UPPER

GASTROINTESTINAL
BLEEDING (UGIB)
MUHAMMAD IZZAT BIN FATAS
 Definition
• Hemorrhage in the upper gastrointestinal tract.
• The anatomic cut-off for upper GI bleeding is the ligament of
Treitz, which connects the fourth portion of the duodemum to
the diaphragm near the splenic flexure of the colon.
• Common. Incidence about 300 per 100000
• Mortality 5-10% and increased in elderly
 Classification
VARICEAL BLEED NON VARICEAL BLEED
Esophageal Varices Peptic Ulcers
Gastric Varices Erosions
Esophagitis
Mallory-Weiss tear
Malignancy
 ETIOLOGY BY ANATOMIC CLASSIFICATION

ESOPHAGUS STOMACH DUODENUM

Oesophageal ulcer Gastric ulcer Duodenal ulcer

Mallory-Weiss tear Gastric erosion Aorta-duodenal fistula
Reflux oesophagitis Dieulafoy’s lesion Polyps
Barret’s ulcer Gastric cancer Ampullary/pancreas cancer
Cameron ulcer

The most common cause for non variceal UGIB is peptic

ulcer disease.
 RISK FACTORS

• Aspirin / NSAIDS / anticoagulant / steroid

• Cigarettes , alcohol
• Recurrent vomiting
• Burn / trauma
• Liver disease , hx of PUD , esophageal varices, portal hypertension
 Clinical features
Period-wise
Acute Chronic
1.Haemetemesis with or without 4.Iron deficiency anaemia with or
melaena without evidence of visible blood loss

2.Melaena with or without 5.Blood loss detected by positive

haemetemesis Occult Blood Test

3.Rarely Haematochezia indicating

massive life threatening bleed
Hematemesis is the vomiting of blood that is either
bright red or resembling coffee-ground in appearance. Usually
indicates a bleeding source proximal to the ligament of treitz.
Coffee-ground hematemesis indicates that the blood has been in
contact with gastric acid long enough to become converted from
hemoglobin to methemoglobin.
Melena is the passage of black, usually tarry, stools.
Although melena signifies a longer time within the GI tract than
bright red blood, it does not guarantee that the bleeding is from
the upper tract.
• Hematochezia is the passage of bright red blood by
rectum. Although it indicates GI bleeding, it does
not specify the level within GI tract. (if profuse,
UGIB)
 Clinical presentations

Coffee ground
Maelena Hemetemesis
vomitus

• Haematochezia
• Anemia with or without
evidence of visible blood loss
 Presentation
 Vomiting blood
 Black, tarry or bloody stools
 Shock (in severe case)
 Abdominal pain.
 Features of liver disease and specific underlying condition
 Dysphagia/odynophagia (pain on swallowing; uncommon)
 Confusion secondary to encephalopathy (even coma)
 Pallor.
 Hypotension and tachycardia (ie shock).
 Reduced urine output.
 Reduced Glasgow Coma Scale.
 Signs of sepsis may also commonly be present.
 Patient assessment
• History:
• Bleeding from where? How much patient has
bled?
• Risk factor: NSAID, blood thinning agents,
traditional meds, alcohol, PUD, hepatitis
• Physical examination:
• General examination
• PR: “fresh” vs “stale” malena
 General Management
(New England Journal- 2008)

• Assess of haemodynamic status

• Resuscitation
• Blood investigation
• Early OGDS
• Initiating IV PPI
• Risk stratification
 Resus, resus, resus! (ABC)
• Aim to stabilize hemodynamic status
1. Insert at least 2 large bore branulla into large
peripheral veins
2. Give O2: NPO2, VM, HFM
3. Take bloods for IX: FBC, RP, LFT, COAG, BG,
GXM/GSH
4. Fluid resus with crystalloids or packed cell
5. Correct coagulopathy
6. Monitoring: Ryles tube, CVP, CBD, strict I/O
• Start PPI
• Consider intubation when:
• severe uncontrollable bleeding
• encephalopathic
• inability to maintain O2 saturation adequately
• to prevent aspiration

• ICU bed and facilities should be made available

• Close monitoring in ward
• Once patient stable -> OGDS within 24H
When to transfuse blood or blood products?
• Why transfuse?
• To restore blood volume, BP and to correct anemia to
maintain oxygen carrying capacity
• Indication for packed cell transfusion:
1. Systolic BP < 110 mmHg
2. Postural hypotension
3. Pulse > 110/min
4. Hb <7g/dl
5. Angina or cardiovascular disease with a hb <10g/dl
• Maintain Hb ~10g/dL
• Transfuse platelet if patient actively bleeding and PLT count is
<50,000/mm3
• Give FFP if PT is at least 1.5x higher than control value
 Endoscopy for Risk Assessment

