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Urinary Calculi and

Endourology
EPIDEMIOLOGY OF STONES
 Sex: men are affected thrice as
commonly as women.
 Age : Peak incidence is between 3rd to
5th decade.
 Race ; Whites are affected 4 to 5
times in comparison to places.
 Urolithiasis is a life long disease with
an average of 9 year intervening
between episodes.
ETIOLOGY AND PATHOGENESIS
 Development of stones in urinary tract is a complex, poorly
understood multifactorial process.
 Supersaturation
 Ovur abundance of solute in solution.
 This occurs fairly well for uric acid, cysteine and xanthine
calculi.
 Inhibitiory substances in urine that black crystallization eg :
Pyrophosphates, citrate, zinc, magnesium; lack of sufficient
urinary inhibition may cause precipitation of stones.
 Matrix : Non crystalline mucoprotein often associated with
urinary calculi. Pure matrix calculi may be seen in association
with proteus infection.
 Exogenous substances like indinavir and Triamterene may lead
to formation of stones.
STONES OF THE UPPER URINARY
TRACT
Clinical presentation :
 Usually silent.
 When stone moves within urinary tract it produces either
haematuria, or some degree of urinary obstruction which
may be accompanied by pain, urinary infection,
generalized sepsis, nausea or vomiting.
 Sudden onset, severe colicky in flanks or abdominal pain
which may radiate to groin, testis , or tip of penis
depending on the location of obstruction.
 Gross or microscopic haematuria.
STONES OF THE UPPER URINARY
TRACT
Diagnosis :
 Initial evaluation includes urinalysis, urine culture
and plain x-ray of KUB.
 Renal ultrasonogram demonstrates the presence of
stone along with any evidence of hydronephrosis if
present.
 Axial spinal CT confirmes the presence of calculus,
and demonstrates the degree of obstruction.
 Spiral CT is rapid, does not require bowel
preparation and avoids use of IV & it has gradually
replaced IVU as primary imaging modality for acute
renal colic.
URINARY CALCULI AND COMPOSITION,
FREQUENCY AND ETIOLOGIC FACTORS
S.No. Type of Stone Frequency Effect of pH Etiologic Factors
1. Calcium stones 80% Solubility Supersaturation of urine with
a. Oxalate 35% Little effect calcium due to
b. Phosphate 10% Increased at pH <5.5 2.Renal leak
c. Oxalate and Phosphate 35% Variable 3.Intestinal absorption.
2. Oxalate and Phosphate 10% Increaed at pH <5% 4.Bone resorption.
3. Struvite 8% Increased at pH >6.8 Alkaline urine due to urea
4. Uric acid 1% Increased at pH >7.5 splitting organisms.
5. Cysteine 1% Hyperuricosuria
Other Cystinuria
Matrix Alkaline urine due to urea
Xanthime splitting organisms
Triamtene
STONES OF THE UPPER URINARY
TRACT
Treatment :
 Depends on size, location, degree of obstruction and patients clinical
status :
 Common sites of stone impaction are :
 Ureteropelvic junction .
 Pelvic brim where ureter crosses pelvic vessels.
 Ureterovesical junction.
 Patients with infection in high grade obstruction require prompt
intervention in the form of retrograde ureteral catheter or
percutaneous nephrostomy drainage.
 About 90% of ureteral calculi measuring less than 4 mm pass
spontaneously whereas only 20% of calculi measuring more than 6 mm
pass.
 Expectant treatment in indicated in asymptomatic, non obstructed, non
infective with stone size less than 4 mm diameter in the lower third of
ureter.
STONES OF THE UPPER URINARY
TRACT
Treatment :
 Patient is asked to drink copious amount of water, four to six weeks
duration is allowed for passage of stone.
 Stone extraction is indicated for ureteral stones that do not pass
spontaneously.
 Small stones may be grasped directly or engaged in stone basket and
extracted. Longer stones may be fragmented using ultrasound,
electrohydraulic, pneumatic or laser lithotripsy.
