Urolithiasis lecture DR TARIK ELDARAT

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  • 1. UROLITHIASIS Dr: Wael El Orfi. Urologist Hawari Hospital
  • 2. factors intrinsic to the individual and by extrinsic (environmental) factors.  Intrinsic factors  Age. the ages of 20-50 years.  Sex. Males are affected 3 times as frequently as females. Testosterone ( oxalate in the liver) / higher urinary citrate  ~25% of patients with kidney stones report a family history of stone disease  Extrinsic (environmental) factors  more common in hot climates  Ureteric stones become more prevalent during the summer. Concentrated urine / Exposure to sunlight )  Water intake.  Diet. High animal protein intake (high urinary oxalate, low pH, low urinary citrate).  High salt intake causes hypercalciuria.  Occupation. Sedentary occupations predispose to stones compared with manual workers.
  • 3. Kidney stones: types and predisposing factors Stones may be classified according to composition, X- ray appearance, or size and shape.
  • 4. Radiodensity on X-ray  Radio-opaque 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. 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.
  • 5. Factors predisposing to specific stone types  Calcium oxalate (~85% of stones)  Hypercalciuria/3 types: 1. Absorptive: increased intestinal absorption of calcium 2. Renal: renal leak of calcium 3. Resorptive:increased demineralization of bone (due to hyperparathyroidism)  Hypercalcaemia (primary hyperparathyroidism).  Hyperoxaluria Due to: 1. Increased oxalate absorption in short bowel syndrome or malabsorption (enteric hyperoxaluria) .  Hypocitraturia  Hyperuricosuria (on the surface of which calcium oxalate crystals form).
  • 6. Uric acid :10% of stones.  uric acid is essentially insoluble in acid urine and soluble in alkaline urine.  Human urine is acidic and this combined with supersaturation of urine with uric acid, predisposes to uric acid stone formation.  %20 of patients with gout have uric acid stones.  Myeloproliferative disorders. Particularly following treatment with cytotoxic drugs  Idiopathic uric acid stone .
  • 7. Calcium phosphate (calcium phosphate + calcium oxalate = 10% of stones(  renal tubular acidosis (RTA)  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.
  • 8. Struvite and cystine stones  Struvite (infection or triple phosphate stones) (2-20% of stones) 1. magnesium, ammonium, and phosphate. 2. urease-producing bacteria which produce ammonia from breakdown of urea (urease hydrolyses urea to carbon dioxide and ammonium) 3. alkalinize urine .  Cystine (1% of all stones). 1. only in 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. 2. Cystine is very insoluble, so reduced absorption of cystine from the proximal tubule results in supersaturation with cystine and cystine crystal formation.
  • 9. Evaluation of the stone former  stone type and a metabolic evaluation .  Stone type is analysed by polarizing microscopy, X-ray diffraction, and infrared spectroscopy, rather than by chemical analysis. radiological appearance (e.g. a completely radiolucent stone is likely to be composed of uric acid) or from more detailed metabolic evaluation.
  • 10. Risk factors for stone disease  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.
  • 11. Risk factors for stone disease  Systemic disease. Gout, primary hyperparathyroidism, sarcoidosis.  Family history. Cystinuria, RTA.  Renal anatomy. PUJO, horseshoe kidney, medullary sponge kidney .  Previous bowel resection or inflammatory bowel disease. Causes intestinal hyperoxaluria.
  • 12. Metabolic evaluation of the stone former  High risk: previous history of a stone, family history of stones, GI disease, gout, chronic UTI, nephrocalcinosis.  Urea and electrolytes.  FBC (to detect undiagnosed haematological malignancy).  serum calcium (corrected for serum albumin).  Serum uric acid.  urine culture, urine dipstick for pH .  High-risk patient evaluation:  As for low-risk patients plus 24-h urine for calcium, oxalate, uric acid, cystine; evaluation for RTA.
  • 13. Kidney stones: presentation and diagnosis  with symptoms or incidentally  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).