• Early OGDS (within 12-24h) help in management

• Roles:
1. Diagnosis (source of bleeding)
2. Treatment
3. Risk stratification
Forrest Classification For Bleeding Peptic Ulcer
• Ia : Spurting bleeding
• Ib : Non spurting active bleeding
• IIa : Visible vessel (no active bleeding)
• IIb : Non bleeding ulcer with overlying clot
• IIc : Ulcer with haematin covered base
• III : Clean base ulcer
 Forrest classification for bleeding peptic ulcer:

Source: Jain V, Agarwal P N, Singh R, Mishra A, Chugh A, Meena M. Management of Upper Gastrointestinal Bleed.
MAMC J Med Sci 2015;1:69-79
 Use of Risk Stratification Scoring Systems

• There are a number of scoring system for outcome

• Rockall risk assessment score:

• ≤2 : mortality of 0.1%, rebleeding of 4.3%
• >8 : mortality of 41%, rebleeding of 42.1%
• Glassgow-Blatchford Score:
• 0 : Low risk and suitable for outpatient management and deferred an
OGDS treatment
• ≥6 : ≥50% risk of needing an intervention
Parameter Level Score
Blood Urea ≥6·5 <8·0 2
≥8·0 <10·0 3
≥10·0 <25·0 4
≥25 6
Hemoglobin (g/L) for men ≥12.0 <13.0 1
≥10.0 <12.0 3
<10.0 6
Hemoglobin (g/L) for women ≥10.0 <12.0 1
<10.0 6
Systolic blood pressure (mm 100–109 1
Hg)
90–99 2
<90 3
Pulse ≥100 (per min) 1
Presentation with melaena 1
Presentation with syncope 2
Hepatic disease 2
Cardiac failure 2
Therapeutics
• Mechanical
• Hemoclips
• Injection
• Injection therapy with diluted
epinephrine
• Results in local tamponade and va
sospasm
• Thermal
• Unipolar diathermy
• Thermal coagulation uses argon
plasma coagulation (APC)
 Pharmacological Therapy

• Platelet aggregation, coagulation and fibrinolysis are highly dependent on

gastric pH

• In low pH:
• Peptic may digest thrombus (pH 1-3.5)
• Pepsin still functioning (up to pH 5)
• Platelet aggregation is impaired
1. H2 – Receptor Antagonist

• Eg: Ranitidine, Cimetidine

• Competitive antagonist of histamine at parietal cells H2
receptor reduce production of gastric acid
• A meta-analysis (27 randomised trial) showed there is no
significance benefit in treatment of UGIB by using H2-
receptor antagonist compared with placebo

Protocol: The use of H2-antagonist in UGIB is not

recommended
2. Proton Pump Inhibitor

• Eg: Omeprazole, Pantoprazole

• Irriversibly blocking H+/K+ ATPase (proton pump) of gastric
parietal cells (which is the terminal stage in gastric acid
secretion)
• More effective than H2 antagonist
• Can reduce gastric acid secretion up to 99%
• In a meta-analysis comparing PPI with H2-antagonist
• Persistent or recurrent bleeding was less frequent with PPI (6.7%) than with H2-
antagonist (13.4%)
• The need for surgery and mortality rates are reduced with PPI

 Protocol: After endoscopic therapy, to give IV Omeprazole 80mg stat and

infusion of 8mg/hour for 72h
• According to Lau NEJM 2000, 30 days rebleed rate:
• With the use of PPI: 6.7%
• With placebo: 22.5%
 PPI reduce rebleeding rate

• According to Sung Ann Intern Med 2003, 30 days rebleed rate:

• With PPI only: 11.6%
• With PPI and endoscopic therapy: 1.1%
 Combination of endoscopic therapy and PPI is better
 Management of other Causes of UGIB

1. Mallor-Weiss Tears
• Endoscopic therapy – with adrenaline, thermal methods, mechanical clips

2. Vascular Malformations
• Argon plasma coagulation, heater probe therapy
 Surgery

Indications
• Massive bleeding
• Uncontrolled by endoscopic procedure
• Failure of endoscopic visualization due to profuse haemorrhage

• Ulcer inaccessible by endoscopy

• Duodenum – deformed and narrowed
Type of surgery
• Local
• Over-sewing of ulcer
• Excision of ulcer

