is passed down the track and into the calyx, and through this a nephroscope can be advanced into the kidney (Fig. 9.10). An ultrasonic lithotripsy probe is used to fragment the stone and remove the debris. A posterior approach is most commonly used; below the 12th rib (to avoid the pleura and far enough away from the rib to avoid the intercostals, vessels, and nerve). The preferred approach is through a posterior calyx, rather than into the renal pelvis, because this avoids damage to posterior branches of the renal artery which are closely associated with the renal pelvis. General anaesthesia is usual, though regional or even local anaesthesia (with sedation) can be used. Indications for PCNL PCNL is generally recommended for stones >3cm in diameter, those that have failed ESWL and/or an attempt at flexible ureteroscopy and laser treatment. It is the first-line option for staghorn calculi,17 with ESWL and/or repeat PCNL being used for residual stone fragments. For stones 2–3cm in diameter, options include ESWL (with a JJ stent in situ), flexible ureteroscopy and laser treatment, and PCNL. PCNL gives the best chance of complete stone clearance with a single procedure, but this is achieved at a higher risk of morbidity. Some patients will opt for several sessions of ESWL or flexible ureteroscopy/laser treatment and the possible risk of ultimately requiring PCNL because of failure of ESWL or laser treatment, rather than proceeding with PCNL ‘up front’. ~50% of stones >2cm in diameter will be fragmented by flexible ureteroscopy and laser treatment. Outcomes of PCNL For small stones, the stone-free rate after PCNL is in the order of 90–95%. For staghorn stones, the stone-free rate of PCNL, when combined with post-operative ESWL for residual stone fragments, is in the order of 80–85%.

Fig. 9.7 A ureteric catheter is inserted into the renal pelvis to dilate it with air or fluid
Fig. 9.8 A nephrostomy needle has been inserted into a calyx
Fig. 9.9 A guidewire is inserted into the renal pelvis and down the ureter; over this guidewire the track is dilated
Fig. 9.10 An access sheath is passed down the track and into the calyx, and through this a nephroscope can be advanced into the kidney

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Kidney stones: open stone surgery Indications

  • Complex stone burden (projection of stone into multiple calyces, such that multiple PCNL tracks would be required to gain access to all the stone)
  • Failure of endoscopic treatment (technical difficulty gaining access to the collecting system of the kidney)
  • Anatomic abnormality that precludes endoscopic surgery (e.g. retrorenal colon)
  • Body habitus that precludes endoscopic surgery (e.g. gross obesity, kyphoscoliosis—open stone surgery can be difficult)
  • Patient request for a single procedure where multiple PCNLs might be required for stone clearance
  • Non-functioning kidney

Non-functioning kidney Where the kidney is not working, the stone may be left in situ if it is not causing symptoms (e.g. pain, recurrent urinary infection, haematuria). However, staghorn calculi should be removed, unless the patient has comorbidity that would preclude safe surgery because of the substantial risk of developing serious infective complications. If the kidney is non-functioning, the simplest way of removing the stone is to remove the kidney. Functioning kidneys—options for stone removal Small- to medium-sized stones

  • Pyelolithotomy
  • Radial nephrolithotomy

Staghorn calculi

  • Anatrophic (avascular) nephrolithotomy
  • Extended pyelolithotomy with radial nephrotomies (small incisions over individual stones)
  • Excision of the kidney, ‘bench’ surgery to remove the stones, and autotransplantation

