GAWAT DARURATGASTRO ENTERO HEPATOLOGI Dr.H.ALI IMRON YUSUF, SpPD,FINASIM,KGEH DIVISI GASTRO-HEPATOLOGI BAG- I. P. DALAM,FK.UNILA/ RSUD Dr.H.ABDUL MOELOEK BANDAR LAMPUNG GAWAT DARURAT GASTRO ENTERO-HEPATOLOGI. • HEMATEMESIS MELENA • PANKREATITIS AKUT • KOMA HEPATIKUM • DILATASI LAMBUNG AKUT • KOLESISTITIS AKUT • KOLITIS PESEUDOMEMBRANOSA • ILEUS PARALITIKUS • SPASME DAN TROMBOSIS A. MESENTRIKA • HEMATOKHESIA • KERACUNAN ZAT KOROSIF HEMATEMESIS – MELENA • MERUPAKAN KEADAAN GAWAT DARURAT DIBIDANG PENYAKIT DALAM DENGAN ANGKA KEMATIAN YANG MASIH CUKUP TINGGI. • DI RSCM I987- ’88 ANGKA KEMATIAN :26 %. • DI EROPA DAN A.S. 8 – 10 % DEFINISI • HEMATEMESIS ADALAH MUNTAH DARAH BERWARNA HITAM TER YG BERASAL DARI SCBA TEPATNYA PROKSIMAL LIG-TREIZ • MELENA YAITU BUANG AIR BESAR BERWARNA HITAM • PROKSIMAL LIG- TREIZ Y.I.MULAI PROKSIMAL YEYUNUM- ESOPAGUS HEMATEMESIS-MELENA • WARNA DARAH TERGANTUNG JML AS-LAMBUNG YG ADA DAN LAMANYA KONTAK DGN DARAH. • HITAM SEPERTI TER ATAU ASPAL BILA BERCAMPUR AS- LAMBUNG, SHG TERJADI OKSIDASI DR HB YG BERCAMPUR DGN ENZYM PENCERNA’AN MENJADI HEMATIN. MAROON STOOLS • FAESES WARNA MERAH KEHITAMAN AKIBAT PERDARAHAN SCBB TERUTAMA DAERAH KOLON KANAN ATAU DAERAH ILOSEKAL. KRITERIA DIAGNOSIS/PENDEKATAN KLINIK • MUNTAH DAN BAB WARNA HITAM #DICARI RIWAYAT PENYAKIT# • SINDROM DISPEPSIA,RWYT MINUM OBAT,JAMU PEGEL LINU-ALKOHOL • K.U.PEND-: SAKIT-RINGAN SAMPAI BERAT,DPT DISERTAI KESADARAN • DAPAT TERJADI SYOK HIPOVOLEMIK :TAKIKARDI,PUCAT,AKRAL DINGIN,APATIS- MENINGGAL ETIOLOGI • 1 PECAH VARISES ESOPAGUS ±70% • 2 GASTROPATI HIPERTENSI PORTAL • 3 GASTRITIS EROSIF • 4 TUKAK PEPTIK • 5 TUKAK STRESS • 6 ROBEKAN MALLORY WEISS • 7 KEGANASAN SCBA • 8 PENYAKIT SISTEMIK • DIF-DIAGN:HEMOPTOE, HEMATOKHEZIA PEMERIKSAAN PENUNJANG • LAB-: DPL(HB,HT,TROMBOSIT),CT,BT, • K,Na,Cl, LFT:SGOT,SGPT,HEPATITIS B/C,ALBUMIN-GLOBULIN • ENDOSKOPI • OMD FOTO,JIKA ENDOS- TDK BISA • BILA PERLU: USG,CT SCAN ATAU FOTO DADA PENATALAKSANAAN • NON FARMAKOLOGIS • FARMAKOLOGIS NON FARMAKOLOGIS • PENYULUHAN • TIRAH BARING • PUASA SAMPAI PERDARAHAN STOP • NUTRISI PARENTERAL TOTAL DHI,DHII,DHIII,DHIV ATAU DLI,DLII DLIII,DLIV JIKA PERDARAHAN DIDUGA NON VARISES FARMAKOLOGIS • TRANFUSI DARAH PRC /WB • INFUSCAIRAN Sbb:JIKA SYOK DITEMUKAN POSISI BERBARING,KEHILANGAN CAIRAN ±50%: 1JAM I GUYUR, TD SISTOLIK>100 TTSAN CAIRAN SESUAI KONDISI PASIEN. JK SYOK POSISI DUDUK, KEHILANGAN CAIRAN ± 30%, CAIRAN GUYUR 2 KOLF, BILA TD >100 SISTOLIK, TTS SESUAI KONDISI PASIEN . • PS NGT,KUMBAH LAMBUNG DGN AIR ES, PS MONITOR CVP JK MUNGKIN. UTK NON VARISES: 1.INJEKSI H2 BLOKER/PPI. 2. SITOPROTEKTOR. • BILA ADA GGUAN HEMOSTASIS : OBATI SESUAI KELAINAN, FIBRINO LISIS: AS.TRANEKSAMAT,DEF-FAK TOR PEMBEKUAN:FFP DLL, DIC: HEPARIN. • UTK PENYEBAB VARISES/PENYAKIT HATI: LAKTULOSE 4X1C, NEOMISIN 4X500 MG. • PROPANOLOL 2X10MG, ISDN 3X10MG. • JIKA MAMPU DAPAT DIBERIKAN SOMATOSTATIN BOLUS 250 UG +DRIP 3000 µg DALAM 12 JAM SAMPAI PERDARAHAN STOP. TINDAKAN