Acute gastrointestinal bleeding

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Chapter 36 Acute gastrointestinal bleeding

Acute gastrointestinal (GI) bleeding is a common admission to the intensive care unit (ICU) and a major cause of morbidity and mortality. Peptic ulcer disease accounts for 75% of upper GI bleeding.^1,² Bleeding from varices, oesophagitis, duodenitis and Mallory–Weiss syndrome each account for between 5% and 15% of cases. About 20% of GI bleeding arises from the lower GI tract. Common aetiological causes for GI bleeding are listed in Table 36.1. Mortality from upper GI bleeding has remained at approximately 10% for decades, but recent reports suggest that mortality from bleeding ulcers has fallen substantially to about 5%.³ On the other hand, variceal bleeding has a much higher mortality of about 30%. Risk factors for mortality include old age, associated medical problems, coagulopathy and magnitude of bleeding.

Table 36.1 Common causes of acute gastrointestinal bleeding

Upper gastrointestinal bleeding

Peptic ulcers (DU:GU 3:1)

Varices (oesophageal varices:gastric varices 9:1)

Portal hypertensive gastropathy

Mallory–Weiss syndrome

Gastritis, duodenitis and oesophagitis

Lower gastrointestinal bleeding

Diverticular bleeding

Angiodysplasia and arteriovenous malformation

Colonic polyps or tumours

Meckel’s diverticulum

Inammatory bowel diseases

DU, duodenal ulcer; GU, gastrointestinal ulcer.

UPPER GASTROINTESTINAL BLEEDING

CLINICAL PRESENTATION

The patient may or may not present with a history of upper GI problems. There may be pain but bleeding ulcers can be painless, especially in elderly patients and users of non-steroidal anti-inflammatory drugs. Frequently, the symptoms of hypovolaemia such as tachycardia, pallor, sweating, cyanosis, mental confusion and oliguria may be present, especially in massive GI bleeding. A history of vomiting and retching preceding haematemesis suggests Mallory–Weiss syndrome.

Haematemesis and melaena are the most common presentations of acute upper GI bleeding. Haematochezia is the passage of bright red or maroon blood from the rectum, in the form of pure blood or admixed with stool. It usually represents a lower intestinal source of bleeding, but can also be a feature of massive upper GI bleeding.

INVESTIGATION

ENDOSCOPY OR BARIUM STUDY

As history and physical examination are seldom useful in identifying the source of bleeding, investigations are necessary in most cases of GI bleeding. Endoscopy has replaced barium studies as the investigation of choice. It should be performed as soon as the patient is haemodynamically stabilised, and adequate supportive personnel are available. Endoscopy is preferred to barium X-rays for the following reasons:

• Endoscopy allows more precise identification of the site and nature of bleeding.

• Endoscopic appearance often predicts the risk of recurrent bleeding from ulcer and varices (see below).

• Lesions such as gastritis, portal hypertensive gastropathy and duodenitis are difficult to diagnose by barium X-ray.

• Treatments such as injecting ulcers may be instigated during endoscopy (see below).

• Barium X-ray is notoriously unreliable in patients with previous gastric surgery.

However, endoscopy can induce serious hypoxia in patients with cardiorespiratory diseases. Continuous monitoring of blood pressure, pulse and oxygen saturation with a pulse oximeter is mandatory. Oxygen should be administered by nasal cannula when necessary.

ANGIOGRAPHY

Angiography is seldom used for the diagnosis of upper GI bleeding. Theoretically, when the bleeding is very brisk and obscures the endoscopic view, angiography may help to identify the sources of bleeding and may sometimes be used to embolise the bleeding point. In practice, however, most patients with this degree of haemorrhage should be considered for emergency laparotomy.

MANAGEMENT OF NON-VARICEAL UPPER GI BLEEDING

The goals of managing a patient with acute GI bleeding are first, to resuscitate; second, to control active bleeding; and third, to prevent recurrence of haemorrhage.

Stigmata of haemorrhage	% recurrent bleeding
Spurter or oozer	85–90
Protuberant vessel	35–55
Adherent clot	30–40
Flat spot	5–10
None	5

TREATMENT

Pharmacological control

Acid-suppressing drugs such as H₂-receptor antagonists and proton pump inhibitors are very effective drugs to promote ulcer healing. An acidic environment impairs platelet function and haemostasis. Therefore, reducing the secretion of gastric acid should reduce bleeding and encourage ulcer healing. A recent study has shown that potent acid suppression using intravenous proton pump inhibitors reduces recurrent bleeding after endoscopic therapy.⁴ Proton pump inhibitors should be recommended in high-risk peptic ulcer bleeding patients as an adjuvant to endoscopic therapy. In contrast, antifibrinolytic agents such as tranexamic acid have not been effective in reducing the operative rate and mortality of acute GI haemorrhage. Recent studies show that in patients at high risk of recurrent bleeding, pharmacologic control without endoscopic hemostasis is inadequate.⁵ Thus a combination of endoscopic and pharmacologic therapy offers the best therapy for ulcer bleeding patients.^6,⁷