Specific complications of open stone surgery Wound infection (the stones operated on are often infection stones); flank hernia; wound pain. (With PCNL these problems do not occur, blood transfusion rate is lower, analgesic requirement is less, mobilization is more rapid and discharge earlier—all of which account for PCNL having replaced open surgery as the mainstay of treatment of large stones.) There is a significant chance of stone recurrence after open stone surgery (as for any other treatment modality) and the scar tissue that develops around the kidney will make subsequent open stone surgery technically more difficult. P.379
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Kidney stones: medical therapy (dissolution therapy) Uric acid and cystine stones are potentially suitable for dissolution therapy. Calcium within either stone type reduces the chances of successful dissolution. Uric acid stones Urine is frequently supersaturated with uric acid (derived from a purine-rich diet—i.e. animal protein). 50% of patients who form uric acid stones have gout. The other 50% do so because of a high protein and low fluid intake (‘Western’ lifestyle). In patients with gout, the risk of developing stones is ~1% per year after the first attack of gout. Uric acid stones form in concentrated, acid urine. Dissolution therapy is based on hydration, urine alkalinization, allopurinol, and dietary manipulation—the aim being to reduce urinary uric acid saturation. Maintain a high fluid intake (urine output 2–3L/day), ‘alkalinize’ the urine to pH 6.5–7 (sodium bicarbonate 650mg 3 or 4 times daily or potassium citrate 30–60mEq/day, equivalent to 15–30ml of a potassium citrate solution 3 or 4 times daily). In those with hyperuricaemia or urinary uric acid excretion >1200mg/day, add allopurinol 300–600mg/day (inhibits conversion of hypoxanthin and xanthine to uric acid). Dissolution of large stones (even staghorn calculi) is possible with this regimen. Cystine stones Cystinuria is an inherited kidney and intestinal transepithelial transport defect for the amino acids cystine, ornithine, arginine, and lysine (‘COAL’) leading to excessive urinary excretion of cystine. Autosomal recessive inheritance; prevalence of 1 in 700 are homozygous (i.e. both genes defective); occurs equally in both sexes. ~3% of adult stone formers are cystinuric and 6% of stone-forming children. Most cystinuric patients excrete about 1g of cystine per day, which is well above the solubility of cystine. Cystine solubility in acid solutions is low (300mg/l at pH 5, 400mg/l at pH 7). Patients with cystinuria present with renal calculi, often in their teens or twenties. Cystine stones are relatively radiodense because they contain sulphur atoms. The cyanide nitroprusside test will detect most homozygote stone formers and some heterozygotes (false +ves occur in the presence of ketones). Treatment of existing stones and prevention of further stones The aim is to:

  • Reduce cystine excretion (dietary restriction of the cystine precursor amino acid methionine and also of sodium intake to <100mg/day).
  • Increase solubility of cystine by alkalinization of the urine to >pH 7.5, maintenance of a high fluid intake, and use of drugs which convert cystine to more soluble compounds.

D-penicillamine, N-acetyl-D-penicillamine, and mercaptopropionylglycine bind to cystine—the compounds so formed are more soluble in urine than is cystine alone. D-penicillamine has potentially unpleasant and serious side-effects (allergic reactions, nephrotic syndrome, pancytopenia, P.381
proteinuria, epidermolysis, thrombocytosis, hypogeusia). Therefore reserved for cases where alkalinization therapy and high fluid intake fail to dissolve the stones. Treatment for failed dissolution therapy Cystine stones are very hard and are therefore relatively resistant to ESWL. Nonetheless, for small cystine stones, a substantial proportion will still respond to ESWL. Flexible ureteroscopy (for small) and PCNL (for larger) cystine stones are used where ESWL fragmentation has failed. P.382
Ureteric stones: presentation Ureteric stones usually present with sudden onset of severe flank pain which is colicky (waves of increasing severity are followed by a reduction in severity, but it seldom goes away completely). It may radiate to the groin as the stone passes into the lower ureter. ~50% of patients with classic symptoms for a ureteric stone do not have a stone confirmed on subsequent imaging studies, nor do they physically ever pass a stone. Examination Spend a few seconds looking at the patient. Ureteric stone pain is colicky—the patient moves around, trying to find a comfortable position. They may be doubled-up with pain. Patients with conditions causing peritonitis (e.g. appendicitis, a ruptured ectopic pregnancy) lie very still: movement and abdominal palpation are very painful. Pregnancy test Arrange a pregnancy test in pre-menopausal women (this is mandatory in any pre-menopausal woman who is going to undergo imaging using ionizing radiation). If +ve, refer to a gynaecologist; if negative, arrange imaging to determine whether they have a ureteric stone. Dipstick or microscopic haematuria Many patients with ureteric stones have dipstick or microscopic haematuria (and, more rarely, macroscopic haematuria), but 10–30% have no blood in their urine.18,19 The sensitivity of dipstick haematuria for detecting ureteric stones presenting acutely is ~95% on the first day of pain, 85% on the second day, and 65% on the third and fourth days.19 Therefore, patients with a ureteric stone whose pain started 3–4 days ago may not have blood detectable in their urine. Dipstick testing is slightly more sensitive than urine microscopy for detecting stones (80% versus 70%) because blood cells lyse, and therefore disappear, if the urine specimen is not examined under the microscope within a few hours. Both ways of detecting haematuria have roughly the same specificity for diagnosing ureteric stones (~60%). Remember, blood in the urine on dipstick testing or microscopy may be a coincidental finding because of non-stone urological disease (e.g. neoplasm, infection) or a false +ve test (no abnormality is found in ~70% of patients with microscopic haematuria, despite full urological investigation). P.383
Temperature The most important aspect of examination in a patient with a ureteric stone confirmed on imaging is to measure their temperature. If the patient has a stone and a fever, they may have infection proximal to the stone. A fever in the presence of an obstructing stone is an indication for urine and blood culture, intravenous fluids and antibiotics, and nephrostomy drainage if the fever does not resolve within a matter of hours. P.384
Ureteric stones: diagnostic radiological imaging The intravenous urogram (IVU), for many years the mainstay of imaging in patients with flank pain, has been replaced by CT urography (CTU) (Fig. 9.11). Compared with IVU, CTU:

