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DAN KOMPLIKASINYA
Nyoman Purwadi
Divisi Gastro Hepatologi
Bag./SMF Penyakit Dalam
FK Unud/ RS Sanglah
Denpasar
VESICLE COMPOSITION
GALL STONE
Harvest Time
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
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
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)
Cullens sign
Evaluation
amylaseNonspecific !!!
Amylase levels > 3x normal very suggestive of
pancreatitis
May be normal in chronic pancreatitis!!!
lipase
More sensitive & specific than amylase
Radiographic Evaluation
Plain Foto - sentinel loop or small bowel ileus
US or CT may show enlarged pancreas with
Therapy
Remove offending agent (if possible)
Supportive !!!
#1- NPO (until pain free)
NG suction for patients with ileus or emesis
TPN may be needed
Therapy continued
#3- Narcotic analgesics usually necessary for pain
TERIMA KASIH