Et. 2.Perdarhan Saluran Cerna

7/28/2019 Et. 2.Perdarhan Saluran Cerna

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Dr. LEONARDO DAIRY, SpPD KGEH


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INTRODUCTION

PSCBA (UGI BLEEDING)

PSCBB (LGI BLEEDING)

OCCULT BLEEDING

OBSCURE BLEEDING


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Gastrointestinal (GI) bleeding is an extremely

common clinical problem

resulting in significant morbidity, mortality, and cost.There are over 300,000 hospitalizations annually in theUnited States for GI bleeding, accounting for 12% of

all hospital admissions. A conservative estimate of the overall annual cost of

hospital admissions for GI bleeding is $900 million, butthe true overall cost, including outpatient endoscopic

and radiologic investigations, clinic visits, and work dayslost, far exceeds.


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Upper GI bleeding (UGI) Incidence of UGI is approximately 100 cases per 100,000

population.Acid peptic disease (e.g., gastric,duodenal ulcers andgastritis) is the most common cause of upper GI bleeding,accounting for 5075% of all cases). Acid peptic disease isfollowed by variceal bleeding, gastric and duodenal erosivedisease, and Mallory-Weiss tears in prevalence. Furthermore, thepredominance of peptic ulcer bleeding has not been affected bythe advent of improved acid suppression with medical therapy.

The elderly appear to be at particular risk, as the proportion ofelderly patients who present with upper GI bleeding has steadily

increased, with persons older than age 60 years accounting for3545% of all cases. This increase cannot be explained bydemographics alone, as increasing age directly correlates with anincreased rate of hospitalization for upper gi bleeding.

.


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Lower GI bleeding less common, around 2027 per 100,000 .

80% of patients with GI bleeding pass heme per rectum as bright red blood,

maroon stools, or melena, only 24% of all GI bleeding is from a lower GI

source. The incidence of LGI bleeding is higher in men and elderly .

The rate of hospitalization for LGI bleeding increases more than 200-fold

from the third to the ninth decades, probably because of an increased

incidence of the most common etiologies; diverticulosis, angiodysplasia,

and neoplasia in the elderly. In most studies, diverticulosis is the most

common cause of acute LGI bleeding, accounting for 4255% of cases.

However, in one large series of patients with severe, persistent

hematochezia, angiodysplasia was the most common diagnosis, accounting

for 30%. Other, less common etiologies include colorectal neoplasia,

colonic ischemia, IBDi, infectious causes, radiation proctitis,, iatrageniccauses (e.g. postpolypectomy, endoscope trauma, and so on),

intussusception, solitary rectal ulcer syndrome, colonic varices, and

endometriosis .Hemorrhoidal bleeding is probably the most prevalent cause

of acute GI bleeding in the ambulatory setting, accounting for up to 76% of

cases, but it represents only 2

9% of admissions for lower GI bleeding.


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Definition

Bleeding derived from any sourceproximal to the Ligament of Treitz

1 in 1000 in us who

experienced upper GI

bleedingMen :women

2 : 1

Mortality rate 10%


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PSCBA PERDARAHAN SEPANJANG SAL. CERNAPROK. DARI LIG.TREITZ.

KEGAWAT-DARURATAN

INSIDENS 50

100/100.000 PDDK (USA), 20.000KEMATIAN/TAHUN

TINGKAT MORTALITAS 10% - 36%, 33% (UK)

80% BERHENTI SPONTAN PERDARAHAN SALURAN CERNA ATAS

PERDARAHAN SALURAN CERNA ATAS

VARISESPERDARAHAN SALURAN CERNA ATAS

NON VARISES


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Sebuah studi meta analisis terapi endoskopi

pada PSCBA secara bermakna mengurangifrekuensi perdarahan lanjut, pembedahan danmortalitas.

Angka morbiditas dan mortalitas juga sangatdipengaruhi oleh bagaimana optimalnyatatalaksana kasus dalam 24-48 jam pertama di

sarana pelayanan kesehatan.

Sass AD, Chopra KB. Portal hypertension and variceal hemorrhage. Med Clin N Am. 2009;93:83753.