  • Has greater specificity (95%) and sensitivity (97%) for diagnosing ureteric stones20—it can identify other, non-stone causes of flank pain (Fig. 9.12).
  • Requires no contrast administration so avoiding the chance of a contrast reaction (risk of fatal anaphylaxis following the administration of low-osmolality contrast media for IVU is in the order of 1 in 100,000).21
  • Is faster, taking just a few minutes to image the kidneys and ureters. An IVU, particularly where delayed films are required to identify a stone causing high-grade obstruction, may take hours to identify the precise location of the obstructing stone.
  • Is equivalent in cost to IVU, in hospitals where high volumes of CT scans are done.22

If you only have access to IVU, remember that it is contraindicated in patients with a history of previous contrast reactions and should be avoided in those with hay fever, a strong history of allergies, or asthma who have not been pre-treated with high-dose steroids 24h before the IVU. Patients taking metformin for diabetes should stop this for 48h prior to an IVU. Clearly, being able to perform an alternative test, such as CTU in such patients, is very useful. Where 24-h CTU access is not available, admit patients with suspected ureteric colic for pain relief and arrange a CTU the following morning. When CT urography is not immediately available (between the hours of midnight and 8 a.m.) we arrange urgent abdominal ultrasonography in all patients aged >50 years who present with flank pain suggestive of a possible stone, to exclude serious pathology such as a leaking abdominal aortic aneurysm and to demonstrate any other gross abnormalities due to non-stone associated flank pain. Plain abdominal X-ray and renal ultrasound are not sufficiently sensitive or specific for their routine use for diagnosing ureteric stones. MR urography This a very accurate way of determining whether a stone is present in the ureter or not.23 However, at the present time, cost and restricted availability limit its usefulness as a routine diagnostic method of imaging in cases of acute flank pain. This may change as MR scanners become more widely available.

Fig. 9.11 A CT urogram
Fig. 9.12 A leaking aortic aneurysm identified on a CTU in a patient with loin pain

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Ureteric stones: acute management While appropriate imaging studies are being organized, pain relief should be given.

  • A non-steroidal anti-inflammatory (e.g. diclofenac—Voltarol) by intramuscular or intravenous injection, by mouth or per rectum. Provides rapid and effective pain control. Analgesic effect—partly anti-inflammatory, partly by reducing ureteric peristalsis.
  • Where NSAIDS are inadequate, opiate analgesics such as pethidine or morphine are added
  • Calcium channel antagonists (e.g. nifedipine) may reduce the pain of ureteric colic by reducing the frequency of ureteric contractions.24,25

There is no need to encourage the patient to drink copious amounts of fluids nor to give them large volumes of fluids intravenously in the hope that this will ‘flush’ the stone out. Renal blood flow and urine output from the affected kidney falls during an episode of acute, partial obstruction due to a stone. Excess urine output will tend to cause a greater degree of hydronephrosis in the affected kidney which will make ureteric peristalsis* even less efficient than it already is. Watchful waiting In many instances, small ureteric stones will pass spontaneously within days or a few weeks, with analgesic supplements for exacerbations of pain. Chances of spontaneous stone passage depend principally on stone size. Between 90–98% of stones measuring <4mm will pass spontaneously.26,27 Average time for spontaneous stone passage for stones 4–6mm in diameter is 3 weeks. Stones that have not passed in 2 months are unlikely to do so. Therefore, accurate determination of stone size (on plain abdominal X-ray or by CTU) helps predict chances of spontaneous stone passage. Nifedipine24,25 and tamsulosin (an alpha adrenergic adrenoceptor blocking drug) may assist spontaneous stone passage and reduce frequency of ureteric colic.28 Glyceryl trinitrate patches do not aid stone passage or reduce frequency of pain episodes.29 P.387
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Ureteric stones: indications for intervention to relieve obstruction and/or remove the stone

  • Pain which fails to respond to analgesics or recurs and cannot be controlled with additional pain relief.
  • Fever. Have a low threshold for draining the kidney (usually done by percutaneous nephrostomy).
  • Impaired renal function (solitary kidney obstructed by a stone, bilateral ureteric stones, or pre-existing renal impairment which gets worse as a consequence of a ureteric stone). Threshold for intervention is lower.
  • Prolonged unrelieved obstruction. This can result in long-term loss of renal function30. How long it takes for this loss of renal function to occur is uncertain, but generally speaking the period of watchful waiting for spontaneous stone passage tends to be limited to 4–6 weeks.
  • Social reasons. Young, active patients may be very keen to opt for surgical treatment because they need to get back to work or their childcare duties, whereas some patients will be happy to sit things out. Airline pilots and some other professions are unable to work until they are stone free.

