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UROLITHIASIS

Describes the stone in renal pathway

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BHAJAN MOLLIK
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0% found this document useful (0 votes)
31 views32 pages

UROLITHIASIS

Describes the stone in renal pathway

Uploaded by

BHAJAN MOLLIK
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

UROLITHIASIS

1st documented cystolithotomy – SUSHRUTA, 600 BC

Lifetime prevalence 1-20%, recurrence high 10% within 10 years

Risk factors: Age (40-60), Sex (M), Race ( Whites), Family history (
2.5 times more), environmental ( hot and dry regions), drugs (
steroids, cytotoxic drugs etc)
Pathogenesis : concentration of culprit salts ( Calcium & oxalate)
overcome inhibitory factors ( citrate, K, Mg, Tamm Horsfall
mucoproteins, ph changes) -> precipitates into crystals ->may be
washed off with flow of urine or anchor onto sites like renal papillae
to form Randall’s plaques -> variations in ph may facilitate or
inhibit stone growth ( acidic ph precipitates uric acid stones &
alkaline ph precipitates Calcium phosphate stones)

Stasis of urine -> promotes stone formation-> multiple, round,


smooth ( milk of calcium stones)
TYPES OF STONES
Calcium oxalate
Most common, 60-85%
Hypercalciurea, hypercalcaemia, hyperoxaluria, hyperuricosuria,
hypocitratouria
Hypercalciura – most common-> dysregulation of transport at
various sites like intestine, bone, kidney
Primary hyperparathyroidism-> hypercalcaemia, >PTH causes
increased bone resorption & increased synthesis of 1,25
dihydroxyvitamin D3 -> causes increased intestinal absorption of
calcium-> hypercalcaemia & hypercalciurea
Calcium phosphate
Rare, forms- apatite & brushite stones (calcium phosphate)

Uric acid stones


Hyperuricosurea-> calcium oxalate & uric acid stones
Uric acid precipitates into crystals in acidic urine & remains soluble
in alkaline urine
GOUT, myeloproliferative disorders after cytotoxic treatment
Infection stones
Struvite & apatite stones ( Ammonium Mg phosphate)
Form after urease producing bacterial infections (proteus,
klebsiella, serratia, Enterobacter) -> urease hydrolyses urea to CO2
& ammonium-> alkalinisation of urine
STAGHORN CALCULI – infection stones that grow in branching
pattern, taking form of pelvicalyceal system -> very large size->
obstruction -> renal failure
Recurrence common- long term antibiotic therapy needed
Cystine stones
1%, cystinuria, autosomal recessive inherited disease
Decreased absorption of cystine from intestine and kidney
Insoluble even at normal ph
Worsens with increasing acidity
Very hard because of di sulphide bonds and don’t easily fragment
with lithotripsy
CLINICAL FEATURES
Asymptomatic
Location, size and type of stone, underlying infections, complications
Haematuria
Calculurea (sandy urine)
Ureteric colic – severe abdominal pain in flanks radiating to
groin/scrotum/labia
Urgency, frequency – VUJ calculus
Fever with chills & rigor – UTI
Malaise, weight loss- renal failure
HISTORY
Diet, physical activity, fluid intake, h/o UTIs, GI symptoms, previous
surgery, family history, previous stone disease
Complications- UTI, loss of renal function
B/L ureteric stones- anuria
Infectious – pyelonephritis, pyonephrosis, renal abscess,
septicaemia
Xanthogranulomatous pyelonephritis,
pyeloenteric/pyelocutaneous fistula
Differential diagnoses
Clot colic
Papillary necrosis
Acute appendicitis
Ectopic pregnancy
Ovarian torsion
Acute intestinal obstruction
Abdominal aortic aneurysm
Malingering
INVESTIGATIONS
Urine RE- microscopic haematuria, pyuria, 24 hr urine collection
Blood RE- > TLC
X ray KUB
USG
NCCT KUB- INVESTIGATION OF CHOICE
IVP x ray – to check renal function
Pregnancy test
Blood CS, Urine CS if sepsis
S. Ca, Phosphorus, uric acid
MANAGEMENT
1. Watchful waiting - < 5 mm stones, non obstructive, asymptomatic,
lower pole calculi, with preserved renal function

2.Medical expulsive therapy-


Tamsulosin ( α adrenergic blocker) causes smooth muscle
relaxation of distal ureteric muscle, distal ureteric stones > 5 mm
IV fluids, diuretics like frusemide, steroids, NSAIDs for pain
ESWL
Extra corporeal shock wave lithotripsy- stone localised by USG/C
arm, acoustic pulse waves generated & focussed on stone-
fragmentation
1984 USA
Uncomplicated stones in kidney & ureter
Size < 2cm
2-3 sittings may be needed
Complications- trauma at site in skin/ kidneys, bleeding,
Surgical management
Indications
1. Failure of medical management
2. Impaired renal function
3. Chronic infection & big stones– staghorn calculi, matrix calculi
4. high risk occupation (pilots/sailors)
5. Patient preference

PCNL, RIRS, URSL, OPEN SURGERY


ENDOUROLOGY
Minimally invasive
Energy sources- pneumatic, US, laser
PCNL- PERCUTANEOUS NEPHRO LITHOTRIPSY
Track between skin and pelvicalyceal system
C arm used to localise, pelvis is entered and camera scope
introduced, stones broken down with energy source
Stones> 2 cm, Failed ESWL/RIRS, Staghorn calculi
Contraindications- pregnancy, untreated UTI, Bleeding disorders,
patient on anticoagulation
URSL ( URETEROSCOPIC LITHOTRIPSY)
Ureteroscopes, semirigid/rigid
Working channels for introduction of energy sources, graspers,
baskets
Complications- ureteric perforation/avulsion, retropulsion
RIRS ( RETROGRADE INTRA RENAL SURGERY)
Slimmer and more flexible ureteroscope- access to kidneys via
ureteric orifice
Laser used as energy source
Stones < 2cm, lower pole calculi, obesity, musculoskeletal
deformities, renal abnormalities
Bleeding disorders
OPEN SURGERY
PYELOLITHOTOMY
NEPHROLITHOTOMY

Complex, infected stones

URETEROLITHOTOMY
CYSTOLITHOTOMY
PREVENTION OF RECURRENCE
Fluid intake > 2.5 litres per day
Reduced intake of animal protein and salt
Increasing citrate (lemon/lime juice)
Avoid supplemental vit c, ca
Allopurinol for patients with Gout

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