ABSES HATI

Bentuk infeksi pada hati

Secara umum : Abses hati amubik
Abses hati pyogenik
Causa: bakteri,parasit,jamur,maupun
nekrosis steril yg bersumber dari sistem g.i.
yg di tandai dgn adanya proses supurasi
dgn pembentukan pus yg t.d.: jaringan hati
nekrotik,sel inflamasi .
Abses Hati Amuba
10 % PENDUDUK DUNIA,TERUTAMA NEGARA BERKEMBANG
TERINFEKSI E.Histolytika

10 % MENIMBULKAN GEJALA

Insidens : Thailand 0,17 %
Indonesia 5-15 % /tahun

LAKI LAKI > WANITA




PATOGENESIS
Belum diketahui secara pasti

Diduga a.l. faktor virulensi parasit,nutrisi,
imunodepresi pejamu,penurunan imunitas
seluler dan resistensi parasit

Mekanisme: strain e. histolytika ada yang
patogen dan non patogen
E.histolytika nempel pada mukosa usus
perusakan sawar intestinal sel lysis
Penyebaran amuba dari usus kehati
sebagian besar via vena porta

GEJALA KLINIS
DEMAM
NYERI PERUT KANAN ATAS
HEPATOMEGALI
KADANG GEJALANYA TIDAK KHAS
ANOREKSIA
KADANG DEMAM
PEMERIKSAAN LABORATORIUM
Umumnya leukositosis

Kelainan faal hati ringan sampai sedang

Serologi amuba , spesifik untuk daerah non
endemik
PEMRIKSAAN PENUNJANG
ULTRASONOGRAFI

CT SCAN

THORAK FOTO
DIAGNOSIS
DEMAM
NYERI PERUT KANAN ATAS
HEPATOMEGALI NYERI TEKAN
LEUKOSITOSIS
DIAFRAGMA LETAK TINGGI
SEROLOGI AMUBA MENDUKUNG
USG
KRITERIA SHERLOCK
HEPATOMEGALI YANG NYERI TEKAN
LEUKOSITOSIS
PENINGGIAN DIFRAGMA KANAN DAN
PERGERAKAN YANG KURANG
ASPIRASI ADA PUS
USG ADA GAMBARAN RONGGA
RESPON TERHADAP OBAT AMUBISID
KOMPLIKASI
TERSERING RUPTUR
DAPAT TERJADI KE :
PLEURA
PARU
PERIKARDIUM
USUS
INTRAPERITONEAL
KULIT
PENGOBATAN
DERIVAT NITROIMIDAZOLE
DAPAT DIBERIKAN ORAL DAN INTRA
VENA
DAPAT MEMBUNUH BTK TROPOZOIT
INTESTINAL,EKSTRA INTESTINAL,KISTA
DOSIS ANJURAN 4 x 500-750 mg 5
sampai 10 hari
CHLOROQUIN
TINDAKAN
BISA DILAKUKAN ASPIRASI CAIRAN
ABSES DENGAN GUIDED USG APABILA
ADA ANCAMAN RUPTUR DAN DIAMETER
> 7 CM
DI RSCM TINDAKAN INI MERUPAKAN
PROSEDUR BIASA
TINDAKAN BISA BERULANG-ULANG
13
Kolesistitis/Gallstone
ALI IMRON YUSUF
DIVISI GASTRO-HEPATOLOGI BAG-
I.PENYAKIT DALAM F.K. UNILA/RSUD
Dr.ABD MOELOEK BANDAR LAMPUNG
KOLESISTITIS
Y I :Reaksi inflamasi akut dd
kandung empedu yg disertai
keluhan nyeri perut kanan atas,
nyeri tekan dan panas badan.
ETIOLOGI DAN PATOGENESIS
FAKTOR:STASIS CAIRAN EMPEDU ,INFEKSI
KUMAN DAN ISKEMIA DD KANDUNG EMPEDU.
PENYEBAB UTAMA : BATU KANDUNG EMPEDU
90 %.FAKTOR
LAIN:KEPEKATANCAIRANEMPEDU,KOLESTER
OL,LISOLESITIN,DAN P G YANG MERUSAK
DD K E.
GEJALA KLINIS
NYERI PERUT KANAN ATAS
NYERI TEKAN
PANAS
RASA SAKIT MENJALAR KEPUNDAK
ATAU SKAPULA KANAN
UMUMNYA W- GEMUK> 40 THN.
MURPHY SIGN
DIAGNOSIS
GEJALA KLINIS
ULTRASONOGRAFI
SKINTIGRAFI SAL-EMPEDU DGN RADIO
AKTIF,TP TEHNIK SUKAR.
PENGOBATAN
ISTIRAHAT
OBAT PENGHILANG RASA SAKIT
ANTIBIOTIK
JIKA PERLU KOLESISTEKTOMI
PROGNOSIS
85 % SEMBUH SPONTAN,TAPI
KANDUNG EMPEDU TEBAL,FIBROTIK
PENUH DGN BATU TDK BERFUNGSI.
KADANG MENJADI GANGREN,
EMPYEMA DAN PERFORASI,FISTEL,
ABSES HATI ATAU PERITONITIS.
GALL STONE
SERING DITEMUKANDI NEGARA DIBARAT
SUKU INDIAN TINGGI : 40-70 %
DI BARAT JARANG MENGALAMI KOLIK
DI INDIAN 50% KOLIK DAN KOMPLIKASI:
KOLESISTITIS,KOLANGITIS DAN PANKREATITIS
PATOGENESIS BATU EMPEDU
DIPERLUKAN 3 FAKTOR UTAMA :
1.SUPERSATURASI KOLESTEROL
2.HIPOMOTILITAS KANDUNG
EMPEDU
3.NUKLEASI CEPAT
JENIS BATU EMPEDU