 Shock wave lithotripsy is advantageous for urethral stones less than 8
mm diameter. It may be performed with or without a stent or long as
stone can be adequately visualized.
 Patients are often placed in prone position for distal ureteral stones.
 Ureterolithotomy is rarely needed given the high success rate of non-
operative and minimally invasive technique like SWL, ureteroscopy and
laparoscopy.
BLADDER STONES
Clinical presentation
 Pain felt in hypogastrium or referred to penis.
 Intermittent stream.
 Dysuria.
 Haematuria.
 Recurrent urinary tract infections.

 Commonly found in male patients of western


world and increase the risk of sqaumous
metaplasia or carcinoma in long standing case.
BLADDER STONES
Diagnosis :
 Plain x-ray of KUB
 Bladder ultrasonography
 Cystoscopy

Treatment :
 Lithotrites : Mechanical devices that
permit crushing of large, hard,
bladder stones, under direct vision. It
BLADDER STONES
Treatment :
 Lithotrites : Mechanical devices that permit crushing of large,
hard, bladder stones, under direct vision. It should be done
only with bladder partially filled to prevent bladder wall injury.
Fragments are then worked out through a resectoscope sheath.
 Electrohydraulic Lithotripsy : Hydraulic shock wave is produced
near stone that usually produces fragmentation after delivery
of several shocks.
 Ultrasound Lithotripsy is based on ultrasound energy delivered
through a rigid probe passed through an endoscope causing
fragmentation of stone which is removed by continous suction.
 Cystolithotomy : It is performed through a small suprapubic
incision. It has advantage of removing the entire store rather
than leaving the fragments inside the bladder.
RECURRENT STONE DISEASE
Diagnosis :
 Predisposing factors can be found in 80% of
recurrent stone formation. Passage of single
stone is an indication of screening study
including determination of serum calcium,
phosphorus, uric acid and 24 hourly urinary
creatinine, calculi phosphorus, uric acid and
oxalate levels.
 Patients found to have any abnormality should
have an extensive evaluation.
RECURRENT STONE DISEASE
METABOLIC EVALUATION :
 Baseline studies already mentioned are performed & along
with recording of urinary patient.
 Dietary restriction of calcium to 400 mg and 100 mEq of
sodium for 1 week is done, followed by urine and serum
studies as previously described.
CALCIUM LOADING :
 After on overnight fast during which only distilled water is
permitted patient reports at the clinic at 7 am.
 First urine sample is discarded, a 2 hour pooled specimen is
collected from 7 to 9 am.
 Patient receives 1 gm of calcium gluconate orally at 9 am
and collected of the urine specimen from 9 am to 1 pm in
done.
HYPERCALCIURIA
 Resorptive hypercalciuria : Constant hypercalcuria
regardless of dietary restriction. Hyperparathyroidism is
a common cause and causes calcium urolithiasis. Other
causes include neoplasm metastatic to bone, multiple
myeloma, immobilization, Cushing’s disease etc.
Treatment is by correction of the underlying disorder.
 Absorptive Hypercalciuria : It is the most common cause
and is responsible for formation of stones in more than
50% of patients.
 These patients have an exaggerated intestinal
response to vitamin D leading to hyperabsorption of
ingested calcium. Urinary calcium normalizes on
restriction of oral calcium and increases to abnormal
range under calcium loading.
HYPERCALCIURIA
Treatment :
 Diet and hydration.
 Patients should be placed on a diet restricted to 400 mg of calcium
per day & 100 meq of sodium per day.
 Addition of bran in useful as it binds calcium in the gastro intestinal
tract.
 Drinking of 3 to 4 litres of water daily to reduce urinary concentration
of calcium.
 Cellulose phosphate : It is a calcium binding resin that exchanges
sodium for calcium in the gastrointestinal tract. It must be used in
conjunction with calcium restricted diet.
 Orthophosphates : They act by decreasing urinary excretion of calcium
and increasing excretion of citrate and pyrophosphate both of which act
to inhibit calcium stone formation.
