This document summarizes upper gastrointestinal bleeding (UGIB), including its causes, presentation, evaluation, management, and prognosis. It discusses specific causes like variceal bleeding, peptic ulcer bleeding, Mallory-Weiss syndrome, and Dieulafoy's lesion. For variceal bleeding, it describes treatments like band ligation, TIPS, and beta-blockers for prophylaxis. For peptic ulcers, it notes the role of PPIs, H. pylori treatment, and endoscopic therapies. The document provides an overview of evaluating and treating major causes of UGIB.

1. UPPER GI BLEEDING
PRESENTER: DR. VISHNU THEJA. POSA
MODERATOR: PROF. KARAM ROMEO SINGH

2. INTRODUCTION
• Gastrointestinal (GI) bleeding is a common and potentially life-threatening
problem.
• Mortality rate of upper GI bleeding (6% to 10%) has remained unchanged
over the years.
• Manifestastion of UGIB is Malena and
Haematemesis.

3. HAEMATEMESIS:
• Gastric acid may alter the colour of the vomited blood.
• If vomiting occurs shortly after the onset of bleeding, the vomitus appears red.
• Precipitated blood clots and acid-degraded blood produce a characteristic
‘coffeeground’ appearance of the vomitus.
MELAENA:
• Melaena is black, tarry, foul-smelling stool due to acid haematin (hb degredation
product)
• 60 mL of blood can cause single melaenic stool.
• Melaena may persist a week.

4. CAUSES

5. Initial Assessment
• A,B,C Assessment
• Blood loss of <500 mL is rarely associated with systemic signs.

6. Resuscitation

7. Diagnostic Evaluation
• Stigmata of liver cell failure with painless UGI bleed may indicate Variceal Bleed
• History of NSAID intake, pain epigastrium may indicate Peptic Ulcer Bleed
• A history of retching and vomiting prior to haematemesis may indicate Mallory-
Weiss syndrome
• History of aortic graft can have Aortoenteric Fistula
• History of radiation therapy may indicate Radiation Enteritis
• History of shock before bleeding may indicate Ischemic Enteritis

8. Poor Prognostic Indicator

9. Acute Variceal Hemorrhage
• Oesophageal varices, Gastric varices can bleed.
• IV terlipressin 1 mg every 4 to 6 hourly or octreotide 50 to 100 µg bolus,
followed by infusion at 50 µg/hour.
• Sengstaken Blakemore tube with oesophageal and gastric balloon inflated with
250ml air for mechanical haemostasis.

10. EVL
• Involves the placement of rubber bands around a portion of the varix causing
ischaemic necrosis of the mucosa and submucosa.
• Application of the bands is started at the gastroesophageal junction and progresses
cephalad in a helical fashion.
• Heals in 14 to 21 days.
• EVL sessions are repeated at approximately 2-week intervals until varices are
obliterated, usually requiring 2 to 4 ligation sessions.

12. OTHER MODALITIES
1. Transjugular Intrahepatic Porto-systemic Shunt (TIPSS)
2. Gastroesophageal Devascularisation
3. Balloon-occluded Retrograde Transvenous Obliteration (B-RTO)
Indications for TIPS
• Multiple episodes of variceal bleeding
• Refractory variceal hemorrhage despite adequate endoscopic treatment
• Bleeding portal hypertensive gastropathy
• Bleeding gastric varices

13. Prophylaxis of Variceal Bleeding
• After control of initial haemorrhage, prevention of variceal rebleeding is an
important aspect of the management of portal hypertension. Non-selective
beta-blockers reduce cardiac output and cause splanchnic vasoconstriction,
reducing portal venous pressure

14. Primary Prophylaxis In Esophageal Varices
Ligation is more effective than beta-blocker therapy in reducing first bleeding. @GH
Secondary Prophylaxis In Esophageal Varices
Combined endoscopic and drug therapy is more effective than either therapy alone. @GH
Carvedilol Versus Propranolol For Secondary Prophylaxis Of Variceal Hemorrhage
In Patients With Liver Cirrhosis
Carvedilol was equally efficacious and may be preferred over propranolol due to lower
rate of rebleeding. @ARGH

15. • All patients with cirrhosis should be endoscoped at the time of diagnosis (level
1a).
• If at the time of first endoscopy no varices are seen, endoscopy should be at 2–
3-year intervals (level 2a).
• Grade I varices» should be endoscoped at yearly intervals (level 2a).
• Varices with red signs or grade 2–3 varices primary prophylaxis is must (level
1a).

16. PEPTIC ULCER
• Duodenal > Gastric.
• Up to 80% of duodenal ulcers and 50% of gastric ulcers are caused by H pylori.
• Bleeding stops spontaneously in 80% cases.
• Proton pump inhibitors (PPI) are the mainstay of pharmacological treatment.
• High dose intravenous (IV) omeprazole or pantoprazole (80 mg IV bolus
followed by 8 mg per hour for 72 hours).
• Patients with ongoing bleed, haemodynamic compromise, and high transfusion
requirements need urgent endoscopic therapy

17. • The most popular endoscopic therapy is injection therapy using epinephrine
(1:10,000).
• Newer techniques include application of metal clips, band ligation, argon plasma
coagulation and endoloops.
• Presence of hypotension at admission and an ulcer size larger than 2 cm are
independent predictors of failure of endoscopic therapy
• Eradication of H. pylori and stopping NSAIDS are two factors shown to prevent
recurrent bleeding.

18. Erosive Gastropathy
• Erosive gastropathy refers to endoscopically visualised subepithelial
haemorrhages and erosions.
• Antacids, H2 receptor blockers, proton pump inhibitors and sucralfate decrease
bleeding from gastric erosions.
• Endoscopic argon plasma coagulation

19. Mallory-Weiss Syndrome
• Recurrent vomiting or retching can lead to mucosal tears at the gastro-
oesophageal junction causing haematemesis
• Bleeding is usually not massive and stops spontaneously
• Haemoclips

20. Dieulafoy’s Lesion
• Dieulafoy’s lesions are prominent submucosal vessels.
• These lesions are difficult to identify if they are not bleeding actively during
endoscopy.
• Argon plasma coagulation

21. GAVE
• AKA watermelon stomach.
• It is associated with cirrhosis and scleroderma.
• Endoscopic hemostasis with thermal heat modalities such as laser and argon
plasma coagulation

22. Aortoenteric Fistula
• Communication between the abdominal aorta and duodenum.
• Infected abdominal aortic surgical graft can cause AE fistula
• Diagnostic suspetion history of an abdominal aortic aneurysm or by palpation of a
pulsatile abdominal mass
• Patients with an acute UGIB and a history of an aortic aneurysm repair should
undergo urgent CT with IV contrast or MR angiography.
• Surgical treatment is required to remove the infected graft

25. REFERENCES
• HARRISON PRINCIPLES OF INTERNAL MEDICINE
• THE WASHINGTON MANUAL OF CRITICAL CARE
• API TEXT BOOK OF MEDICINE
• SLEISENGER AND FORDTRAN’S GASTROINTESTINAL AND LIVER
DISEASES
• JOURNAL OF HEPATOLOGY

26. THANK YOU