53
Urology Division, Surgery Department Medical Faculty, University of Sumatera Utara

BEDAH Nephrolithiasis

  • Upload
    enri

  • View
    226

  • Download
    1

Embed Size (px)

DESCRIPTION

Nephrolithiasis

Citation preview

Page 1: BEDAH Nephrolithiasis

Urology Division, Surgery DepartmentMedical Faculty,

University of Sumatera Utara

Page 2: BEDAH Nephrolithiasis

References

Page 3: BEDAH Nephrolithiasis

Epidemiology

Prevalence of kidney stone 1 – 15 %, and in hot

area such as the mountains, desert & tropical areas

: = 2 to 3 : 1, peak age onset 40 - 60 yrs

The third most common affliction of the urinary tract,

after UTI and pathologic conditions of the prostate

Race : Whites > Asian > African

Individual occupations eg. manager and professional

risk of stone (unclear reason)

Page 4: BEDAH Nephrolithiasis

Epidemiology25% stone formers have a family history

Risk of stone correlates with weight and body mass index

Uric acid and Ca stones more frequent in, infectious stones more common in

The most common kinds of stones are calcium oxalate, uric acid, struvite and cysteine

Page 5: BEDAH Nephrolithiasis

Etiology

1. Definitive causes :

Metabolic

Infection

Anatomic

Functional

2. Idiopathic

Page 6: BEDAH Nephrolithiasis

Definitive causes

Defects in purine metabolism (uric acid related disorders)

Hyperoxaluric states

- Primary hyperoxaluria

- Enteric hyperoxaluria

Hypercalcemic states

- Primary hyperparathyroidism

- Hyperthyroidism

- Vitamin D abuse

Page 7: BEDAH Nephrolithiasis

Hypercalcemic states (cont.)

- Immobilization

- Disseminated malignancies

- Sarcoidosis

- Renal tubular acidosis

Chronic diarrheal states

Cystinuria

Urinary infection with urease producing microorganisms

Anatomical and functional abnormalities

Page 8: BEDAH Nephrolithiasis

Risk factors Genetics : Cystinuria : autosomal recessive RTA (renal tubular acidosis) – type IMedullary sponge kidney

Geography : temperature & humidity

Diet : calcium / oxalate intake >>

Profession : sedentary

Page 9: BEDAH Nephrolithiasis

ClassificationDefenition

Non Calcium Stones Infection stones: • Magnesium ammonium phosphate • Carbonate apatite • Ammonium uratea

Uric acidAmmonium urateaSodium uratea

Cystine

Calcium Stones

Page 10: BEDAH Nephrolithiasis

Stone Composition and Relative Occurrence

Stone Composition Occurrence (%)

Calcium-Containing Stones

Calcium oxalate 60

Hydroxyapatite (CaPO4) 20

Brushite 2

Non–Calcium-Containing Stones

Uric acid 7

Struvite 7

Cystine 1–3

Triamterene <1

Silica <1

2,8-Dihyroxyadenine <1

Page 11: BEDAH Nephrolithiasis

Stone formation

Page 12: BEDAH Nephrolithiasis

Stone formation

Crystallization NucleationAggregation

Page 13: BEDAH Nephrolithiasis

Inhibitors and Promoters of Crystal Formation

Inhibitors : Nephrocalcin Uropontin Tamm-Horsfall protein Citrate Magnesium

Promoters : Calcium phospate Calcium oxalate

Page 14: BEDAH Nephrolithiasis

Urinary tract stone

Age Sex

Profession Nutrition Climate Race

Inheritance

Abnormal renal morphologyDisturbed urin flow UTIMetabolic abnormalGenetic factors

Increaseexcretion of : 1.Stone forming constituents2. Crystallization promoters

Decrease :1.Urinary volume2. Excretion of crystallization inhibitors

SUPER SATURATIONSTONE

Page 15: BEDAH Nephrolithiasis

Pathogenesis

CALCIUM STONES

1. Hipercalciuria

2. Hiperoksaluria

3. Hiperuricosuria

4. Hipositraturia

5. Hipomagnesuria

Page 16: BEDAH Nephrolithiasis

URIC ACID STONES 5-10% of all stone

3 factors of uric acid stone formation :

1. Low pH, < 5,5

2. Low urine volume

3. Hyperuricosuria urinary uric acid

less than 600 mg/day

Secondary causes : gout (20%),obesity ,

myeloproliferative cancer and congenital

disorder

Page 17: BEDAH Nephrolithiasis

STRUVITE STONESInfection stones comprise 5% to 15% of all stones Composed of Mg ammonium phosphate crystals

or triple phosphate stoneStaghorn calculi are typically struvite stoneCaused by infection with urease-producing bacteria

