Urology pdf - غير معروف

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Epidemiology

 Sex:

 Metabolic and idiopathic M>F
 Infection F>M

 Age:

 Metabolic and idiopathic, 3

and 4

decade of life

 Infection 5

decade

 Occupation: sedentary work, hot climate
 Diet:

 Fiber rich diet decrease the risk
 Refined CHO and animal pr. Increase the risk

 Family history: double risk (15% vs. 30%)



Stone formation requires SUPERSATURATION

Supersaturation depends on

  Urinary PH
  Ionic strength
  Solute conc.
  complexation

Chemical Terms

• concentration product: multiplying 2 ion conc.
• Solubility product: The point above which ions are metastable and capable

of heterogenous nucleation.

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

• Formation product: the level above which the ions are unstable and capable

of homogenous nucleation.

• Calcification: metastatic vs dystrophic

Causes

• Idiopathic: most common cause
• Abnormalities of urine:

 Congenital: primary hyperoxalurea, cystinurea
 Acquired: dehydration, dietary hypercalciuria

• Abnormalities of the urinary tract:

 Cong: PUJ obstruction, ureteroceles, diverticuli
 Acquired: postoperative or traumatic fibrosis

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Theories Of Stone Formation

Nucleation theory: stones originate from crystals or foreign bodies immersed

in supersaturated urine

Crystals inhibitors theory: stones are formed due to absence or low conc. of

stone inhibitors e.g citrate

Stone Components

A stone consists of crystalline material arranged in layers on an organic scaffold

A. Crystal component: >90%

 Crystal formation occurs in 3 steps: nucleation, growth, and

aggregation

 Nucleation can be either homogenous or hetergenous

B. Matrix component:< 10%
Protiens, hexose, and hexosamines

 Matrix role???

 Matrix stone:

Risk Factors

  Anatomical abnormalities
  Infection: urease producers
  Hormonal imbalance: PTH
  Environmental factors
  Diet: decreased fluid intake, meat,multivitamins
  Metabolic state of the person which influenced by the genetic background
  Drugs: antacids, CS, chemotherapy
  Low mobility: bone demeniralization
  Family history: cystineuria, RTA
  Bowel inflam. conditions and resection: hyperoxaluria

Urinary Ions

: it is the major ion present in urinary stones.

50% of plasma ca

is ionized and filterable, it’s reabsorbed by PT&DT, 2%

excreted.

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

 Normal urinary ca+2 in adults is ≤4mg/kg/day.
 Diuretics decrease u. ca

 Increased monosodium urate increase ca

–oxalate

crystallization.

 Acidic urine increase the crystallization also.

Oxalate:

85% is a metabolic by-product, while only 15% is dietary
IN BOWEL: either absorbed then exclusively excreted by PT, or metabolized by
bacteria, or complex and excreted in feces.
Normal level is less than 45 mg/day.

Phosphate:

 is an important buffer that complexes with ca

in urine

 Part of MAP stone
 Urinary excretion depends on dietary intake (meat), then

filtered by the glomerulus and re absorbed by PT under
influence of PTH

: although it is not a major constituent of urinary stone, it plays a very

important role in the regulation of ca

salts crystallization, a major increase in u.

excretion will dramatically increase u. Ca

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Uric acid: is a byproduct of purine metabolism, it’s Pka is 5.75, so its solubility
increases in alkaline urine
Citrate: is the major stone inhibitor in urine, its level in urine decreases in:

  Metabolic acidosis
  RTA type I
  Chronic diarrhoea
  Thiazide therapy
  Hypokalemia
  Esterogen lack in females

Other inhibitors:

  Mg
  Sulfate
  Urinary proteins (Tamm-Horsfall pr.)
  Pyrophosphate
  Glycoseamineglycans
  uropontine

Stone Varieties

Calcium stones (85%)

•  Hypercalciuric
•  Hyperoxaluric
•  Hyperuricoseuric
•  hypocitraturic

Non calcium stones (15%)

•  Struvite “infection, MAP”
•  Uric acid
•  Cystine
•  Xanthine
•  Others: indinavir

Hypercalciuria

Absorptive:

  Diet independent /cellulose phosph. vs. thiazides
  Diet dependent /mild and respond to dietary modif.
  Renal phosphate leak /orthophosphate suppl.

