Urinary Stone Disease

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Stone Disease
• Incidence
• ▪ Prevalence of 2-3%
• ▪ Male: female = 3:1, peak incidence 30-50 years of age
• ▪ Recurrence rate: 10% at one year, 50% at 5 years, 60-80% life time

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Stone Pathogenesis
• Mechanism of formation: Unknown but theories:
• 1) Saturation of urine by salts:
• • It depends on:
• 1. type of solute (concentration).
• 2. PH of urine.
• 3. Temperature.

• • It's important to decrease recurrence of stone by control of PH and

solute.
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• 2) Super-saturation:
• • Above saturation level.
• • due to absence of:
• a) Inhibitors → inhibit stone formation (organic nephrocalcin,
inorganic → Mg citrate)
• b) Complexing agents e.g. ca citrate
• c) Without nucleus formation.

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• 3) Nucleation: e.g. epithelial cells, urinary crystals, RBCs, WBCs, ....
• 4) Crystal formation:
• 5) Crystal aggregation.
• 6) Crystal retention: factor that increase retention.
• a) Pelvic-ureteric junction obstruction (PUJO)
• b) Medullary sponge kidney
• c) UT obstruction.
• d) Crystals & epithelial adhesion.

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Etiology: (Predisposing factors)
• (I) Pre-renal Causes:
• 1) Hypercalcemia due to:
• A. Idiopathic hypercalciuria (60%):
• 1. Excess absorption of Ca from GIT (commonest)
• 2. Excess excretion of Ca in urine
• B. Hypercalciuric state (40%) e.g.
• 1. Hyper-parathyroidism
• 2. Hyperthyroidism (↑ bone catabolism)
• 3. Cushing syndrome
• 4. Paraneoplastic syndrome (Bronchogenic carcinoma, Renal cell carcinoma)
• 5. Multiple Myeloma → ↑Adrenalin (pheochromocytoma)
• 6. Vit. D toxicity.
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• 2) Hyper-oxaluria: due to:
• a) hyper-oxaluria (oxalosis): due to enzyme deficiency in liver → ↑ oxalate formation.
• b) hyper-oxaluria (dietary): - ↑ intake ↑ absorption (in short bowel syndrome)
• 3) Hyperphosphaturia: - ↑ intake of proteins.
• 4) Hyper-uricosuria: in
• a) Gout
• b) ↑ purine intake → Red meat liver
• c) lead to uric acid nucleus upon which oxalate will ppt.
• 5) Cystinuria: due to ↑ absorption.
• 6) Low citrate level: acidosis → ↓ serum citrate → hypocitraturia as citrate →
precipitation of calcium as ca oxalate.
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• (II) Renal Causes:
• due to renal tubular necrosis → kidney fails to excrete H+ ions →
alkalosis of urine (ppt of Ca phosphate) & acidosis of blood.

• (III) Post-renal Causes:

• a) Infection.
• b) Stasis of urine.

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Classifications of urinary stones
• according to:
• 1. Stone size
• 2. Stone location:
• Stones can be classified according to anatomical position: upper,
middle or lower calyx; renal pelvis; upper, middle or distal ureter; and
urinary bladder.
• 3. X-ray characteristics

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Types of Stones
• (1) Ca Oxalate stone (60 %):
• • Commonest type
• • Oxalate stone is hereditary.

• (2) Ca Phosphate stone (10%):

• • Usually in association with Ca oxalate. (10%)
• • Pure phosphate stone are rare (5%)→ due to renal tubular acidosis.

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• (3) Struvite stone (5-10%)
• • Triple phosphate stone = Ammonium, Mg, Phosphate, Carbonate
"CO3"
• • Infection stone (Mg, PO4, NH4 + CO3)
• • Formed by urea splitting organism: Proteus Mirabilis, Pseudomonas,
Klebsiella.
• • Mechanism: Urea → organism by urease enzyme in bacteria →
ammonium (NH4) + H2O →alkaline urine → ppt of Mg, NH4 & PO4.

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• (4) Uric acid stone. (5-10%) Metabolic stone

• (5) Cystine stone. (1%) Metabolic stone

• (6) Xanthine stone → Radiolucent

• (7) Matrix stone → soft gelatinous material in urine

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• Character of stone in hyper-parathyroidism:
• 1-Radio-opaque. 2-Multiple. 3-Bilateral.

• • Most common stone is Ca oxalate.

