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Non variceal upper GI bleed

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Define upper GI bleed?

Upper GI bleed is that which originates proximal to the ligament of Treitz. It presents with haematemesis, coffee ground vomiting or melaena. Melaena can also be due to small bowel or right colonic bleeding.

Discuss the Rockall system for bleed prognosis?

Rockall scoring system is widely used to identify the risk of death and rebleeding.

Score
Variable 0 1 2 3 Initial score criteria
Age <60 60-79 >=80
Shock No shock
Pulse<100
SBP>=100
(indicates loss of < 15% of blood volume or 750ml)
Tachycardia
Pulse>100
SBP>=100
(indicates loss of 15-30% of blood volume or 750-1500ml)
Hypotension
SBP<100
Co-morbidity No major
Co-morbidity
CCF, IHD,
Any major co morbidity
Renal failure, Liver failure,
Disseminated malignancy
Diagnosis Mallory Weiss tear, no lesion identified, No SRH All other diagnoses Cancer of the upper GIT Additional criteria for full score
Major stigmata of recent haemorrhage (SRH) None or dark spot only Blood in the upper GIT, adherent clot, visible or spurting vessel

If the initial score (pre endoscopic) is above 0, there is significant mortality (score 1: predicted mortality 2.4%, score 2: predicted mortality 5.6%). Thus only those scoring 0 can safely be discharged at this stage.

Patients with a full Rockall score (post endoscopic) of <3 have a low risk of rebleeding (approx 5%) or death (less than 1%) and should be considered for early discharge.
The risk of rebleeding in those with an adherent clot is around 35% and that with a non bleeding visible vessel is 40-50%.

Who could be considered for early discharge or non admission to hospital?

  • Age <60 years
  • No haemodynamic disturbance
  • No major co-morbidity
  • Not a current inpatient or transfer
  • No witnessed haematemesis or haematochezia

What is the role of pre endoscopy PPI?

PPI should not be used prior to endoscopy in patients presenting with an acute upper GI bleed. Pre endoscopy high dose PPI may reduce the need for endoscopic therapy, but there is no evidence that it alters important clinical outcomes. Further the study was done in Asian patients (more sensitive to PPI) and may not be generalisable to this country.

What is the evidence for early endoscopy?

There is no consistent definition of an early endoscopy. The literature describes early endoscopy as one ranging from 1-24 hours of the initial presentation. Early endoscopy is associated with reduced transfusion requirements, reduction in rebleeding, reduced length of stay and a lower need for surgery, however there is no evidence that it reduces mortality. This may be because the major determinant of survival is the number and severity of co-morbidities rather than achievement of haemostasis.

What are the major causes of upper GI bleeding?

Peptic ulcer (commonest cause), oesophagitis, gastritis/erosions, erosive duodenitis, varices, portal hypertensive gastropathy, malignancy, Mallory Weiss tear and vascular malformation.
In approximately 20% of patients presenting with an apparent upper GI bleed endoscopy does not reveal a cause.

Discuss endoscopic treatment of upper GI bleed?

  • Endoscopic therapy should only be delivered to actively bleeding lesions, non bleeding visible vessels and adherent clots.
  • Injection of 1:10,000 adrenaline- Injection alone reduces the rebleeding rate in non bleeding visible vessel (from 50 to 15-20%) and adherent clot (from 35% to 10%). Studies show that at least 13 mls should be injected for optimum haemostasis.
  • Thermal- Heater probe as similar efficacy to injection
  • Mechanical- Clips and thermo coagulation has comparable efficacy.
  • Combination therapy (injection plus one other modality)- A meta analyses  showed that combination therapy reduces the rebleeding rate from 18.4% to 10.6% and emergency surgery from 11.3 to 7.6% and mortality from 5.1% to 2.6%.
  • Combination of endoscopic therapy comprising an injection of least 13 ml of 1:10,000 adrenaline coupled with either a thermal or mechanical method is thus recommended.

Discuss the value of a second look endoscopy?

A second endoscopy should be considered within 24 hours when initial endoscopic treatment was considered sub optimal or in patients in whom rebleeding is likely to be life threatening. A second endoscopy reduces the rebleeding rate without affecting survival or surgical operation rate.