Emergency temporizing and definitive treatment of the stone Where the pain of a ureteric stone fails to respond to analgesics or where renal function is impaired because of the stone, then temporary relief of the obstruction can be obtained by insertion of a JJ stent or percutaneous nephrostomy tube. (Percutaneous nephrostomy tube can restore efficient peristalsis by restoring the ability of the ureteric wall to coapt.) JJ stent insertion or percutaneous nephrostomy tube can be done quickly, but the stone is still present (Fig. 9.13). It may pass down and out of the ureter with a stent or nephrostomy in situ, but in many instances it simply sits where it is and subsequent definitive treatment is still required. While JJ stents can relieve stone pain, they can cause bothersome irritative bladder symptoms (pain in the bladder, frequency, and urgency). JJ stents do make subsequent stone treatment in the form of ureteroscopy technically easier by causing passive dilatation of the ureter. The patient may elect to proceed to definitive stone treatment by immediate ureteroscopy (for stones at any location in the ureter) or ESWL (if the stone is in the upper and lower ureter—ESWL cannot be used for stones in the mid ureter because this region is surrounded by bone, which prevents penetration of the shock waves) (Fig. 9.14). Local facilities and expertise will determine whether definitive treatment can be offered immediately. Not all hospitals have access to ESWL or endoscopic surgeons 365 days a year.

Fig. 9.13 A JJ stent
Fig. 9.14 Ureteroscopic stone fragmentation for a lower ureteric stone

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Emergency treatment of an obstructed, infected kidney The rationale for performing percutaneous nephrostomy rather than JJ stent insertion for an infected, obstructed kidney is to reduce the likelihood of septicaemia occuring as a consequence of showering bacteria into the circulation. It is thought that this is more likely to occur with JJ stent insertion, than with percutaneous nephrostomy insertion. P.390
Ureteric stone treatment Many ureteric stones are 4mm in diameter or smaller and most such stones (90%+) will pass spontaneously, given a few weeks of ‘watchful waiting’, with analgesics for exacerbations of pain.31,32 Average time for spontaneous stone passage for stones 4–6mm in diameter is 3 weeks. Stones that have not passed in 2 months are much less likely to do so, though large stones do sometimes drop out of the ureter at the last moment. Indications for stone removal

  • Pain which fails to respond to analgesics or recurs and cannot be controlled with additional pain relief.
  • Impaired renal function (solitary kidney obstructed by a stone, bilateral ureteric stones, or pre-existing renal impairment which gets worse as a consequence of a ureteric stone).
  • Prolonged unrelieved obstruction (generally speaking ~4–6 weeks).
  • Social reasons. Young, active patients may be very keen to opt for surgical treatment because they need to get back to work or their childcare duties, whereas some patients will be happy to sit things out. Airline pilots and some other professions are unable to work until they are stone free.

These indications need to be related to the individual patient—their stone size, their renal function, presence of a normal contralateral kidney, their tolerance of exacerbations of pain, their job and social situation, and local facilities (the availability of surgeons with appropriate skill and equipment to perform endoscopic stone treatment). 20 years ago, when the only options were watchful waiting or open surgical removal of a stone (open ureterolithotomy), surgeons and patients were inclined to ‘sit it out’ for a considerable time in the hope that the stone would pass spontaneously. Nowadays, the advent of ESWL and of smaller ureteroscopes with efficient stone fragmentation devices (e.g. the holmium laser) has made stone treatment and removal a far less morbid procedure, with a far smoother and faster post-treatment recovery. It is easier for both the patient and the surgeon to opt for intervention, in the form of ESWL or surgery, as a quicker way of relieving them of their pain, and a way of avoiding unpredictable and unpleasant exacerbations of pain. It is clearly important for the surgeon to inform the patient of the outcomes and potential complications of intervention, particularly given the fact that many of stones would pass spontaneously if left a little longer. P.391
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Treatment options for ureteric stones

  • ESWL: in situ; after ‘push-back’ into the kidney (i.e. into the renal pelvis or calyces); or after JJ stent insertion
  • Ureteroscopy
  • PCNL
  • Open ureterolithotomy
  • Laparoscopic ureterolithotomy