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Resorptive hypercalciuria

Due to hyperparathyroidism

Renal induced hypercalciuria
Due to intrinsic renal tubular defect

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Hyperoxaluria

A. Primary hyperoxaluria: a rare AR disease, it is aggressive and ends in RF,

the definitive therapy by combined renal and liver transplantation, however
adequate hydration, oxalate restriction, and pyridoxine all will decrease
urinary excretion

B. Enteric hyperoxaluria: oxalate is poorly absorbed by intestine, but once

absorbed it is exclusively excreted in urine, causes of increased absorption
include:

• IBD, small bowel bypass, mal-absorption syndromes, low

dietary calcium, steatorrhoea, excessive ascorbic acid intake,
and accidental ethylene glycol ingestion

• Oxalate rich food

Hyperuricoseuria

• Due to either excessive oral purine intake, or excessive endogenous

production

• Monosodium urate absorbs and adsorbs urinary inhibitors and facilitates

heterogeneous nucleation

• Patients usually have elevated urinary uric acid and U.pH >5.5
• Treatment includes adequate hydration, urine alkalization, and allopurinol

Hypocitraturia

 Citrate is the major stone inhibitor in urine
 Causes of hypocitraturia are mentioned before

  Metabolic acidosis
  RTA type I
  Chronic diarrhoea
  Thiazide therapy
  hypokalemia

  Normal level: > 320 mg/24 hrs
  Treatment: by potassium citrate suppl.
  6-8 glasses of lemonade per day increase U. citrate by 150 mg/day

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Struvite Stones

  Also called triple phosphate, or infection stones
  Composed of MAP
  It is formation requires the presence of urea splitting bacteria which

alkalinize urine and causes high conc. of bicarbonate and ammonium

  These include: proteus, pseudomonads, klebsiella and staph.
  E.coli is not a urease producer
  MAP crystals ppt. only in high PH>7.2

Struvite stones (cont’d)

Incidence increases in patients with chronic cath, urinary diversion, S.C

injury, and bladder dysfunction

  Presentation: usually as stag-horn, but can be in any form
  On X-ray: faintly opaque due to poor mineralization and large protein matrix
  Treatment: should include complete removal, with control of infection pre,

per and post operatively

Uric acid stones

  5-10 % of all u. stones
  Pure uric acid stones are radiolucent
  Xanthine oxidase converts xanthine into uric acid
  Urinary pH < 5.5
  May be formed in patients with:

  Hyperuricemia
  Hyperuricoseuria
  Chronic dehydration

Corner stones of treat included:

  Good hydration
  Urine alkalization
  Allopurinol

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Cystine stones

1-2% of all stone types
Have faintly opaque ground glass appearance with smooth edges due to

presence of sulfur

AR inborn error of metabolism
There is abnormal renal tubular re-absorption of dibasic amino acids COLA
Its PKa is 8.1, so the more alkaline the urine the more cystine is soluble
May present as single, multiple, or staghorn
Medical therapy may dissolve or prevent stone recurrence by:

  Adequate hydration
  Urine alkalization
  Cystine binding drugs as penicillamine, captopril, thiola, or

bucacillin

Sign and Symptoms

•  Pain:
•  Hematuria: microscopic in up to 90%
•  Infection: affects pain perception, endotoxins and exotoxins affect ureteric

peristalsis, it may range from simple to frank pyonephrosis (emergency)

• Nausea and vomiting

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Signs:

  Pain causes sweating, hypotension, tachypnoea and tachycardia
  Obs,infection,and pyonephrosis cause high temp,rigor and sepsis
  Renal angle tenderness
  Bladder may be tender or with urine retention
  Do full abd. exam and exclude other diff.diagnosis

Investigations:

  GUE
  Renal function
  Abd. US
  EXU
  CT scan
  Stone analysis and work up

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Treatment of renal stones

Decision depends on:

  Stone size, site, and type
  Renal function and anatomy
  Patient clinical condition
  Facility available

Patient’s and doctor’s preference

Indications for hospitalization

High-grade obstruction, (spec. stones >10 mm) will require early

intervention (stenting or PCN).

High fever (>38.5ºC) suggests pyelonephritis, I.V AB should be started

immediately.

  Patients with uncontrollable pain requiring parenteral analgesics.
  Patients with severe nausea and dehydration requiring intravenous fluids.
  Patients with a single functioning kidney at risk of acute renal failure.