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CAUSE OF GI BLEEDING

Common causesGastric ulcer, Duodenal ulcer

Esophageal varices

Mallory-Weiss tear

Rare causes

Esophageal ulcer, Erosive duodenitis

Aortoenteric fistula, Hemobilia

Pancreatic sources

Crohns disease

No lesion identified

Less Frequent Causes

Dieulafoys lesion

Vascular ectasia

Portal hypertensive gastropathy

Gastric antral vascular ectasiaGastric varices

Neoplasia

Esophagitis

Gastric erotions

Rare Causes


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o

AINS

Aspirin

Gastric Acid

Helicobacter pylori Anti-koagulan

Anti-trombotik

Merokok

Alkohol

Penyakit hati kronik

Rockey DC. Gastrointestinal bleeding. Gastroenterol Clin N Am. 2005;34:5818.


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CLINICAL PRESENTATION

HEMATEMESIS :

MUNTAH DARAH WARNA MERAH KECOKLAT COKLATAN KEHITAM HITAMAN (CAFFEIN)

MELENA :

BAB WARNA HITAM (TERRY STOOL) >50CC DARAH

HAEMATOCHEZIA :

BAB WARNA MERAH TERANG GELAP

OCCULT BLEEDING :

TDK ADA PERUBAHAN WARNA BAB, NAMUN BENZIDINETEST (+)


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1. PERDARAHAAN ANAMNESE RIWAYAT COMMON

VOMITING (MENTAL)MALLORYWEISS TEAR ?

HEARTBURN & REGURGITASI REFLUX ESOFAGITIS ?

DYSFAGIA & BBMALIGNANCY PD ESOFAGUS ?

MAKAN OBAT-OBATAN & ALKOHOLGASTRIC EROSIVE ?

ULKUS PEPTIKUM ?

LIVER STIGMATA (CH) VARICES BLEEDING ?

PENYAKIT BERAT (DI ICU) STRESS ULCER ?

DIAGNOSTIK


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GAMBARAN KLINIK

Hematemesis + Melena PSCBA esofagus &gaster

Melena PSCBA duodenum

Berat ringannya perdarahan dinilai dari :

manifestasi klinik yang ada

derajat turunnya kadar hemoglobin, ada tidaknya manifestasi gangguan

hemodinamik.


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2. PEMERIKSAAN FISIK :

Penilaian status hemodinamik & resusitasi Jaundice & Tanda2 liver stigmata & HT portal

Bleeding diathesis : purpura, ekimosis, ptikiae

3. RADIOLOGI

Ba. Swallow, Ba. Follow Through, MDF double contras, Kolon in loop.

Upper & Lower Abdominal Scanning

4. ENDOSKOPI

Gastroduodenoskopi Sigmoidoskopi

Colonoskopi

Push Enteroskopi

Capsule Endoscopy


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Historical Features Important in Assesing the

Etiology of Gastrointestinal Bleeding

Age

Prior Bleeding

Previous gastrointestinal disease

Previous surgery

Underlying medical disorder (especialy liver disease)

Nonsteroidal anti-inflammatory drugs/aspirin

Abdominal pain

Change in bowel habits

Weight loss/anorexia

History of oropharyngeal disease


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Diagnosis

Pemeriksaan fisik

Tanda vital syok?

Stigmata penyakit hatikronik

Ikterus

Hepatomegali

Asites

Spider angioma

Palmar erythema

Pemeriksaan laboratorium

DPL

Prothrombin time

INR

Fungsi hati



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INITIAL PATIENT ASSESMENT

hemodynamics Blood loss (%) Severity of bleed

(vital signs) (fraction of

intravascularvolume)

Shock (Restinghypotension)

Postural(Orthostatictac

hycardia/hypotension)

Normal

20-25

10-20


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HEMORRHAGIC I II III IV

CLASS 15% OR 20-25% OR 30-35% OR 40-50% OR

BLOOD LOSS 750 ML 1000-1250 ML 1500-1800ML 2000-2500 ML

HEART RATE 100 >120 >140

RESPIRATORY 14-19 20-29 30-40 >40

RATEARTERIAL NORMAL 110-80 70-60


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Aspirasi nasogastrik

Membedakan perdarahan

saluran cerna atas danbawah

Sensitivitas 79%,spesifisitas 55%

Modalitas diagnostik danterapeutik

Townsend: Sabiston Textbook of Surgery, 18th ed. 2007.