Basketing of stones (blind or under radiographic ‘control’) are historical treatments (the potential for serious ureteric injury is significant). The ureter can be divided into two halves (proximal and distal to the iliac vessels) or in thirds (upper third from the PUJ to the upper edge of the sacrum; middle third from the upper to the lower edge of the sacrum; lower third from the lower edge of the sacrum to the VUJ). AUA guidelines panel recommendations33 These should be interpreted in the light of:

  • recent (within the last 5 years or so) improvements in ureteroscope design
  • local facilities and expertise

Smaller ureteroscopes with improved optics and larger instrument channels, and the advent of holmium laser lithotripsy have improved the efficacy of ureteroscopic stone fragmentation (to ~95% stone clearance) and reduced its morbidity. As a consequence, many surgeons and patients will opt for ureteroscopy, with its potential for a ‘one-off’ treatment, over ESWL where more than one treatment will be required and post-treatment imaging is required to confirm stone clearance (with ureteroscopy you can directly see that the stone has gone). Most urology departments do not have unlimited access to ESWL and patients may therefore opt for ureteroscopic stone extraction. The stone clearance rates for ESWL are stone-size dependent. ESWL is more efficient for stones <1cm in diameter compared with those >1cm in size. Conversely, the outcome of ureteroscopy is somewhat less dependent on stone size. Recommendations Proximal ureteric stones

  • <1cm diameter: ESWL (in situ, push-back)
  • >1cm diameter: ESWL, ureteroscopy, PCNL

JJ stent insertion does not increase stone free rates and is therefore not required in ‘routine’ cases. Indicated for pain relief, relief of obstruction, and in those with solitary kidneys. Distal ureteric stones

  • Both ESWL and ureteroscopy are acceptable options.
  • Stone free rate <1cm: 80–90% for both ESWL and ureteroscopy; >1cm: 75% for both ESWL and ureteroscopy.

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Failed initial ESWL is associated with a low success rate for subsequent ESWL. Therefore, if ESWL has no effect after 1 or 2 treatments, change tactics.34 Open ureterolithotomy and laparoscopic ureterolithotomy are used where ESWL or ureteroscopy have been tried and failed, or were not feasible. P.394
Prevention of calcium oxalate stone formation A series of landmark papers from Harvard Medical School35 and other groups allow us to give rational advice on reducing the risk of future stone formation in those who have formed one or more stones. The Harvard studies stratified risk of stone formation based on intake of calcium and other nutrients (Nurses Health Study, n = 81,000 women; equivalent male study, n = 45,000). Low fluid intake Low fluid intake may be the single most important risk factor for recurrent stone formation. High fluid intake is protective,35 by reducing urinary saturation of calcium, oxalate, and urate. Time to recurrent stone formation is prolonged from 2 to 3 years in previous stone formers randomized to high fluid vs. low fluid intake (averaging about 2.5 vs. 1L/day) and over 5 years, risk of recurrent stones was 27% in low-volume controls compared with 12% in high-volume patients.36 Dietary calcium Conventional teaching was that high calcium intake increases the risk of calcium oxalate stone disease. The Harvard Medical School studies have shown that low calcium intake is, paradoxically, associated with an increased risk of forming kidney stones, in both men and women (relative risk of stone formation for the highest quintile of dietary calcium intake vs. the lowest quintile = 0.65; 95% confidence intervals 0.5 to 0.83—i.e. high calcium intake was associated with a low risk of stone formation). Calcium supplements In the Harvard studies,37 the relative risk of stone formation in women on supplemental calcium compared with those not on calcium was 1.2 (95% confidence intervals 1.02–1.4). In 67% of women on supplements, the calcium was either not consumed with a meal or was consumed with a meal with a low oxalate content. It is possible that consuming calcium supplements with a meal or with oxalate-containing foods could reduce this small risk of inducing kidney stones. Other dietary risk factors related to stone formation Increased risk of stone formation (relative risk of stone formation shown in brackets for highest to lowest quintiles of intake of particular dietary factor):

  • Sucrose (1.5)
  • Sodium (1.3): high sodium intake (leading to natriuresis) causes hypercalciuria
  • Potassium (0.65)

