Acute Gastrointestinal Bleeding Guidelines
Upper Gastrointestinal (GIT) Bleeding: This accounts for about 80% of the bleeding.
Peptic Ulcer Disease accounts for 50-75% of upper GIT bleeding.
Bleeding from varices 15%, oesophagitis, duodenitis and Mallory-Weiss Syndrome account for about 5% each.
Lower GIT bleeding: The causes of this include diverticular bleeding, angiodysplasia, AV malformations, colonic polyps or tumours, Meckel’s diverticulum or inflammatory bowel disease.
Mortality from upper GIT bleeding has now fallen to 5%, however variceal bleeding still has a risk of about 30%.
Endoscopy remains the best investigation and therapeutic interventions may be performed at the same time.
Angiography seldom used for upper GIT bleeding however in lower GIT bleeding it can be performed with embolisation to control bleeding brisk bleeding. However if bleeding is rapid a laparotomy must be considered.
Second control bleeding.
Third prevent recurrence of haemorrhage.
Fourth prevent other complications.
All these elements must be thought of concurrently however the emphasis of management should always remain on resuscitation and control of bleeding until these are completed satisfactorily.
Two large bore cannulae are placed in. Blood and plasma expanders are given. Crystalloids Hartmann’s or normal saline solution can be used initially however if the patient has ascites change to albumin solutions to reduce the accumulation of ascitic fluid. Blood products should be given to correct haemoglobin levels and coagulopathy. It is important to restore the blood volume however over transfusion may lead to increased bleeding risk. Following adequate resuscitation it is important to identify the high risk patient who is likely to require early endoscopic or surgical treatment.
Identifying the high risk patient; this patient requires early endoscopic or surgical treatment.
Significant GIT bleeding is indicated by syncope, haematemesis, systolic BP below 100mmHg, postural hypotension and if more than 4 units of blood have been transfused in 12 hours to maintain blood pressure.
Management of Bleeding:
Esomeprazole 80mg IV bolus over 1 hour followed by 8mg/h for 72 hours, for high risk patients.
Esomeprazole IVI or omeprazole orally-40mg bd, for all other patients.
Octreotide 50mcg IV bolus followed by a 25mcg/h infusion. Continue in variceal bleeds for a minimum of 48 hours may in persistent bleeding be used for 5-7 days. It has no benefit for peptic ulcer disease and should be stopped in all patients with non variceal bleeds.
Give prophylactic antibiotics 3rd generation cephalosporin, if patient has signs of cirrhosis. IV ceftriaxone 1g daily
Correction of coagulopathy:
FFP if INR >1.5 and drop in Hb >4g/dl
10mg Vitamin K ivi
Platelets if active bleeding and platelet count < 50,000
Endoscopy must be performed immediately if persistent bleeding despite correction of coagulopathy and pharmacological treatment, i.e. within 6 hours.
In high risk patients endoscopy should be performed during the first 24 hours of admission.
This may allow injection with adrenalin at the base of a bleeding ulcer or banding of bleeding varices.
Instituted in patients where:
1) arterial bleeding cannot be controlled at endoscopy
2) Massive transfusion required to maintain blood pressure
3) Recurrent bleeding after initial success with endoscopic treatment with ulcer disease.
4) Evidence suggesting GIT perforation.
Prevention of Recurrent Bleeding:
1) Recognize the high risk patients and the high risk disease
High Risk Ulcer: This is determined at endoscopy by the stigmata of bleeding.
1) Spurter or oozer- 85-90% chance of recurrent bleeding
2) Protuberant vessel 35-55% chance of recurrent bleeding
3) Adherent clot 30-40% chance of recurrent bleeding
4) Flat spot 5-10% chance of recurrent bleeding
5) None <5% chance of recurrent bleeding
The first 3 are considered high risk ulcers.
2) Treat all patients with bleeding varices or upper GIT bleeding with cirrhosis with IVI antibiotics.
3) Test for helicobacter in all ulcer patients and treat all patients with disease.
4) Proton pump inhibitors to be continued if ulcer related disease.
1) Treat any reversible precipitant of chronic liver disease (go through chronic liver disease check list.) All alcohol related liver disease needs to have appropriate counseling. All hepatitis B must be refered for treatment.
2) Treat portal hypertension: The options include B blocker therapy, screening endoscopies and prophylactic banding and TIPPS procedure. B Blocker therapy is the treatment of choice when tolerated and compliance with therapy is good, if concerns about compliance it should not be used as stopping B blockers causes rebound and worsens outcome. If B blockers are not tolerated nitrates can be used (inferior but better tolerated.) All patients not placed on medications to manipulate portal hypertension should be considered for prophylactic banding. TIPPS procedure should only be considered in severe cases and when encephalopathy has not been a problem.
3) Treat other symptoms – such as infection, alcohol withdrawal encephalopathy and other symptoms associated with chronic liver disease (see guidelines.)
4) Consider the patient for work up for liver transplant.
The triage of patients to HDU or ICU should reflect the underlying principle that only patients that will benefit should be offered intensive care. Both the patients that are too well or whose prognosis is too poor to have mortality benefit should not be admitted. All admission requests should be discussed with ICU consultant or senior registrar.
Patient’s to be considered for HDU monitoring:
Significant GIT bleeding with:
2) Hypotension systolic<100mmHg not corrected by moderate fluid resuscitation e.g. 2litres of crystalloid or colloid.
3) Fall in Hb >4g/dl
4) Signs of decompensated liver disease
5) Known variceal bleeding in past
6) Evidence of ongoing bleeding
7) Requirement of octreotide infusion to cease bleeding
8) Significant coagulopathy (platelet count<80 and INR>2.)
9) Patients with an endoscopically proven high risk ulcer.
Understanding Portal Hypertension:
This is the main consequence of cirrhosis and is responsible for its most important complications. Portal hypertension initially increases as a result of increased intrahepatic resistance, but once the collaterals are formed high portal blood flow is maintained by an increased blood flow secondary to vasodilation. Although it is the increased portal pressure that leads to the formation of varices it is the hyperdynamic splanchnic circulation that leads to their growth and eventual rupture.
Ascites is formed from increased sinusoidal pressure and also from sodium retention, secondary to vasodilation and activation of the neurohumoral systems.
Hepatorenal syndrome results from more severe peripheral vasodilation that leads to renal vasoconstriction.
Spontaneous bacterial peritonitis and hepatic encephalopathy are a consequence of portal hypertension and liver insufficiency.
It is important to understand that when dealing with one aspect of portal hypertension such as bleeding varices that the other aspects are present and will almost certainly be affected.
Understanding the causes of portal hypertension:
Portal pressure increases initially as a consequence of an increased resistance to portal flow. There is some intrahepatic vasoconstriction that appears in part to be related to a deficiency in nitric oxide (NO.) Increased portal venous flow is most likely to be triggered by increased splanchnic and peripheral vasodilators mainly NO, which may be exacerbated by bacterial gut translocation.
Prevention of first variceal bleed:
Non selective B blockers are the old standard in prevention of first variceal bleed. The 2 year risk is reduced from 30% to 14% in patients with large varices. No advantage in survival is seen in patients with small varices however the varices grew slower and less hemorrhage. Adding nitrates has not improved survival however there may be an improvement in patients whose hepatic venous pressure gradient does not improve with B blockers.
Prophylactic banding of varices and b blockers had about the same reduction in mortality, therefore this can be considered in patients who are not candidates for long term treatment with B blockers.