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Acute upper gastrointestinal bleeding (UGIB)

This post is based upon two recent review articles, published in 2017 (K Siau) and 2019 (A Stanley) and NICE guideline (updated 2016).


Background

Upper gastrointestinal bleeding UGIB refers to bleeding from the oesophagus, stomach, or duodenum. 

Upper gastrointestinal bleeding (UGIB) has a mortality of 2-10%.

Patients assessed to be very low risk of needing intervention or death can be managed as outpatients.

Causes

Peptic ulcer (gastric, duodenal)
Varices: oesphageal or gastric
Malignancy
Aorto-enteric fistula
Vascular ectasia
Drugs (anti platelet, anti coagulant)

Symptoms and signs

Hematemesis (bloody or coffee ground emesis)
Melena
Hemodynamic instability 



Resuscitation and initial management

  1. ABC

  2. Intravenous fluid resuscitation

  3. Blood and Blood Products
    Red cell transfusion to achieve Hb 70-80 g/L (higher threshold Hb>80 g/L if severe bleeding with hypotension or pre-existing cardiovascular disease)
    Offer platelet transfusion to patients who are actively bleeding and have a platelet count <50 x 10⁹/L
    Offer fresh frozen plasma INR or APTT>1.5 times normal.
    Offer cryoprecipitate If fibrinogen< 1.5 g/L
    Offer prothrombin complex concentrate to patients who are taking warfarin and actively bleeding.

  4. High dose proton pump inhibitors (PPIs) at least 72hr

  5. Prokinetic agent iv erythromycin (250 mg infusion 30-120 minutes before endoscopy; to improve gastric emptying, thereby improving visualization at endoscopy)

  6. Antifibrinolytic therapy (iv tranexamic acid): uncertain if beneficial, awaiting results of HALT-IT trial

  7. If known liver cirrhosis, administer:
    antibiotics
    vasoactive drugs (5 days of terlipressin, somatostatin, or its analogs octreotide and vapreotide)

Do not use recombinant factor Vlla except when all other methods have failed.

Controlling bleeding in patients on NSAIDs, aspirin, clopidogrel, warfarin or direct oral anticoagulants (DOACs) 

Warfarin: reverse effect of warfarin by iv prothrombin complex concentrate (PCC) and iv vitamin K

INR>2.5: normalise INR by iv prothrombin complex concentrate (PCC) or fresh frozen plasma and iv vitamin K

DOAC: stops DOAC
give antidote if severe bleeding: idarucizumab (for dabigatran, a thrombin/Factor 2a inhibitor) and andexanet alfa (for factor Xa inhibitors: apixaban, rivaroxaban, fondaparinux)

Low-dose aspirin for secondary prevention: continue, once haemostasis has been achieved.

NSAIDs: Stop

Clopidogrel: discuss risk/benefits of discontinuing or continuing with patient and appropriate specialist (cardiologist or stroke specialist)

Risk assessment

Glasgow-Blatchford score at first assessment

Rockall score after endoscopy.

Glasgow-Blatchford score ≤1 consider outpatient endoscopy and management 

GLASGOW-BLATCHFORD SCORE

ROCKALL SCORE POST ENDOSCOPY


Endoscopy should be undertaken within 24 hours (and possibly within 2 hours)

Immediate endoscopy (<2hr) for people who are haemodynamically unstable

Haemodynamically unstable People who are haemodynamically unstable are those with active bleeding whose blood pressure or pulse cannot be normalised or who need rapid intravenous fluids to maintain haemodynamic stability.

People with severe acute upper gastrointestinal bleeding who are haemodynamically unstable are given an endoscopy within 2 hours of optimal resuscitation.

Endoscopy (<24hr) for people who are haemodynamically stable

Haemodynamically stable means stabilised blood pressure and pulse.

This will help to avoid re-bleeding, and can reduce the length of their hospital stay.


Managing non-variceal bleeding (e.g. duodenal or gastric ulcer)

A peptic ulcer may present with high risk stigmata:

  • active bleeding

  • a non-bleeding visible vessel

  • adherent clot

Endoscopic haemostasis of such lesions has been shown to reduce mortality, rebleeding risk and the need for surgery.

Endoscopic treatment

Endoscopic treatment involves:

  • a mechanical method (e.g.clips) with or without adrenaline

  • thermal coagulation with adrenaline

  • fibrin or thrombin with adrenaline.

  • haemostatic spray therapy

Adrenaline injection should always be followed by a second modality

Proton pump inhibitors

Offer proton pump inhibitors for non-variceal UGI after endoscopy.

Treatment after first or failed endoscopic treatment

Recurrent ulcer bleeding is treated with repeat endoscopic therapy, with subsequent bleeding managed by interventional radiology or surgery


Managing variceal bleeding

TIPSS procedure. A: Insertion of a catheter- guided needle passed from the internal jugular to right hepatic vein to puncture the portal vein. B: Insertion of guide-wire into the portal system. C: Dilatation of hepatic parenchyma between the portal vein and hepatic vein. D: Stent placement in the newly formed tract

  1. Terlipressin 2mg every 4hr
    Vasoactive drugs (terlipressin, somatostatin, or its analogs octreotide and vapreotide) cause splanchnic artery vasoconstriction
    Stop treatment after definitive haemostasis has been achieved, or after 5 days.

  2. Prophylactic antibiotic (Intravenous ceftriaxone) therapy (7 day duration)

Oesophageal varices

Use band ligation

For massive refractory oesophageal variceal bleeding consider using a removable covered self-expanding metal stent (Danis stent) instead of balloon tamponade as a temporising measure

Gastric varices

Offer endoscopic injection of N-butyl-2-cyanoacrylate (tissue adhesive glue) or thrombin injection

Recurrent variceal bleeding (oesophageal or gastric)

Recurrent variceal bleeding is generally treated with transjugular intrahepatic portosystemic shunt (TIPSS)


Post-endoscopic management

  1. High dose proton pump inhibitors for 72 h

  2. Patients with cirrhosis should continue antibiotics for up to seven days

  3. Variceal bleeding should be treated with vasoactive drugs for up to five days

  4. Non-selective beta blockers to reduce portal pressures (propranolol or carvedilol).

  5. Early commencement of antithrombotic drugs (e.g. aspirin, DOACs, clopidogrel), after hemostasis is achieved, to reduce thrombotic events and death