Animal proteins High intake of animal proteins causes increased urinary excretion of calcium, reduced pH, high urinary uric acid, and reduced urinary citrate, all of which predispose to stone formation.38 P.395
Alcohol Curhan’s studies from Harvard39 suggest small quantities of wine decrease risk of stones. Vegetarian diet Vegetable proteins contain less of the amino acids phenylalanin, tyrosine, and tryptophan that increase the endogenous production of oxalate. A vegetarian diet may protect against the risk of stone formation.40,41 Dietary oxalate A small increase in urinary oxalate concentration increases calcium oxalate supersaturation much more than does an increase in urinary calcium concentration. Mild hyperoxaluria is one of the main factors leading to calcium stone formation.42 P.396
Bladder stones Composition Struvite (i.e. they are infection stones) or uric acid (in non-infected urine). Adults Bladder calculi are predominantly a disease of men aged >50 and with bladder outlet obstruction due to BPE. They also occur in the chronically catheterized patient (e.g. spinal cord injury patients), where the chance of developing a bladder stone is 25% over 5 years (similar risk whether urethral or suprapubic location of the stone).43 Children Bladder stones are still common in Thailand, Indonesia, North Africa, the Middle East, and Burma. In these endemic areas they are usually composed of a combination of ammonium urate and calcium oxalate. A low-phosphate diet in these areas (a diet of breast milk and polished rice or millet) results in high peaks of ammonia excretion in the urine. Symptoms May be symptomless (incidental finding on KUB X-ray or bladder ultrasound or on cystoscopy)—the common presentation in spinal patients who have limited or no bladder sensation). In the neurologically intact patient—suprapubic or perineal pain, haematuria, urgency and/or urge incontinence, recurrent UTI, LUTS (hesitancy, poor flow). Diagnosis If you suspect a bladder stone, they will be visible on KUB X-ray or renal ultrasound (Fig. 9.15). Treatment Most stones are small enough to be removed cystoscopically (endoscopic cystolitholapaxy), using stone-fragmenting forceps for stones that can be engaged by the jaws of the forceps and EHL or pneumatic lithotripsy for those that cannot. Large stones (see Fig. 9.15) can be removed by open surgery (open cystolitholapaxy).

Fig. 9.15 A bladder stone

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Management of ureteric stones in pregnancy While hypercalciuria and uric acid excretion increase in pregnancy (predisposing to stone formation), so too do urinary citrate and magnesium levels (protecting against stone formation). ‘Net’ effect—incidence of ureteric colic is the same as in non-pregnant women.44 Ureteric stones occur in 1 in 1500–2500 pregnancies, mostly during the 2nd and 3rd trimesters. They are associated with a significant risk of pre-term labour45 and the pain caused by ureteric stones can be difficult to distinguish from other causes. The hydronephrosis of pregnancy 90% of pregnant women have bilateral hydronephrosis from weeks 6–10 of gestation and up to 2 months after birth (smooth muscle relaxant effect of progesterone and mechanical obstruction of ureter from the enlarging fetus and uterus). Hydronephrosis is taken as surrogate evidence of ureteric obstruction in non-pregnant individuals, but because it is a normal finding in the majority of pregnancies, its presence cannot be taken as a sign of a possible ureteric stone. Ultrasound is unreliable for diagnosing the presence of stones in pregnant (and in non-pregnant) women (sensitivity 34%—i.e. it ‘misses’ 66% of stones; specificity 86%—i.e. false +ve rate of 14%).46 Differential diagnosis of flank pain in pregnancy Ureteric stone, placental abruption, appendicitis, pyelonephritis, and all the other (many) causes of flank pain in non-pregnant women. Diagnostic imaging studies in pregnancy Exposure of the fetus to ionizing radiation can cause fetal malformations, malignancies in later life (leukaemia), and mutagenic effects (damage to genes causing inherited disease in the offspring of the fetus). Fetal radiation doses during various procedures are shown in Table 9.3. While the recommended maximum radiation levels shown in Table 9.3 are well above those occuring during even CT scanning, and a dose of 50mGy or less is regarded as ‘safe’, every effort should be made to limit exposure of the fetus to radiation. Pregnant women may be reassured that the risk to the unborn child as a consequence of radiation exposure is likely to be minimal. Radiation doses of <100mGy are very unlikely to have an adverse effect on the fetus.47 In the United States, the National Council on Radiation Protection has stated that ‘Fetal risk is considered to be negligible at <50mGy when compared to the other risks of pregnancy, and the risk of malformations is significantly increased above control levels at doses >150mGy’.48 The American College of Obstetricians and Gynecologists has stated that ‘X-ray exposure to <50mGy has not been associated with an increase in fetal anomalies or pregnancy loss’.49

Table 9.3 Fetal radiation dose after various radiological investigations
Procedure Fetal dose (mGy) (mean) Risk of inducing cancer (up to age 15 years)
KUB X-ray 1.4 –
IVU 6 shot 1.7 1 in 10,000
IVU 3 shot – –
CT: abdominal 8 –
CT: pelvic 25 –
Fluoroscopy for JJ stent insertion 0.4 1 in 42,000