KHUSUS • PEMASANGAN BALON SB-TUB • ENDOSKOPI • TINDAKAN BEDAH: EMERGENSI JIKA GAWAT I : 8 JAM PERTAMA TRANFU SI > 2L DAN GAWAT II: 24 JAM PERTA MA PERLU 2 LITER LEBIH. GAWAT III-ELEKTIF JIKA 3X24 JAM PERDARAHAN (+) KOMPLIKASI • SYOK HIPOVOLEMIK • ASPIRASI PNEUMONIA • GAGAL GINJAL AKUT • SINDROM HEPATORENAL • KOMA HEPATIKUM • ANEMIA HEMATOCHEZIA • PERDARAHAN WARNA MERAH. • UMUMNYA SEGAR, KADANG AGAK SEDIKIT MERAH TUA ETIOLOGI • 1.KOLITIS ULCERATIF • 2. DIVERTIKULOSIS KOLON • 3.ANGIODISPLASIA • 4. TUMOR KOLON • 5. KOLITIS CROHN • 6. HEMORROID GEJALA KLINIS • UMUMNYA B A B DARAH SEGAR • KADANG KOLIK (KOLITIS) • KADANG BERCAMPUR LENDIR • DIARE • ANEMIA DIAGNOSIS • KOLONOSKOPI • FOTO KOLON DENGAN KONTRAS GANDA • ARTERIOGRAFI KOMA HEPATIKUM • DAPAT TIMBUL AKIBAT PENYAKIT HATI YG BERAT AKUT ATAU KRONIS • AKUT: TERUTAMA AKIBAT KERUSAKAN SEL HATI YANG LUAS • KRONIK: KERUSAKAN SEL + FAKTOR PENCETUS (ENDOGEN ) DEFINISI • SINDROMA NEUROPSIKIATRIK YG DI TANDAI DENGAN PERUBAHAN KESADARAN, PENURUNAN INTELEKTUAL DAN KELAINAN NEUROLOGIS YG DAPAT TERJADI SECARA SPONTAN ATAU PASCA BEDAH.DITEMUKAN PD KEGAGA LAN SEL HATI AKUT/KRONIK,PSE DGN ATAU TANPA SIRKULASI KOLATERL PATOGENESIS 1.MERUPAKAN GGUAN PROSES METABOLIK DAN NEUROFISIOLOGIK,TANPA DISERTAI LESI STRUKTURAL OTAK . 2.MRPKAN KELAINAN YG DIPENGARUHI BERBAGAI FAKTOR.DPT OLEH INTERAKSI SECARA SINERGIS PADA OTAK: AMONIA,AS.LEMAK RANTAI PDK/PANJANG.MERKAPTAN,GGUAN KESEIMBANGAN AS. AMINO DAN NEURO TRANSMITER. PD PSE . BEBERAPA ZAT PE RUSAK SPT AZOTEMA,INFEKSI DAN ALKALOSIS HIPOKA LEMI DPT BEKERJA SAMA DGN TOKSIN2 YG DI DUGA SBG PENCETUS KOMA HEPATIKUM • 3 MEKANISME YG DIDUGA MENDA SARI KOMA HEPATIKUM YAITU: PERUBAHAN ENERGI MET- OTAK,GGUAN FUNGSI MEM BRAN NEURON,PERUBAHAN TRANSMISI SINAPTIK SBGAI AKIBAT GANG GUAN NEUROTRANSMITER OTAK . INI MEMPUNYAI EFEK MENGHAMBAT TRANMISI IMPULS. FAKTOR PENCETUS PSE • 1 AZOTEMIA • 2 SEDATIF,TRANSQUILIZER,ANALG- • 3 PERDARAHAN G.I. • 4 ALKALOSIS METABOLIK • 5 PROTEIN YG BERLEBIHAN • 6 INFEKSI • 7 OBSTIPASI TOKSIN PENYEBAB K. H. • 1.AMONIA • 2.MERKAPTAN • 3.ASAM ASAM LEMAK • 4.BERBAGAI MACAM ASAM AMINO • 5.SUBSTANSI LAIN ( BENZODIAZE PIN LIKE SUBSTANCE ) GAMBARAN KLINIS • 1 TINGKAT PRODROMAL • 2 IMPENDING KOMA • 3 TINGKAT STUPOR • 4 KOMA YANG DALAM DIAGNOSIS K.H. 1.ADANYA KELAINAN NEURO PSIKIA- TRIK,TREMOR,FLAPING TREMOR,EEG 2.ADA TANDA GAGAL HATI 3.ADA FAKTOR PENCETUS 4.AMONIA YG MENINGKAT DIAGNOSA BANDING • 1 KOMA UREMIA/DIABETIKUM • 2 KOMA AKIBAT OBAT2AN • 3 TRAUMA KEPALA • 4 TUMOR OTAK • 5 EPILEPSI PENATALAKSANAN • OBATI PENYAKIT DASAR • HILANGKAN FAKTOR PENCETUS • CEGAH/KURANGI PEMBTK /INFLUK TOKSIN NITROGEN KEDALAM OTAK • MENJAGA KECUKUPAN KALORI,ME NGOBATI KOMPLIKASI KEGGLN HA TI:HIPOGLIKEMI,PERDRH SAL-CERNA ATUR KESEIMBANGAN ELEKTROLIT PROGNOSIS • PADA PSE,DGN PENGOBATAN STAN DAR,80% SADAR.BURUK JIKA ADA IKTERIK,ASITES,ALBUMIN RENDAH • KH PD HEPATITIS FULMINAN HANYA 20% YG BISA SADAR DI PRWT YG SUDAH MAJU.DI