Endoscopic therapy

Most patients with acute upper GI haemorrhage stop bleeding spontaneously and have an uneventful recovery. No specific intervention is required in these patients. Endoscopic haemostasis should be used in patients with a high risk of persistent or recurrent bleeding. In the last two decades, endoscopic haemostasis, with its high efficacy and low morbidity, has resulted in a dramatic decrease in emergency surgery, and has reduced the mortality of ulcer bleeding. The three most popular methods of haemostasis are as follows.

Adrenaline (epinephrine) injection

Endoscopic injection of adrenaline (1:10 000 dilution) at 0.5–1.0-ml aliquots (up to 10–15 ml) into and around the ulcer bleeding point has achieved successful haemostasis in over 90% of cases.⁶ Debate exists as to whether the haemostatic effect is a result of local tamponade by the volume injected, or vasoconstriction by adrenaline. Absorption of adrenaline into the systemic circulation has been documented, but without any significant effect on the haemodynamic status of the patient.⁸ Adrenaline injection is an effective, cheap, portable and easy-to-learn method of haemostasis, and has acquired worldwide popularity.

Coaptive coagulation

This method uses direct pressure and heat energy (heater probe) or electrocoagulation (bipolar coagulation probe (BICAP)) to control ulcer bleeding. The depth of tissue injury induced by these devices is minimised, as the bleeding vessel is tamponaded prior to coagulation. The overall efficacy of the adrenaline injection, heater probe and BICAP probe methods is comparable.⁹ Occasionally, it is not possible to obtain a view en face of the bleeding ulcers, particularly those on the lesser curve or on the posterior wall of the duodenal bulb. In these situations, direct pressure cannot be applied, and the failure rate of coaptive coagulation in these situations is expected to be higher.

Haemoclips

Endoscopic clipping of a bleeding vessel is an appealing alternative treatment which has gained popularity in recent years. The advantage of haemoclips over thermocoagulation is that there is no tissue injury induced and hence the risk of perforation is reduced. Studies comparing haemoclips against injection and thermocoagulation have shown favourable results.^10,¹¹ However, the application of haemoclips in certain sites, for example lesser curve, gastric fundus and posterior wall of the duodenum, is technically difficult. Loading of clips on to the application device is cumbersome and time-consuming and transfer of torque from the handle to the tip of the device is limited.

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 treatment is so effective. Accordingly, good cooperation among intensivists, gastroenterologists and surgeons is essential. Indications for surgery can be:

• 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 hemostasis

• evidence suggestive of GI perforation

Surgical procedures include underrunning of the ulcer, underrunning plus vagotomy and drainage, and various types of gastrectomy. The overall mortality of emergency surgery for GI bleeding is about 15–20%. In a study investigating the best salvage treatment for patients with recurrent bleeding after endoscopic therapy, surgery was found to be comparable to repeating endoscopic treatment in securing hemostasis.¹² However, morbidity is significantly higher in surgical patients than in endoscopic patients. Early surgery should be considered in patients with hypovolaemic shock and/or large peptic ulcer with protuberant vessels. A protocol to manage bleeding peptic ulcer is shown in Figure 36.1.¹³

Figure 36.1 Management of peptic ulcer bleeding.

ACUTE STRESS ULCERATION

Acute stress ulceration is associated with shock, sepsis, burns, multiple trauma, head injuries, spinal injuries and respiratory, renal and hepatic failure. Lesions are most commonly seen in the gastric fundus, and range from mild erosions to acute ulcerations. The exact mechanism leading to acute mucosal erosion/ulceration in critically ill patients is still unclear. Hypoxia and hypoperfusion of the gastroduodenal mucosa are probably the most important factors. Besides haemodynamic instability, respiratory failure and coagulopathy are also strong independent factors in critically ill patients. The incidence of stress-related mucosal bleeding in ICU patients has reported to range from 8 to 45%.¹⁴ It has been declining in the last decade as a result of highly effective management of hypotension and hypoxaemia. Bleeding may be occult or overt, from ‘coffee-grounds’ aspirates to frank haemorrhage.