Modalities

Conservative observation:

 Small calculi without obstruction need no urgent intervention, and have

great chance of spontaneous passage, specially if <7 mm.

 Analgesia is the corner stone of treatment, the best is indomethasin supp.

(Keotrolac??).

  Anti-emetics
  AB if associated infection
  Diuretics and antispasmodics are not preferred
  Keep the patient well hydrated
  Encourage normal movement

Indication for early intervention

  High-grade urinary obstruction
  Persistent infection despite antibiotics
  Uncontrollable pain
  Impairment of renal function

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

ESWL

• Has revolutionized the stone management
• Shock waves: unharmonic, with steep rise in pressure amplitude that results

in compressive forces.

• It includes:

  Energy source: to create the shock waves
  Coupling mechanism: transfer the energy into the human body
  Localization technique: help localize the stone, either by US, or

flouroscopy

Shock wave sources

 Supersonic emitters (point source of shock waves): releasing energy in a

confined space creating expanding plasma bubble that emits shock waves.

 Finite amplitude emitters (surface source of shock waves)

 Piezoceramic plates that elongate on electrical stimulation and

displace to generate the shock waves.

 Electromagnetic membrane that displace on electrical

stimulation and generates the shock waves.

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Patient preparation:

  EXU to exclude distal obstruction
  GUE and urine culture
  Bleeding profile
  In some cases ureteric stent (single kidney or large stone burden)

Contraindication:

  Pregnancy
  Uncontrolled bleeding tendency
  Large abd. aortic aneurysm
  Distal obstruction
  Uncontrolled hypertension?????

Complications:

Early:

•  Heamturia
•  Heamatoma: perirenal, subcapsular or parenchymal
•  Steinstrass
•  Skin echymosis

Late:

• Accelerated hypertension
• Renal impairment

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Post ESWL care:

•  Abd. examination
•  Don’t let the pt. leave before passes urine
•  Analgesia
•  Adequate oral hydration
•  Instruct the pt to monitor his urine for stone gravels

Percutaneous Nephrolithotomy

•  Greatly replaced open surgical procedures
•  Done under flouroscopic guidance
•  creation of a nephrostomy tract toward the targeted calyx, the tract then

dilated and used to pass a nephroscope into the collecting system, through
which litholapaxy or lithotripsy is done.

• Mainly used for staghorn calculi, and those who failed ESWL treatment.
• Advantages:

  No surgical wound and scar
  Short hospitalization
  Less blood transfusion

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Surgery:

Laparoscopy

 Transperitoneal
 retroperitoneal

Open surgery

  Pyelolithotomy
  Nephrolithotomy
  Extended pyelo-nephrolithotomy
  Anatrophic nephrolithotomy
  Partial nephrectomy
  Nephrectomy

Ureteric Stones:

Additional factors affecting management decision:
  Obstruction
  Symptom severity
Modalities:
  Conservative, (expulsive therapy)
  ESWL can be used for all ureteric stones sp. upper, limitation when over

bone

 Ureteroscopy sp. for lower ureteric stones
 Open surgery (ureterolithotomy)

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Vesical Stones

• Childrean:

Dietary cause: low pr. High CHO diet, formation of ammonium urate

stones

Urine is sterile
Males>females

• Adults:

Obstruction: ca-ox stone e.g: BPH, urethral stricture, neuropathic

bladder

  Urine is infected
  F.B as stitches
  Or descended stone

Presentation:
•  Asymptomatic
•  Hesitancy, frequency, dysuria
•  Hematuria
•  Pain referred to tip of penis
•  Urine retention

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Diagnosis:
US, EXU, CYSTOSCOPY

TREATMENT
•  Treat the primary cause
•  Cystolitholapaxy
•  Lithotripsy
•  ESWL
•  Vesicolithotomy

Prevention of Urolithiasis
General measures:
  Drink suff. water to keep UOP > 3L/d
  Limit daily intake of meet
  Limit daily intake of table salt
  Increase fiber diet and cereals
  Limit intake of oxalate rich food
  Normal intake of dairy products
  Increase intake of citrus fruit juices

Surgery

Renal Stone Disease

Dr. Hasanain Farhan

Lec. 30

Specific measures:

  Alkalinize urine for uric acid and cystine stones by potassium citrate
  Treat hypercalciuria according to the cause
  Allopurinol for hyperuricemia
  Urease inhibitors for MAP stones e.g AHA
  Cystine binding drugs for cystineuria