The main causes of haematemesis are listed in Box 10.1. So how do these patients present? They may feel nauseous and even continue to vomit during the initial assessment or have symptoms related to blood loss including sweating, dizziness and confusion.

Management

The first goal in managing a patient with haematemesis is to resuscitate him or her and ensure that the haemodynamic state is stable. Limited time is available for detailed history-taking and physical examination. The most important initial steps are as follows:

• Ensure that the patient’s airway is clear.

• Check for shock and hypotension and organise blood or fluid replacement.

• Check if the patient is still actively bleeding.

• Look for clues as to the source of bleeding.

These important steps will be considered in more detail below. Delays in assessment and the institution of proper management may prove fatal.

Airway

The mental state should be noted carefully because a drowsy or comatose patient is at high risk of aspiration if he or she continues to vomit blood. The mental state may be impaired by a number of factors, including:

• severe, acute blood loss leading to cerebral hypoperfusion;

• concomitant chronic liver disease or renal failure leading to encephalopathy; and

• alcohol or drug intoxication or overdose.

If the patient is unconscious or has an impaired gag reflex, the airway must be protected, especially if vomiting continues. The patient should be kept flat on his or her side. A cuffed endotracheal tube may need to be inserted. Such patients should be managed in an intensive care facility.

Hypotension and shock

Assessment of hypovolaemia involves simple bedside clinical observations. The patient may be clammy and sweaty with cold peripheries and a fast thready pulse. There may be associated confusion. The blood pressure will be low, often under 90 mmHg systolic. If any of these signs are seen, resuscitation should commence immediately. At least two large-bore intravenous cannulae should be inserted into large peripheral veins. A central venous line should be placed in high-risk cases (see below). Rapid infusion of isotonic saline followed by a plasma expander such as Haemaccel® should be commenced and blood samples should be drawn urgently for full blood count, coagulation screen, blood group and cross-matching of four to six units of packed cells, and urea, electrolytes and liver function tests.

As a rule of thumb, patients who have obvious signs of shock, with clammy peripheries and low blood pressure, may have lost up to 50% of their circulating blood volume. If these signs are not present, the patient may be sat up carefully and a check made for a postural drop in blood pressure. If this is present, it is likely that 10–20% of blood volume has been lost. Remember that with haemoconcentration immediately after a bleed, the haemoglobin may initially be near normal despite the loss of a considerable amount of blood.

Patients with a gastrointestinal bleed have lost ‘whole blood’ and there is, therefore, logic in transfusing them with whole blood (Box 10.2). In practice, however, donated blood is separated into packed cells and other products, such as platelets and plasma, which may be used in different clinical situations. Thus, in current clinical practice, patients with a significant bleed are given packed cells alternating with a plasma expander such as Haemaccel if they are hypovolaemic and packed cells alone if they are normovolaemic but anaemic. The aim of transfusion is to restore circulating blood volume so that the blood pressure is normal and to correct anaemia so that the oxygen carrying capacity of the blood is satisfactory. This generally means maintaining a haemoglobin level of approximately 100 g/L. One unit of packed cells will increase the haemoglobin level by 10 g/L (haematocrit by 3%).

Box 10.2 Indications for blood transfusion in patients with gastrointestinal bleeding

Consider transfusing if:

• blood pressure < 110 mmHg or

• postural hypotension (> 10 mmHg) or

• pulse > 110/min or

• haemoglobin < 70 g/L ^∗

^∗ May be a normal haemoglobin level with severe bleeds initially.

In hypovolaemic patients, packed cells are transfused rapidly until the patient is haemodynamically stable. Rarely, group-specific uncross-matched blood or O rhesus-negative blood will be required. In haemodynamically stable patients, packed cells are transfused slowly, approximately one unit every 2 hours.

If the patient is coagulopathic or needs more than four units of packed cells, fresh frozen plasma (two units initially) should also be given to provide clotting factors.

Upper gastrointestinal endoscopy is the single most useful test. If performed within 24 hours of presentation, the cause of bleeding will be found in 90–95% of patients (Figs 10.1 to 10.3). Furthermore, it may permit the endoscopist to perform therapeutic interventions that in turn may arrest the bleeding or minimise the chance of further bleeding. It requires considerable expertise, especially in the situation of an actively bleeding lesion, and is not without some risk.

Figure 10.1 Arterial spurting from a gastric ulcer.

Figure 10.2 Gastric varices.