• • Most opaque stone is Ca phosphate (as composition of bone)

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Clinical Features
• 1. Urinary obstruction ± upstream distention ± pain
• ▪ Flank pain from renal capsular distention (non-colicky).
• ▪ Severe waxing and waning pain radiating from flank to groin, testis, or tip
of penis due to stretching of collecting system or ureter (ureteral colic)
• 2. Writhing, never comfortable, nausea, vomiting, hematuria (90%
microscopic), diaphoresis, tachycardia, tachypnea
• 3. Occasionally symptoms of trigonal irritation (frequency, urgency).
• 4. Bladder stones result in: storage and voiding, terminal hematuria,
suprapubic pain.
• 5. If fever, rule out concurrent pyelonephritis or obstruction.
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Differential Diagnosis of Renal Colic
• 1. Acute ureteral obstruction (other causes):
• a) UPJ obstruction
• b) sloughed papillae
• c) clot colic from gross hematuria

• 2. acute abdominal crisis: biliary, bowel, pancreas, abdominal aortic aneurysm.

• 3. Gynecological: ectopic pregnancy, torsion/rupture of ovarian cyst, pelvic
inflammatory disease (PID)
• 4. pyelonephritis (fever, chills, pyuria)
• 5. radiculitis: herpes zoster, nerve root compression

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Location of Stones
• A. Kidney
• ▪ Calyx
• - May cause flank discomfort, recurrent infection or persistent hematuria
• - May remain asymptomatic for years and not require treatment
• ▪ Pelvis
• - Tend to cause obstruction at ureteropelvic junction (upj)
• - Staghorn calculi (renal pelvis and one or more calyces)
• - Often associated with infection that will not resolve until stone is cleared
• ▪ Ureter: <5 mm diameter will pass spontaneously in 75% of patients
• C. Bladder
• D. Urethra
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Complications:
• 1- Haematuria: due to injury to mucosa.
• 2- Infection: pyonephrosis, pyelonephritis, pyelitis, cystitis.
• 3- Migration, repeated attack of colic.
• 4- Obstruction: hydronephrosis, retention or anuria.
• 5- Malignancy: due to chronic irritation.
• 6- Renal Failure.

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Investigations

• screening labs
CBC elevated WBC in presence of fever suggests infection
Electrolytes, Cr, BUN ± to assess renal function
Urinalysis: R&M (WBCs, RBCs, crystals), C&S

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• 2. imaging
• (KUB) kidneys, ureters, bladders x-ray
• • to differentiate opaque from non-opaque stones (e.g. uric acid)
• 90% of stones are radiopaque.

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• CT scan: accurate method of diagnosing renal and ureteric stones
(except) indinavir stones. Allows accurate determination of stone size
and location and good definition of pelvicalyceal anatomy
• Abdominal ultrasound
• • May demonstrate stone (difficult in ureter)
• • May demonstrate hydronephrosis
• IVP:
• • Anatomy of urine collecting system, degree of obstruction,
extravasation

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• 3. cystoscopy for suspected bladder stone
• 4. stone analysis
• 5. metabolic studies: if recurrent stone formers:
• ✓ serum electrolytes, Ca, PO4, uric acid, creatinine and urea
• ✓ PTH if hypercalcemic
• ✓ 24 hour urine: for creatinine, Ca, PO4 , uric acid, Mg, oxalate,
citrate

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Management of urolithiasis:
• Acute
• 1. medical
• ▪ analgesic (NSAID and morphine) ± antiemetic
• ▪ alpha-blockers: increase rate of spontaneous passage in distal
ureteral stones
• ▪ antibiotics for UTI
• ▪ IV fluids if vomiting (note: IV fluids do NOT promote stone passage)

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Management of urolithiasis:
• 2. interventional: if obstruction endangers patient (i.e. sepsis, renal
failure)
• ▪ ureteric stent (via cystoscopy)
• ▪ percutaneous nephrostomy (image-guided or US guided)

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• Elective managment
• ▪ Medical (conservative)
• ▪ ESWL. (Extracorporeal shock wave lithotripsy)
• ▪ Endoscopy.
• ▪ Open Surgery.

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indication hospitalization:
• 1. intractable pain
• 2. intractable vomiting
• 3. Fever ( infection)
• 4. Compromised renal function
• 5. Single kidney with ureteral obstruction
• 6. bilateral obstructing stones

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Management of Renal stones
• 1) Medical.
• 2) Extra-corporeal Shock Wave Lithotripsy (ESWL)
• 3) Percutaneous nephrolithotomy (PCNL)
• 4) Combined PCNL and ESWL
• 5) Open renal stone surgery
• a) Pyelolithotomy.
• b) Extended pyelolithotomy
• c) Nephrolithotomy.
• d) Pyelonephrolithotomy
• e) Partial nephrectomy.
• f) Simple nephrectomy.
• 6) Laparoscopic stone extraction.