PROPHYLAXIS AND TREATMENT

Significant ulcerations are managed as above. Minor bleeding and prophylactic treatment are considered together. Prophylactic treatment aims for gastric alkalinisation (gastric pH > 3.5), with the rationale that gastric acidity is the main cause of stress ulceration.¹⁴ The incidence of stress ulcerations appears to be lower with prophylactic gastric alkalinisation than with placebos, although an improvement in survival has not been shown.^15,¹⁶ Gastric bacterial overgrowth and the associated nosocomial pneumonia have been concerns, but have not been substantiated by existing data. On balance, prophylactic treatment should probably be reserved only for at-risk patients. Scoring systems to estimate the risk of stress-ulcer bleeding have been proposed, for example Zinner and Tryba scores.^17,¹⁸ The mainstay of prophylaxis and treatment for minor bleeding remains supportive – optimise oxygenation and tissue perfusion and control of infection. There is little consensus among critical care experts in the choice of prophylactic treatment used.¹⁹ Drugs given include the following:

Antacids

Antacids given hourly via a nasogastric tube can maintain gastric alkalinisation. Gastric pH monitoring is necessary. Antacids contain magnesium, aluminium, calcium or sodium, and complications may arise from excessive intake of these minerals. Bowel stasis and diarrhoea can also be problems. They are used less commonly now.

Sucralfate

This is a basic aluminium salt of sucrose octasulphate. It is effective in healing ulcers by increasing mucus secretion, mucosal blood flow and local prostaglandin production. These effects promote mucosal resistance against acid and pepsin (i.e. they are cytoprotective). As it does not alter gastric pH, Gram-negative bacterial colonisation of gastric juice is less likely. The incidence of nosocomial pneumonia may be less with sucralfate than with antacids or H₂-receptor antagonists, but this is debatable and there is a potential risk of aspiration.¹⁵ Sucralfate is given via a nasogastric tube as 1.0 g every 4–6 hours. Constipation is a side-effect, and aluminium toxicity may arise from renal dysfunction.

H₂-receptor antagonists

These drugs suppress acid secretion by competing for the histamine receptor on the parietal cell. Cimetidine is less potent and has interactions with anticonvulsants, theophyllines and warfarin. Famotidine and nizatidine are newer agents but have no particular advantage over ranitidine. The problem of H₂-receptor antagonists is the development of tachyphylaxis after the first day of administration, leading to reduction of effectiveness in acid suppression. At least one meta-analysis showed that ranitidine did not confer any protection against stress ulcer in intensive care patients.²¹

Proton pump inhibitors

These are potent acid-suppressing agents as they block the final common pathway of acid secretion by the parietal cell, namely the proton pump. All proton pump inhibitors (omeprazole, lansoprazole, pantoprazole and rabeprazole) can be given as oral medication. Omeprazole and pantoprazole are also available in intravenous form for those who cannot be fed orally. In two non-randomized studies, intravenous omeprazole has been shown to protect critically ill patients who required ventilation from the development of stress-related mucosal bleeding from the upper GI tract.²⁰ Yet, there are no prospective data indicating which are the high-risk patients who might benefit from this treatment.

VARICEAL BLEEDING

Acute variceal bleeding is a serious complication of portal hypertension, with a high mortality. About 50% of patients with bleeding varices have had an earlier bleed during hospitalisation. The degree of liver failure, using Child–Pugh’s classification (see Chapter 38), is the most important prognostic factor for early rebleeding and survival.

RESUSCITATION

Immediate resuscitation with whole blood and fluid is mandatory. Overtransfusion may cause a rebound increase in portal pressure (with a consequent increased risk of rebleeding) and must be avoided. Fresh frozen plasma and platelet concentrates transfusion may be indicated. A nasogastric cannula is often inserted for the removal of blood (and also drug administration). Forceful aspiration through the nasogastric tube should be discouraged as bleeding may be induced. Lactulose (15–30 ml every 4–6 hours) should be given to prevent or correct hepatic encephalopathy. A colonic wash-out can be used, but a magnesium-containing enema should be avoided in the presence of renal failure. Close attention must be given to haemodynamic monitoring.

When the patient is haemodynamically stable, upper endoscopy should be performed to identify the source of bleeding. Patients with portal hypertension could bleed from oesophageal or gastric varices, peptic ulcers and portal hypertensive gastropathy.

PHARMACOLOGICAL CONTROL

Vasopressin (0.2–0.4 U/min) used to be 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.²² Infusion of somatostatin and its analogue (octreotide, vapreotide) reduces portal blood pressure and azygous blood flow. They are safe and effective vasoactive agents to be used in acute variceal bleeding.²³ The benefit is more prominent if these vasoactive agents are given early, even before endoscopy.^22,²⁴ Octreotide has also been shown to be effective when used as an adjuvant therapy in combination with endoscopic therapy.²⁵ Recurrent bleeding episodes and hence requirement of transfusion are significantly reduced.