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Plain radiography and IVU Limited usefulness (fetal skeleton and the enlarged uterus obscure ureteric stones; delayed excretion of contrast limits opacification of ureter; theoretical risk of fetal toxicity from the contrast material). CTU Very accurate method for detecting ureteric stones, but most radiologists and urologists are unhappy to recommend this form of imaging in pregnant women. MRU The American College of Obstetricians and Gynecologists and the US National Council on Radiation Protection state that ‘although there is no evidence to suggest that the embryo is sensitive to magnetic and radiofrequency at the intensities encountered in MRI, it might be prudent to exclude pregnant women during the first trimester’.48,49 MRU can therefore potentially be used during the second and third trimesters, but not during the first trimester. Involves no ionizing radiation. Very accurate (100% sensitivity for detecting ureteric stones50), but expensive, and not readily available in most hospitals, particularly out of hours. Management Most (70–80%) will pass spontaneously.46 Pain relief: opiate-based analgesics; avoid non-steroidal anti-inflammatory drugs (NSAIDs) (can cause premature closure of the ductus arteriosus by blocking prostaglandin synthesis). Indications for intervention: the same as in non-pregnant patients (pain refractory to analgesics, suspected urinary sepsis (high fever, high white count), high-grade obstruction and obstruction in a solitary kidney). Options for intervention Depend on stage of pregnancy and on local facilities and expertise:

  • JJ stent urinary diversion47
  • Nephrostomy urinary diversion
  • Ureteroscopic stone removal