:

- proteus is the most common

- urease hydrolized urea to form ammonia

alkalinizes the urine, pH and allows crystals to form

Page 18: BEDAH Nephrolithiasis

CYSTINE STONES

1% of all stones

Congenital disorders, autosomal recessive

Caused by a defect in cystine reabsorption in

the proximal tubule

Cystine poorly soluble at normal pH (pKa 8.3)

Crystal form benzene ring on microscopy

Page 19: BEDAH Nephrolithiasis

CALCIUM PHOSPHATE STONE Urine pH > 5.5

Hypocitraturia

70% of adults with type 1 RTA have stones

80% are women

Associated with renal cyst

Page 20: BEDAH Nephrolithiasis

Medications That directly Promote Stone Formation

Indinavir Stones

Triamterene Stones

Guaifenesin and Ephedrine

Silicate Stones

Page 21: BEDAH Nephrolithiasis

Anatomic Predisposition

Ureteropelvic Junction Obstruction :

20 % cases

Horseshoe Kidneys

Caliceal Diverticula

Page 22: BEDAH Nephrolithiasis

DIAGNOSIS

History

Physical examination

Additional :

● Urine, microbiology

● Serum : kidney function, uric acid

● Plain x-ray / USG /IVP

Recently : Computed tomography (CT),

Magnetic resonance imaging (MRI), and

endourology

Page 23: BEDAH Nephrolithiasis

HISTORY

The chief complaint is a constant reminder to the urologist as to why the patient initially sought care

In obtaining the history of the present illness, the duration, severity, chronicity, periodicity, and degree of disability are important considerations

Page 24: BEDAH Nephrolithiasis

  Indications for a Metabolic Stone Evaluation

Recurrent stone formers  

Strong family history of stones   

Intestinal disease (particularly chronic diarrhea)

  

Pathologic skeletal fractures  

Osteoporosis   

History of urinary tract infection with calculi

Page 25: BEDAH Nephrolithiasis

 Indications for a Metabolic Stone Evaluation

Personal history of gout   

Infirm health (unable to tolerate repeated

stone episodes)

Solitary kidney

Anatomic abnormalities  

Renal insufficiency   

Stones composed of cystine, uric acid, or

struvite

Page 26: BEDAH Nephrolithiasis

Basic Metabolic Evaluation

HISTORY : Hyperparathyroidism or

hypercalcaemia, Hyperuricemia, Renal

tubular acidosis

X-RAY

STONE ANALYSIS : Ca, Uric Acid,

Cystein, Carbonate etc.

BLOOD : Serum Creatinin, Calcium, Uric

Acid

Page 27: BEDAH Nephrolithiasis

Basic Metabolic EvaluationURINE :Urinary sediment/dipstick test for :

- Red cells- White cells- Bacteriuria (nitrite)- Urine culture in case of a possible

bacteriuria- pH

Page 28: BEDAH Nephrolithiasis

CLINICAL PRESENTATION

PAINClassically : flank pain, often acute in onsetLocated in the ipsilateral costoverteral angelCaused by distension of renal capsuleMay radiated to upper abdomen, umbilicus, testis or labiumPain by ureteral obstruction is typically colicky in nature and intensifies with ureteral peristalsis

Page 29: BEDAH Nephrolithiasis

PAIN

Associated with gastrointestinal symptoms

Ureteral pain is usually acute and secondary to

obstruction

Site of ureteral obstruction different referred

pain

- Right mid ureteral stone McBurney”s point

- Distal ureteral stones Ipsilateral groin,

testicular (can mimic torsion or epididimytis),

vulvar

pain, supra pubic, urethra and tip of penis

Page 30: BEDAH Nephrolithiasis

PAIN

- waxes & wanes - frequently move about to find a more comfortable position

Sudden onset, no relief with change of position

Page 31: BEDAH Nephrolithiasis

CLINICAL PRESENTATION

Nausea & vomiting

Irritative voiding symptom

Hematuria (gross or microscopic)

Urinary infection

Fever, esp if infection present

Occasionally asymptomatic, with stones

detected incidentally

Page 32: BEDAH Nephrolithiasis

PHYSICAL EXAMINATION

1. Inspection : General overview of patient Local position ?? Systemic component tachycardia, sweating

and nausea

2. Palpation :Bimanual palpation of the kidney abdominal massDRE : To exclude other patological conditions

Page 33: BEDAH Nephrolithiasis

URINALYSIS AND URINE CULTURE

RBC usually present, WBC may be presentpH : < 5.5 + radioluscent stone uric acid stone