• Radical surgery
• Gastric resection
• Vagotomy
Interventional Radiology
• Embolization therapy
• In patients whom endoscopic therapy was failed
• Bleeding stopped in 83% cases
• Rate of complications: 14%
• Use: sodium diatrizoate, metal coils, tissue adhesives, Gelfoam particles
 Varices
 Esophageal varice are dilated veins of the esophagus that form as a
consequence of portal hypertension, preferentially in the submucosa of
the lower esophagus.
 collateral veins within the wall of the esophagus that project directly
into the lumen
 Rupture and bleeding from esophageal varices are major complications
of portal hypertension and are associated with a high mortality rate.
 Gastric varices are dilated submucosal veins in the stomach
 Variceal bleeding accounts for 10–30% of all cases of upper
gastrointestinal bleeding
 Investigation
 Endoscopy is required at an early stage
 FBC - haemoglobin may be low; MCV may be high, normal or low; platelets may
also be low; WCC may be raised.
 Clotting including INR.
 Renal function.
 LFTs.
 Group and cross-match.
 CXR - patients may have aspirated or have chest infection.
 Ascitic tap may be needed if bacterial peritonitis is suspected.
 Management
1) Prophylaxis
Reducing pressure in the portal vein - beta blockers[propranolol (Inderal, Innopran)
and nadolol (Corgard)] markedly reduced risk of variceal bleeding as well as
slowing the progression of small varices into larger ones.
Banding - Using an endoscope, the doctor snares the varices and wraps them with an
elastic band, which essentially "strangles" the veins so they can't bleed. Esophageal
band ligation carries a small risk of complications, such as scarring of the
esophagus.
 Management
2) Management of active variceal bleed
Resuscitation and initial management
Resuscitate – A,B,C. Look for early signs of shock(tachycardia, postural HPT)
Assess mental state (if altered such as in encephalopathy – protect airway)
Correct fluid losses (place two wide-bore cannulae and also send bloods at the same time).
Transfuse patients with massive bleeding with blood, platelets and clotting factors
Offer platelet transfusion to patients who are actively bleeding and have a platelet count of
less than 50 x 109/litre.
Offer fresh frozen plasma to patients who have either:
a fibrinogen level of less than 1 g/litre, or
a prothrombin time (international normalised ratio) or activated partial thromboplastin time
greater than 1.5 times normal
Offer prothrombin complex concentrate to patients who are taking warfarin and actively
bleeding.
Emergency endoscopy- Timing of Endoscopy


Offer endoscopy to unstable patients with severe acute upper gastrointestinal

bleeding immediately after resuscitation.
Offer endoscopy within 24 hours of admission to all other patients with upper
gastrointestinal bleeding.
Urgent endoscopy is necessary for variceal haemorrhage - confirms the diagnosis
and source of bleeding, allowing the bleeding point to be visualised and treated:
Band ligation is the first choice of treatment
Vasoactive drugs
 The use of vasoactive agents (terlipressin, octreotide or somatostatin) is associated with
a significantly lower risk of acute all-cause mortality and transfusion requirements, and
improved control of bleeding and shorter hospital stay.
 Terlipressin is an analogue of vasopressin and is considered the vasoactive agent of
choice in acute variceal bleeding. It should be given to all patients presenting with
suspected variceal bleeding prior to endoscopy and following confirmation.
*Vasopressin and terlipressin should not be used in severe hypovolaemic shock and patients
with severe cardiac disease.
Variceal obturation with glue
This involves embolisation of varices with a glue-like substance (N-butyl-2-cyanoacrylate).
It is particularly good for gastric or gastro-oesophageal variceal bleeding.
However, there is a risk of embolisation to the lung, spleen or brain.
Balloon tube tamponade (Sengstaken-Blakemore tube)

 Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled

variceal haemorrhage.
 The Sengstaken tube is inserted through the mouth and into the stomach.
 The gastric balloon is inflated with air and the gastric balloon in then pulled up against the
oesophagogastric junction, compressing submucosal varices.

If bleeding continues, it may be that the tube is wrongly positioned or bleeding is from another source.
Transjugular intrahepatic portosystemic shunt (TIPS)- recommended as the treatment of choice for
uncontrolled variceal haemorrhage.

The hepatic vein is cannulated percutaneously via the internal jugular vein, using a needle under
ultrasound or fluoroscopic guidance.
 A tract is created through the liver from the hepatic to the portal vein - thus reducing portal pressure.
This is dilated and an expandable metal stent inserted to create a shunt.
 This has a high success rate but encephalopathy is found in 25% of cases (as portal blood diverted
from the liver) and shunt occludes within one year in up to 50% of cases.