gawat darurat gastro hepatologi

8/13/2019 Gawat Darurat Gastro Hepatologi

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GAWAT DARURAT

GASTRO ENTERO HEPATOLOGIDr.H.ALI IMRON YUSUF,

SpPD,FINASIM,KGEH

DIVISI GASTRO-HEPATOLOGIBAG- I. P. DALAM,FK.UNILA/

RSUD Dr.H.ABDUL MOELOEK

BANDAR LAMPUNG


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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


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HEMATEMESISMELENA

MERUPAKAN KEADAAN GAWATDARURAT DIBIDANG PENYAKIT

DALAM DENGAN ANGKAKEMATIAN YANG MASIH CUKUPTINGGI.

DI RSCM I987- 88 ANGKAKEMATIAN :26 %.

DI EROPA DAN A.S. 810 %


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DEFINISI

HEMATEMESIS ADALAH MUNTAHDARAH BERWARNA HITAM TER YG

BERASAL DARI SCBA TEPATNYAPROKSIMAL LIG-TREIZ

MELENA YAITU BUANG AIR BESARBERWARNA HITAM

PROKSIMAL LIG- TREIZ Y.I.MULAIPROKSIMAL YEYUNUM- ESOPAGUS


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HEMATEMESIS-MELENA

WARNA DARAH TERGANTUNG JMLAS-LAMBUNG YG ADA DAN

LAMANYA KONTAK DGN DARAH. HITAM SEPERTI TER ATAU ASPAL

BILA BERCAMPUR AS- LAMBUNG,

SHG TERJADI OKSIDASI DR HB YGBERCAMPUR DGN ENZYMPENCERNAAN MENJADI HEMATIN.


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MAROON STOOLS

FAESES WARNA MERAH KEHITAMAN

AKIBAT PERDARAHAN SCBB

TERUTAMA DAERAH KOLON KANAN

ATAU DAERAH ILOSEKAL.


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KRITERIA

DIAGNOSIS/PENDEKATAN

KLINIK MUNTAH DAN BAB WARNA HITAM

#DICARI RIWAYAT PENYAKIT#

SINDROM DISPEPSIA,RWYT MINUM OBAT,JAMUPEGEL LINU-ALKOHOL

K.U.PEND-: SAKIT-RINGAN SAMPAI BERAT,DPTDISERTAI KESADARAN

DAPAT TERJADI SYOK HIPOVOLEMIK:TAKIKARDI,PUCAT,AKRAL DINGIN,APATIS-MENINGGAL


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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


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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


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PENATALAKSANAAN

NON FARMAKOLOGIS

FARMAKOLOGIS


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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


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PS NGT,KUMBAH LAMBUNG DGN AIRES, PS MONITOR CVP JK MUNGKIN.

UTK NON VARISES: 1.INJEKSI H2BLOKER/PPI. 2. SITOPROTEKTOR.

BILA ADA GGUAN HEMOSTASIS :OBATI SESUAI KELAINAN, FIBRINOLISIS: AS.TRANEKSAMAT,DEF-FAKTOR PEMBEKUAN:FFP DLL, DIC:

HEPARIN.


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UTK PENYEBAB VARISES/PENYAKIT HATI:LAKTULOSE 4X1C, NEOMISIN 4X500 MG.

PROPANOLOL 2X10MG, ISDN 3X10MG.

JIKA MAMPU DAPAT DIBERIKAN

SOMATOSTATIN BOLUS 250 UG +DRIP 3000g DALAM 12 JAM SAMPAI PERDARAHANSTOP.


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TINDAKAN KHUSUS

PEMASANGAN BALON SB-TUB

ENDOSKOPI

TINDAKAN BEDAH: EMERGENSI JIKAGAWAT I : 8 JAM PERTAMA TRANFUSI > 2L DAN GAWAT II: 24 JAM PERTA

MA PERLU 2 LITER LEBIH. GAWATIII-ELEKTIF JIKA 3X24 JAMPERDARAHAN (+)


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KOMPLIKASI

SYOK HIPOVOLEMIK

ASPIRASI PNEUMONIA

GAGAL GINJAL AKUT

SINDROM HEPATORENAL

KOMA HEPATIKUM ANEMIA


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HEMATOCHEZIA

PERDARAHAN WARNA MERAH.