  • 14. Diagnostic tests  Plain abdominal radiography:  Radiodensity of in decreasing order: calcium phosphate > calcium oxalate > struvite >> cystine.  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 by ultrasound, CTU, or MRU.  Renal ultrasound: its sensitivity is ~95%.  A combination of plain abdominal radiography and renal ultrasonography is a useful screeing test for renal calculi.  IVU: increasingly being replaced by CTU.  CTU: a very accurate method of diagnosing all but indinavir stones.  MRU: cannot visualize stones, but is able to demonstrate the presence of hydronephrosis.
  • 15. Kidney stone treatment options  indications for intervention are pain, infection, and obstruction.  Options for stone treatment are:  Watchful waiting.  ESWL.  Flexible ureteroscopy.  PCNL.  Open surgery.  Medical (dissolution) therapy.
  • 16. When to watch and wait and when not to?  the younger the patient, the larger the stone, and the more symptoms it is causing, the more inclined are we to recommend treatment.  the patient's job. Airline pilots are not allowed to fly if they have kidney stones.  Watchful waiting is NOT recommended for staghorn calculi unless patient comorbidity is such that surgery would be a higher risk than watchful waiting.
  • 17. Stone fragmentation techniques: extracorporeal lithotripsy (ESWL(  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.  electrohydraulic, electromagnetic, and piezoelectric.  X-ray, ultrasound, or a combination of both .  oral or parenteral analgesia.  Efficacy of ESWL:  depends on stone size and location, anatomy of renal collecting system, degree of obesity, and stone composition.  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).
  • 18. Side-effects of ESWL  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).  ESWL may increase the likelihood of development of hypertension.  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).
  • 19. potential complications after ESWL  Common:  Bleeding on passing urine for short period after procedure  Pain in the kidney as small fragments of stone pass .  UTI from bacteria released from the stone.  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.  Stone fragments occasionally get stuck in the tube between the kidney and the bladder (steine strasse)  Severe infection requiring intravenous antibiotics and sometimes drainage of the kidney by a small drain placed through the back into the kidney.
  • 20. Intracorporeal techniques of stone fragmentation (fragmentation within the body(  Electrohydraulic lithotripsy (EHL).  Pneumatic (ballistic) lithotripsy.  Ultrasonic lithotripsy.  Laser lithotripsy (The holmium: YAG laser).  Used with ureteroscopy ,cystoscopy and nephroscopy (PCNL)
  • 21. Kidney stone treatment: ureteroscopy (intracorporeal, endoscopic treatment of kidney stones(.  small-calibre ureteroscopes .  laser technology  stone baskets and graspers .  requires a general anaesthetic .
  • 22. 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.  percutaneous puncture of a renal calyx with a nephrostomy needle  An access sheath is passed down the track and into the calyx, and through this a nephroscope can be advanced into the kidney (  An ultrasonic lithotripsy probe is used to fragment the stone and remove the debris.  Indications for PCNL  stones >3cm in diameter.  failed ESWL and/or flexible ureteroscopy.  It is the first-line option for staghorn calculi with ESWL .
  • 23. Kidney stones: open stone surgery  Indications  Complex stone burden (projection of stone into multiple calyces)  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(open stone surgery can be difficult)  Patient request for a single procedure where multiple PCNLs might be required for stone clearance  Non-functioning kidney  In case of Non-functioning kidney  the stone may be left in situ if it is not causing symptoms .  If the kidney is non-functioning, the simplest way of removing the stone is to remove the kidney.
  • 24. Functioning kidneys (options for stone removal(  Pyelolithotomy  Radial nephrolithotomy  Staghorn calculi  Anatrophic (avascular) nephrolithotomy  Excision of the kidney (bench) surgery to remove the stones, and autotransplantation  Specific complications of open stone surgery  Wound infection  flank hernia  wound pain.  With PCNL these problems do not occur  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.
  • 25. Kidney stones: medical therapy (dissolution therapy): Uric acid and cystine stones are potentially suitable for dissolution therapy.  Uric acid stones:  Dissolution therapy is based on hydration, urine alkalinization, allopurinol, and dietary manipulation  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.  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 is possible with this regimen.
  • 26. 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.  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 has potentially unpleasant and serious side- effects (allergic reactions, nephrotic syndrome, pancytopenia, proteinuria, epidermolysis, thrombocytosis, hypogeusia).