Figure 10.3 Gastric arteriovenous malformation.

So who should be endoscoped and when should it be done? This decision is more easily made if consideration is given to why the endoscopy is being done. First, the aim is to make an accurate diagnosis. Secondly, a prognosis for further bleeding may be given, based on the endoscopic findings. Finally, a bleeding lesion or one at high risk of re-bleeding may be able to be treated. However, if the patient is not in a high-risk category, it may not be necessary to do an emergency procedure. In general terms, endoscopy should always be done within 24 hours but, for patients considered being at ‘high risk’, particularly if there is a possibility of oesophageal varices, emergency endoscopy should be arranged once the patient has been adequately resuscitated.

Risk factors for greater morbidity and mortality from haematemesis are now well known and are listed in Box 10.3.

Box 10.3 High risk features in patients with haematemesis

• Older age (over 60 years old)

• Associated serious medical conditions (e.g. chronic lung disease, cerebrovascular disease, recent myocardial infarction)

• Coagulopathy

• Magnitude of bleed (patients presenting with hypotension or shock are a high-risk group—this includes those patients with syncope, systolic blood pressure below 100 mmHg and if more than four units of blood are required over a 12-hour period)

• Re-bleeding after the initial bleed

• Endoscopic findings (variceal bleeding, peptic ulcer with arterial spurting, oozing, visible vessel or clot in the ulcer base)

These patients should be targeted for the most aggressive management with emergency endoscopy. Endoscopy for acute haematemesis requires a high level of skill and experience. The main risk to the patient is of aspiration of blood, especially if sedation is used, and all staff must be aware of the need to protect the patient’s airway with a cuffed endotracheal tube, if necessary. There is some evidence to support the administration of intravenous erythromycin (approximately 250 mg) prior to endoscopy. The prokinetic effect of this drug clears blood from the stomach, thereby potentially improving visualisation of bleeding lesions and probably also reducing aspiration risk.

It should be noted that in about 80% of patients bleeding has stopped spontaneously upon presentation. In the remaining 20% of patients, bleeding persists or recurs during their period of hospitalisation. The mortality in this group increases as much as eightfold compared to those without further bleeding.

Common causes of haematemesis

Oesophageal varices

Oesophageal varices are dilated submucosal veins forming a portal systemic circulation anastomosis in patients with portal hypertension. They look like large varicose veins and bulge into the oesophageal lumen. Arising from these veins are very thin-walled vascular channels, lined only by endothelium, extending into the squamous epithelium of the oesophagus. These have a high risk of rupture, which is considered to be mainly precipitated by sudden pressure rises.

About 50% of patients with cirrhosis of the liver have oesophageal varices, and 30% of these varices bleed within 2 years of their diagnosis. After bleeding, the risk of further bleeding is very high—about 70% over the ensuing 2 years. The mortality rate from bleeding oesophageal varices ranges from 40% to 70%. Predictors of haemorrhage include the presence of very large varices and varices with ‘cherry red spots’. These red spots represent the intraepithelial vascular channels arising from the varices. Ongoing alcohol ingestion, thrombocytopenia and poor liver synthetic function are also predictors of variceal bleeding.

If bleeding oesophageal varices are found during endoscopy, rubber band ligation is the current treatment of choice. Bleeding can be controlled in 80–90% of cases with a relatively low risk of complications. If passage of the rubber band ligating device mounted on the tip of the endoscope is not feasible or if equipment and expertise for rubber band ligation are not available, injection sclerotherapy may be performed (Fig 10.4). This involves direct injection of a sclerosant such as ethanolamine oleate or sodium tetradecyl sulfate into the varices. Injection sclerotherapy has a very high success rate in controlling the bleeding, although with a greater risk of complications including sepsis, oesophageal stricture and mediastinitis.

Figure 10.4 Injection sclerotherapy equipment for variceal bleeding.

Pharmacological treatment is frequently used in the control of variceal bleeding. The most widely used drug in this situation is intravenous octreotide, which is an analogue of somatostatin. It can be given acutely in the emergency room if there is a high index of suspicion that varices are the cause of the bleed, even before endoscopic confirmation. It is given by an initial bolus injection of approximately 25–50 mcg, followed by an infusion of 25–50 mcg octreotide per hour in 5% dextrose. An octreotide infusion is regarded as part of the resuscitation process. It works by decreasing portal venous blood flow and has been shown to control variceal bleeding in over 70% of cases. Octreotide is a safe and effective vasoactive agent. The benefit is more prominent if octreotide is prescribed 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 requirement of transfusion are significantly reduced.