UMUMNYA SEGAR, KADANG AGAK

SEDIKIT MERAH TUA


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ETIOLOGI

1.KOLITIS ULCERATIF

2. DIVERTIKULOSIS KOLON

3.ANGIODISPLASIA

4. TUMOR KOLON

5. KOLITIS CROHN 6. HEMORROID


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GEJALA KLINIS

UMUMNYA B A B DARAH SEGAR

KADANG KOLIK (KOLITIS)

KADANG BERCAMPUR LENDIR

DIARE

ANEMIA


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DIAGNOSIS

KOLONOSKOPI

FOTO KOLON DENGAN KONTRAS

GANDA

ARTERIOGRAFI


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KOMA HEPATIKUM

DAPAT TIMBUL AKIBAT PENYAKIT

HATI YG BERAT AKUT ATAU KRONIS

AKUT: TERUTAMA AKIBATKERUSAKAN SEL HATI YANG LUAS

KRONIK: KERUSAKAN SEL + FAKTOR

PENCETUS (ENDOGEN )


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DEFINISI

SINDROMA NEUROPSIKIATRIK YG DI

TANDAI DENGAN PERUBAHAN

KESADARAN, PENURUNAN INTELEKTUALDAN KELAINAN NEUROLOGIS YG DAPAT

TERJADI SECARA SPONTAN ATAU PASCA

BEDAH.DITEMUKAN PD KEGAGA LAN SEL

HATI AKUT/KRONIK,PSE DGN ATAUTANPA SIRKULASI KOLATERL


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PATOGENESIS

1.MERUPAKAN GGUAN PROSES METABOLIK DANNEUROFISIOLOGIK,TANPA DISERTAI LESI

STRUKTURAL OTAK .2.MRPKAN KELAINAN YG DIPENGARUHI BERBAGAI

FAKTOR.DPT OLEH INTERAKSI SECARASINERGIS PADA OTAK: AMONIA,AS.LEMAKRANTAI PDK/PANJANG.MERKAPTAN,GGUANKESEIMBANGAN AS. AMINO DAN NEUROTRANSMITER. PD PSE . BEBERAPA ZAT PE RUSAKSPT AZOTEMA,INFEKSI DAN ALKALOSIS HIPOKALEMI DPT BEKERJA SAMA DGN TOKSIN2 YG DI

DUGA SBG PENCETUS KOMA HEPATIKUM


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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 . INIMEMPUNYAI EFEK MENGHAMBAT

TRANMISI IMPULS.


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FAKTOR PENCETUS PSE

1 AZOTEMIA

2 SEDATIF,TRANSQUILIZER,ANALG-

3 PERDARAHAN G.I.

4 ALKALOSIS METABOLIK

5 PROTEIN YG BERLEBIHAN

6 INFEKSI

7 OBSTIPASI


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TOKSIN PENYEBAB K. H.

1.AMONIA

2.MERKAPTAN

3.ASAM ASAM LEMAK

4.BERBAGAI MACAM ASAM AMINO

5.SUBSTANSI LAIN ( BENZODIAZE

PIN LIKE SUBSTANCE )


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GAMBARAN KLINIS

1 TINGKAT PRODROMAL

2 IMPENDING KOMA

3 TINGKAT STUPOR

4 KOMA YANG DALAM


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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


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DIAGNOSA BANDING

1 KOMA UREMIA/DIABETIKUM

2 KOMA AKIBAT OBAT2AN

3 TRAUMA KEPALA

4 TUMOR OTAK

5 EPILEPSI


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PENATALAKSANAN

OBATI PENYAKIT DASAR

HILANGKAN FAKTOR PENCETUS

CEGAH/KURANGI PEMBTK /INFLUKTOKSIN NITROGEN KEDALAM OTAK

MENJAGA KECUKUPAN KALORI,ME

NGOBATI KOMPLIKASI KEGGLN HATI:HIPOGLIKEMI,PERDRH SAL-CERNAATUR KESEIMBANGAN ELEKTROLIT


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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 BELUMMAJU HAMPIR 100% MENINGGAL.


