UPPER

GASTROINTESTINAL
BLEEDING

by
Fajar Yuwanto
SMF Penyakit Dalam
RSUD abdul Moeloek
DEFINITIONS
* HEMATEMESIS : is vomiting fresh red blood
A site of bleeding proximal to the duodenal-
jejunal junction ( Upper Treitz Ligament )
The Colour of vomitus depends on how long
the blood has been in the stomach
* Coffee ground vomiting is vomiting of altered
black blood
* Melena is the passage of black tarry stools
 Causes of Haematemesis
and Melaena
Oesophagus
Oesophageal Varices
Mallory-Weiss tear
Oesophageal carcinoma
Reflux oesophagitis
Foreign body
 Causes of Haematemesis
and Melaena
Stomach
Peptic ulcer
Erosions/ Gastritis
Gastric varices
Portal hypertensive gastropathy
Gastric carcinoma
Lymphoma
Leiomyoma
Angiodysplasia (including Osler’s disease)
Dieulafoy’s erosion
 Causes of Haematemesis
and Melaena
Duodenum/jejunum
Peptic ulcer
Erosions/ Gastritis
Vascular malformations
Haemofilia
Polyps (including Peutz-Jeghers
syndrome and other polyposis syndromes)
Aorto-enteric fistula
Causes of massaive upper
gastrointestinal bleeding

Oesophageal or gastric varices

Gastric ulcer
Duodenal ulcer
Stress ulceration
Dieulafoy’s erosion
Aorto-enteric fistula
 Causes of acute upper gastrointestinal haemorrhage
in Sardjito Hospital 2004

1%1%1%

22%

9%
66%

VE Stress Ulcer Gastritis

Duodenitis Ulkus Peptik Esofagitis

Endoscopic stigmata associated with
high risk of further gastrointestinal bleeding.
Top left : an active, spurting haemorrhage from
a peptic ulcer is associated with an 80% risk of
Continuing bleeding or rebleeding in shocked
patients. Top right : a non-bleeding, visible vessel
Represents either a pseudoaneurysm of an eroded
artery or a closely adherent clot, and 50% of such
patients rebleed in hospital. Left: large varives
with red spots are also strongly associated with bleeding
Risk factors for death after hospital admission
for acute upper gastrointestinal haemorrhage

Advanced age
Shock on admission (pulse rate > 100 beats/min;
systolic blood pressure < 100 mmHg
Comorbidity (particularly hepatic or renal failure and
disseminated cancer)
Diagnosis (worst prognosis for advanced upper
gastrointestinal malignancy)
Endoscopic findings (active, spurting haemorrhage
from peptic ulcer; non-bleeding, visible vessel; large
varices with red spots)
Rebleeding (increases mortality 10-fold)
Faktor resiko varises ruptur
Besar varises  F3 > 5 mm
Tekanan intra varises > 15 mmHg
Warna varises :
Cherry red spot (CRS)
Red wale marking (RWM)
Hemato cystic spot (HCS)
 Blood tests taken urgently at initial
presentation

Haemoglobin, platelet count, and white

blood cell count
Urea and electrolytes
Liver function test
Cross match
Prothrombin time
 PENATALASANAAN AWAL
Anannesis & pemeriksaan fisis
Tanda vital, Jalan infus yg sangat besar
Selang nasogastrik Hb, Ht, trombosit,
hemostaisis
Hemodinamik stabil
Tidak ada perdarahan aktif Hemodinamik tidak stabil
Perdarahan aktif
Pengobatan empirik RESUSITASI
Cairan krostaloid, cairan koloid,
Transfusi darah, koreksi
faktor koagulasi

Hemodinamik stabil
Perdarahan berhenti Hemodinamik stabil
Perdarahan tetap berlangsung Obat Vasoaktif
Perdarahan berhenti Octreotide, Somat ostatin,
Vasopressin
Elektif Emergensi atau Dini
Endoskopi SCBA Endoskopi SCBA