Sometimes, the above approaches fail and the patient continues to bleed. This is a very high-risk situation and a long-term management plan must be prepared. Important questions are:

• What other methods of bleeding control are available?

• Is the patient suitable for an urgent liver transplant?

• Is the patient’s general condition so poor and the severity of underlying liver disease so advanced that ongoing resuscitation is inappropriate?

If ongoing aggressive management is decided upon, the next step should be to insert a Minnesota or Sengstaken-Blakemore tube (balloon tamponade) into the oesophagus and stomach (Fig 10.5). This can be passed through the nose, preferably with the patient anaesthetised, though in practice the tube is often inserted in an emergency situation without a general anaesthetic.

Figure 10.5 Sengstaken-Blakemore tube.

Once the position of the tube has been confirmed by x-ray examination to be in the stomach, the gastric balloon is inflated to 300 mL with air or with water and the tube withdrawn so that the gastric balloon is snug against the cardia. This can be maintained in position by gentle traction using a weight of approximately 0.5 kg. Most variceal bleeding will stop since the oesophageal varices are ‘fed’ from veins passing up across the cardia and these are compressed by the gastric balloon. If bleeding continues, the oesophageal balloon should be inflated to a pressure of 30–40 mmHg using a sphygmomanometer to monitor the pressure achieved.

Patients who have a Minnesota or Sengstaken-Blakemore tube in situ need special monitoring in an intensive care environment and have a nurse dedicated to the care of the tube. It is imperative that the nurse watch carefully for displacement of the tube and regularly check the pressure in the oesophageal balloon. This technique may stabilise the patient until alternative treatments can be given. A further attempt at endoscopic sclerotherapy or rubber band ligation is the next step. If this fails to control the bleeding, other strategies must be considered.

TIPS (transjugular intrahepatic portal systemic stent) is a radiological procedure that involves the creation of a fistula within the liver substance between the hepatic and portal veins, followed by insertion of an expandable metal stent. This forms a portal systemic shunt and lowers the pressure in the portal venous system. The technique is being increasingly used after failed banding or sclerotherapy and buys time for definitive long-term management such as liver transplantation. It certainly requires the presence of a highly experienced interventional radiologist.

Mortality from bleeding oesophageal varices is still very high despite the advances in endoscopic and radiological management. The severity of the underlying liver disease is the main determinant of outcome. For those patients who do respond well to the initial banding or sclerotherapy, careful follow-up is required with ongoing endoscopic treatment at 1–3 weekly intervals until the varices are obliterated. These treatments can be given on a day-case basis. This treatment approach should be supplemented by a beta-blocking agent such as propranolol.

Bleeding from gastric varices is a less frequent event. Injection therapy with cyanoacrylate (‘glue’) is frequently used.

Gastric or duodenal ulceration

Ulcers bleed when an artery or other vessels in the base of the ulcer are eroded. If the bleeding is arterial in origin, it may be very brisk and rapidly lead to shock. In a young patient, there is good arterial contractility, which can cause spasm of the damaged vessel and bleeding may cease spontaneously. In an elderly patient with atherosclerotic arteries, this ability to induce arterial spasm is impaired and bleeding is more likely to continue.

Endoscopic interventions may be used if a gastric or duodenal ulcer is found at endoscopy. These are particularly appropriate if there is active bleeding with oozing or arterial spurting, or an adherent blood clot, or a flat pigmented spot on the ulcer base or if there is a visible blood vessel in the base of the ulcer crater. These are stigmata, which predict a high risk of ongoing or recurrent bleeding. Several studies support aggressive management combining adrenaline injection therapy, clot removal and thermal ablation using a heater probe and haemostatic clips. The most widely used agent for injection is 1:10,000 adrenaline, which probably works by causing spasm of any feeding arteriole or artery and encourages platelet plugging and thrombosis.

For actively spurting vessels or visible vessels in a peptic ulcer, thermal ablation therapy using a heater probe or bipolar electrocoagulation probe, often in combination with adrenaline injection and/or endoclips, is now the most widely utilised technique.