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BAHAN BACAAN

1.AKIL,HAM,KOMAHEPATIK,DALAM BUKUAJAR I.P.DALAM JILID I EDISI 3 ED-SAYAIFULLAH NOER,JKT,BALAI PENERBITFKUI,1997,300-3009

2 PENATALAKSAAN KEDARURATAN DIBIDANGI.P.DALAM,PUSAT INFORMASI DAN PENERBITBG I.P.DALAM FKUI, 2000

3SIMPOSIUM PENATALAKSANAANKEDARURATAN 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


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Acute pancreatitis :

Sudden

Severe abdominal painSystemic upset

Varies : Clinically mild to fulminating

disease cause sudden

death


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Aetiological factors in acute pancreatitis

Cholelithiasis

Microlithiasis

AlcoholTrauma (blunt and penetrating)

Endoscopic retrograde cholangiopancrea-

tographyObstruction (ampullary stenosis, duodenal

diverticulum, neoplasm, parasites)


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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


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Cholelithiasis - pressure pancreatic ductobstructing 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


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painvomiting

dehydration

epigastric tendernessconfusion (a result of hypoxia)

hypovolaemic shock

jaundice (10-20%)

Grey - Turner/Cullen sign (discoloration of

the flanks and/or periumbilical area, < 5%).


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Serum amylase/ lipase

Other biochemical tests

Radiology

Ultrasonography

CT


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Early administration of improved a. biotik

Cytokine inhibitors

Endoscopic/ surgical techniques

Treat complication

reduced mortality rate 5% - 10%


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Critical anatomic areas : 41. The glands

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 : 21. Pancreas divisum

2. Annular pancreas


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Etiology & severity of the attack

ex : alcohol induced pancreatitis

gallstones


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Abdominal pain with

fever or

abdominal mass

Vomiting

constipation

diarrhea


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1. Alcohol and gallstones

2. Medications

3. Cancer of the pancreas

4. ERCP

5. Idiopathic pancreatitis6. Other causes


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Duct obstruction

Direct toxic effect on acinar cells

Neurohormonal mechanisms

Vascular insufficiencyEnzyme - cytokine cascade


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Cellular changes only

Edematous pancreatitis

Necrotic and hemorrhagic pancreatitis

Infected necrosis


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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


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Ransons Signs

Ransons 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/LAST > 250 U/L > 250 U/L

48 h HCT < 10% < 10%

BUN > 5 mg/100 mL 2 mg/100 mL

Ca2+ < 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


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Banks Criteria

Banks 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 ++


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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

Chrohns disease


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Causes of Hyperamylasemia

Physiologic

Pregnancy

? Genetic S hyperamylasemia

Protein-Bound Hyperamylasemia

Inborn macroamylasemia attached to albumin orglobulin (macroamylase)

IgA-bound : chronic disease, lymphoma, IPSID

IgG-bound : chronic infections, liver disease

Immune-complex-bound : AIDS, collagen disease,Sjogrens syndrome

Decreased Excretion of Amylase

Acute and chronic renal failure


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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)

Diff ti l Di i f A t P titi


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Differential Diagnosis of Acute Pancreatitis

EthanolGallstones

CholedocholelithiasisBilliary sludgeMicrolithiasis

Mechanical/structural injury

Sphincter of Oddi dysfunctionPancreas divisumTraumaPost-endoscopic retrograde cholangiopancreatographyPancreatic malignancyPeptic ulcer diseaseInflammatory bowel disease

MedicationsAzathioprine/6-mercaptopurine DideoxyinosinePentamidineSulfonamides

L-Asparaginase

Thiazide diuretics


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Differential Diagnosis of Acute Pancreatitis

Metabolic

Hyperlipidemia

Hypercalcemia

Infectious

Viral

Bacterial

ParasiticVascular

Vasculitis

Atherosclerosis

Miscellaneous

Scorpion bite

Heretary pancreatitis

Idiopathic pancreatitis

Cystic fibrosis Coronary bypass

Tropical pancreatitis

Prognostic Criteria for Acute Pancreatitis


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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/dlArterial Po2 < 60 mmHg

