Haematemesis and melaena

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Chapter 8 HAEMATEMESIS AND MELAENA

KEY POINTS

• Resuscitation should be instituted irrespective of the underlying cause of gastrointestinal bleeding.
• A multidisciplinary approach to management is key.
• Patients over 60 years of age and patients with comorbid conditions have a higher risk of mortality.
• Endoscopic examination should be made available to the patient within 24 hours or when the patient is stabilised.
• A combination of adrenaline injection with either thermal coagulation or haemoclips reduces the risk of recurrent bleeding.
• Proton pump inhibitors are recommended as an adjuvant to endoscopic therapy in peptic ulcer patients with a high risk of bleeding.
• Somatostatin or octreotide are effective therapy for acute variceal bleeding.
• Angiography may help identify bleeding from an unknown source.
• Indications for surgery include arterial bleeding that cannot be controlled by endoscopic haemostasis, and patients requiring massive transfusions.

INTRODUCTION

Acute gastrointestinal (GI) bleeding is one of the most common emergency conditions and is associated with significant morbidity and mortality. Haematemesis is the vomiting of fresh blood. Haematemesis indicates that bleeding originates from a site proximal to the ligament of Treitz. A history of fresh haematemesis usually implies a significant bleed. Vomiting altered blood that appears like coffee grounds arises from the breakdown of haemoglobin by gastric acid, and often indicates that active bleeding may have ceased. Melaena is the passage of black, tarry stool. It occurs when haemoglobin is converted to haematin by bacterial degradation. Ingestion of as little as 200 mL of blood can produce melaenic stool. Although melaena generally connotes bleeding proximal to the ligament of Treitz, bleeding from the small intestine or proximal colon may also cause melaena, especially when colonic transit is slow. Haematochezia is the passage of pure red blood or blood admixed with stool. It usually occurs as a result of bleeding in the lower GI tract. It can also be present in massive upper GI bleeding (in 10%–15% of cases).

RESUSCITATION

Irrespective of the underlying cause of GI bleeding, a patient should be resuscitated. Vital signs (blood pressure, pulse, oxygenation) should be carefully monitored. A large bore peripheral drip should be inserted for fluid replacement and, if the patient is in shock, a central line inserted. Blood transfusion should not be delayed if there is evidence of substantial volume loss. Patients with chronic liver diseases might also benefit from fresh frozen plasma and platelet transfusion. A patient with GI bleeding is best cared for by a joint team with gastroenterologists, GI surgeons and intervention radiologists. Patients with severe acute bleeding require admission to a high dependency or intensive care unit.

AETIOLOGY

The most common cause of upper GI bleeding is peptic ulcer. This is followed by mucosal erosions, Mallory-Weiss tear, oesophagitis and oesophageal/gastric varices. In the lower GI tract, the most common causes of bleeding are diverticular disease, vascular malformation, inflammatory bowel disease and colorectal neoplasia (Table 8.1). In general, bleeding from the upper GI tract is more common than lower GI tract bleeding.

TABLE 8.1 Causes of acute upper and lower gastrointestinal (GI) bleeding

Upper GI bleeding Lower GI bleeding
Common
• Gastric/duodenal ulcer
• Oesophageal/gastric varices

• Diverticular disease
• Angiodysplasia
• Haemorrhoids
Less common
• Gastroduodenal erosions
• Oesophagitis
• Mallory-Weiss tear
• Colonic neoplasms
• Inflammatory bowel disease
• Ischaemic colitis
• Radiation colitis
• Upper GI bleeding
• Small intestine diseases
Rare
• Upper GI malignancy
• Vascular malformation
• Colonic ulcers
• Rectal varices

High-risk patients

Significant GI bleeding is indicated by syncope, haematemesis, tachycardia (pulse rate >100 beats per minute), systolic blood pressure below 100 mmHg (13.3 kPa), postural hypotension and requiring more than 4 units of blood to be transfused within 12 hours to maintain blood pressure. Patients over 60 years of age with multiple underlying diseases (comorbidities) are at higher risk of mortality. Those admitted for comorbid medical problems (e.g. heart or respiratory failure, or a cerebrovascular bleed) who develop GI bleeding during hospitalisation also have a higher mortality risk.

