GALL STONE

DAN KOMPLIKASINYA
Nyoman Purwadi
Divisi Gastro Hepatologi
Bag./SMF Penyakit Dalam
FK Unud/ RS Sanglah
Denpasar

VESICLE COMPOSITION

GALL STONE

Harvest Time

Acute and Chronic Cholecystitis and Cholelithiasis

Pathogenesis pigment stone

RISK FACTORS

CLINICAL MANIFESTATION

KOLESISTITIS AKUT
Adalah reaksi inflamasi akut dinding
kandung empedu dgn ditandai adanya:
= Nyeri perut kanan atas
= Panas badan
Faktor yg berperan :
= stasis cairan
= infeksi kuman
= iskemia dinding

PEMBAGIAN
Berdasar penyebab dibagi 2:
= Kolesistitis akut kalkulus : (90%) terjadi
karena ada batu yg menyumbat ductus
cysticus
= Kolesistitis akut akalkulus : didapat pd
pasien yg dirawat cukup lama dan dgn
nutrisi parenteral, keganasan GB, atau
merupakan komplikasi demam tifoid
atan
DM

GEJALA KLINIS
Keluhan yg khas adalah :
= Kolik perut kanan atas
= Nyeri tekan perut kanan atas
= kenaikan temperatur
= Rasa sakit menjalar ke pundak atau
scapula kanan
Keluhan bervariasi mulai dari keluhan
ringan
Sampai keluhan berat seperti perforasi

Pd pemeriksaan fisis :
= Nyeri tekan perut kanan atas
= Demam
= Murphy sign
Laboratorium :
= lekositosis

MURPHY SIGN
Pasien terlentang dan pemeriksa ada di sisi
kanan penderita
Dilakukan penekanan dengan tangan kanan
di
perut kanan atas, tahan pada posisi ini, dan
pasien diminta menarik nafas dalam : nafas
terhenti krn pasien kesakitan, Murphy sign
positif

DIAGNOSIS
PLAIN

FOTO ABDOMEN
KOLESISTOGRAFI
USG
SKINTIGRAFI
CT- SCAN

PAIN PHOTO ABDOMEN

ULTRASONOGRAPHY

PENGOBATAN
= Bedrest
= Nutrisi parenteral
= Pain killer
= Antibiotik sistemik
= Kolesistektomi

ACUTE CHOLANGITIS
Inflammatory
process
involving the
bile ducts that
usually results
from biliary
obstruction
and associated
biliary
infection and
can be life
threatening

PATHOPHYSIOLOGY
Sterile bile in healthy
individuals
Biliary tract
compromised
(e.g. stone, stricture,
endoprosthesis)
Bacteria in the bile

Obstruction
Biliary pressure rises
Bacteria & products
(e.g.endotoxin) in the
bile systemic
circulation
Endotoxaemia &
septicaemia

Van Lent AUG et al. Gastrointest Endosc 2002;55:518-22; Lee DWH, Chung SCS. Baillieres Clin Gastroenterol
1997;11(4).

AETIOLOGY
Obstruction Can Cause by:
Stone (the most common)
Benign strictures
Neoplasm
Direct cholangiography
Sclerosing cholangitis
Foreign bodies
Lee DWH, Chung SCS. Baillieres Clin Gastroenterol 1997;11(4).

CLINICAL FEATURES
CHARCOTS TRIAD
Abdominal (right upper quadrant) pain
Fever
Jaundice
REYNOLDS PENTAD Charcots triad +
Mental confusion
Hypotension
Severe cholangitis

Other symptoms

Chills
Rigors
Tea-coloured urine
Pruritus
Pale stools

Lee DWH, Chung SCS. Baillieres Clin Gastroenterol 1997;11(4).

DIAGNOSIS
History (Charcots Triad)
Complete Physical Findings
Charcots Triad
Reynolds Pentad
Laboratory Examination
Plain Foto Abdomen
Ultrasound Examination
CT Scan
PTC and ERCP

MANAGEMENT
IV fluids and IV antibiotics + monitoring blood
pressure, pulse, and urinary output
Antibiotic therapy
75% of patients will respond to IV antibiotics
Mortality of acute cholangitis has decreased from
100% to 9-40% with the introduction of antibiotics
and biliary decompression
Empirical therapy broad-spectrum

Endoscopic drainage
Percutaneous transhepatic drainage
Surgical drainage
Lee DWH, Chung SCS. Baillieres Clin Gastroenterol 1997;11(4).

Acute pancreatitis
Etiologies
Idiopathic
Gallstones (or other
obstructive lesions)
EtOH
Trauma
Steroids
Mumps (& other
viruses: CMV, EBV)
Autoimmune (SLE,
polyarteritis nodosa)

Scorpion sting
Hyper Ca, TG
ERCP (5-10% of pts
undergoing procedure)
Drugs (thiazides,
sulfonamides, ACE-I,
NSAIDS, azathioprine)

EtOH and gallstones

account for 60-70%
of cases

Signs & Symptoms

Severe epigastric abdominal pain - abrupt onset

(may radiate to back)

Nausea & Vomiting
Weakness
Tachycardia
+/- Fever; +/- Hypotension or shock

Grey Turner sign - flank discoloration due to

retroperitoneal bleed in pt. with pancreatic necrosis
(rare)
Cullens sign - periumbilical discoloration (rare)

 Grey Turner sign

Cullens sign

Evaluation
amylaseNonspecific !!!
Amylase levels > 3x normal very suggestive of
pancreatitis
May be normal in chronic pancreatitis!!!

Enzyme level severity

False (-): acute on chronic (EtOH); HyperTG
False (+): renal failure, other abdominal or salivary gland
process, acidemia

lipase
More sensitive & specific than amylase

Radiographic Evaluation
Plain Foto - sentinel loop or small bowel ileus
US or CT may show enlarged pancreas with

stranding, abscess, fluid collections, hemorrhage,

necrosis or pseudocyst
MRI/MRCP newest fad
Decreased nephrotoxicity from gadolinium
Better visualization of fluid collections
MRCP allows visualization of bile ducts for stones
Does not allow stone extraction or stent insertion

Endoscopic US (even newer but used less)

Useful in obese patients

CT Scan of acute pancreatitis

CT shows
significant
swelling
and
inflammation
of the
pancreas

Gall stone pancreatitis by ERCP

Therapy
Remove offending agent (if possible)
Supportive !!!
#1- NPO (until pain free)
NG suction for patients with ileus or emesis
TPN may be needed

#2- Aggressive volume repletion with IVF

Keep an eye on fluid balance/sequestration
and electrolyte disturbances

Therapy continued
#3- Narcotic analgesics usually necessary for pain

relieftextbooks say Meperidine

NO conclusive evidence that morphine has
deleterious effect on sphincter of Oddi pressure
#4- Urgent ERCP and biliary sphincterotomy within
72 hours improves outcome of severe gallstone
pancreatitis
Reduced biliary sepsis, not actual improvement of
pancreatic inflammation

#5- Dont forget PPI to prevent stress ulcer

TERIMA KASIH