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ABSES HATI 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 Amuba
10 % PENDUDUK DUNIA,TERUTAMA NEGARA BERKEMBANG TERINFEKSI E.Histolytika
10 % MENIMBULKAN GEJALA
Insidens : Thailand 0,17 % Indonesia 5-15 % /tahun
LAKI LAKI > WANITA
Abses Hati Amuba 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
Kolesistitis/Gallstone ALI IMRON YUSUF DIVISI GASTRO-HEPATOLOGI BAGI.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,NYERI 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 EUS 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
RISK FACTOR
PROPOSED METABOLIC ABNORMALITY
Older Age
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
Female Gender Obesity Weight Loss
Total Parenteral Nutrition Pregnancy
Increased cholesterol gallbladder hypomotility
secretion
and
Table
Risk Factors Associated with Cholesterol Gallstone Formation
RISK FACTOR Drugs Clofibrate
Oral contraceptives Estrogen treatment in women Estrogen treatment in men Progestogens Ceftriaxone Octreotide
PROPOSED METABOLIC ABNORMALITY Decreased bile acid concentration as a result of suppression of 7 -hydroxylase activity and decreased ACAT activity Increased cholesterol secretion
Cholesterol hypersecretion into bile reduced bile acid synthesis Cholesterol hypersecretion into bile
and
Diminished ACAT activity and increased cholesterol secretion Precipitation of an insoluble calciumceftriaxone salt Decreased gallbladder motility
Table
Risk Factors Associated with Cholesterol Gallstone Formation
RISK FACTOR Genetic Predisposition Native Americans
Scandinavians
PROPOSED METABOLIC ABNORMALITY
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
Diseases of the Terminal Ileum Lipid Profile Increased activity of HMG-CoA reductase Decreased HDL Increased activity of HMG-CoA reductase Increased triglycerides Apolipoprotein E-4 Proposed pronucleator
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 Charcot’s 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 < 102OF 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 gramnegative sepsis
Table
Common Clinical Manifestations of Gallstone Disease
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
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 Amuba
10 % PENDUDUK DUNIA,TERUTAMA NEGARA BERKEMBANG TERINFEKSI E.Histolytika
10 % MENIMBULKAN GEJALA
Insidens : Thailand 0,17 % Indonesia 5-15 % /tahun
LAKI LAKI > WANITA
Abses Hati Amuba 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
Kolesistitis/Gallstone ALI IMRON YUSUF DIVISI GASTRO-HEPATOLOGI BAGI.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,NYERI 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 EUS 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
RISK FACTOR
PROPOSED METABOLIC ABNORMALITY
Older Age
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
Female Gender Obesity Weight Loss
Total Parenteral Nutrition Pregnancy
Increased cholesterol gallbladder hypomotility
secretion
and
Table
Risk Factors Associated with Cholesterol Gallstone Formation
RISK FACTOR Drugs Clofibrate
Oral contraceptives Estrogen treatment in women Estrogen treatment in men Progestogens Ceftriaxone Octreotide
PROPOSED METABOLIC ABNORMALITY Decreased bile acid concentration as a result of suppression of 7 -hydroxylase activity and decreased ACAT activity Increased cholesterol secretion
Cholesterol hypersecretion into bile reduced bile acid synthesis Cholesterol hypersecretion into bile
and
Diminished ACAT activity and increased cholesterol secretion Precipitation of an insoluble calciumceftriaxone salt Decreased gallbladder motility
Table
Risk Factors Associated with Cholesterol Gallstone Formation
RISK FACTOR Genetic Predisposition Native Americans
Scandinavians
PROPOSED METABOLIC ABNORMALITY
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
Diseases of the Terminal Ileum Lipid Profile Increased activity of HMG-CoA reductase Decreased HDL Increased activity of HMG-CoA reductase Increased triglycerides Apolipoprotein E-4 Proposed pronucleator
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 Charcot’s 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 < 102OF 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 gramnegative sepsis
Table
Common Clinical Manifestations of Gallstone Disease
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