In about 80% of patients, bleeding stops spontaneously before presentation. In the remaining 20% of patients, bleeding continues or recurs during hospitalisation. The mortality in this latter group increases as much as eight-fold compared with patients without further bleeding. Peptic ulcers are a very common cause of GI bleeding and haematemesis. High-risk peptic ulcers, those actively bleeding or that have bled recently, may show stigmata of haemorrhage on endoscopy. These stigmata of recent haemorrhage include active localised bleeding (i.e. pulsatile, arterial spurting or simple oozing), an adherent blood clot, a protuberant vessel or a flat pigmented spot on the ulcer base. Stigmata of haemorrhage are important predictors of recurrent bleeding.

INVESTIGATIONS

Endoscopy

Endoscopic examination offers three functions. It:

1. Gives the most accurate diagnosis of the source of bleeding
2. Assesses the risk of recurrent bleeding (from an ulcer or varices)
3. Offers endoscopic therapy when a source of bleeding is found.

Endoscopic examination should be made available to the patient within 24 hours or when the patient has been stabilised haemodynamically. For triage, it is the best tool to determine whether a patient should be treated at home or admitted.

The following should be done during endoscopy.

• Emptying of blood and blood clot. A single dose of erythromycin (3 mg/kg) can assist visualisation by increasing gastric emptying in a massive bleed.
• Lavage of potential bleeding source (e.g. ulcer, varices, tumour) to assess the risk of recurrent bleeding.
• Endoscopic haemostasis:

– For peptic ulcers (either actively bleeding or showing protuberant vessel or fresh clot):

• Injection therapy using adrenaline
• Thermocoagulation using heater probe or electrocoagulation
• Haemostatic clips.

– For gastric or oesophageal varices:

• Banding ligation using single or multiple band ligators
• Injection of sclerosant (e.g. ethanolamine, sodium tetradecyl sulfate [STD]) if banding is not possible
• Injection of cyanoacrylate for gastric varices is an option. Balloon tamponade can buy time to provide other definitive therapy (e.g. TIPS—see below).

– For vascular malformation:

• Argon plasma coagulation
• Haemostatic clips.

MANAGEMENT

Pharmacological therapy

In patients with a high risk of recurrent bleeding, pharmacologic control without endoscopic haemostasis is inadequate. Thus a combination of endoscopic and pharmacologic therapy is best practice for patients with bleeding ulcers.

Acid suppressing drugs

Acid suppressing drugs such as H2-receptor antagonists and proton pump inhibitors (PPIs) are effective drugs to promote ulcer healing, however H2-receptor antagonists do not control acute bleeding. As an acidic environment impairs platelet function and haemostasis, reducing the secretion of gastric acid should reduce bleeding. Potent acid suppression using intravenous PPIs (e.g. esomeprazole, lansoprazole, omeprazole, pantoprazole or rabeprazole) reduces recurrent bleeding after endoscopic therapy. PPIs should be recommended as an adjuvant to endoscopic therapy in patients with peptic ulcers with a high risk of bleeding.

Vasoactive agents

Previously, vasopressin (0.2–0.4 U/min) was the most widely used agent to reduce portal blood pressure and control variceal bleeding. Adverse effects of vasopressin such as cardiac ischaemia (in about 10% of patients) and worsening coagulopathy (by release of plasminogen activator) have discouraged the use of this drug in recent years. Terlipressin, a triglycyl synthetic analogue of vasopressin, has a longer half-life and fewer cardiac side effects and appears more effective and safe when used in combination with glyceryl trinitrate. Infusion of somatostatin and its analogue (octreotide, vapreotide) reduces portal blood pressure and azygous blood flow. They are safe and effective vasoactive agents for acute variceal bleeding. The benefit is more prominent if these vasoactive agents are given early, even before endoscopy. Octreotide has also been shown to be effective when used as an adjuvant therapy in combination with endoscopic therapy. Recurrent bleeding episodes and, hence, transfusion requirements are significantly reduced.

Antifibrinolytic agents

Antifibrinolytic agents such as tranexamic acid have not reduced the operative rate and mortality of acute GI haemorrhage. Recombinant activated factor VII (rFVIIa, eptacog alfa) may be useful in difficult cases of bleeding from oesophageal varices.