If there is an index of suspicion of a bleeding peptic ulcer, an intravenous proton pump inhibitor infusion is usually initiated in the emergency department while waiting for an endoscopic diagnosis. Many studies have shown a clear reduction in the risk of re-bleeding when a proton pump inhibitor is used as primary therapy for bleeding ulcers without concomitant endoscopic therapy. Best results appear to occur with high-dose infusion (e.g. omeprazole 8 mg per hour) over a period of 3–5 days. There is also theoretical evidence to support high-dose intravenous infusions, which elevate gastric juice pH to above 6, a level at which fibrinolysis of adherent clots is inhibited. Both regular and high-dose intravenous infusions of omeprazole have been shown to be effective at preventing re-bleeding in patients whose peptic ulcers have been treated initially by endoscopic therapy.

Since there is a high risk of re-bleeding it is common practice in some centres to have a ‘second-look’ endoscopy 24 hours after the first endoscopic intervention.

After bleeding has stabilised, definitive ulcer healing treatment is introduced; this comprises avoidance of ulcerogenic medications, such as aspirin or NSAIDS, administration of oral proton pump inhibitor therapy at standard dosage and eradication of Helicobacter pylori if identified on initial assessment (but note active bleeding can cause false negative testing). An endoscopy to document healing is often performed 4–6 weeks after treatment has been given, especially in a high-risk patient whose ulcer has bled without warning symptoms.

The discovery that most peptic ulcers are caused by an infection in the stomach, courtesy of the bacterium H. pylori, has led to the frequent adoption of antibacterial therapy (Ch 5). Treatment of H. pylori in patients with peptic ulcer markedly reduces the risk of subsequent ulcer relapse and associated bleeding, without the need for long-term maintenance drug treatment. The current regimens will work in up to 80% of patients, eradicating the infection, healing the ulcer and markedly reducing the risk of ulcer recurrence. In the immediate aftermath of a haematemesis, clinicians may choose to use the simpler drug regimen of an H₂-receptor antagonist or proton pump inhibitor alone to heal the ulcer and then, when the patient has stabilised and out of hospital, follow on with H. pylori eradication, or treat the infection as soon as the patient can eat at the same time as giving acid suppression drug therapy.

The success of the treatment can be documented in the patient with a bleeding ulcer by taking gastric biopsies to look for the organism during a subsequent endoscopy 4 or more weeks after stopping therapy. Alternatively, a ¹⁴C or ¹³C urea breath test or stool antigen can be done.

If a peptic ulcer is found in a patient receiving NSAID therapy, these drugs should be discontinued at least in the short term and, ideally, long term. Ulcer healing can then proceed along the lines outlined above. Some patients cannot manage without regular NSAIDs and, in that case, long-term prophylactic treatment with a proton pump inhibitor should be considered. Misoprostol can also be used to protect against recurrent gastric ulceration in a patient on NSAIDs. The COX-2 inhibitors can be used in these patients in place of traditional NSAIDs, but the risk of further bleeding is only reduced, not abolished, by this substitution and ideally these patients should also remain on a proton pump inhibitor.

Other causes of haematemesis

Acute gastric erosions and a Mallory-Weiss tear are usually self-limiting lesions that will heal fully over a matter of days. In the case of erosions, withdrawal of gastric irritants such as aspirin or NSAIDs should be done. A short course of a proton pump inhibitor is often prescribed.

Ulcerative oesophagitis that bleeds sufficiently to cause an overt haematemesis is usually severe and requires aggressive acid suppression. Rarely, a chronic ulcer in a Barrett’s oesophagus may bleed (Ch 1). By far the most effective treatment for oesophageal ulceration is with the proton pump inhibitors such as omeprazole, esomeprazole, rabeprazole or pantoprazole. Long-term therapy is likely to be needed. Laparoscopic fundoplication may also be considered as an alternative to long-term medical treatment.

Role of surgery in bleeding peptic ulcers

Modern endoscopic treatments have reduced the need for surgical intervention in bleeding peptic ulcers. Nonetheless, some patients will be bleeding so massively at presentation that endoscopic therapy cannot be applied due to poor visualisation of the lesion, or endoscopic interventions fail to control the bleeding. A major arterial bleed (e.g. from the gastroduodenal artery in a posterior wall duodenal ulcer) is unlikely to respond to endoscopic therapy. Therefore, it is imperative that all high-risk patients be assessed early by a gastrointestinal surgeon.