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Medical (conservative):
• Aim:
• • Spontaneous passage.
• • ↓ metabolic activity →↓stone recurrence.
• Indications:
• • Small stone < 5 mm
• • No infection
• • No distal obstruction

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• Include:
• 1) Antispasmodic: e.g. buscopan.
• 2) Analgesic: up to morphia.
• 3) Antiseptic: to guard against infection.
• 4) ↑fluid intake: esp. water (3-4 litre / day)

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• 5) Diet:
• • Ca containing stone → ↓use of milk & milk products.
• • Oxalate stone → ↓ Tomato, Mango, Strawberry, Coffee
• • Uric acid →↓ Red meat, Liver, Coffee, Tea, Soup.

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• 6) Drugs:
• • Ca oxalate stone → Vit. B6 (pyridoxine)
• • Phosphate stone → Aceto hydroxamic acid (urease inhibitor)
• • Uric acid stone → Xanthine oxidase inhibitors (Allopurinol)
• • Cystine stone → D-penicillamine, Mercapto-propionyl glycine (Best),
Acetyl cystein.

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• 7) PH of urine:
• • Dilution of urine: slight alkalinization of urine.
• • Alkalinization of urine: in uric acid & cystein stone by potassium
citrate
• • Acidification of urine: in Ca & PO4 stone by vit.C.

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Extra-corporeal Shock Wave Lithotripsy (ESWL)
• Objective
• • To treat renal calculi, proximal calculi, and mid ureteral calculi which cannot pass through the urinary
tract naturally
• • Shockwaves are generated and focused onto stone fragmentation, allowing stone fragments to pass
spontaneously and less painfully
• Methods:
• A. Ultrasonic lithotripsy:
• ▪ Explosion of the stone using ultrasonic waves.
• ▪ The micro-fragments will pass spontaneously in the urine.
• B. Electro-hydraulic lithotripsy:
• ▪ Explosion of the stone by shock waves, directly at the calculus.
• ▪ Micro-fragments will pass spontaneously in the urine.

• Indication: potential first-line therapy for renal and ureteral calculi less than 2 cm in size
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Extra-corporeal Shock Wave Lithotripsy (ESWL)
• Contraindication:
• 1) Acute urinary tract infection or urosepsis
• 2) Bleeding disorder or coagulopathy
• 3) Pregnancy
• 4) Obstruction distal to stone
• 5) Impaired renal function.

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Extra-corporeal Shock Wave Lithotripsy (ESWL)
• Complications
• 1) bacteriuria and bacteremia
• 2) post-procedure hematuria
• 3) ureteric obstruction (by stone fragments)
• 4) peri-nephric hematoma

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PCNL - Percutaneous nephrolithotomy
• Indications:
• 1. Stone > 2 cm (especially hard)
• 2. Urinary obstruction.
• 3. Cystine stones
• 4. ESWL failure.

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PCNL Method
• 1. Establish a track for percutaneous endoscopy,
• 2. A nephroscope is introduced at the location of the stone.
• 3. Small stone extracted with forceps.
• 4. Large stone fragmented by lithotripsy (either laser ultrasonic or
pneumatic)
• 5. lnsertion of a nephrostomy tube for 48 hours for drainage.

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PCNL
• Advantages:
• 1. small incision
• 2. Short hospital stay.
• 3. minimal operative and postoperative complications.
• Complications
• 1. Hemorrhage.
• 2. Extravasations of irrigation used fluid.
• 3. Residual stones.
• 4. injury of Renal or other organs injury e.g. colon, pleura.
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Open renal stone surgery
• It becomes 3rd choice method for renal stone management.
• Indications:
• ▪ Failure of previous lines of treatment.
• ▪ Complex renal stones
• ▪ Presence of congenital anomalies as horse shoe kidney
• Incision: flank incision (mainly)
• Technique:
• Pyelolithotomy.
• ▪ Always tried first especially with extra-renal pelvis.
• ▪ lt can to be done in intra-renal pelvis using Gil Vernet retractor.
• ▪ incision in the posterior aspect of the renal pelvis then the stone is removed.

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• Advantages:
• a) Minimal bleeding.
• b) No damage for renal parenchyma.
• c) Rapid healing

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• Nephrolithotomy.
• Indicated when pyelolithotomy cannot be done:
• ▪ Stone in a calyx with narrow neck.
• ▪ lntra-renal pelvis.
• ▪ Dense adhesions around the pelvis.

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• Disadvantages: The reverse of advantages of pyelolithotomy.
• ▪ The incision is in the substance of the kidney may be through
• ln Brodel's line (in the posterior aspect of the kidney between lateral
1/3 and medial 2/3).
• ▪ Radial incision directly on the stone.

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• Partial nephrectomy. if multiple stones impacted in nonfunction part
of the kidney.

• Simple nephrectomy. lf the kidney is non-functioning provided that

the other kidney is normal.