Aim to minimize radiation exposure to the fetus, and to minimize the risk of miscarriage and pre-term labour. General anaesthesia can precipitate pre-term labour and many urologists and obstetricians will err on the side of temporizing options such as nephrostomy tube drainage or JJ stent placement, rather than on operative treatment in the form of ureteroscopic stone removal. References 1 Curhan GC, Willett WC, Rimm EB, Stampfer MJ (1997). Family history and risk of kidney stones. J Am Soc Nephrol, 8:1568–73. 2 Borghi L, et al. (1996) Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol 155:839–43. 3 Curhan GC, et al. (1997) Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Int Med 126:497–504. 4 Borghi L, et al. (2002) Comparison of 2 diets for the prevention of recurrent stones in idiopathic hypercalciuria. NEJM 346:77–84. 5 Curhan GC, et al. (1993) A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. NEJM 328:833–38. 6 Ramakumar S, Patterson DE, LeRoy AJ, et al. (1999) Prediction of stone composition from plain radiographs: a prospective study. J Endo Urol 13:397–401. 7 Millman S, Strauss AL, Parks JH, Coe FL (1982) Pathogenesis and clinical course of mixed calcium oxalate and uric acid nephrolithiasis. Kidney Int 22:366–70. 8 Haddad MC, Sharif HS, Abomelha ME, et al. (1992) Management of renal colic: redefining the role of the urogram. Radiology 184:35–36. 9 Burgher A et al. (2004) J Endourol 18:534–39. 10 Blandy JP, Singh M (1976) The case for a more aggressive approach to staghorn stones. J Urol 115:505–6. 11 Rous & Turner (1977) Retrospective study of 95 patients with staghorn calculus disease. J Urol 118:902. 12 Teichmann J (1995) Long-term renal fate and prognosis after staghorn calculus management. J Urol 153:1403–7. 13 Chaussy CG, Brendel W, Schmidt E (1980) Extracorporeal induced destruction of kidney stones by shock waves. Lancet 2:1265–68. 14 Walsh PC, Retik AB, Vaughan D, et al. (2002) Campbell’s Urology, 8th Edition. W.B. Saunders/Elsevier, pp. 3395–97. 15 Kupeli B, Isen K, Biri H, et al. (1999) Extracorporeal shockwave lithotripsy in anomalous kidneys. J Endourol 13:39–52. 16 Dasgupta P, et al. (2004) Flexible ureterorenoscopy: prospective analysis of the Guy’s experience. Annals of the Royal College of Surgeons 86:367–70. 17 Segura JW, Preminger GM, Assimos DG, et al. (1994) Nephrolithiasis clinical guidelines panel summary report on the management of staghorn calculi. J Urol 151:1648–51. 18 Luchs JS, Katz DS, Lane DS, et al. (2002) Utility of hematuria testing in patients with suspected renal colic: correlation with unenhanced helical CT results. Urology 59:839. 19 Kobayashi T, Nishizawa K, Mitsumori K, Ogura K (2003) Impact of date of onset on the absence of hematuria in patients with acute renal colic. J Urol 1770:1093–96. 20 Smith RC, Verga M, McCarthy S, Rosenfield AT (1996) Diagnosis of acute flank pain: value of unenhanced helical CT. Am J Roentgen 166:97–101. 21 Caro JJ, Trindale E, McGregor M (1991) The risks of death and severe non-fatal reactions with high vs low osmolality contrast media. Am J Roentgen 156:825–32. 22 Thomson JM, Glocer J, Abbott C, et al. (2001) Computed tomography versus intravenous urography in diagnosis of acute flank pain from urolithiasis: a randomized study comparing imaging costs and radiation dose. Australas Radiol 45:291–97. 23 Louca G, Liberopoulos K, Fidas A, et al. (1999) MR urography in the diagnosis of urinary tract obstruction. Eur Urol 35:102–8. 24 B Borghi L et al. (1994) Nifedipine and methylprednisolone in facilitating ureteral stone passage: a randomised, double-blind, placebo controlled study. J Urol 152:1095–98. 25 Porpiglia F et al. (2000) Effectiveness of nifedipine and deflazacort in the management of distal ureteric stones. Urology 56:579–82. 26 Segura JW et al. (1997) Ureteral stones guidelines panel summary report on the management of ureteral calculi. J Urol 158:1915–21. 27 Miller OF et al. (1999) Time to stone passage for observed ureteral calculi. J Urol 162:688–91. 28 Dellabella M et al. (2003) Efficacy of tamsulosin in the medical management of juxtavesical ureteral stones. J Urol 170:2202–5. 29 Hussain Z et al. (2001) Use of glyceryl trinitrate patches in patients with ureteral stones: a randomized, double-blind, placebo-controlled study. Urology 58:521–25. 30 Holm-Nielsen A, Jorgensen T, Mogensen P, Fogh J (1981) The prognostic value of probe renography in ureteric stone obstruction. Br J Urol 53:504–7. 31 Segura JW et al. (1997) Ureteral stones guidelines panel summary report on the management of ureteral calculi. J Urol 158:1915–21. 32 Miller OF et al. (1999) Time to stone passage for observed ureteral calculi. J Urol 162:688–91. 33 Segura JW, Preminger GM, Assimos DG, et al. (1997) Ureteral stones clinical guidelines panel summary report on the management of ureteral calculi. J Urol 158:1915–21. 34 Pace KT et al. (2000) Low success rate of repeat shock wave lithotripsy for uretal stones after failed initial treatment. J Urol 164:1905–7. 35 Curhan GC, et al. (1993) A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. NEJM 328:833–38. 36 Borghi L, et al. (1996) Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: A 5-year randomized prospective study. J Urol 155:839–43. 37 Curhan G, et al. (1997) Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Int Med 126:497–504. 38 Kok DJ (1990) The effects of dietary excesses in animal protein and in sodium on the composition and crystallization kinetics of calcium oxalate monohydrate in urines of healthy men. J Clin Endocrinol Metab 71:861–67. 39 Curhan G, et al. (1998) Beverage use and risk for kidney stones in women. Ann Intern Med 128:534–40. 40 Robertson WG, et al. (1982) Prevalence of urinary stone disease in vegetarians. Eur Urol 8:334–39. 41 Borghi, L (2002) Comparison of two diets for prevention of recurrent stones in idiopathic hypercalciuria. NEJM 346:77–84. 42 Robertson WG, Peacock M, Ouimet D, et al. (1981) The main risk for calcium oxalate stone disease in man: hypercalciuria or mild hyperoxaluria? In: Smith LH, Robertson WG, Finlayson B (eds.) Urolithiasis: Clinical and Basic Research. New York: Plenum Press, pp. 3–12. 43 Ord J (2003) Bladder management and risk of bladder stone formation in spinal cord injured patients. J Urol. 170:1734–37. 44 Coe FL, Parks JH, Lindhermer MD (1978) Nephrolithiasis during pregnancy. N Engl J Med 298:324–26. 45 Hendricks SK (1991) An algorithm for diagnosis and therapy of urolithiasis during pregnancy Surg Gyne Obst 172:49–54. 46 Stothers L, Lee LM (1992) Renal colic in pregnancy. J Urol 148:1383–87. 47 Hellawell GO, Cowan NC, Holt SJ, Mutch SJ (2002) A radiation perspective for treating loin pain in pregnancy by double-pigtail stents. Br J Urol Int 90:801–8. 48 National Council on Radiation Protection and Measurement (1997) Medical radiation exposure of pregnant and potentially pregnant women. NCRP Report no. 54. Bethesda, MD: NCRPM. 49 American College of Obstetricians and Gynecologists Committee on Obstetric Practice (1995) Guidelines for Diagnostic Imaging During Pregnancy. ACOG Committee Opinion no. 158. Washington DC: ACOG. 50 Roy C (1996) Assessment of painful ureterohydronephrosis during pregnancy by MR urography. Eur Radiol 6:334–38.

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