BATU KOLESTEROL

BATU Ca BILIRUBINAT( PIG-COKLAT)

BATU PIGMEN HITAM
GEJALA KLINIK
1 A SIMPTOMATIK

2 SIMPTOMATIK

3 DGN KOMPLIKASI Y I :
KOLESISTITIS AKUT,IKTERUS,
KOLANGITIS DAN PANKREATITIS.
MANIFESTASI KLINIK
1 KOLIK BILIER, INI O.K.SPASME TONIK AKIBAT
OBSTRK-TRANSIEN DUKTUS SISTIKUS OLEH BATU,
BIASANYA TIMBUL MALAM HARI,NYE-
RI T.U. DIDAERAH EPIGASTRIUM.
2 KOLESISTITIS AKUT(90-95%)
3 KOLESISTITIS KRONIK
4 KOLEDOKOLITIASIS DAN KOLANGITIS,INI O.K.
MIGRASI BATU KE DUK- KOLEDOKUS, GEJALA
UTAMA: NYERI 97%,IKTERIK-69%,TRIAS CHARCOT
39%.
DIAGNONIS
YANG PALING TEPAT DENGAN

E U S
KEBERHASILAN: 97 % DIBANDING
USG BIASA.
PE MERIKSAAN -RADIOLOGI
FOTO POLOS ABDOMEN
KOLESISTOGRAFI
PENATAHAN HATI DGN HIDA
CT SCAN
PTC(PERKUTANIUS TRANS-KOLANG-
ERCP
Table Risk Factors Associated with Cholesterol
Gallstone Formation
Older Age

Female Gender

Obesity

Weight Loss


Total Parenteral
Nutrition
Pregnancy
Increased cholesterol secretion and decresed
bile acid synthesis
Increased cholesterol secretion and
increased intestinal transit time
Cholesterol hypersecretion into bile and
increased cholesterol synthesis via
increased HMG-CoA reductase activity
Cholesterol hypersecretion into bile, reduced
bile acid synthesis and gallbladder
hypomotility
Gallbladder hypomotility

Increased cholesterol secretion and
gallbladder hypomotility
RISK FACTOR PROPOSED METABOLIC ABNORMALITY
Table Risk Factors Associated with Cholesterol
Gallstone Formation
Drugs
Clofibrate


Oral contra-
ceptives
Estrogen treat-
ment in women
Estrogen treat-
ment in men
Progestogens

Ceftriaxone

Octreotide
Decreased bile acid concentration as a result
of suppression of 7 -hydroxylase activity
and decreased ACAT activity
Increased cholesterol secretion

Cholesterol hypersecretion into bile and
reduced bile acid synthesis
Cholesterol hypersecretion into bile

Diminished ACAT activity and increased
cholesterol secretion
Precipitation of an insoluble calcium-
ceftriaxone salt
Decreased gallbladder motility
RISK FACTOR PROPOSED METABOLIC ABNORMALITY

Table Risk Factors Associated with Cholesterol
Gallstone Formation
Genetic Predis-
position
Native Americans


Scandinavians
Diseases of the Ter-
minal Ileum
Lipid Profile
Decreased HDL
Increased trigly-
cerides
Apolipoprotein E-4
Increased cholesterol synthesis and
reduced conversion of cholesterol into
bile salts
Increased cholesterol secretion into bile
Hyposecretion of bile salts from diminished
bile acid pool