  • 27. Ureteric stones:  presentation  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. 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.  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.
  • 28. 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)  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).21  Is faster, taking just a few minutes to image the kidneys and ureters.  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.
  • 29.  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.
  • 30. 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.  Where NSAIDS are inadequate, opiate analgesics such as pethidine or morphine are added  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. measuring <4mm will pass  tamsulosin (an alpha adrenergic adrenoceptor blocking drug) may assist spontaneous stone passage and reduce frequency of ureteric colic.
  • 31. 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.
  • 32. Emergency temporizing and definitive treatment of the stone  temporary relief of the obstruction can be obtained by insertion of a JJ stent or percutaneous nephrostomy tube.  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)
  • 33. Emergency treatment of an obstructed, infected kidney  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.
  • 34.  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.
  • 35. Treatment options for ureteric stones  ESWL.  Ureteroscopy  PCNL  Open ureterolithotomy  Laparoscopic ureterolithotomy
  • 36. Bladder stones  Composition  Struvite (i.e. they are infection stones) or uric acid (in non- infected urine).  Adults  a disease of men aged >50  bladder outlet obstruction due to BPE.  in the chronically catheterized patient (e.g. spinal cord injury patients).  Children  common in Thailand, Indonesia, North Africa, the Middle East, and Burma.  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.
  • 37.  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 (  Treatment  endoscopic cystolitholapaxy) using stone-fragmenting forceps for stones that can be engaged by the jaws of the forceps )  Large stones- can be removed by open surgery (open cystolitholapaxy .
  • 38. Management of ureteric stones in pregnancy  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 labour and the pain caused by ureteric stones can be difficult to distinguish from other causes.  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).
  • 39. 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).  every effort should be made to limit exposure of the fetus to radiation.
  • 40. Diagnostic imaging studies in pregnancy:  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  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.
  • 41. Management  Most (70-80%) will pass spontaneously.  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).
  • 42. Options for intervention  Depend on stage of pregnancy and on local facilities and expertise:  JJ stent urinary diversion.  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.
  • 43. PATHOPHYSIOLOGY  two basic phenomena: supersaturation of the urine by stone-forming constituents( calcium, oxalate, and uric acid(. Crystals can act as nidi.  Calcium phosphate precipitates in the basement membrane of the thin loops of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal papilla(Randall plaques).  eventually erode through the papillary urothelium.
  • 44. Frequency  approximately 10%.  rare in Greenland and the coastal areas of Japan.  In developing countries, bladder calculi are more common than upper urinary tract calculi.  diet-related.
  • 45. Mortality/Morbidity  obstruction with its associated pain.  obstructing calculi may be asymptomatic.  Stone-induced hematuria .  The most morbid and potentially dangerous aspect is the combination of urinary tract obstruction and upper urinary tract infection. Pyelonephritis, pyonephrosis, and urosepsis can ensue.
  • 46. Renal stone : sex and age  In general, more common in males (male-to-female ratio of 3:1.  cystinuria, hyperparathyroidism and stone disease in children are equally prevalent between the sexes.  Stones due to infection (struvite calculi) are more common in women than in men.  Most urinary calculi develop in persons aged 20-49 years.  An initial stone attack after age 50 years is relatively uncommon.
  • 47. CLINICAL: 1. History  pain, infection, or hematuria.  Small nonobstructing stones only occasionally cause symptoms.  The passage of stones into the ureter is associated with classic renal colic.  severe pain ( nausea and vomiting).  the pain moves from the flank to the lower abdomen, down to the groin, scrotal or labial areas.  Associated irritative bladder symptoms ( intramural ureter).  NO peritonitis .  staghorn calculi are often relatively asymptomatic.  Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure.
  • 48. Important historical features are as follows:  Duration, characteristics, and location of pain  History of urinary calculi  Prior complications related to stone manipulation  Urinary tract infections  Loss of renal function  Family history of calculi  Solitary or transplanted kidney  Chemical composition of previously passed stones
  • 49. CLINICAL: Physical  costovertebral angle tenderness is common.  Peritoneal signs are usually .  urinary extravasation, abscess formation.  the specific location of tenderness does not always correlate with the exact location of the stone.
