Dr.

LEONARDO DAIRY, SpPD KGEH

INTRODUCTION
PSCBA (UGI BLEEDING) PSCBB (LGI BLEEDING) OCCULT BLEEDING OBSCURE BLEEDING

Gastrointestinal (GI) bleeding is an extremely common clinical problem

resulting in significant morbidity, mortality, and cost. There are over 300,000 hospitalizations annually in the United 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, but the true overall cost, including outpatient endoscopic and radiologic investigations, clinic visits, and work days lost, far exceeds.

Upper GI bleeding (UGI)

Incidence of UGI is approximately 100 cases per 100,000 population. Acid peptic disease (e.g., gastric,duodenal ulcers and gastritis) is the most common cause of upper GI bleeding, accounting for 5075% of all cases). Acid peptic disease is followed by variceal bleeding, gastric and duodenal erosive disease, and Mallory-Weiss tears in prevalence. Furthermore, the predominance of peptic ulcer bleeding has not been affected by the advent of improved acid suppression with medical therapy. The elderly appear to be at particular risk, as the proportion of elderly patients who present with upper GI bleeding has steadily increased, with persons older than age 60 years accounting for 3545% of all cases. This increase cannot be explained by demographics alone, as increasing age directly correlates with an increased rate of hospitalization for upper gi bleeding.
.

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,, iatragenic causes (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 29% of admissions for lower GI bleeding.

Definition
Bleeding derived from any source proximal to the Ligament of Treitz

1 in 1000 in us who experienced upper GI bleeding Men :women 2 : 1 Mortality rate 10%

 PSCBA PERDARAHAN SEPANJANG SAL. CERNA PROK. DARI LIG.TREITZ. KEGAWAT-DARURATAN INSIDENS 50 100/100.000 PDDK (USA), 20.000 KEMATIAN/TAHUN TINGKAT MORTALITAS 10% - 36%, 33% (UK) 80% BERHENTI SPONTAN PERDARAHAN SALURAN CERNA

ATAS PERDARAHAN SALURAN CERNA ATAS VARISES PERDARAHAN SALURAN CERNA ATAS NON VARISES

 Sebuah studi meta analisis terapi endoskopi pada PSCBA secara bermakna mengurangi frekuensi perdarahan lanjut, pembedahan dan mortalitas.

Angka morbiditas dan mortalitas juga sangat dipengaruhi oleh bagaimana optimalnya tatalaksana 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.

CAUSE OF GI BLEEDING
Common causes
Gastric ulcer, Duodenal ulcer Esophageal varices Mallory-Weiss tear
Rare RareCauses 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 ectasia Gastric varices Neoplasia Esophagitis Gastric erotions

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.

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 BENZIDINE TEST (+)

DIAGNOSTIK
1. PERDARAHAAN ANAMNESE RIWAYAT COMMON
VOMITING (MENTAL) MALLORY WEISS TEAR ? HEARTBURN & REGURGITASI REFLUX ESOFAGITIS ? DYSFAGIA & BB MALIGNANCY PD ESOFAGUS ?

MAKAN OBAT-OBATAN & ALKOHOL GASTRIC EROSIVE ?

ULKUS PEPTIKUM ? LIVER STIGMATA (CH) VARICES BLEEDING ?

PENYAKIT BERAT (DI ICU) STRESS ULCER ?

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.

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

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

Diagnosis
Pemeriksaan fisik
Tanda vital syok? Stigmata penyakit hati kronik
Ikterus Hepatomegali Asites Spider angioma Palmar erythema

Pemeriksaan laboratorium DPL Prothrombin time INR Fungsi hati

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

INITIAL PATIENT ASSESMENT

hemodynamics Blood loss (%) Severity of bleed

(vital signs)

(fraction of intravascularvolume)

Shock (Resting hypotension) Postural(Orthostatictac hycardia/hypotension)

