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