 Renal Hypercalciuria : This disorder is caused by inability of kidney to
absorb calcium from tubular fluid. Thus, placing the patient on calcium
restricted diet will not reduce loss of calcium in the urine. Calcium
loading may increase urinary calcium even further.
HYPERURICOSURIA
Pure uric acid stones account for approximately 10% of calculi. Uric acid
becomes insoluble in urine at pH less than 5.8.
ETIOLOGY :
 Approximately 25% of patients with uric acid calculi are found to have
gout.
 However most of them neither have hyperuricemia or hyperuricosuria.
 Calculi are probably caused by constantly acidic urine, dehydration or
both.
Treatment :
 Hydration : Oral intake of atleast 3 litres water daily.
 Alkalinization of urine is usually achieved by oral or I.V. sodium
bicarbonate.
 Reduction of uric acid load may be achieved by dietary restriction and
use of allopininol. It is indicated in patients urine passive to hydration
and alkalination of urine, who have meloproliferative disorders, those
receiving chemotherapy.
HYPEROXALURIA
Oxalic acid is an extremely insoluble end product of metabolism.
 Primary hyperoxaluria : Autosomal recessive disorder
characterized by early onset of nephrocalcinasis due to enzymatic
defect. Widespread deposition of oxalate in the kidneys and other
soft tissue eventually occurs. Pyridoxine daily has reported
reduction in oxalate excretion in some patients.
 Enteric Hyperoxaluria : May occur in patients with malabsorption
from any cause like inflammatory bowel disease, small bowel
bypass surgery. Increased amount of fatty acids in bowel binds
calcium leaving increased oxalate for absorption. Treatment
includes low oxalate, low fat diet with oral fluid hydration and
calcium supplementation. Cholestyramine binds oxalate and has
good results in patients with malabsorption.
 Exogenous hyperoxaluria : When substances metabolized to
oxalate are ingested in large quantities such as ethylene glycol, as
carbolic acid etc.
STRUVITE STONES
 Composed of magnesium ammonium phosphate and
carbonate.
 They may grow to fill the entire renal pelvis and collecting
system.
 They form when urinary pH is markedly elevated and increased
concentration of ammonia, carbonate & bicarbonate are
present in the urine. Such conditions are caused by urea
splitting organisms producing urease enzyme. Proteis species
are most common with others like Klebsiella, pseudomonas
etc.
 Female are affected more in ratio of 2:1 as compared to males
 Other at risk group are spinal cord injury patients, patients
having indwelling catheter for many year, patients with ileal
conduit and other supravesical diversions
STRUVITE STONES
Diagnosis :
 Struvite stones should be suspected in
any patient with high urinary pH caused
by infection.
 Plain X-ray of KUB will usually
demonstrate the calculi.
 IVU should be performed to determine
whether obstruction is present and
causing persistence of infection.
STRUVITE STONES
Treatment :
 Aim of treatment is to achieve complete elimination of stones,
correction of any obstruction and eradication of infection.
 Surgical Modalities :
 Nephrolithotomy.
 Nephrectomy in case of little or no renal function.
 Partial staghorn causing renal parenchymal damage requires
partial nephrectomy.
 Percutaneous lithotripsy : Recently it has replaced open surgery in
many patients and approximately 85% of patients can be rendered
stone free at 3 months.
 ESWL : ESWL alone produces stone free rates in range of 40 to
60% and multiple treatments are usually required. Sandwich
technique used effectively involves percutaneous lithotripsy,
followed by ESWL followed by secondary percutaneous lithotripsy,
extraction on chemolysis.
STRUVITE STONES
CHEMOLYSIS :
 Generally ineffective in calcium stones but can be used very effectively
to dissolve uric acid, cysteine, struvite and carbonate stones.