NEGARA YG BELUM MAJU HAMPIR 100% MENINGGAL. BAHAN BACA’AN • 1.AKIL,HAM,KOMAHEPATIK,DALAM BUKU AJAR I.P.DALAM JILID I EDISI 3 ED- SAYAIFULLAH NOER,JKT,BALAI PENERBIT FKUI,1997,300-3009 • 2 PENATALAKSAAN KEDARURATAN DIBIDANG I.P.DALAM,PUSAT INFORMASI DAN PENERBIT BG I.P.DALAM FKUI, 2000 • 3SIMPOSIUM PENATALAKSANAAN KEDARURATAN DI BIDANG I.P.DALAM,ED- IDRUS ALWI DKK,B.P.FKUI,2002 • 4 GASTROENTEROLOGI HEPATOLOGI,ED- ALI SULAIMAN DKK,CV AGUNG SETO 1997,8-14 Acute pancreatitis : Sudden Severe abdominal pain Systemic upset Varies : Clinically mild to fulminating disease cause sudden death Aetiological factors in acute pancreatitis Cholelithiasis Microlithiasis Alcohol Trauma (blunt and penetrating) Endoscopic retrograde cholangiopancrea- tography Obstruction (ampullary stenosis, duodenal diverticulum, neoplasm, parasites) ¤ ¤ ¤ ¤ ¤ ¤ Hypercalcaemia Hypertriglyceridaemia (types I and V) Infection (coxsackievirus, mumps, Mycoplasma) Ischaemia (vasculitis, hypotension) Hypothermia Cardiopulmonary bypass Drugs1 Miscellaneous (scorpion bite, hereditary, pregnancy) Aetiological factors in acute pancreatitis ¤ ¤ ¤ ¤ ¤ ¤ ¤ ¤ ¤ Cholelithiasis - pressure pancreatic duct obstructing stone Alcohol - interfering the tone of sphincter of Oddi - toxin - acinar cells or - trigger autodigestion. 3 phases : 1. Local inflammation 2. Systemic inflammation 3. Sepsis pain vomiting dehydration epigastric tenderness confusion (a result of hypoxia) hypovolaemic shock jaundice (10-20%) Grey - Turner/Cullen sign (discoloration of the flanks and/or periumbilical area, < 5%). C C C C C C C C Serum amylase/ lipase Other biochemical tests Radiology Ultrasonography CT _ _ _ _ _ Early administration of improved a. biotik Cytokine inhibitors Endoscopic/ surgical techniques Treat complication reduced mortality rate 5% - 10% 4 4 4 4 Critical anatomic areas : 4 1. The gland’s 2. Relationship pancreas - duodenal loops & greater curvature and splenic flexure 3. Common bile duct and pancreatic duct 4. Ductal acinar and islets of langerhans Anatomic abnormalities : 2 1. Pancreas divisum 2. Annular pancreas Etiology & severity of the attack ex : alcohol induced pancreatitis gallstones 4 4 Abdominal pain with fever or abdominal mass Vomiting constipation diarrhea _ _ 4 4 4 4 1. Alcohol and gallstones 2. Medications 3. Cancer of the pancreas 4. ERCP 5. Idiopathic pancreatitis 6. Other causes Duct obstruction Direct toxic effect on acinar cells Neurohormonal mechanisms Vascular insufficiency Enzyme - cytokine cascade E E E E E Cellular changes only Edematous pancreatitis Necrotic and hemorrhagic pancreatitis Infected necrosis E E E E Hormonal pancreatic stimuli 1. Secretion volume and bicarbonate 2. Cholecystokinin (CCK) enzymes Alcohol p.o / I.V Vagal or local release CCK ampullary spasm/ excessive enzym secretion for for Ranson’s Signs Ranson’s early objective sign (1974) Alcohol and other Gallstone 0 h Age > 55 y > 70 y Leukocyte