  • 50. Causes  Hypercalciuria:  Absorptive.  Resorptive.
  • 51. Causes  Most research ( role of elevated urinary levels of calcium, oxalate, and uric acid in stone formation, as well as reduced urinary citrate levels).  Hypercalciuria is the most common metabolic abnormality.  increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive calcium absorption mechanisms).  excess resorption of calcium from bone (ie, hyperparathyroidism).  inability of the renal tubules to properly reclaim calcium in the glomerular filtrate (renal-leak hypercalciuria).  Magnesium and citrate are important inhibitors of stone formation in the urinary tract.  A low fluid intake ( the most important).  24-hour urine studies include hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume.  high urinary sodium and low urinary magnesium concentrations.
  • 52. Differential Diagnoses: Appendicitis Pancreatitis, Acute Biliary Colic Cholecystitis Diverticulitis Duodenal Ulcers Gastritis, Acute Urinary Tract Infection, Inflammatory Bowel Disease Liver Abscess Lumbar Disc Disease
  • 53. Workup: Laboratory Studies Evaluate the urine for evidence of hematuria and infection. Complete blood cell count :elevated white blood cell count suggests renal or systemic infection. Serum electrolytes, creatinine, calcium, uric acid, parathyroid hormone (PTH), and phosphorus studies A high serum uric acid level may indicate gouty diathesis or hyperuricosuria, while hypercalcemia suggests either renal- leak hypercalciuria (with secondary hyperparathyroidism) or primary hyperparathyroidism. If the serum calcium level is elevated, serum PTH levels should be obtained.
  • 54. Imaging Studies  Plain abdominal radiography [KUB] radiography: 1. total stone burden, size, shape, and location of urinary calculi 2. the progress of the stone . 3. Calcium-containing stones (85% of all upper urinary tract calculi) are radiopaque, but pure uric acid, indinavir-induced, and cystine calculi are relatively radiolucent on plain radiography.  Renal ultrasonography 1. adequate (in pregnancy ) 2. not visible on the plain radiograph may be a uric acid or cystine stone. 3. in the distal ureter, and smaller than 5 mm are not easily observed with ultrasonography.
  • 55.  Intravenous urography (IVU) also known as an intravenous pyelography (IVP).  has been the standard for determining the size and location of urinary calculi up until recently.  IVU provides both anatomical and functional information.  Up to 6 hours may be required to complete the study in the presence of severe obstruction.  For optimal results, IVU requires a bowel preparation.  It involves intravenous injection of potentially allergic and mildly nephrotoxic contrast material.
  • 56.  Helical CT scanning without contrast material  imaging of the entire abdomen in a single breath hold.  the most sensitive clinical imaging modality for calcifications. Even for radiolucent on a plain radiograph (except for indinavir-induced stones) are clear and distinct on a CT scan.  Contrast is not used in the initial screening study because (masking the stones).  CT scanning has replaced IVU for the assessment of urinary tract stone disease, especially for acute renal colic.  A lucent stone that is not visible on the KUB radiograph that is clearly visible on the CT scan may indicate a uric acid calculus.
  • 57. Advantages of a CT scanning include the following:  It can reveal other pathology (eg, abdominal aneurysms, appendicitis, cholecystis.  It can be performed quickly.  It avoids the use of intravenous contrast materials. Disadvantages of CT scanning include the following:  It cannot be used to assess individual renal function.  It can fail to reveal some unusual radiolucent stones, such as those caused by indinavir.  It is relatively expensive.  It exposes the patient to a relatively high radiation dose.  It is not suitable for tracking the progress of the stone over time, supporting the recommendation for KUB radiography along with the CT scan.
  • 58. Treatment Medical Care  Emergency management of renal (ureteral) colic.  Medical therapy for stone disease.  both short- and long-term forms (the former to dissolve the stone [possible only with noncalcium stones] and the latter to prevent further stone formation).  stone formation before age 30 years.  family history of stones.  multiple stones at presentation.  renal failure.  residual stones after surgical treatment.