20-25

Massive

10-20

Moderate

Normal

<10

Minor

Table : Hemorrhagic Classes

HEMORRHAGIC I CLASS 15% OR BLOOD LOSS 750 ML

II 20-25% OR

III 30-35% OR

IV 40-50% OR 2000-2500 ML

1000-1250 ML 1500-1800ML

HEART RATE
RESPIRATORY RATE ARTERIAL PRESSURE CAPILLARY FILLING TIME DIURESIS (ML/H) NEUROLOGIC STATUS

<100
14-19

>100
20-29

>120
30-40 70-60

>140
>40 <60

NORMAL 110-80

NORMAL INCREASED INCREASED INCREASED 35-30 30-25 25-5 CONFUSED 0 LETHARGIC

MILDLY VERY ANXIOUS ANXIOUS

Aspirasi nasogastrik
Membedakan perdarahan saluran cerna atas dan bawah Sensitivitas 79%, spesifisitas 55% Modalitas diagnostik dan terapeutik
Townsend: Sabiston Textbook of Surgery, 18th ed. 2007.

Diagnosis
Esofagogastroduodenoskopi (EGD)
Modalitas utama Menentukan lokasi & penyebab perdarahan saluran cerna atas: 90% - 95%

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

Tabel 2. KLASSIFIKASI FORREST PSCBA

Forrest class Ia Ib II a II b II c Type of lesion Arterial Spurting Arterial Oozing Visible Vessel Sentinel Clot Haematin covered flat spot Risk of rebleed if untreated (%) 100 17-100 8-81 14-36 0-13

III

No Stigmata

0-10

MANAGEMENT
RESUSCITATION
VASCULAR ACCESS INTRAVENOUS FLUIDS BLOOD TESTS TYPING & CROSS MATCHING CORRECT COAGULOPATHY BLOOD TRANSFUSION

Rockall scoring system for risk of rebleeding and death

Variable 0 point
Age (yrs) Shock <60 Systolic BP>100 Pulse <100 None

1 point
60-79 Systolic BP>100 Pulse>100

2 points
>80 Systolic BP<100 Pulse>100 Cardiac failure Coronary heart disease Other major co morbidity

3 points

Comorbidity

Renal failure Hepatic Failure Metastatic cancer

Diagnosis

MW tear No lesions

All other diagnoses

Malignancy of upper GI tract Fresh blood Ulcer with adherent clot, visible or spurting vessel

Major stigmata of recent bleeding (SRH)

None

Rockall Score Clinical Implication

Rockall score ranges 0-11

A total score<3 is associated with an excellent prognosis rebleeding <5% mortality <1% A score>8 is associated with a poor prognosis rebleeding >50%
mortality >30%
reeburg EM, Tarwee CB, Suel P, et al. Gut 1999;44:331-5

PENATALAKSANAAN
Prinsip Umum : 1. Penilaian hemodinamik disertai resusitasi cairan dan stabilisasi hemodinamik 2. Penilaian onset dan derajat perdarahan 3. Usaha menghentikan perdarahan secara umum (stop gap treatment) 4. Usaha identifikasi lokasi sumber perdarahan dengan modalitas sarana penunjang yang tersedia 5. Mengatasi sumber perdarahan secara defenitif 6. Minimalisasi komplikasi yang dapat terjadi 7. Upaya pencegahan terjadinya perdarahan ulang dalam jangka pendek maupun jangka panjang.

PENATALAKSANAAN Penatalaksanaan
Penatalaksanaan pada PSCBA terbagi atas penatalaksanaan medik dan penatalaksanaan bedah. A. PENATALAKSAAN MEDIK 1. Penatalaksanaan non-farmakologis : memperbaiki keadaan umum, tanda vital, infus cairan parenteral/nutrisi, transfusi darah dan lain-lain. 2. Penatalaksanaan farmakologis : ARH2 atau PPI, sitoprotektor, antibiotika, obat hemostatik (tranexamic acid, adona AC dan somatostatin).