Increased activity of HMG-CoA reductase
Increased activity of HMG-CoA reductase

Proposed pronucleator
RISK FACTOR PROPOSED METABOLIC ABNORMALITY
Table Common Clinical Manifestations of Gallstone Disease
Symptoms
BILIARY COLIC
Severe, poorly localized epigastric or right upper quadrant visceral pain
growing in intensity over 15 min and remaining constant for 1-6 hr,
often with nausea
Frequency of attacks varies from days to months
Gas, bloating, flatulence, and dyspepsia are not related to stones
ACUTE CHOLECYSTITIS
75% are preceded by attacks of biliary colic
Visceral epigastric pain gives way to moderately severe, localized pain in
the right upper quadrant, back, shoulder, or, rarely, chest
Nausea with some emesis is frequent
Pain lasting > 6 hr favors cholecystitis over colic
CHOLEDOCHOLITHIASIS
Often asymptomatic
Symptoms (when present) are indistinguishable from biliary colic
Predisposes to cholangitis and acute pancreatitis
CHOLANGITIS
Charcots triad of pain, jaundice, and fever is present in 70%
Pain may be mild and transient and is often accompanied by chills
Mental confusion, lethargy, and delirium are suggestive of bacteremia
Table Common Clinical Manifestations of Gallstone Disease
Natural history
BILIARY COLIC
After initial attack, 30% have no further symptoms
The remainder develop symptoms at a rate of 6% per year and
severe complications at rate of 1% per year
ACUTE CHOLECYSTITIS
50% resolve spontaneously in 7-10 days without surgery
Left untreated, 10% are complicated by a localized perforation and
1% by a free perforation and peritonitis
CHOLEDOCHOLITHIASIS
Natural history is not well defined, but complications are more
frequent and severe than for asymptomatic stones in the
gallbladder
CHOLANGITIS
High mortality if unrecognized, with death from septicemia
Emergent decompression of the CBD (usually by ERCP) dramatically
improves survival.
Table Common Clinical Manifestations of Gallstone Disease
Physical findings
BILIARY COLIC
Mild-to-moderate gallbladder tendermess during an attack with mild
residual tenderness lasting days
Often a completely normal examination
ACUTE CHOLECYSTITIS
Febrile but usually < 102
O
F unless complicated by gangrene or perforation
Right subcostal tenderness with inspiratory arrest (Murphy sign)
Palpable gallbadder in 33%, especially in patients having their first attack
Mild jaundice in 20%, higher frequency in elderly

CHOLEDOCHOLITHIASIS
Often a completely normal examination if the obstruction is intermittent
Jaundice with pain suggests stones, whereas painless jaundice and a
palpable gallbladder favor malignancy
CHOLANGITIS
Fever in 95%
Right upper quadrant tenderness in 90%
Jaundice in only 80%
Peritoneal signs in only 15%
Hypotension and mental confusion coexist in 15% and suggest gram-
negative sepsis
Laboratory findings
BILIARY COLIC
Usually normal
In patients with findings of only uncomplicated biliary colic, an elevated
bilirubin, alkaline phosphatase, or amylase suggests coexisting CBD
stones
ACUTE CHOLECYSTITIS
Leukocytosis of 12,000 to 15,000 with bandemia iscommon
Bilirubin may be 2-4 mg/dL and transaminase and alkaline phosphatase may
be elevated even in the absence of CBD stone orhepatic infection
Mild amylase elevation is seen even in absence of pancreatitis
If bilirubin >4 or amylase > 1000, suspect CBD stone
CHOLEDOCHOLITHIASIS
Elevated bilirubin and alkaline phosphatase seen with CBD obstruction
Bilirubin >10 mg/dL suggests malignant obstruction or coexisting hemolysis
Transient spike in transaminases or amylase suggests passage of a stone
CHOLANGITIS
Leukocytosis in 80%, but remainder may have normal WBC count with
bandemia as the only hematologis finding
Bilirubin >2 mg/dL in 80%, but when < 2 mg/dL the diagnosis may be
missed
Alkaline phosphatase is usually elevated
Blood cultures are usually positive, especially during chills or fever spike,
and grows two organisms in half of patients
Table Common Clinical Manifestations of Gallstone Disease
DAFTAR PUSTAKA
BUKU AJAR IPD JILID 1 ED- IV
FUNDAMENTAL OF GASTROENTROLOGI, ALIH
BAHASA DALDIONO DKK
KULIAH IPD Dr. YUKE, FK.UNPAD
GREENBERGER,JN,PAUMGARTNER,G;
DESEASE OF THE GALLBLADDER AND BILE
DUCT in PRINCIPLES OF INTERNAL
MEDICINE,HORRISONS 15 th ED,VOL-2,ed-
BRAUNWALD ETALL,2001.
THANKS FOR YOUR ATTENTION.