Varises esophagus Sumber perdarahan

lambung Tukak Tak tervisualisasi
Skleroterapi Injeksi, Radiologi, Intervensional
Atau ligasi hemostatik Diagnostik & terapeutik
Pengobatan
Bedah Jika Atau “SB tube” Atau bedah segera Atau bedah segera
definitif
gagal
Resuscitation
a. Mild or Moderate Bleed
* Pulse and blood pressure : N
* Hb > 10 mg/ml
* Without comorbidity
* Less than 60 years of age
b. Severe Bleed
Pulse > 100 beats/min
Sistolic blood pressure < 100
mmHg
Hb < 10 mg/ml
Aged > 60 years
 Table 1. Hypovolaemic shock: symptoms, sign, and fluid replacement
Blood loss (ml) <750 750-1500 1500-2000 >2000
Blood loss (%bv) <15% 15-30% 30-40% <40%
Pulse rate <100 >100 >120 >140
Blood pressure Norma Norma Decreased Decreased
Pulse pressure Normal or increased Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30 20-30 30-40 >35
Mental status Slightly anxious Mildly anxious Anxious & confused Confused & letargic
Fluid replacement Crystalloid Crystalloid Crystalloid & blood Crystalloid blood

Adapted from Grenvick A, Ayres SM, Holbrook PR,

et al. Textbook of critical care. 4th edition. Philadelphia WB Saunders Company; 40-5
Drug Therapy
1. Acid suppressing drugs
2. Somatostatin
3. Antifibrinolytic drugs
 Pasien dengan Perdarahan Saluran
Gastrointestinal Bagian Atas

Singkirkan :
Riwayat penyakit A Hematemesis atau melena C
B Hemoptisis
Pemeriksaan fisik
Epitaksis

Pasien scr hemodinamik tidak stabil Pasien yg scr hemodinamik stabil

Resusitasi : Oksigen, intubasi pm

D Hematokrit, gol & skrining darah
Jalur intravena x 2 Jalur intravena, sifat pembekuan
Gol darah & crossmatch, transfusi
Perbaiki koagulopati, EKG
E Lavase nasogastrik

E Lavase nasogastrik
Positif, Positif, jernih dg
Tidak jernih negatif
Perawatan di ICU <500-1.000 cc
Dg lavase
F Konsultasi dokter ahli Observasi psn 6 jam
Gastroenterologi/bedah
Rawat Hematokrit  Hematokrit stabil
Perub tanda vital Tanda vital stabil

Perdarahan berlanjut Perdarahan berhenti Transfusi pm

Pemeriksaan elektif H Follow-up

G Endoskopi Terapi spesifik Rawat jalan
Management of bleeding peptic ulcer
Peptic ulcer

Low risk of rebleeding Active bleeding or high risk of

Rebleeding (shock, visible vessel)

Endoscopic therapy
Monitor

No further bleeding Rebleed Unable to control bleeding

Repeat endoscopic therapy

Rebleed Surgery
Endoscopic treatment for non-variceal bleeding

Thermal
Heater probe
Multipolar electrocoagulation
Injection
Adrenaline (1:10.000 to 1:100.000)
Alcohol (98%)
Sclerosants (ethanolamine, 1% Polidoconal)
Procoagulants (thrombin, fibrin glue)
Mechanical
Clips
Sutures
Staples
Combination
 Management of non-bleeding varices
Varices present but bleeding

Band ligation

Rebleeding No further bleeding

Repeat band ligation (or sclerotherapy)

Octreotide, 25 ug/hour

Further bleeding No further bleeding Repeat within 1 week

Consider:
•Transcutaneous intrahepatic portosystemic shunt Repeat every 3-4 weeks
•Shunt surgery/liver transplantation Until varices are obliterated
•Withdrawal of therapy
 Management of actively bleeding varices
Actively bleeding varices

Band ligation or injection sclerotherapy

Commence octreotide, 25 ug/hour

Bleeding controlled Bleeding not controlled

Insert Sengstaken-Blakemore
Tube (admit to ICU)

Deflate Sengstaken-Blakemore tube at 24 hours

Attemp band ligation or sclerotherapy

unsuccesful Succesful

Re-inflate Sengstaken-Blakemore tube Consider:

•Transcutanous intrahepatic portosystemic shunt
• Shunt surgery
• Transplantation

Deflate Sengstaken-Blakemore
Tube at 24 hours
Attemp ligation or sclerotherapy
Consider :
•Transcutaneous intrahepatic portosystemic shunt
•Shunt surgery
Unsuccesful •Transplantation
•Withdrawal of therapy
Penanganan Perdarahan Akut VE