 Mempertahankan pH lambung > 6 Proses koagulasi Agregasi trombosit Pembentukan fibrin Dosis, Bolus 80 mg IV dilanjutkan dengan infus 8 mg/jam selama 72 jam Menurunkan angka kejadian perdarahan berulang Menurunkan mortalitas
Barkun AN, Badou M, Kuipers EJ, Sung J, Hunt RH, et al. International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2010;152:101-13.

Seven-day intravenous low-dose omeprazole infusion reduces peptic ulcer rebleeding for patients with comorbidities
Ceng H, et al. Gastrointest Endosc 2009;70:433-

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

 Injeksi sklerosan seperti etanol, polidocanol, dan etanolamin, dapat menyebabkan trombosis pembuluh darah sehingga tercapai hemostasis. Pada perdarahan saluran cerna atas akibat nonvarises, efektivitas sklerosan sama dengan adrenalin dalam mencapai hemostasis dan mencegah rekurensi. Penggunaan sklerosan lebih terbatas karena dapat mengakibatkan ulkus atau striktur iatrogenik.

 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.

 Pemanasan dengan teknik kontak menggunakan elektrokoagulasi bipolar dan heater probe thermocoagulation. Kombinasi elektrokoagulasi bipolar dan injeksi adrenalin dapat menurunkan risiko terjadinya rekurensi. Kombinasi heater probe thermocoagulation dan injeksi adrenalin dapat mencapai hemostasis pada 98.6% kasus dengan angka rekurensi sebesar 8,2%.

 Endoloop, clip, dan rubber band ligation merupakan alat yang digunakan untuk menghentikan perdarahan secara mekanik. Penggunaan clip dapat mencapai hemostasis pada 100% kasus perdarahan saluran cerna atas dengan rekurensi yang lebih rendah dibandingkan injeksi adrenalin.

Kombinasi penggunaan hemoclips 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.

Endoscopic clipping for acute nonvariceal upper-GI bleeding: a meta-analysis and critical appraisal of randomized controlled trials
Yuan Y, et al. Gastrointest Endosc 2008;68:339-51

Lo C, et al. Gastrointest Endosc 2006;63Comparison of hemostatic efficacy for epinephrine injection alone and injection combined with hemoclip therapy in treating high-risk bleeding ulcers:767-73

Penatalaksanaan
B.PENATALAKSAAN BEDAH,OPERASI dilakukan bila perdarahan tetap berlangsung atau sudah masuk dalam keadaan gawat I s/d II maka merupakan indikasi operasi.

Varices Esofagus
Ligasi banding Skeleroterapi Varices Gaster Injeksi argon plasma

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

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

TERAPI FARMAKOLOGI
1. 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 jam setelah 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 jam bebas perdarahan.10 Ocreotide 50 g diikuti oleh infus 25-50 g/jam Menurunkan angka rebleeding 3. REKOMBINAN faktor VIIa

MANAJEMEN NON FARMAKOLOGI

ENDOSKOPI 1. EST ( Endoskopi Skleroterapi ) 2. EVL ( Endoskopi Variceal Ligation) TIPS ( Transjugular Intrahepatic Portosystemic Shunts ) BALOON TAMPONADE

Endoscopic Sclerotherapy

Endoscopic Band Ligation

ENDOSCOPIC VARICEAL LIGATION ( EVL)

Endoscopy shows two varices in the distal esophagus that have been banded. The bands are indicated with the green arrows. The two strings in the right of the field control the trigger device used to deploy the bands.

BALOON TAMPONADE

Linton tube dan Sengstaken-Blakemore Tube

Algorithm for cirrhosis Without Bleeding

Algorithm For Cirrhosis Without Bleeding
Cirrhosis Established
Upper Endoscopy

No varices

Small or Medium Varices

Large Varices

(2 3 years Evaluation)

Observe

(1 2 years Evaluation)

Observe

Primary Bleeding Prophylaxis

Reguler Interval Usually one week

Non Selectne Blockers (and /or Nitrates) Ligation

Algorithm For Bleeding Cirrhotis

Resuscitae

Begin Octreotide (or Vasopressin) Early endoscopy Esophagel Non-Portal Gastric Varices Portal Varices Hypertensive Cause Hypertensive Gastropathy Treat appropriately