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Diagnosis

Esofagogastroduodenoskopi (EGD)

Modalitas utama

Menentukan lokasi & penyebab perdarahan saluran

cerna atas: 90% - 95%



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Forrest class Type of lesion Risk of rebleed ifuntreated (%)

I a Arterial Spurting 100

I b Arterial Oozing 17-100

II a Visible Vessel 8-81

II b Sentinel Clot 14-36

II c Haematin covered flat spot 0-13

III No Stigmata 0-10

Tabel 2. KLASSIFIKASI FORRESTPSCBA


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MANAGEMENT

RESUSCITATION

VASCULAR ACCESS

INTRAVENOUS FLUIDS BLOOD TESTS

TYPING & CROSS MATCHING

CORRECT COAGULOPATHY

BLOOD TRANSFUSION

Rockall scoring system for risk of


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Rockall scoring system for risk ofrebleeding and death

Variable 0 point 1 point 2 points 3 points

Age (yrs) 80

Shock Systolic BP>100

Pulse 100

Pulse>100

Systolic BP100

Comorbidity None Cardiac failure

Coronary heart

disease

Other major co

morbidity

Renal failure

Hepatic Failure

Metastatic cancer

Diagnosis

Major

stigmata of

recent

bleeding

(SRH)

MW tear

No lesions

None

All other

diagnoses

Malignancy of

upper GI tract

Fresh blood

Ulcer with

adherent clot,

visible or

spurting vessel


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Rockall score ranges 0-11

A total score30%

reeburg EM, Tarwee CB, Suel P, et al. Gut 1999;44:331-5

Rockall Score Clinical Implication


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Prinsip Umum :1. Penilaian hemodinamik disertai resusitasi cairan dan

stabilisasi hemodinamik2. Penilaian onset dan derajat perdarahan

3. Usaha menghentikan perdarahan secara umum (stopgap treatment)4. Usaha identifikasi lokasi sumber perdarahan dengan

modalitas sarana penunjang yang tersedia

5. Mengatasi sumber perdarahan secara defenitif6. Minimalisasi komplikasi yang dapat terjadi7. Upaya pencegahan terjadinya perdarahan ulang dalam

jangka pendek maupun jangka panjang.

PENATALAKSANAAN


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Penatalaksanaan

Penatalaksanaan pada PSCBA terbagi atas penatalaksanaanmedik dan penatalaksanaan bedah.

A. PENATALAKSAAN MEDIK1. Penatalaksanaan non-farmakologis : memperbaiki

keadaan umum, tanda vital, infus cairanparenteral/nutrisi, transfusi darah dan lain-lain.

2. Penatalaksanaan farmakologis : ARH2 atau PPI,sitoprotektor, antibiotika, obat hemostatik (tranexamicacid, adona AC dan somatostatin).

PENATALAKSANAAN


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Mempertahankan pH lambung > 6

Proses koagulasi

Agregasi trombosit

Pembentukan fibrin

Dosis, Bolus 80 mg IV dilanjutkan dengan infus8 mg/jam selama 72 jam

Menurunkan angka kejadian perdarahanberulang

Menurunkan mortalitas

Barkun AN, Badou M, Kuipers EJ, Sung J, Hunt RH, et al. International consensus recommendations on the management ofpatients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010;152:101-13.


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Seven-day intravenous low-dose omeprazole infusion

reduces peptic ulcer rebleeding for patients with

comorbiditiesCeng H, et al. Gastrointest Endosc 2009;70:433-

3 PENATALAKSANAAN KHUSUS


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3. PENATALAKSANAAN KHUSUS

TOPICAL THERAPY

-Tissue adhesives

-Clotting factors

-Collagen

-Ferromagnetic tamponade

MECHANICAL THERAPY

-Snares

-Sutures

-Balloons

-Hemoclips

INJECTION THERAPY

-Variceal bleeding

-Non variceal bleeding

- Ethanol

- Other sclerosants

THERMAL THERAPY

-Electrocoagulation

- monopoloar

- electrohydrothermal

bipolar (multipolar)

-Heater probe

-Laser


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Injeksi sklerosan seperti etanol, polidocanol, dan

etanolamin, dapat menyebabkan trombosispembuluh darah sehingga tercapai hemostasis.