For patients with uncontrollable massive bleeding, emergency surgery can be life-saving and the decision to operate is usually straightforward. For patients whose bleeding continues at a slower rate or who have episodic re-bleeds despite initial endoscopic treatment, the timing of surgical intervention is more difficult and requires careful consideration of the risks of ongoing conservative management and blood transfusion balanced against the risks of an anaesthetic and operation. An experienced surgeon can give far better input to this decision if he or she has been reviewing the patient from admission rather than being called in at the last moment. Often the ultimate decision regarding surgical intervention depends on the expertise of the endoscopist, the endoscopy facilities and the experience of the surgeon and gastroenterologist.

The choice of operation will vary according to the clinical circumstances. In most instances, an oversewing of the bleeding artery is all that is performed since it is assumed that medical therapy afterwards will deal with the ulcer effectively. In some instances, especially if there is a history of recurrent bleeding or ulceration despite medical therapy, a more definitive operation will be performed, such as a partial gastrectomy for a gastric ulcer (Ch 6).

Discharge from hospital

As a general rule, patients with bleeding should be admitted to hospital. There is a growing body of literature supporting same-day discharge in carefully selected patients following clinical and endoscopic evaluation. This would be an appropriate strategy for young, otherwise healthy individuals with clinically small bleeds in whom endoscopy shows minor erosive gastritis, mild oesophagitis or peptic ulceration without any high-risk stigmata. These patients can resume eating normally after the endoscopy. A long-term management strategy should be instituted.

Patients with bleeding varices comprise the highest risk group and these patients should remain in hospital for up to a week, during which time the risk of massive re-bleeding is highest. Treatment also has to be directed to the underlying liver disease and its complications (Ch 24). Patients with high-risk peptic ulcers are at increased risk of re-bleeding for at least 72 hours after the initial bleed. Discharge from hospital is reasonable after 4–5 days if the patient’s course in hospital has been uncomplicated.

Passing Melaena Alone

This is a common clinical situation, sometimes badly managed, because the patient or the doctor underestimates the seriousness of the complaint. The patient may blame the colour of the motions on something eaten and not appreciate that the black colour is due to altered blood. The characteristic strong odour of melaena should help the clinician distinguish it from other causes of black-coloured motions (e.g. the use of iron supplements, bismuth or liquorice).

Most cases of melaena are due to bleeding from the upper gastrointestinal tract, mainly from peptic ulceration. Oesophageal varices rarely present in this way, because they bleed so briskly that bright red haematemesis occurs long before melaena is seen. However, some patients with portal hypertension ooze blood more slowly from dilated blood vessels in the stomach (portal gastropathy, Fig 10.2) or intestine (portal enteropathy), and melaena may be the first sign.

Therefore, all patients with active melaena should be assumed to have an upper gastrointestinal cause and be managed in exactly the same way as the patient who presents with haematemesis (including appropriate resuscitation as described above). Admission to hospital is warranted, even if the patient is haemodynamically stable, since the melaena from a mild initial bleed may herald a more severe life-threatening bleed to follow. If the melaena has been transient and is over a week old, it may be safe to investigate on an outpatient basis, though endoscopic evaluation should be done promptly, within a few days, so that an accurate diagnosis can be made and definitive treatment started.

Some patients with melaena will not be bleeding from the upper gastrointestinal tract and the endoscopy will fail to show a lesion. Blood loss from the right colon or the small intestine may also present as melaena. Colonic lesions such as polyps, cancer, angiodysplasia and diverticula are much more common than small bowel lesions and the next step should, therefore, be a colonoscopy. If polyps are found, these can be removed by polypectomy during the examination. Bleeding angiodysplastic lesions can be treated by argon plasma coagulation or by injection sclerotherapy.

If no abnormality is found on upper endoscopy and colonoscopy, a decision to investigate the small bowel has to be made. If there are any associated small bowel symptoms, small bowel evaluation with double or single balloon enteroscopy or capsule endoscopy should be considered. These tests can identify vascular lesions and angiodysplasia, small bowel tumours and inflammatory bowel disease. In some cases, more extensive evaluation with enteroclysis, Meckel’s scanning and angiography will be required. This will be discussed further in the next section.

If patients with melaena have associated iron deficiency anaemia secondary to chronic blood loss, iron replacement therapy may be necessary. It is important to warn the patient that oral iron will colour the motions black and mimic the appearances of melaena. Iron-containing stools, though black in colour, do not have the characteristic odour of melaena and most patients will be able to distinguish at least a more severe melaena stool from the effects of iron tablets. If the patient is severely iron-deficient, an intravenous iron infusion may be more beneficial.