  • 59. General guidelines for emergency management  Obstruction ( managed with analgesics).  Infection ( managed with antimicrobial therapy(.  If neither obstruction nor infection is present( the stone will likely pass from the upper urinary tract if its diameter is smaller than 5-6 mm (.  If both obstruction and infection are present, emergent decompression of the upper urinary collecting system is required  Hydration.  Analgesia with parenteral narcotics or nonsteroidal anti-inflammatory drugs (NSAID).  the alpha-1 selective blockers, such as tamsulosin, also relax musculature of the ureter and lower urinary tract, markedly facilitating passage of ureteral stones.
  • 60. Long-term medical treatment of calcium-containing urinary calculi  calcium-containing urinary calculi cannot be dissolved with current medical therapy but long-term chemoprophylaxis of further calculus growth or formation.  avoid excessive salt and protein intake and to increase fluid intake.  Uric acid and cystine calculi can be dissolved with medical therapy. with alkalization of the urine.  Sodium bicarbonate , but potassium citrate is usually preferred because of the availability of slow-release tablets and the avoidance of a high sodium load.  The dosage adjusted to maintain the urinary pH between 6.5 and 7.0.  Roughly 1 cm per month dissolution can be achieved.  If hyperuricosuria or hyperuricemia :allopurinol (300 mg qd) .  D-penicillamine help reduce stone formation in cystinuria.
  • 61. Surgical Care  The primary indications : pain, infection, and obstruction. (occupational reasons. (  General contraindications :  Active, untreated urinary tract infection  Uncorrected bleeding diathesis  Pregnancy (a relative, but not absolute, contraindication).  Specific contraindications : do not perform ESWL if a ureteral obstruction is distal to the calculus or in pregnancy.  For an obstructed and infected collecting system secondary to stone disease: either by ureteral stent DJ (Duoble J) placement or by percutaneous nephrostomy.  Infection combined with urinary tract obstruction is an extremely dangerous situation, with significant risk of urosepsis and death, and must be treated emergently in virtually all cases.
  • 62.  majority are now treated with noninvasive or minimally invasive techniques.  stones that are 4 mm in diameter or smaller will probably pass spontaneously, and stones that are larger than 8 mm are unlikely to pass without surgical intervention.  Extracorporeal shockwave lithotripsy  Most urinary tract calculi that require treatment are currently managed with this ESWL.  The shock head delivers shockwaves developed from an electrohydraulic, electromagnetic, or piezoelectric source.  focused on the calculus, produces fragmentation. The resulting small fragments pass in the urine.  A stone larger than 1.5 cm in diameter or one located in the lower section of the kidney is treated less successfully.
  • 63. Ureteroscopy  A small endoscope, which may be rigid, semirigid, or flexible, is passed into the bladder and up the ureter to directly visualize the stone.  directly extracted using a basket or grasper or broken into small pieces using various lithotrites (eg, laser, ultrasonic, electrohydraulic, ballistic).
  • 64. Percutaneous nephrostolithotomy  allows fragmentation and removal of large calculi from the kidney and ureter and is often used for the many ESWL failures.  A needle, and then a wire, over which is passed a hollow sheath, are inserted directly in the kidney through the skin of the flank.  Because of their increased morbidity compared with ESWL and ureteroscopy, percutaneous procedures are generally reserved for large and/or complex renal stones and failures from the other two modalities.  In some cases, a combination of ESWL and a percutaneous technique is necessary to completely remove all stone material from a kidney. This technique, called sandwich therapy, is reserved for staghorn or other complicated stone cases.
  • 65. Diet  increase in fluid intake and, therefore, an increase in urine output is recommended. This is likely the single most important aspect of stone prophylaxis.  to avoid excessive salt and protein intake.  Dietary calcium should not be restricted beyond normal unless specifically indicated based on 24-hour urinalysis findings.  more oxalate is absorbed from the GIT in the absence of sufficient intestinal calcium to bind with it. This results in a net increase in oxalate absorption and hyperoxaluria, which tends to increase new kidney stone formation in patients with calcium oxalate calculi.  adversely affect bone mineralization and may have osteoporosis implications, especially in women.
  • 66. Follow-up: Postsurgical issues