Pada perdarahan saluran cerna atas akibat non-

varises, efektivitas sklerosan sama dengan adrenalindalam mencapai hemostasis dan mencegahrekurensi.

Penggunaan sklerosan lebih terbatas karena dapatmengakibatkan ulkus atau striktur iatrogenik.


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Pemanasan menimbulkan penekanan pada arteri sehingga

perdarahan berhenti. Teknik pemanasan dibagi atas non-kontak dan kontak.

Pemanasan dengan teknik non-kontak menggunakan laser(neodymium:yttrium-aluminum-garnet) atau argon plasma

coagulation. Teknik pemanasan menggunakan laser kini jarang

digunakan.

Hemostasis pada pemanasan dengan argon tercapai pada

75,9% kasus dengan rekurensi pada 5,7% kasus.


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Pemanasan dengan teknik kontak menggunakanelektrokoagulasi bipolar dan heater probethermocoagulation.

Kombinasi elektrokoagulasi bipolar dan injeksiadrenalin dapat menurunkan risiko terjadinyarekurensi.

Kombinasi heater probe thermocoagulation dan injeksiadrenalin dapat mencapai hemostasis pada 98.6%kasus dengan angka rekurensi sebesar 8,2%.


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Endoloop, clip, dan rubber band ligation merupakanalat yang digunakan untuk menghentikanperdarahan secara mekanik.

Penggunaan clip dapat mencapai hemostasis pada100% kasus perdarahan saluran cerna atasdengan rekurensi yang lebih rendahdibandingkan injeksi adrenalin.


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Kombinasi penggunaanhemoclips dan endoloops Perdarahan berhenti

Racz I, et al. Endoscopic hemostasis of bleeding gastric ulcer with a combination of multiple hemoclips and endoloops. Gastrointest Endosc; 2009.


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Endoscopic clipping for acute nonvariceal upper-GI bleeding: a

meta-analysis and critical appraisal of randomized controlled trialsYuan Y, et al. Gastrointest Endosc 2008;68:339-51


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Lo C, et al. Gastrointest Endosc 2006;63Comparison of hemostatic efficacy for

epinephrine injection

alone and injection combined with hemoclip therapyin treating high-risk bleeding ulcers:767-73


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Penatalaksanaan

B.PENATALAKSAAN BEDAH,OPERASIdilakukan bila perdarahan tetap berlangsung atausudah masuk dalam keadaan gawat I s/d II makamerupakan indikasi operasi.


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Varices Esofagus

Ligasi banding

Skeleroterapi

Varices Gaster

Injeksi argon plasma


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Toubia N, Sanyal AJ. Portal Hypertension and Variceal Hemorrhage. Med Clin N Am 92 (2008) 551574


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Bendtsen F, Krag A, Moller S. Treatment of Acute Variceal Bleeding. Digestive and Liver Disease 40 ( 2008 ) 328-336


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TERAPI FARMAKOLOGI1. TERLIPRESSIN

menurunkan tekanan portal sekitar 20 % setelah single dose

Dosis 2 mg/4 jam selama 48 jam pertama

Dapat dilanjutkan sampai 5 hari dengan dosis yang lebih rendah yaitu 1 mg/4 jam atau 12-24 jamsetelah perdarahan berkurang

2. SOMATOSTATIN DAN ANALOG

Somatostatin

Mengurangi tekanan portal sekitar 17 % tanpa mempengaruhi hemodinamik sistemik.

Diawali dengan 250 g bolus diikuti oleh infus 250 g/jam yang dapat dipertahankan sampai 24 jambebas perdarahan.10

Ocreotide

50 g diikuti oleh infus 25-50 g/jam

Menurunkan angka rebleeding

3. REKOMBINAN faktor VIIa


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MANAJEMEN NON FARMAKOLOGI

ENDOSKOPI

1. EST ( Endoskopi Skleroterapi )

2. EVL ( Endoskopi Variceal Ligation)

TIPS ( Transjugular Intrahepatic Portosystemic

Shunts )

BALOON TAMPONADE


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Endoscopic Sclerotherapy Endoscopic Band Ligation


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ENDOSCOPIC VARICEAL LIGATION (

EVL)

Endoscopy shows two

varices in the distal

esophagus that have

been banded. Thebands are indicated with

the green arrows. The

two strings in the rightof the field control the

trigger device used to

deploy the bands.