count > 16,000 mm > 18,000 mm Blood sugar > 200 mg/100 mL > 220 mg/100 mL LDH > 350 U/L > 250 U/L AST > 250 U/L > 250 U/L 48 h HCT < 10% < 10% BUN > 5 mg/100 mL 2 mg/100 mL Ca 2+ < 8 mg/100 mL < 8 mg/100 mL P0 < 60 mmHg - Base deficit > 4 mEq/L > 5 mEq/L Fluid sequestration > 6000 mL > 4000 mL Bank’s Criteria Bank’s clinical criteria (1983) Cardiac Shock, tachycardia > 130, arrhytmia, EcG changes Pulmonary Dyspnea, rates P0 < 60, adult respiratory distress syndrome Renal Urine output < 50 mL/h, rising BUN or serum creatinine level Metabolic Low or falling Ca2+, pH, serum albumin decrease Hematologic Falling HCT, diffuse intravascular coagulation (low platelets, split products) Neurologic disease On physical (Grey Turner, Cullen) signs or peritoneal tap Tense distention Severe ileus, fluid ++ Causes of Hyperamylasemia Acute Atdominal Emergencies Penetrating peptic ulcer Acute cholecystitis with hyperamylasemia Intestinal obstruction with strangulation Intestinal infarction Ruptured aortic aneurysm or dissection Ruptured ectopic pregnancy Acute salpingitis Tonsion of ovarian cyst or carcinoma Abdominal trauma with hematoma formation Perforated diverticulitis Postgastrectomy afferent loop obstruction Chrohn’s disease Causes of Hyperamylasemia Physiologic Pregnancy ? Genetic S hyperamylasemia Protein-Bound Hyperamylasemia Inborn macroamylasemia attached to albumin or globulin (macroamylase) IgA-bound : chronic disease, lymphoma, IPSID IgG-bound : chronic infections, liver disease Immune-complex-bound : AIDS, collagen disease, Sjogren’s syndrome Decreased Excretion of Amylase Acute and chronic renal failure Benefits of Treatment Options Definite benefits Possible benefit Experimental benefit ICU therapy Dextran 60 O-Radical scavengers Surgery Peritoneal lavage (allopurinol, dismutase, for complications for 7 days and catalase) Angiography Antibiotics, Interleukins 10, 11, for bleeding antifungals TNF- antibody Octreotide Calcium channel blockers Gabexate ERCP and stone removal Platelet factor inhibitor (Lexipifant) Differential Diagnosis of Acute Pancreatitis Ethanol Gallstones Choledocholelithiasis Billiary sludge Microlithiasis Mechanical/structural injury Sphincter of Oddi dysfunction Pancreas divisum Trauma Post-endoscopic retrograde cholangiopancreatography Pancreatic malignancy Peptic ulcer disease Inflammatory bowel disease Medications Azathioprine/6-mercaptopurine Dideoxyinosine Pentamidine Sulfonamides L- Asparaginase Thiazide diuretics Differential Diagnosis of Acute Pancreatitis Metabolic Hyperlipidemia Hypercalcemia Infectious Viral Bacterial Parasitic Vascular Vasculitis Atherosclerosis Miscellaneous Scorpion bite Heretary pancreatitis Idiopathic pancreatitis Cystic fibrosis Coronary bypass Tropical pancreatitis Prognostic Criteria for Acute Pancreatitis RANSON CRITERIA SIMPLIFIED GLASGOW CRITERIA On admission Within 48 hrs of admission Age > 55 yrs Age > 55 yrs Leukocyte count > 16,000/ l Leukocyte count > 15,00/ l Lactate dehydrogenase > 350 IU/liter Lactate dehydrogenase > 600 IU/liter Glucose > 200 mg/dl Glucose > 180 mg/dl Aspartate aminotransferase Albumin < 3,2 g/dl > 250 IU/liter Calcium < 8 mg/dl Arterial Po2 < 60 mmHg Serum urea nitrogen > 45 mg/dl 48 hrs after admission Hematocrit decrease by > 10% Serum urea nitrogen increase by > 5 mg/dl Calcium < 8 mg/dl Arterial Po2 < 60 mmHg Base deficit > 4 mEq/liter Estimated fluid sequenstration > 6 liter Prognosis Ranson criteria simplified Glasgow criteria Prognostic accuracy : similar 2 or < : mortality < 1 % 3 - 5 : mortality 5 % 6 > : mortality 20 % Complication Severe peripancreatic fluid collections or pancreatic necrosis infected Prophylactic antibiotic - controversial Combination : quinolone & metronidazole ¤ ¤ Complications Pancreatic abscesses Pseudocyst 10% Several weeks - pain - compressing organs eroding mediastinum. > 5-6 cm 30% - 50% : rupture, hemorrhage, infection Persisten (> 6weeks), large, expanding drained surgical - endoscopie or percutaneous Somatostatin analog ocreotide : risk fistula formation pancreatic secretions Pulmonary processes Stress gastritis, renal failure, hypocalemia, delirium, disseminated fat necrosis Thrombosis - gastric varices & GI hemorrhage ¤ ¤ ¤ ¤ ¤ - - Supportive - most cases crystalloid Severe cases : volume replection colloids nutrition & electrolyte IV NOT ENTERALLY > 2 - 3 days : TPN P.E meperidine > morphine Sphincter of Oddi spasm NG suctioning - : intractable vomiting No evidence : routine antibiotics or somatostatin Reinitiate feeding : Not serum enzym fevels clinical status Resolution pain & emergence hunger ready to eat Gallstone pancreatitis : ERCP sphineterotomy & stone extraction Note : ERCP worsen pancreatitis. ¤ ¤ Mild gallstone : conservativelly ERCP : after recovery to asses retained bile duct stones Risk recurrent gallstone ------- 33% definitive surgical therapy. Poor operative risk : endoscopic sphincterotomy without cholecyctectomy Common sequelae of acute pancreatitis Systemic Local Manifestation Complication Hypovolemia Hypocalcemia Hyperglycemia Coagulopathy Hepatic dysfunction Respiratory failure Cardiovascular insufficiency Renal failure Pain Nausea and vomiting Pancreatic enlargement Peripancreatic fluid Pancreatic infection Pseudocyst Gastric outlet obstruction Biliary obstruction ACUTE PANCREATITIS EDEMATOUS NECROTIZING (Interstitial) (Hemorrhagic) INFLAMMATORY MASS (Phlegmon) STERILE ABSCESS/ NECROSIS HEALING CHRONIC INFECTED PSEUDOCYST ABSCESS/NECROSIS PSEUDOCYST ABSCESS Pathologic classification of acute pancreatitis Hyperamylasemia & abdominal pain 1. Is the hyperamylasemia due to pancreatitis, another abdominal emergency or concomitant concidental disease ? 2. Is pancreatitis is present, how severe is the attack ? 