Bright Red Blood Per Rectum

This is also an extremely common clinical complaint affecting patients of all ages. In the vast majority of cases, the bleeding is trivial in quantity, although in some patients a large volume of blood is passed and, rarely, the bleeding is massive and associated with hypotension or shock.

Causes of rectal bleeding in patients under the age of 40 years are listed in Box 10.4. In older patients, the differential diagnosis is wider, and more serious conditions such as colorectal cancer are much more prevalent (Box 10.4).

A careful history should be taken, focusing on the following points:

• amount of bleeding and colour of blood;

• blood on toilet paper only (suggesting anal pathology) or blood mixed in with the stool;

• associated perianal pain suggesting local anal pathology;

• pattern of bowel habit—constipation and straining at stool point towards haemorrhoids or anal fissure; diarrhoea and mucus per rectum suggest ulcerative colitis

• family history of colorectal diseases such as carcinoma.

Examination should include a check for an abdominal mass arising from the colon and a careful inspection of the anal area to look for any signs of an anal fissure. A rectal examination should be done, feeling with the finger for any palpable lumps and any local tenderness. A proctoscopy and/or rigid or flexible sigmoidoscopy should follow. This is an extremely useful test in this situation, especially if done acutely. If a bleeding source is clearly identified, such as bleeding haemorrhoids or fissure, further immediate investigation may be avoided. If no lesion is found or if a possible source is seen but with no evidence of recent bleeding (e.g. non-bleeding haemorrhoids), further investigation will be necessary in most instances. Remember that haemorrhoids are common and it is dangerous to assume that they are the source of the bleeding, especially in a more elderly patient, if no evidence of recent bleeding is seen at the time of the examination.

For patients over the age of 40 years, a colonoscopy should be arranged if the initial local inspection and sigmoidoscopy have not clearly identified the source of bleeding. A barium enema is not an appropriate investigation in this situation. It is less accurate than colonoscopy, especially in the detection of vascular lesions such as angiodysplasia. Barium also obscures the views if subsequent colonoscopy or angiography is required, and therapeutic interventions, such as polypectomy, cannot be performed.

For younger patients, discretion and clinical judgment are needed if the initial work-up is negative. The yield from colonoscopy in this group is small and serious pathology, such as colorectal cancer, is very rare. If the bleeding is persistent or recurrent, a colonoscopy is clearly warranted.

Causes of rectal bleeding

Specific points related to the individual causes of rectal bleeding are given below.

Haemorrhoids

These are particularly associated with constipation and straining at stool. They are vascular cushions that form in the venous plexuses at the anorectal junction. Bleeding is typically intermittent. Blood is seen on the toilet paper, as a splash in the toilet bowl or on the outside of the stools. For minor bleeding, reassurance is all that is necessary after the clinical evaluation has been performed. Attention to diet and treatment of associated constipation is appropriate. If bleeding is more persistent or recurrent, local treatment of the haemorrhoids can be given. The most common interventions include injection of the haemorrhoids with sclerosant, and rubber band ligation. For more severe prolapsing haemorrhoids, haemorrhoidectomy is appropriate (Ch 12).

Anal fissure

Treatment again is directed towards the underlying constipation. Fibre supplements and stool softeners are used and the patient is encouraged to avoid straining at stool. Glyceryl trinitrate ointment will relax anal spasm and allow some fissures to heal. This conservative approach will work in many cases but for more chronic recurrent fissures, surgical intervention is necessary (Ch 12).

Rectal polyps

If these are seen at sigmoidoscopy, the patient should be fully prepared for a colonoscopy so that a search for more proximal polyps can be made. Most polyps can be removed at colonoscopy using a snare or biopsy forceps. Since approximately 90% of colorectal cancers arise from preexisting adenomatous polyps, the rationale for polyp excision is not only control of the rectal bleeding but also cancer prevention. If the polyps are found at histology to be adenomatous, colonoscopic surveillance is warranted, especially in patients with multiple polyps or large polyps, as there is an increased risk of new polyp formation and colorectal cancer. Repeat examinations should be done at 3- to 5-yearly intervals in most cases (Ch 22).