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BALOON TAMPONADE

Linton tube dan Sengstaken-Blakemore

Tube

Algorithm for cirrhosis Without Bleeding


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Algorithm for cirrhosis Without Bleeding

Algorithm For

Cirrhosis Without

Bleeding

Cirrhosis

Established

Reguler Interval

Usually one week

Upper Endoscopy

No varices Small or Medium

Varices

Large Varices

Observe Observe

(1

2 years Evaluation)

Primary Bleeding

Prophylaxis

Non Selectne Blockers

(and /or Nitrates)

Ligation

(2

3 years Evaluation)

Algorithm For


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Algorithm For

Bleeding Cirrhoti

Algorithm For

Bleeding CirrhotisResuscitae

Begin Octreotide

(or Vasopressin)

Early endoscopy

Non-Portal

HypertensiveCause

Gastric Varices Esophagel

VaricesPortal

Hypertensive

Gastropathy

Treat appropriatelyContinue octreotide 5 daysBegin beta-blocker when stable

Band ligation or injectionSclerotheraphy

Ballon Tamponade

Rebleeding No rebleeding

Shunt (Child A)

TiPSS. or

Liver transplantation (Child B or C)

Continue treatment

Preventation of Rebleeding Pharmacological Treatment

Ligation /SclerotheraphyReguler Interval

Usually one week

Repeated Endoscopy

3 6 month

Eradication

Shunt (Child A)

TIPSS Or OLT (Child B or C)

Rebleeding


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Peptic ulcer hemorrhage

Surgical intervention Only 10% of patients

Indications Failure of endoscopy Significant rebleeding after 1st endoscopy

Ongoing transfusion requirement

Need for >6 units over 24 hours

Earlier for elderly, multiple co-morbidities


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Ulcus Pepticum Bleeding


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Gastric ulcer 10% are maliganant

30% will rebleed with simple ligation

Need Resection

Distal gastrectomy with Bilroth I or II Subtotal gastrectomy for 10% high on lesser curve


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Doudenal ulcer Expose ulcer with duodenotomy or duodenopyloromyotomy

Direct suture ligation, four quadrent ligation, ligation ofgastroduodenal artery

Anti-secretory procedure Truncal, parietal cell vagotomy

If unstable can use meds


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Tatalaksana Perdarahan Saluran Cerna Atas


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Rumah Sakit Tipe A dan BAnamnesis

Pemeriksaan tanda vitalPasang IV line, NGT

Periksa DPL, hemostasis

Hemodinamik tidak stabil,perdarahan aktif

Resusitasi

Kristaloid; koloid

Transfusi darahKoreksi faktor koagulasi

Terapi Empirik

Hemodinamik stabil, tidakada perdarahan aktif

Hemodinamik stabil,perdarahan berhenti

Hemodinamik tidak stabil,perdarahan tidak berhenti

Emergency endoscopy

Perdarahan berhenti

Elective endoscopy

Terapi definitif

Varises esofagus Ulkus

Bleeding site non-visualized

EVL, ES, SB tube

Bedah

Injeksihemostasis

Interventional diagnostic &therapeutic radiology

Obat vasoaktifOcreotide, somatostatin,

vasopressin

Konsensus Nasional Perkumpulan Gastroenterologi Indonesia 2007

Tatalaksana Perdarahan Saluran Cerna Atas


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Rumah Sakit Tipe CAnamnesis

Pemeriksaan tanda vitalPasang IV line, NGT

Periksa DPL, hemostasis

Hemodinamik tidak stabil,perdarahan aktif

Resusitasi

Kristaloid; koloid

Transfusi darahKoreksi faktor koagulasi

Terapi Empirik

Hemodinamik stabil, tidakada perdarahan aktif

Hemodinamik stabil,perdarahan berhenti

Hemodinamik tidak stabil,perdarahan tidak berhenti

Perdarahan berhenti

Foto abdomen dg kontras Baatau

Rujuk untuk Endoskopi

Terapi definitif

Obat vasoaktifOcreotide, somatostatin,

vasopressin

Konsensus Nasional Perkumpulan Gastroenterologi Indonesia 2007

Perdarahan tidak berhenti

Balloon tamponadeSB tube

Perdarahan berhenti

Perdarahan tidak berhenti Bedah


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Summary of consensus Recommendation Management