Antibiotics

Antibiotics have been recommended in management of variceal bleeding. Bacteraemia is a common occurrence after endoscopic therapy. Prophylactic antibiotics (e.g. cephalosporin or quinolone) can prevent the development of infected ascites in these patients.

Radiological therapy

Angiography is an important tool for diagnosing GI bleeding when endoscopy fails to identify the source. The advantages of angiography include accurate localisation of rapidly bleeding lesions and the potential to achieve immediate control with several treatment modalities:

• Highly-selective coil embolisation for bleeding ulcer and vascular malformation using:

– Gelatin sponge pledgets
– Microcoils
– Polyvinyl alcohol particles

• Transjugular intrahepatic porto-systemic shunt (TIPS) for gastric or oesophageal varices.

Surgery

Surgery remains the most definitive method of stopping haemorrhage. However, there is little agreement on the exact indications and best timing for surgical intervention. These issues are even less clear now that endoscopic and radiological intervention are so effective. Accordingly, good cooperation among intensivists, gastroenterologists, intervention radiologists and surgeons is essential. Indications for surgery include:

• arterial bleeding that cannot be controlled by endoscopic haemostasis
• massive transfusion (i.e. total of 6–8 units of blood) required to maintain blood pressure
• recurrent clinical bleeding after initial success in endoscopic and/or angiographic haemostasis
• evidence suggestive of GI perforation.

A multidisciplinary approach to the management of upper GI bleeding is shown in Figure 8.1.

image

FIGURE 8.1 Management of common causes of acute upper gastrointestinal bleeding.

PPI = proton pump inhibitor; TIPS = transjugular intrahepatic portosystemic shunt.

BLEEDING OF OBSCURE ORIGIN

The source of bleeding remains unidentified after gastroscopy and colonoscopy in about 5% of patients. The most common causes include angiodysplasia, small intestine neoplasms, Meckel’s diverticulum, ectopic varices and conditions causing haemobilia. Bleeding as a result of these conditions is often difficult to manage. In the past, red blood cell scintigraphy and angiography were the two commonly used diagnostic tools, but the yields were very low. With the advent of capsule endoscopy and double balloon enteroscopy, the diagnosis and treatment success of these conditions is much improved. While capsule endoscopy is much more comfortable and, hence, better tolerated by patients, double balloon enteroscopy offers an opportunity to control the bleeding when a source is found.

SUMMARY

Acute GI bleeding is one of the common emergencies encountered and is associated with significant morbidity and mortality. It is important that a team approach is adopted comprising gastroenterologists, GI surgeons and interventional radiologists.

The most common cause of upper GI bleeding is peptic ulcer, followed by mucosal erosions, Mallory-Weiss tear, oesophagitis and oesophageal/gastric varices.

High-risk patients with peptic ulcers are those actively bleeding or which have bled recently and show stigmata of haemorrhage at endoscopy. There is a high mortality in approximately 20% of patients in whom bleeding has not stopped spontaneously or recurs during hospitalisation.

Endoscopic examination should be done within 24 hours or when the patient is stabilised. A combination of endoscopic and adjuvant pharmacologic therapy (PPIs and octreotide) is optimal therapy for patients with bleeding ulcers. Surgery is indicated when arterial bleeding cannot be controlled by endoscopic haemostasis and when massive transfusion is required.

FURTHER READING

Chung SS, Lau JY, Sung JJ, et al. Randomized comparison between adrenaline injection alone and adrenaline injection plus heat probe treatment for actively bleeding ulcers. Brit Med J. 1997;314:1307-1311.

Gross M, Schiemann U, Muhlhofer A, et al. Meta-analysis: efficacy of therapeutic regimens in ongoing variceal bleeding. Endoscopy. 2001;33:737-746.

Leontiadis GI, Sharma VK, Howden CW. Proton pump inhibitors for acute peptic ulcer bleeding. Cochrane Database Syst Rev. (1):2006. CD002094

Rollhauser C, Fleischer DE. Nonvariceal upper gastrointestinal bleeding. Endoscopy. 2004;36:52-58.

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