 Uric acid and cysteine stones : They are readily soluble in alkaline
solution by local irrigation through urethral or ureteral cather /
Nephrostomy. Uric acid stones can be treated with solution of sodium
bicarbonate in normal saline. Oral alkalinizing agent such as potassium
citrate are better tolerated for long term maintenance of an alkaline
pH. Cysteine stones may be treated with solution containing
acetylcysteine, sodium bicarbonate and normal Saline.
 Struvite and carbonate apatite calculi. They are amenable to dissolution
by acidic solution having pH of less than 5.5. The most widely used
solution is 10% hemiacridin delivered to store via nephrostomy tube or
ureteral catheter. Normal saline infusion should be done priorly to
determine response of collecting system.
STRUVITE STONES
Important precautions while doing chemolysis :
 Intrapelvic pressure must be below 30 cm water, monitored
through a manometer. Treatment should be discontinued if
patient complaints flank pain.
 Infusate must have adequate egress which may be a problem
in infusion through a single ureteral catheter.
 Chemolysis is contraindicated in presence of urinary tract
infection .
 Hemocridin contains magnesium that can be absorbed to cause
hypermagnesemia.
 Prevention : Prevention of struvite calculi depends an
elimination of infection with urea splitting organisms. Urease
inhibitor such as acetohydroxamic acid may be used to
decrease urinary pH and ammonia levels.
RENAL TUBULAR ACIDOSIS
 Urolithiasis occurs only in type I, a
disorder in which distal tubule is
unable to maintain adequate
hydrogen ion gradients. It accounts
for approximately 1% of calcium
stone forming patients.
ENDOUROLOGIC TECHNIQUES
 Percutaneous access to the upper
urinary tract is the cornerstone of
endourologic technique.
 The combination of rigid and flexible
endoscopes with ultrasound or
electrohydraulic lithotripsy allows
virtually all stones to be treated by
percutaneous means. It offers lower cost
discomfort and reduced recovery time in
comparison with open surgery.
ENDOUROLOGIC TECHNIQUES
 Percutaneous puncture techniques
 patient is placed on fluroscopy table in prone
position and imaging of kidney is carried out
by fluoroscopy on ultrasonography.
 Puncture site is most commonly on posterior
axillary line midway between 12th rib and
iliac crest.
 Nephrostomy tube is placed through a renal
pyramid into a posterior calyx
ENDOUROLOGIC TECHNIQUES
 Ultrasound Lithotripsy :
 High frequency sound waves cause
fragmentation after delivery through a
rigid probe passed through nephroscope.
 Small fragments are removed by
continuous suction.
 Larger fragments are extracted with
grasping forceps or stone baskets under
direct vision.
ENDOUROLOGIC TECHNIQUES
 Electrohydraulic lithotripsy –
 Useful in stones resistant to US lithotripsy.
 Hydraulic shock wave is produced near stone
producing fragmentation.
 Its probe is flexible and can be passed through both
rigid and fibreoptic endoscopes.
 Fragments produced tend to scatter widely and
retrieval is not as easy as with US lithotripsy.
 Pneumatic Lithotripsy – Delivery of jack hammer effect
with compressed in causing stone fragmentation.
 Laser Lithotripsy – Holmium laser in used which is an
effective incisor of tissue and additionally may be used
for cutting scars and uretheral strictures.
EXTRACORPOREAL SHOCK
WAVE LITHOTRIPSY
 It was developed in Germany in the early 1980s.
 Propogation of focussed shock wave through the body, which
fragment the stones.
 Shock is produced by either discharging a high voltage or
deforming a piezocrystal or moving a membrane by
electromagnetic energy.
 Average patient requires 1000 to 4000 shocks to fragment
stones completely.
 In some cases fragments may cause obstruction of the ureter.
 Combination of percutaneous techniques may be required to
reduce large staghorn calculi to smaller fragments before ESWL
is performed.
 Third generation machines are characterized by more compact
designs, lower pressure and narrower focussing allowing
anaesthesia free lithotripsy.
CONTRAINDICATIONS OF ESWL
 Infundibular obstruction.
 Obstruction of ureter
 Active urinary tract infection.

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