Tindakan Umum
Resusitasi : cairan kristaloid
Transfusi darah mengandung faktor pembekuan
darah segar, whole blood, fresh frozen plasma,
pached red cell
Bilas lambung  NGT
Vitamin K intramuskuler : obat hemostasis (asam
traneksamat)
Penyekat reseptor H2
Sterilisasi usus : kanamisin, neomisin oral
Laktulosa oral / klisma
Pengobatan Farmakologis
Menurunkan tekanan porta  perdarahan
berhenti
Vasopresin, vasokonstriktor pembuluh darah
splangnik  aliran darah ke Vena porta .
Dosis : 20  dalam 100 cc selama 10-20 menit
diulang tiap 4 jam atau per infus 0,2-0,5 /menit
 120 menit
Somatostatin. Bolus 250 g  infus 250 g/jam.
Octeotrid, 100 g  infus 25 g/jam
Nitrat organik, ISDN 20 mg (2 ampul) + 500 cc
NaCl 0,9% (detrose 5%) per drip  2 mg/jam
syarat : tekanan sistolik > 90 mmHg, Nadi < 90
x/mnt.
Tindakan khusus:
• SB Tube
• Skleroterapi/ligasi
Minnesota tube
Endoscopic treatment of varices. Intravariceal injection of sclerosant
(left) and band ligation of oesophageal varices (right)
Traneksamat
Menghambat aktivitas plasminogen dan plasmin

Plasmin
Meningkatkan proses fibrinolisis
Menurunkan aktifitas faktor koagulopati
Meningkatkan permeabilitas pembuluh
darah
Menurunkan agregasi platelet
Figure : Antifibrinolytic Action of Aminocaproic Acid and Tranexamic Acid
N.Engl.J Med. 1998 : 339(4)245-253
Table 2. Indications for the use the Antifibrinolytic drugs
tranexamic acid and aminocaproic acid in the treatment
of excessive bleeding

Clinical Situation Study Grade of

Evidence*
Primary menorrhagia Bonnar and Sheppard A
Upper gastrointestinal Henry and O’Connell A
bleeding
Dental extraction in patients Walsh et al A
with coagulation disorders Forbes et al
Sinder-Pedersen et al

Bleeding associated with Gardner and Helmer B

thrombocytopenia Bartholomew et al

N.Engl.J.Med. 1998: 339(4)245-253

Klasifikasi V.E.
I. Kl. Degradi
II. Kl. Palmer & Brick
III. Kl. Omed
IV. Kl. Perhimpunan Endoskopi GI
Jepang
 Kl. Perhimpunan Endoskopi GI
Jepang

1. Warna (colour)
2. Tanda Warna merah (red colour sign)
3. Bentuk (form)
4. Lokalisasi
 Warna

Colour White (CW)

Colour Blue (CB)
 Tanda warna merah
(red colour sign/RCS)

Red Wale Marking (RMW)  gambar 1

Cherry Red Spot (CRS)  gambar 2
Hemato Cystic Spot (HCS)  gambar 3
Diffuse Redness (DR)
 (RWM)
Red Wale Marking)

Gambar 1
 (CRS)
Cherry Red Spot

Gambar 2
 (HCS)
Hemato Cystic Spot

Gambar 3
 (DR)
Diffuse Redness

Gambar 4
 Bentuk

Tingkat I : VE lurus (straight line

varises/F1)  gambar 5
Tingkat 2 : VE bentuk untaian tasbeh
menempati 1/3 lumen (F2)  gambar 6
Tingkat 3 : VE yang besar, berkelok-
kelok >1/3 lumen (F3)  gambar 7
Tingkat 1, varises yg lurus
(Straight line varicess/F1)
Tingkat 2, varices berbentuk
untaian manik-manik (rosary like varicess)
yg menempati 1/3 lumen(F2)
Tingkat 3, varices yg besar dan berkelo-kelok
Menempati lebih dari 1/3 lumen (F3)
 Lokalisasi
VE sp diatas bifurkasi trakhea (LS)
VE yg menempati daerah dibawah
bifurkasi trakhea (Lm)
VE yg menempati daerah dibawah 1/3
distal (Li)
VE yang menempati cardia lambung (lg)
 Ls
superior

Lm
middle

Li
inferrior

Lg
gastric