Discus the role of high dose PPI following endoscopic therapy?

High dose of IV PPI (omeprazole or pantoprazole 80 mg stat and then 8 mg/hour for 72 hours) should be used in patients with major peptic ulcer bleeding (non bleeding visible vessel, active bleeding ) following endoscopic therapy. The aim of PPI therapy in this group of patients is to maintain intragastric pH above 6 to stabilise clots and prevent rebleeding.
A meta analyses of 24 RCTs involving 4373 patients confirmed that PPIs significantly reduce rebleeding (NNT=13), the need for surgery (NNT=34) and requirement for further endoscopic treatment (NNT=10). There was also a significant reduction in mortality when analysis was confined to 7 trials in high risk patients (active bleeding or non bleeding visible vessel) following endoscopic treatment. The reduction in mortality remained significant when analysis was confined to 4 trials that used high dose PPI treatment following endoscopic treatment. There was no effect on mortality in the other 3 trials that used low dose IV PPI or oral doses.

What is the role of tranexamic acid or somatostatin analogues in non variceal upper GI bleed?

Tranexamic acid may be of value however there is insufficient evidence to recommend its use in non variceal upper GI bleed.
Similarly there is insufficient evidence for the use of somatostatin or its analogues in non variceal bleed.

Discuss treatment options for rebleeding following endoscopic therapy?

Optimum management is based upon clinical judgement, local expertise and is best undertaken following discussion between surgeons and physicians. Options include:

  • Repeat endoscopic treatment- one trial randomised 100 patients who re bled following endoscopic therapy for ulcer bleed to operative surgery or repeat endoscopic treatment. 30 day mortality and transfusion requirements were low and similar in both groups
  • Selective arterial embolization- a single retrospective comparison between surgery and embolization showed no difference in mortality or rebleeding.  Embolisation in small cohort studies shows high rates (98%) of technical success and low (4-5%) complication rates (hepatic/splenic infarction, duodenal ischaemia)
  • Surgery

Discuss prevention strategy?

Approximately one third of patients who present with ulcer bleed will develop recurrent bleeding within 2 years and 40-50% within 10 years if left untreated after ulcer healing.
Patients with peptic ulcer bleeding should be tested for Helicobacter Pylori (HP) and one week eradication treatment prescribed for those who test positive. A further three weeks ulcer healing treatment should be given. In non NSAIDs users’ maintenance PPI treatment should not be continued after ulcer healing and HP eradication.
The NNT with eradication to prevent one episode of rebleeding is 6 when compared with no long term maintenance and 20 when compared with long term antisecretory treatment.

Discuss NSAIDS, COX 2 inhibitor, aspirin, long term PPI etc?

  • Patients with healed bleeding ulcers who test negative for HP require concomitant PPI treatment at the usual daily dose (like esomeprazole 20mhs a day), if NSAIDs, aspirin or COX- 2 inhibitors are indicated.
  • Aspirin and HP eradication- Eradication of HP alone is as effective as maintenance treatment with omeprazole in preventing recurrent upper GI bleed in patients taking low dose aspirin. The probability of recurrent bleeding was 1.9% after HP eradication and 0.9% on omeprazole. A further RCT showed further reduction in frequency of rebleeding by adding lansoprazole after HP eradication.
  • In patients with aspirin induced ulcer bleeding aspirin plus esomeprazole is superior to clopidogrel in preventing recurrent ulcer bleeding.
  • Omeprazole (2mg daily) is superior to HP eradication in preventing recurrent bleeding in patients taking non aspirin NSAIDs.

Discuss SSRI, steroids and anticoagulants?

There is weak evidence that SSRI may be associated with an increased risk of upper GI bleed particularly in patients at high risk and those taking concomitant NSAIDS or aspirin. Thus SSRI drugs should be used with caution in this group of patients.
Anticoagulant use is associated with a threefold increase in risk of bleeding ulcer. Steroids double the risk of GI bleed in patients taking NSAIDs. Thus steroids and anticoagulants should be used with caution in patients at risk of GI bleed, especially in those taking aspirin or NSAIDs.