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Management of ureteric stones

• Conservative management
• Active management:
• Indications:
• 1. Stone large than 5mm
• 2. Distal obstruction
• 3. Persistent pain
• 4. Failure of medical treatment
• 5. Evidence of infection

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• Type of management: depend on site size and effect of the stone
• 1. ESWL
• 2. Push bang technique: pushed to kidney then PCNL
• 3. Ureteroscopy (URS):
• Aim: Stone extraction or fragmentation.
• Technique;
• ▪ Cystoscope and insertion of guide wire to ureteric orifice
• ▪ dilatation of distal ureter and introduction of URS
• ▪ visualization of stone then extraction by forceps or Dormia basket.
• ▪ Fragmentation may be needed
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• Types of lithotripsy
• c. U/S waves.
• d. Electro-hydrolytic.
• a. Laser.
• b. Pneumatic (lithoclast)

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• Complications
• ▪ Infection
• ▪ Perforation
• ▪ Avulsion
• ▪ Stricture ureter
• ▪ Migration of stone
• ▪ Difficulty to introduce guide wire

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• 1. Open ureterolithotomy
• Incision :
• ▪ Stone upper 1/3 → flank incision (stone is best extracted by
pyelolithotomy)
• ▪ Stone middle 1/3 → abernathy incision 2 inches above the asis and
passes downwards and medially to mid-inguinal point (muscle
cutting).
• ▪ Stone lower 1/3 → midline supra-pubic incision.
• 2. Laparoscopic ureterolithotomy

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Management of bladder stones
• Instrumental: lf < 2 cm
• ▪ Cystolitholapaxy (Trans-urethral): mechanical compression of the
stone using lithotrate then removal of the fragments by Ellik's
evacuator.
• ▪ Cystolithotripsy: fragmentation by lithotripsy U/S waves, Electro-
hydrolytic, Laser or Pneumatic (lithoclast)
• Surgical: suprapubic cystotolithotomy

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• Indications
• a. Larger and harder stones
• b. Cases where open prostatectomy or bladder diverticulectomy is
indicated.
• c. Failure of stone fragmentation
• d. In children

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Management of urethral stones:
• ▪ Posterior urethra: Supra-pubic cystolithotomy for stone firmly
impacted supported by urethral dilator & removed trans-vesical.
• ▪ Penile urethra: trial of removal by forceps if failed, External
urethrotomy will be done
• ▪ Glandular urethra: External meatotomy.

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Prevention of stone formation
• 1. dietary modification:
• ▪ Increase fluid (>2 L/day), potassium intake
• ▪ Reduce animal protein, oxalate, sodium, sucrose, and fructose intake
• ▪ Avoid high-dose vitamin C supplements
• 2. The stone should be chemically analyzed.
• 3. Treating infection and other causes of stone formation.
• 4. Follow up of stone formers to detect early recurrence.

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• 5. Metabolic work-up to know etiology of the stone.
• ▪ Serum Ca and phosphorus to exclude hyperparathyroidism.
• ▪ 24-hour urine collection for the following whose normal values are:
• a. Ca <300 mg.
• b. Uric acid <800 mg.
• c. Oxalates <40 mg.
• d. Citrates 300-900 mg.

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• 6. medications:
• Thiazide diuretics for hypercalciuria
• Allopurinol for hyperuricosuria
• Potassium citrate for hypocitraturia

• Although hypercalciuria is a risk factor for stone formation. decreasing

dietary calcium is NOT recommended to prevent stone formation.
Low dietary calcium lead to increased oxalate absorption and higher
urinary levels of calcium oxalate.

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• - Ca oxalate stone is ppt in neutral PH.
• - Ca phosphate & Struvite stones are ppt in alkaline PH.
• - Cystine & Uric acid stones are ppt in acidic PH.
• - Citrate inhibit ppt of Ca.
• - Mg inhibit ppt of oxalate.
• - Pyrophosphate inhibit ppt of phosphate.
• - Hyper-oxaluria is an inborn error of metabolism of glycine.

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• Calcium oxalate stones:
• 1. Avoid diet rich in oxalates.
• 2. Hydrochlorothiazide 50 mg/d aids in the dissolution of Ca oxalate
stones.
• 3. Citrates 5 mg bid inhibits crystallization of oxalates.

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• ✓ Uric acid stones
• 1. Avoid diet rich in purines.
• 2. Rule out myeloproliferative or neoplastic diseases.
• 3. Urine should be kept alkaline, e.g. by NaHCO3 1 gm tds.
• 4. Allopurinol 30 mg/day is indicated in patients with hyperuricemia.

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• ✓ Struvite stones
• 1. Aluminum hydroxide orally restricts phosphate absorption.
• 2. Long term antibiotics to eradicate UTl.
• 3. Avoid indwelling catheters.
• 4. Increase urine acidity by vitamin c

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