patients with non variceal UGI Bleeding

a. Resusitasi, risk assesment, and pre endoscopic management1. Immediately evaluate and initiate appropriate resusitation.

2. Prognostic scales

3. Consider placement of NGT

4. Blood transfution

5. Correction of coagulopathy

6. Promotility agents should not be used7. Preendoscopic PPI therapy

b. Endoscopic management

1. Early endoscopy

2. Endoscopic therapeutic not indicated with low risk stigmata

3. Endoscopic therapy for ulcer with cloth is kontroversial.

4. Endoscopic therapy with high risk stigmata

5. Epinephrine injection sub optimal

6. No single endoscopic thermal is superior

7. Clips thermocoagulation or sclerosan injection alone or combination

8. Endoscopic therapy recommended in rebleeding


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c. Pharmacologic management

1. H2 RA are not recommended

2. Somatostatin and ocretide are not routine recommended

3. IV bolus followed continuous infusion should be use to the decrease rebleeding

and mortality.

d. Non endoscopic and non pharmacologic in hospital management

1. Patients with endoscopic therapy should be hospitalized at least 72 hours

2. Surgical consultation if endoscopic therapy failed

3. Percutaneus embolisation can be consider4. Peptic ulcer bleeding with HP (+) be should eradication therapy

5. HP (-) diagnostic test should be repeat

e. Postdischarge, ASA, and NSAID

1. Previous PUB with NSAID, combination PPI and Cox-2 is recommended

2. Previous PUB with NSAID, NSAID plus PPI or cox-2 alone

3. PUB with low dose ASA, ASA therapy ???

4. Previous PUB who require cardiovascular prophylaxis, clopidogrel alone higherrisk than ASA with PPI


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LGI hemorrhage

Sites Colon 95-97%

Small bowel 3-5%

Only 15% of massive GI bleeding Finding the site

Intermittent bleeding common

Up to 42% have multiple sites


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Bleeding

diverticulosis

Colonic angiodysplasia


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LGI hemorrhage diagnostics

Colonoscopy Within 12 hours in stable patients without large

amounts of bleeding

Selective viseral angiography Need >0.5 ml/min bleeding

40-75% sensitive if bleeding at time of exam

Tagged RBC scan

Can detect bleeding at 0.1 ml/min 85% sensitive if bleeding at time of exam

Not accurate in defining left vs right colon


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Meckels Diverticulum

Cecal angiodysplasia

with extravasation

Small bowel ulceration

due to NSAIDS


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LGI hemorrhage treatment


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LGI hemorrhage treatment

Endoscopy Great for angiodysplasia and polypectomy sites

Angiographic

Selective embolization for poor surgical

candidates Surgery

Ongoing hemorrhage >6 units or ongoing

transfusion requirement


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Hemodynamic instability despitevigorous resuscitation (>6 unitstransfusion)

Failure of endoscopictechniques to arrest

hemorrhage Recurrent hemorrhage after

initial stabilization (with up to twoattempts at obtainingendoscopic hemostasis)

Shock associated with recurrenthemorrhage

Continued slow bleeding with atransfusion requirementexceeding 3 units/day

One of the criteria used to determine the need for surgical intervention isthe number of units of transfused blood required to resuscitate the patient.The more units required, the higher the mortality rate (Larson, 1986).Operative intervention is indicated once the blood transfusion numberreaches more than 5 units, as noted in the following table (Larson, 1986).

Number of UnitsTransfused

Need forSurgery, %

MortalityRate, %

0 4 4

1-3 6 14

4-5 17 28

>5 57 43


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Et. 2.Perdarhan Saluran Cerna

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