3. What is the etiology of the pancreatitis and does it need urgent correction ? Assesment of Severity : 30% severe attack : hypotension tachycardia acidosis abdominal ileus hemorrhagic pancreatitis : Grey Turner’s sign or Cullen’s sign central loop distended bowel colon cutoff sign Ranson’s early objective signs (1974) Bank’s clinical criteria (1982) or signs of MOSF The Apache II physiologic score 4 4 4 Early mortality 2 - 7 days (extra-abdominal organ failure) Delayed mortality 7 - 21 days (intra-abdominal complications) Infected necrosis or abscess Non infected continued massive necrosis Gastrointestinal or intra-abdominal hemorrhage Cyst formation, ascites and massive pleural effusion ICU or in-hospital therapy 6-12 months 4 4 4 4 Transient minor complications Acute diabetes Peripheral fat necrosis Retinal changes SPECIAL TEST Serologic Test Other than Serum Amylase serum esterase phospholipase A 2 salivary (S) fractionation Serum Amylase pancreatic P isoenzym Serum lipase Computed Tomography Scan ERCP 4 4 4 ¤ ¤ ¤ ¤ E E E 2 definitive treatment periods Early Treatment 20% severe - ICU - anticipate extra-abdominal organ system failure NG suction nasal O 2 IAO (intake and output) frequent Serum electrolytes evaluation metabolic function E - - - - - in addition : blood reflacement dextran supp PE nutrition Antibiotic : Still uncertain now appears : is warranted Ulm (Germany) : bacterial colonization 5 th day of disease ¤ ¤ ¤ Administration antibiotik before imiperem and ciprofloxacin morbidity & perhaps mortality Star antibiotics early in the attack More spesific th/ : Peritoneal dialysis antitrypsin (eg. aprotinin or gabexate) ocreotide(universal inhibitor of secretion) - spesific centers - not yet gained wide acceptance. Multicenter trials England & USA : Cytokines & inhibitors : PAF inhibitor (lexipafant) morbidity & mortality ¤ ¤ ¤ OO Late Treatment Continuing Necrosis failed bacterial contamination “septic course” : ICU monitoring, a.biotik th/, TPN continued CT scans repeated some centers : Organ failure develop surgery (necrosectomy) difference mortality rates (30%) Infected necrosis or Abscess Gastrointestinal Hemorrhage Pancreatic cyst, Ascites and Pleural Effusion Transient Diabetes _ _ _ _ _ During the Attack Stop : alcohol & pancreatitis - producing drugs hyperlipidemia After the Attack Has Subsided Recurrent Attacks _ _ _ 80 % Acute attacks - mild episode 7 - 10 days 1 - 3 % progress to severe or complication 20 % acute attacks - severe 2 - 3% : 72 hours - MOF prolanged by PD U U 30 - 50% severe attack Mortality Long Island Yewish Medical Centre 13,5 % 1978 - 1982 8 % 1986 - 1990 Scottish and German 5 % dissappointoments < 5% -10% pat O O U Diagnosis ditegakkan dari adanya peningkatan amilase dan terapi ocreotide Penyakit yang mendasari relatif sama dengan penelitian lain : DM 4 penderita, batu bilier 3 penderita. Tidak didapatkan alkohol sebagai penyakit yang mendasari. Pengobatan dengan ocreotide menunjukkan hasil baik, namun perlu penelitian lebih lanjut secara prospektif.