Algorithm For Bleeding Cirrhotis

Continue octreotide 5 days

Begin beta-blocker when stable

Band ligation or injection Sclerotheraphy Ballon Tamponade Rebleeding No rebleeding Continue treatment Shunt (Child A) Preventation of Rebleeding TiPSS. or Pharmacological Treatment Liver transplantation (Child B or C) Ligation /Sclerotheraphy Reguler Interval Usually one week Eradication Repeated Endoscopy 3 6 month Rebleeding Shunt (Child A) TIPSS Or OLT (Child B or C)

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

Ulcus Pepticum Bleeding

Peptic ulcer hemorrhage

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

Peptic ulcer hemorrhage

Doudenal ulcer
Expose ulcer with duodenotomy or duodenopyloromyotomy Direct suture ligation, four quadrent ligation, ligation of gastroduodenal artery Anti-secretory procedure Truncal, parietal cell vagotomy If unstable can use meds

Tatalaksana Perdarahan Saluran Cerna Atas Rumah Sakit Tipe A dan B

Anamnesis Pemeriksaan tanda vital Pasang IV line, NGT Periksa DPL, hemostasis Hemodinamik stabil, tidak ada perdarahan aktif Terapi Empirik Hemodinamik tidak stabil, perdarahan aktif Resusitasi Kristaloid; koloid Transfusi darah Koreksi faktor koagulasi Hemodinamik stabil, perdarahan berhenti Perdarahan berhenti Elective endoscopy Varises esofagus
EVL, ES, SB tube

Hemodinamik tidak stabil, perdarahan tidak berhenti Obat vasoaktif Ocreotide, somatostatin, vasopressin Emergency endoscopy Ulku s Injeksi
hemostasis

Bleeding site non-visualized

Interventional diagnostic & therapeutic radiology

Terapi definitif

Bedah
Konsensus Nasional Perkumpulan Gastroenterologi Indonesia 2007

Tatalaksana Perdarahan Saluran Cerna Atas Rumah Sakit Tipe C

Anamnesis Pemeriksaan tanda vital Pasang IV line, NGT Periksa DPL, hemostasis Hemodinamik stabil, tidak ada perdarahan aktif Terapi Empirik Hemodinamik tidak stabil, perdarahan aktif Resusitasi Kristaloid; koloid Transfusi darah Koreksi faktor koagulasi Hemodinamik stabil, perdarahan berhenti Perdarahan berhenti Foto abdomen dg kontras Ba atau Rujuk untuk Endoskopi Perdarahan tidak berhenti Perdarahan berhenti Balloon tamponade SB tube Bedah Hemodinamik tidak stabil, perdarahan tidak berhenti Obat vasoaktif Ocreotide, somatostatin, vasopressin

Perdarahan tidak berhenti Terapi definitif

Konsensus Nasional Perkumpulan Gastroenterologi Indonesia 2007

Summary of consensus Recommendation Management patients with non variceal UGI Bleeding
a. Resusitasi, risk assesment, and pre endoscopic management 1. 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 used 7. 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

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 consider 4. 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 higher risk than ASA with PPI

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

Colonic angiodysplasia Bleeding diverticulosis

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

Meckels Diverticulum

Cecal angiodysplasia with extravasation

Small bowel ulceration due to NSAIDS

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

 Hemodynamic instability despite vigorous resuscitation (>6 units transfusion) Failure of endoscopic techniques to arrest hemorrhage Recurrent hemorrhage after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis) Shock associated with recurrent hemorrhage Continued slow bleeding with a transfusion requirement exceeding 3 units/day

One of the criteria used to determine the need for surgical intervention is the 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 number reaches more than 5 units, as noted in the following table (Larson, 1986). Number of Units Need for Mortality Transfused Surgery, % Rate, % 0 1-3 4-5 >5 4 6 17 57 4 14 28 43