ENDOSCOPIC SCLEROTHERAPY

Endoscopic injection sclerotherapy is the mainstay of treatment. At endoscopy, sclerosants can be injected directly into the variceal columns (intravariceal injection) or into the mucosa adjacent to the varices (paravariceal injection) to cause venous thrombosis and inflammation, and tissue fibrosis. Commonly used sclerosants are ethanolamine oleate, sodium tetradecyl sulphate (1–3%), polidocanol and ethyl alcohol. None has appreciable advantage over the others and the choice is very much a personal preference of the endoscopist, and depends also on availability. Endoscopic sclerotherapy controls 80–90% of acute variceal bleeding. Complications such as ulcer formation, fever, chest pain and mediastinitis are common. Bleeding from gastric varices is more difficult to control by injection sclerotherapy because of difficult access. Butylcyanoacrylate (Histoacryl) has recently been used for gastric variceal injections, with a claimed superior haemostatic effect. It is mixed with lipiodol to delay the rate of polymerisation and allow radiological monitoring of the injection.

ENDOSCOPIC VARICEAL LIGATION

Endoscopic variceal ligation was introduced in the late 1980s as a mechanical method to control bleeding from varices. Rubber bands mounted on the banding device at the tip of the endoscope are released to strangulate the bleeding varices. Numerous studies comparing endoscopic variceal ligation with endoscopic sclerotherapy showed that the technique is as effective as injection sclerotherapy in acute bleeding.⁹ Procedure-related complications are significantly fewer, as there is no tissue chemical irritation. An overtube to facilitate banding avoids aspiration during the procedure, but may result in serious oesophageal injury if used improperly. The tunnel vision produced by the banding device as originally designed restricts visibility, and thus makes the procedure technically difficult when bleeding is heavy. With the introduction of multiple banding devices which are loaded with 5–10 rubber bands, and the use of transparent caps, the problems of overtube injury and tunnel vision have been overcome. In many centres, endoscopic variceal ligation has replaced injection sclerotherapy as the first choice for variceal haemorrhage. Many have combined the two endoscopic treatments together in an attempt to improve the outcome. Existing data so far do not support this combined therapy to be better. Combined endoscopic therapy cannot be recommended.

BALLOON TAMPONADE

Variceal bleeding can be controlled by exerting pressure directly on the bleeding point using a balloon. The Sengstaken–Blackmore tube has been replaced by the four-lumen Minnesota tube which allows aspiration of gastric and oesophageal contents. Inflation of the gastric balloon (by 250–350 ml of water) is often sufficient to stop the bleeding by occluding the feeding veins to the oesophageal varices. If bleeding continues, the oesophageal balloon can be inflated by air and kept at a pressure of 50–60 mmHg (6.7–8.0 kPa). Duration of using balloon tamponade should be limited to 24 hours to avoid tissue pressure necrosis. Because of available effective pharmacological and endoscopic therapies, balloon tamponade should only be used in the exceptional cases when these therapies fail to effect control of bleeding.

TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS)

Using a transjugular approach, a catheter is inserted into the hepatic vein, and advanced under fluoroscopic guidance into a branch of the portal vein.²⁶ By means of a guidewire and dilators, a self-expandable metal stent is introduced to create an intrahepatic portosystemic shunt. In good hands, success can be achieved in over 90% of cases. This procedure significantly reduces portal blood pressure and thus bleeding from varices. Major complications include intra-abdominal haemorrhage and stent occlusion. Hepatic encephalopathy has been reported in 25–60% of patients. Nevertheless, this is an effective salvage treatment for uncontrolled variceal bleeding. Meta-analysis comparing TIPS with endoscopic therapy showed that the former has secure haemostasis but at the cost of increasing risk of hepatic encephalopathy.²⁷

A number of markers of outcome after TIPS have been under investigation, including the Acute Physiology, Age and Chronic Health Evaluation (APACHE) score, presence of hyponatraemia and Child C liver disease, hepatic encephalopathy before TIPS, presence of ascites and serum albumin. Before a reliable marker of outcome can be identified, TIPS should be reserved for the subset of patients who continue to bleed or develop recurrent bleeding after endoscopic therapy. Unlike shunt surgery, TIPS will not reduce the chance of future liver transplantation.

SURGERY

Surgical treatments for variceal bleeding include direct devascularisation of the lower oesophagus plus the proximal stomach and a variety of surgical shunts. The role of surgery has diminished since the advent of endoscopic treatment and TIPS.²⁸ Surgery is now used as a second-line treatment, when bleeding continues or recurs after two sessions of injection sclerotherapy or banding ligation. Both staple transection of the oesophagus and portocaval shunt surgery are highly effective emergency measures. Despite successful control of bleeding, long-term survival is not significantly improved. Hepatic encephalopathy is one of the major complications of shunting operations. Expectations that the Warren distal splenorenal shunt will preserve antegrade portal flow and avoid accelerated deterioration of liver function have not been realised. The Warren shunt is technically more difficult, especially if performed as an emergency. Choice of surgery should be carefully made in those who are potential transplant candidates, as it may complicate subsequent surgery. A protocol to manage variceal bleeding is shown in Figure 36.2.