Example case histories:

Case 1:

68 M presented with an upper GI bleed. He is on warfarin for AF. His INR on admission is 2.4

Do we need to correct the INR to achieve endoscopic haemostasis?

Endoscopic therapy is very effective in patients with elevated INR (even in variceal bleed). Rebleeding rate does not seem to be affected by pre procedure INR (unless supratherapeutic) or attempts at correcting it pre procedure. However, attempts to correct INR do delay endoscopy. Thus, the patient in question should have his INR reversed, however his endoscopy should not be delayed till his INR is corrected (as his INR is therapeutic)

International Consensus Recommendations on the Management of Patients with Nonvariceal Upper Gastrointestinal Bleeding 2009 (archived copy) recommends that endoscopy should not be delayed while correcting INR unless the INR is supratherapeutic, because correction in these patients may facilitate endoscopic treatment. This approach should not be generalized to patients with cirrhosis because the prothrombin time does not seem to predict bleeding risk in this setting.

Case 2:

65 F presented with 3 day h/o melaena. She is on aspirin for secondary prophylaxis. Her Hb on admission is 7.4 gms/dl. While awaiting an endoscopy, she has chest with ECG changes and rise in troponin. A cardiac catheterisation is planned. You are requested to perform and endoscopy prior to cardiac catheterisation.

Lin S et al (Dig Dis Sci. 2006 Dec;51(12):2377-83) in a study showed that UGIB as the inciting event and patients suffering from haematemesis and hemodynamic instability were significantly associated with requiring endoscopic therapy. The authors thus concluded that in patients suffering from concomitant UGIB and AMI, urgent endoscopy was most beneficial in patients with UGIB as the initial event and those presenting with haematemesis and hemodynamic instability. In patients without these clinical features, urgent endoscopy may be delayed, unless cardiac management decisions are dependent on endoscopic findings.

Case 3:

73 M admitted with h/o upper GI bleed. He is on aspirin for secondary prophylaxis. OGD showed a bleeding peptic ulcer. When would you restart aspirin?

The benefits-risk ratio favours restarting anti-platelet treatment within a week. Hence, anti-platelet treatment should not be stopped for more than a week.

International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding 2009 (archived copy)  recommends that in patients who receive low-dose ASA and develop acute ulcer bleeding, ASA therapy should be restarted as soon as the risk for cardiovascular complication is thought to outweigh the risk for bleeding. Data from RCTs (209, 210) suggest that the cardiovascular benefits of early reintroduction of ASA or clopidogrel may outweigh the gastrointestinal risks.

Case 4

65 M admitted with melaena. He was started on PPI pre endoscopy. Endoscopy performed 24 hrs later showed a duodenal ulcer with an adherent clot in the base.

What is the role of pre endoscopy PPI?

International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding 2009 (archived copy)  recommends Preendoscopic PPI therapy may be considered to downstage the endoscopic lesion and decrease the need for endoscopic intervention but should not delay endoscopy.

Although preendoscopic PPI therapy has not been shown to affect rebleeding, surgery, or mortality, the beneficial effects on the need for intervention, supportive cost effectiveness analyses, and excellent safety profile suggest that these agents may be useful, particularly in those suspected of having high-risk stigmata.

Discuss the treatment of adherent clot?

International Consensus Recommendations on the Management of Patients with Nonvariceal Upper Gastrointestinal Bleeding 2009 (archived copy) recommends

Statement B5

A finding of a clot in an ulcer bed warrants targeted irrigation in an attempt at dislodgement, with appropriate treatment of the underlying lesion.

Statement B6

The role of endoscopic therapy for ulcers with adherent clots is controversial. Endoscopic therapy may be considered, although intensive PPI therapy alone may be sufficient.

Ref

  1. British Society of Gastroenterology and SIGN guidelines
  2. http://www.bsg.org.uk/clinical-guidelines/endoscopy/guidelines-for-non-variceal-upper-gastrointestinal-haemorrhage.html
  3. International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding 2009 (archived copy at WebCite)


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