Serum urea nitrogen > 45 mg/dl

48 hrs after admission

Hematocrit decrease by > 10%

Serum urea nitrogen increaseby > 5 mg/dl

Calcium < 8 mg/dl

Arterial Po2 < 60 mmHg

Base deficit > 4 mEq/liter

Estimated fluid sequenstration > 6 liter


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PrognosisRanson criteriasimplified Glasgow criteria

Prognostic accuracy : similar

2 or < : mortality < 1 %

3 - 5 : mortality 5 %

6 > : mortality 20 %

Complication

Severe peripancreatic fluid collectionsor pancreatic necrosis

infected

Prophylactic antibiotic - controversial

Combination : quinolone & metronidazole

Complications


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Complications

Pancreatic abscessesPseudocyst 10%

Several weeks - pain - compressing organseroding mediastinum.

> 5-6 cm 30% - 50% :rupture, hemorrhage, infection

Persisten (> 6weeks), large, expandingdrained surgical - endoscopie or

percutaneous

Somatostatin analog ocreotide :

risk fistula formation pancreatic secretionsPulmonary processesStress gastritis, renal failure, hypocalemia, delirium,

disseminated fat necrosisThrombosis - gastric varices & GI hemorrhage


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Supportive - most casescrystalloid

Severe cases : volume replection colloids

nutrition & electrolyte IV NOT ENTERALLY

> 2 - 3 days : TPNP.E meperidine > morphine

Sphincter of Oddi spasmNG suctioning - : intractable vomiting

No evidence : routine antibiotics or somatostatinReinitiate feeding : Not serum enzym fevels

clinical statusResolution pain & emergence hunger ready to eat

Gallstone pancreatitis : ERCP sphineterotomy & stone extraction

Note : ERCP worsen pancreatitis.


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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


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Common sequelae of acute pancreatitis

Systemic Local

Manifestation

Complication

Hypovolemia

Hypocalcemia

Hyperglycemia

Coagulopathy

Hepatic dysfunction

Respiratory failure

Cardiovascular

insufficiencyRenal failure

Pain

Nausea and

vomiting

Pancreatic

enlargement

Peripancreatic fluid

Pancreatic infection

Pseudocyst

Gastric outletobstruction

Biliary obstruction


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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 ?


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Assesment of Severity :

30% severe attack :hypotension

tachycardia

acidosis

abdominal ileushemorrhagic pancreatitis : Grey Turners sign

or Cullens sign

central loop distended bowel

colon cutoff signRansons early objective signs (1974)

Banks clinical criteria (1982) or signs of MOSF

The Apache II physiologic score


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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

Transient minor complications


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Transient minor complications

Acute diabetes

Peripheral fat necrosisRetinal changes

SPECIAL TEST

Serologic Test Other than Serum Amylase

serum esterasephospholipase A 2

salivary (S)

fractionation Serum Amylase

pancreatic Pisoenzym

Serum lipase

Computed Tomography Scan

ERCP


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2 definitive treatment periods

Early Treatment

20% severe - ICU - anticipate

extra-abdominal organ system failure

NG suction

nasal O2

IAO (intake and output)

frequent Serum electrolytes

evaluation metabolic function


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in addition : blood reflacement

dextran suppPE nutrition

Antibiotic : Still uncertainnow appears : is warranted

Ulm (Germany) : bacterial colonization5thday of disease

Ad i i t ti tibi tik b f


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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

Late Treatment


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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 AbscessGastrointestinal Hemorrhage

Pancreatic cyst, Ascites and Pleural Effusion

Transient Diabetes


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During the Attack

Stop : alcohol & pancreatitis - producingdrugs hyperlipidemia

After the Attack Has Subsided

Recurrent Attacks


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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


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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


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Diagnosis ditegakkan dari adanya peningkatanamilase dan terapi ocreotide

Penyakit yang mendasari relatif sama dengan

penelitian lain : DM 4 penderita, batu bilier 3penderita. Tidak didapatkan alkohol sebagai

penyakit yang mendasari.

Pengobatan dengan ocreotide menunjukkanhasil baik, namun perlu penelitian lebih lanjut

secara prospektif.

gawat darurat gastro hepatologi

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