urinary stone

Urinary Stones

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 contributes 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.
Genetic. ~25% of patients with kidney stones report a family history of stone disease.
Extrinsic (environmental) factors
Geographical location, climate, and season.
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.
Diet. High animal protein intake increases risk of stone disease (high urinary oxalate, low pH, low urinary citrate). High salt intake causes hypercalciuria. Contrary to conventional teaching, low calcium diets predispose to calcium stone disease, and high calcium intake is protective.
Occupation. Sedentary occupations predispose to stones compared with manual workers.
Kidney stones: types and predisposing factors
Stone composition% of all renal calculiCalcium oxalate85%Uric acid5-10%Calcium phosphate + calcium oxalate 10%Struvite (infection stones)2-20%Cystine1%Stones may be classified according to composition, X-ray appearance, or size and shape.

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
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 radiodense
Cystine stones are relatively radiodense because they contain sulphur. 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 centimeters. 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. 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.

Kidney stones: mechanisms of formation

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.
Factors predisposing to specific stone types
Calcium oxalate (~85% of stones)
Hypercalciuria
Hypercalcaemia: Almost all patients with hypercalcaemia who form stones have primary hyperparathyroidism.
Hyperoxaluria
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

Uric acid (~5-10% of stones)

Gout: 50% of patients with uric acid stones have gout.
Myeloproliferative disorders. Particularly following treatment with cytotoxic drugs.
Idiopathic uric acid stones (no associated condition).
Calcium phosphate (calcium phosphate + calcium oxalate = 10% of stones)
Occur in patients with distal renal tubular acidosis (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. 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 
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. Stone type is analyzed 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.

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.
Previous bowel resection or inflammatory bowel disease. Causes intestinal hyperoxaluria.
Urine pH
Urine pH in normal individuals shows variation, from pH 5-7. After a meal, pH is initially acid. 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).
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 radiodense 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 , and the diagnosis may be confirmed by ultrasound, or CTU.
Renal ultrasound: its sensitivity for detecting renal calculi is ~95%. A combination of plain abdominal radiography and renal ultrasonography is a useful screening 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.
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.
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. 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.
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).
Stone fragmentation: extracorporeal shock wave 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. ESWL revolutionized kidney and ureteric stone treatment. X-ray, ultrasound, or a combination of both are used to locate the stone on which the shock waves are focused. 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).
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, 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).

Intracorporeal techniques of stone fragmentation (fragmentation within the body)
Electrohydraulic lithotripsy (EHL)
Pneumatic (ballistic) lithotripsy
Ultrasonic lithotripsy
Laser lithotripsy: The holmium: YAG laser.


Kidney stone treatment: flexible ureteroscopy and laser treatment
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
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.
Musculoskeletal deformities such that stone access by PCNL or ESWL is difficult or impossible (e.g. kyphoscoliosis).
Stone in a calyceal diverticulum.
Bleeding diathesis where reversal of this diathesis is potentially dangerous or difficult.
Patient preference.
Kidney stone treatment: percutaneous nephrolithotomy (PCNL)
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. 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, 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.

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
Anatomic abnormality that precludes endoscopic surgery (e.g. retrorenal colon)
Body habitus that precludes endoscopic surgery (e.g. gross obesity, kyphoscoliosis)
Patient request for a single procedure where multiple PCNLs might be required for stone clearance
Non-functioning kidney
Non-functioning kidney
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)
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.

Kidney stones: medical therapy (dissolution therapy)

Uric acid and cystine stones are suitable for dissolution therapy. Calcium within either stone type reduces the chances of successful dissolution.
Uric acid stones
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. In those with hyperuricaemia, add allopurinol 300mg/day. Dissolution of large stones (even staghorn calculi) is possible with this regimen.
Cystine stones
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.
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. Examination
Spend a few seconds looking at the patient. Ureteric stone pain is colicky the patient moves around, trying to find a comfortable position. Patients with conditions causing peritonitis (e.g. appendicitis, a ruptured ectopic pregnancy) lie very still: movement and abdominal palpation are very painful. Many patients with ureteric stones have dipstick or microscopic haematuria (and, more rarely, macroscopic haematuria. 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.

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). Compared with IVU, CTU:
Has greater specificity (95%) and sensitivity (97%) for diagnosing ureteric stones: it can identify other, non-stone causes of flank pain .
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).
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.
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.
Plain abdominal X-ray and renal ultrasound are not sufficiently sensitive or specific for their routine use for diagnosing ureteric stones.


Ureteric stones: acute management
While appropriate imaging studies are being organized, pain relief should be given.
A non-steroidal anti-inflammatory (e.g. diclofenac) 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
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 .
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. 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.

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 function. 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. Stone 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).

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. 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.
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
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
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.
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.
Open ureterolithotomy and laparoscopic ureterolithotomy are used where ESWL or ureteroscopy have been tried and failed, or were not feasible.


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 BPH. They also occur in the chronically catheterized patient (e.g. spinal cord injury patients).
Children
Bladder stones are still common in Thailand, Indonesia, North Africa, and the Middle East. 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. 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 .
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 can be removed by open surgery (open cystolithotomy).

Prevention of calcium oxalate stone formation

Low fluid intake
Low fluid intake may be the single most important risk factor for recurrent stone formation. High fluid intake is protective, 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.

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


Calcium supplements
It is possible that consuming calcium supplements with a meal or with oxalate-containing foods could reduce this small risk of inducing kidney stones.
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.
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.
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.

This Lecture Collected By Omer Ahmed Al-Samrrai, 5th Grade of T.U.C.O.M









Tikrit Medical College, Urology, Fifth year, 2009

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Dr.MMA