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UGI bleed is defined as the bleeding originating proximal to ligament of treitz.90% of patients presenting with GI haemorrhage has an UGI source.

Etiology

• Variceal bleed

  • Gastric

  • Esophageal

• Non variceal bleed

  • Peptic ulcer disease

  • Erosive gastritis

  • Mallory weiss syndrome

  • Stress ulcer

  • AV malformation

  • Malignancy

Clinical Presentation

• Hematemesis

• Malena

• Vitals : Tachycardia, hypotension , decreased pulse pressure may be present.

• Cold & clammy skin due to hypotension may be present.

• Look for features of CLD.

• Vomiting and retching followed by hematemesis suggest Mallory weiss tear.

• H/o of glucocorticoids, NSAID's or anticoagulant intake.

• Blood urea nitrogen levels are elevated due to GI bleed and absorption of Hb. BUN: Creatinine ratio >30 is suggestive of UGI bleeding.

Variceal Bleeding

• It is defined as bleeding from esophageal or gastric varix at the time of endoscopy or presence of large esophageal varices with blood in stomach and no other recognisable cause of bleeding.

• Two factors that appear to determine the development of varices are continued hepatic injury and degree of portosystemic shunting.

• Portal pressure reflects intravariceal pressure and a hepatic venous pressure gradient greater than 12mm Hg is needed for development and bleeding from esophageal varices.

Management of Active variceal bleed

• Airway, Breathing has to addressed.

• Circulation :

  • Secure a two large borer IV cannula

  • IV fluid resuscitation

  • Blood products to be transfused.

• Endoscopy

  • As soon as patient is hemodynamically stable preferably within 24hrs is the standard of care.

  • Variceal band ligation is the method of first choice.

  • Other methods like sclerotherpy , tissue adhesive like cyanoacrylate or bucrylate are used.

• Octerotide

  • It is a stomatostatin analogue .

  • It causes selective spalnchic vasoconstriction and reduces portal pressure and portal blood flow.They also reduce secretion of gastric acid & pesin.Stimulates mucus production.

• DOSE : 25 - 50 mcg IV stat ; followed by 50 mcg/h IV infusion.

• Adverse effect:

  • Arrythmia, Bradycardia

  • Vomiting, flatulence, losse stools, abdominal pain

  • Hypoglycemia & hypergylcemia

• Availability : Ampoules 50, 100mcg.

Terlipressin

• It is the only agent which have proven to improve survival in acute variceal bleeding.

Vasopressin

Antibiotic in variceal bleeding

• Bacterial infection occurs in about 20% of patients with cirrhosis with UGI bleed within 48hrs.

• The suggested drug is ciplox 1gm/day for seven days orally.

Primary Prophylaxis

• Propranolol : It is used as main stay agent in grade2 or grade 3 varices. It reduces portal pressure gradient, reduces azygous blood flow and also variceal pressure. It achieves this by splanchic vasoconstriction and reducing cardiac output. Dose : 40mg BD – 80mg BD.

• Alternative drugs : Nadalol or isosorbide mononitrate

Secondary prophylaxis of variceal hemorrhage

TIPSS (Transjugular Intrahepatic Portosystemic Stent Shunting)

• This technique uses a stent placed between portal vein & hepatic vein within liver to provide a portosystemic shunt and therefore reduce portal pressure.

• It is associated with more chance for hepatic encephalopathy.

• It is done when other methods fail to control variceal bleeding & recurent bleeding.

Portosystemic shunt surgery

• Surgery prevents recurrent bleeding but carries a high mortality and often leads to encephalopathy.

Management of Non variceal bleed

Proton Pump Inhibitors

• They reduce both basal and stimulated acid secretion by inhibiting H+K+ ATPase, the proton pump of parietal cells.

• IV PPI achieves more profound and sustained supression.

• DOSE

  • Pantoprazole/omeprazole : 80mg IV bolus followed by 8mg/hr IV infusion for 72hrs. (increased risk of rebleed during 2-3 day)

Reference

• UK Guidelines on management of variceal hemorrhage: BMJ

• Tintinalli

• Davidson