> 5.5 + metabolic acidosis, hypokalemia & hyper chloremia RTA > 6.0 struvit

Crystals : - Ca oxalate dumbbell/hourglass/bipyramidal

- Ca phosphate needle-shaped/amorphous - uric acid amprphous/rosettes - struvite coffin lid - cystine benzene ring/hexagonal

Page 34: BEDAH Nephrolithiasis

SERUM STUDIES

Complete blood count

Electrolytes

Calcium

Phosphate

Uric acid

Page 35: BEDAH Nephrolithiasis

IMAGING

KUB - 5 typical location of stone impaction : calyx ureteropelvic junction (UPJ) pelvic brim (iliacs) posterior pelvis (broad ligament, females) ureterovesical junction (UPJ)

Page 36: BEDAH Nephrolithiasis

KUB

Page 37: BEDAH Nephrolithiasis

Intravenous pyelogram (IVP) - nowadays, rarely used in the acute

setting

Page 38: BEDAH Nephrolithiasis

Ultrasound - pregnancy & pediatrics : avoids radiation - poor visualization of small renal & ureteral stones

Page 39: BEDAH Nephrolithiasis

Non-contrast computed tomography - 97% sensitive & 97% specific for stone - 4 signs of obstruction : hydroureter perinephric stranding hydronephrosis nephromegaly

Page 40: BEDAH Nephrolithiasis

Imaging modalitiesPreference number

Examination LE

1. Non-contrast CT

1

2. Excretory urography (IVP)

Standard Procedure

3.. KUB + USG 2a

Page 41: BEDAH Nephrolithiasis

ACUTE MANAGEMENTPain control : - narcotics - NSAIDSIV fluidsAB if urinary infection (+)Strain urineRecommended indication for admission : - uncontrolled pain - unremitting nausea/vomiting with inability to tolerate PO - obstructed, infected renal unit - obstructed, solitary renal unit - bilateral obstruction - anuria

Page 42: BEDAH Nephrolithiasis

Pain relief for patients with acute stone colic

Pharmacological agent

LE

1. Diclofenac sodium

1b

2. IndomethacinIbuprofen

1b

3. Hydromorphine

hydrochloride (+ atropine)MethamizolPentazocine

Tramadol

4

Page 43: BEDAH Nephrolithiasis

Recommended indication for watchful waiting

- no evidence of infection - pain well-controlled with oral medication - stone < 5 mm - no obstructionSpontaneous stone passage rates based on

location : - proximal : 20% - distal : 70%

Page 44: BEDAH Nephrolithiasis

Spontaneous passage rates within 1 year : < 4 mm 90% 4 – 6 mm 60% > 6 mm 20%

Page 45: BEDAH Nephrolithiasis

Obstruksi ureter akut

Peningkatan tekanan pelvis renalis

Nyeri meningkat

prostaglandin

diuresis

Suspresi hormon anti diuretikVaso dilatasi ginjal

Page 46: BEDAH Nephrolithiasis

Obstruksi ureter akut

Peningkatan tekanan pelvis renalis

Edema perirenal dan periureter

Kerusakan ginjal :terjadi oleh karena iskhemia infark / nekrosis pada duktus koligentes dan

tubulus proksimalis

Dilatasi pelvis renalis

Page 47: BEDAH Nephrolithiasis

MEDICAL OPTIONS DURING EXPECTANT MANAGEMENTPain controlAB prophylaxisAlpha blockersCa channel blockerssteroids

Page 48: BEDAH Nephrolithiasis

INDICATIONS FOR ACTIVE STONE REMOVALThe stone diameter is > 7 mm (because of a

low rate of spontaneous passage)Pain relief cannot be achievedStone obstruction associated with infectionPyonephrosis or urosepsisIn single kidneys with obstructionBilateral obstruction

Page 49: BEDAH Nephrolithiasis

SURGERYESWLUreteroscopyPercutaneous nephrolithotomy (PNL)LaparascopyOpen surgery

Page 50: BEDAH Nephrolithiasis

SURGERYESWL - imaging : fluoroscopy - anesthesia : sedation or general - potential long-term renal effect : renal injury/scar, hypertension

- complications : hematoma (<1%) UTI/sepsis obstruction injury to organ

- contraindications : pregnancy calcified

aneurysm morbid obesity bleeding diathesis

Page 51: BEDAH Nephrolithiasis

ESWL : Extra Corporeal Shock Wave Lithotripsy

Page 52: BEDAH Nephrolithiasis

STONE FREE RATES

proximal distal ureter ureter

<1.0 cmESWL 84% 85%Ureteroscopy 56% 89%PCNL 76% -

≥1.0 cmESWL 72% 74%Ureteroscopy 44% 73%PCNL 74% -

Page 53: BEDAH Nephrolithiasis