Angiodysplasia or vascular ectasia of the bowel

These vascular lesions are increasingly common with advancing age. About 25% of patients over the age of 60 years have angiodysplasia but only a small proportion bleed. Vascular lesions are most commonly found in the right colon, but are occasionally found in the small intestine or left colon. They may present with occult bleeding leading to iron deficiency anaemia or with more brisk bleeding leading to moderate or even massive rectal bleeding. The cause of these lesions is unclear. They are dilated, thin-walled vascular lesions in the submucosa of the colon and may develop in response to chronic pressure changes, especially in the right colon. Bleeding is typically intermittent and ceases spontaneously, only to recur at a later date in most patients. Sometimes the bleeding is torrential and emergency intervention is required. If detected at colonoscopy, argon plasma coagulation, injection therapy or laser may be used to stop the bleeding. At angiography, injection of vasopressin or embolisation techniques may be used successfully. In some patients, surgical intervention, often a right hemicolectomy, may prove necessary. Delineation of the extent of angiodysplasia by investigation, such as capsule endoscopy for small bowel involvement, is appropriate before surgical intervention is planned.

Diverticulosis

This is a condition with pseudodiverticula or mucosal herniations through the colonic wall, at sites of relative weakness caused by penetrating blood vessels. They become increasingly common with age; 5% of 50-year-old people and more than 50% of 90-year-old people have colonic diverticula. It is widely believed that the Western refined diet, low in fibre, is a significant predisposing cause for diverticula formation. They develop most commonly in the sigmoid colon although, for reasons that are not understood, bleeding is more commonly seen with right colonic diverticula. In the vast majority of patients, bleeding settles spontaneously and management is conservative. Fewer than 25% of patients will have further episodes of bleeding, although those patients that do have further episodes tend to continue with bleeding and require surgical resection. Diagnosis is usually presumptive, made at colonoscopy when other colonic causes have been excluded. Active bleeding is rarely seen at colonoscopy; it can be treated using thermal ablation or injection therapy.

Inflammatory bowel disease

Ulcerative proctitis may present as rectal bleeding without any associated change in bowel habit, though most patients also have diarrhoea. The condition may be due to ulcerative colitis or Crohn’s disease and is easily diagnosed by sigmoidoscopy (Ch 15). If there are other symptoms suggesting the presence of more proximal disease, the patient may need a colonoscopy. Local treatment of proctitis with steroid enemas, 5-aminosalicylic acid enemas or oral sulfasalazine treatment works well in most patients. Resistant cases need more aggressive immunosuppression with high-dose oral steroids.

Ischaemic colitis

This usually occurs in the setting of widespread peripheral vascular disease or cardiac disease. The rectal bleeding is often associated with mild lower abdominal cramps. Characteristic changes are seen on colonoscopy or barium enema usually at the level of the splenic flexure and descending colon because this is a watershed area in the blood supply to the colon (Fig 10.6). Treatment is conservative and the condition settles spontaneously in most cases. Some patients develop a stricture at the site of the ischaemia, which rarely requires subsequent excision (Ch 4).

Figure 10.6 Ischaemic colitis of the splenic flexure on barium enema.

Massive rectal bleeding

This is a relatively uncommon clinical problem. The clinical management is more complex and acute. The patient may be hypotensive or in shock and require urgent resuscitation, as has been described above for patients with haematemesis. The most frequent cause of this clinical presentation is massive bleeding from colonic diverticula or angiodysplasia. However, the site of bleeding may be virtually anywhere in the gastrointestinal tract since massive bleeding even from the stomach or duodenum may pass rapidly to the rectum without becoming discoloured to form melaena. History taking should focus not only on colorectal symptoms, but also on any symptoms that might suggest an upper gastrointestinal origin for the bleeding.

A rectal examination and sigmoidoscopy should start the diagnostic work-up because occasionally a local perianal cause will be found. If the findings are negative, it is appropriate to proceed to an upper gastrointestinal endoscopy so that a gastroduodenal cause is fully excluded. This can be accomplished quickly and prepares the way for more complex and invasive investigation of the small and large intestine.

Colonoscopy (after rapid colon cleansing in 12 hours), radiolabelled red cell scan, selective mesenteric angiography and computed tomogram angiography can all be used to try to identify the site of bleeding. Red cell scan and angiography can localise the site of bleeding if it is faster than 0.5–1 mL/minute. Colonoscopic intervention or angiographic embolisation can be used to stop bleeding if an active site is identified.

Recent studies have demonstrated that it is safe to give these patients bowel preparation and to proceed to emergency or urgent colonoscopy within 12–24 hours. Since most colonic lesions will stop bleeding spontaneously, there is still debate about the appropriateness of emergency, as opposed to urgent, colonoscopy. If a bleeding lesion is identified during emergency colonoscopy, it can be treated using similar techniques to those described for upper endoscopy. Adrenaline injections, argon plasma coagulation, thermal probes and endoscopic clips all have a role.

The next step in the work-up depends on the clinical condition. If the patient is haemodynamically stable and colonoscopy fails to identify the source of bleeding, a technetium-labelled red cell scan is often performed. In this test, a sample of the patient’s blood is taken and labelled with a radioisotope before being injected back into the patient’s bloodstream. Abdominal scans can then be taken at intervals, looking for extravasation of radiolabelled blood into the bowel. The technique can detect bleeding at rates as low as 0.5 mL per minute. If bleeding is intermittent, the patient can be sent for repeated scans over the next 24–48 hours in the hope of catching a fresh bleed. The object is to localise the source of bleeding to the small or large bowel and give some indication to the surgeon of the precise site in the event of surgery being necessary. The accuracy of the test has been questioned by some clinicians and false localisation of the site of bleeding is a problem in some cases.

A Meckel’s scan (⁹⁹Tc pertechnetate) should be considered in young patients with massive rectal bleeding. The ⁹⁹Tc is taken up by the ectopic acid-secreting gastric mucosa of a Meckel’s diverticulum, which rarely ulcerates and bleeds.

A positive red cell scan may lead to a mesenteric angiogram, which may be both diagnostic and therapeutic. The radiologist may identify not only the site of bleeding but also the cause. Vascular lesions such as angiodysplasia may be seen. An abnormal tumour circulation may be identified.

Active bleeding may be controlled by a vasopressin or terlipressin infusion into the appropriate feeding artery, or by embolisation, and thus avoid the need for surgery.

Growing experience with capsule endoscopy has highlighted a beneficial role for this procedure in patients with large-volume rectal bleeds who are relatively stable. The capsule test provides the best mucosal imaging of the small intestine and is particularly useful for the detection of vascular lesions such as angiodysplasia. A capsule endoscopy study takes many hours to perform and then report. Accordingly, the patient must be in a stable condition to allow the procedure to be performed. Small bowel endoscopy can now be performed by using a colonoscope (push enteroscopy) or special small bowel scopes (e.g. double-balloon enteroscope).

If the above techniques identify the lesion but fail to control the bleeding, an operation will be necessary. In some instances, a laparotomy is combined with an on-table endoscopy or colonoscopy, as the endoscopist may be able to assist the surgeon in the precise localisation of a small bleeding point, particularly in the case of angiodysplasia.

Iron Deficiency Anaemia

In all patients over the age of 40 years, iron deficiency anaemia should be assumed to be due to gastrointestinal bleeding. Investigation gives a high yield of gastrointestinal lesions in this age group, even if the anaemia is not associated with any gastrointestinal symptoms.

Young menstruating women, however, have a very high incidence of iron deficiency and pathology in the gastrointestinal tract is rarely found. Thus, empirical treatment of the anaemia without full investigation in the absence of gastrointestinal symptoms is usually appropriate.

The presentation may be vague with ill-defined symptoms, such as lethargy, dizziness or depression. Some patients will present with shortness of breath or angina. A careful search for signs of anaemia is warranted although often none is found. The skin creases, buccal mucosa and conjunctivae should be examined for pallor. There may rarely be spooning of the fingernails present (koilonychia) if the condition is chronic. Blood tests confirm the presence of anaemia and show that the blood is iron-deficient.

The key elements are:

• microcytic hypochromic anaemia; and

• low serum iron and serum ferritin with decreased transferrin saturation.

Sometimes a high platelet count occurs in patients with chronic active blood loss.

A wide range of gastrointestinal lesions (see Box 10.5) may be responsible for the anaemia, from ulcerative oesophagitis to colonic angiodysplasia. A great concern in elderly patients is the possibility of a caecal carcinoma. Usually, distal colonic lesions or oesophageal lesions present with overt blood loss from respective ends of the gastrointestinal tract leading to haematemesis or rectal bleeding and are uncommon causes of isolated iron-deficiency anaemia. Non-bleeding lesions should also be considered. Malabsorption of iron in patients with coeliac disease, previous gastrectomy or atrophic gastritis may occur.