Haematemesis and melaena

Upper gastrointestinal haemorrhage remains a major medical problem and in spite of improvements in diagnosis and the proliferation in treatment modalities over the last few decades is still attended by significant mortality. A hospital mortality in the region of 5 per cent can be expected. In patients in whom the cause of bleeding can be found the most common causes are bleeding peptic ulcer, erosions, Mallory—Weiss tear and bleeding oesophageal varices (Table 51.4).

Whatever the cause the principles of management are identical. First, the patient should be adequately resuscitated and following this investigated urgently to determine the cause of the bleeding. Only then should treatment of a definitive nature be instituted. For any significant gastrointestinal bleed intravenous access should be established and, for those with severe bleeding, central venous pressure monitoring set up and bladder catheterisation performed. Blood should be cross matched and the patient transfused as clinically indicated. As a general rule most gastrointestinal bleeding will stop, albeit temporarily, but there are sometimes instances when this is not the case. In these circumstances resuscitation, diagnosis and treatment should be carried out in quick succession. There are occasions when life-saving manoeuvres have to be undertaken without the benefit of an absolute diagnosis. For instance, in patients with known oesophageal varices and uncontrollable bleeding, a Sengstaken—Blakemore tube may be inserted before an endoscopy has been carried out. This practice is not to be encouraged, except in extremis. In some patients bleeding is secondary to a coagulopathy. The most important current causes of this are liver disease and inadequately controlled warfarin therapy. In these circumstances the coagulopathy should be corrected, if possible, with fresh frozen plasma.

Upper gastrointestinal endoscopy should be carried out by an experienced operator as soon as practicable after the patient has been stabilised. In patients in whom the bleeding is relatively mild, endoscopy may be carried on the morning after admission. In all cases of severe bleeding it should be carried out immediately.

Bleeding peptic ulcers

The epidemiology of bleeding peptic ulcers exactly mirrors that of perforated ulcers. The population affected has in recent years become much older and the bleeding is commonly associated with the ingestion of NSAIDs. Diag­nosis can normally be made endoscopically, although occa­sionally the nature of the blood loss precludes accurately identifying the lesion. However, the more experienced the endoscopist the less likely this is to be a problem.

Medical and minimally interventional treatments

Medical treatment has limited efficacy. All patients are com­monly started on either an H2 antagonist or a proton pump antagonist, but well-performed studies have failed to show that such treatments influence rebleeding, operation rate or mortality. Meta-analysis of studies, however, does suggest that tranexamic acid, an inhibitor of fibrinolysis, reduces the rebleeding rate. Octreotide, a somatostatin analogue, has not proved effective.

Numerous endoscopic devices are now available which can be used to achieve haemostasis ranging from expensive lasers to inexpensive injection apparatus. There are few conclusive studies available but a review of the literature suggests that these modalities may have some utility, although they will probably never be effective in patients who are bleeding from large vessels and with which the majority of the mortality associated with the condition is associated.

Surgical treatment

Criteria for surgery are well worked out. A patient who con­tinues to bleed requires surgical treatment. The same applies to a significant rebleed. Patients with a visible vessel in the ulcer base, a spurting vessel or an ulcer with a clot in the base are statistically likely to require surgical treatment to stop the bleeding. Elderly and unfit patients are more likely to die as a result of bleeding than younger patients. Ironically, they should have early surgery. A patient who has required more than 6 units of blood in general needs surgical treatment. Various scoring systems have been devised which predict the probability of rebleeding and mortality with some degree of accuracy.

The aim of the operation is to stop the bleeding. The advent of endoscopy has greatly helped in the management of upper gastrointestinal bleeding as a surgeon can usually be confident about the site of bleeding prior to operation. The most common site of bleeding from a peptic ulcer is the duodenum. In tackling this it is most important essential that the duodenum is fully Kocherised. This should be done before the duodenum is opened as it makes the ulcer much more accessible and also allows the surgeon’s hand to be placed behind the gastroduodenal artery that is commonly the source of major bleeding. Following mobilisation, the duodenum and usually the pylorus are opened longitudinally as in a pyloroplasty. This allows good access to the ulcer, which is usually found posteriorly or superiorly. Accurate haemostasis is important. It is the vessel within the ulcer that is bleeding and this should be controlled using well-placed sutures which under run the vessel. The placing of more and more inaccurately positioned sutures is counter productive. Following under running it is possible often to close the mucosa over the ulcer. The pyloroplasty is then closed with interrupted sutures in a transverse direction as in the usual fashion.

The principles of management of bleeding gastric ulcers are essentially the same. The stomach is opened at an appropriate position anteriorly and the vessel in the ulcer under run. If the ulcer is not excised then a biopsy of the edge needs to be taken to exclude malignant transformation. Sometimes the bleeding is from the splenic artery and if there is a lot fibrosis present then the operation may be challenging. Most patients, however, can be managed by conservative surgery. Gastrectomy for bleeding has been widely practised in the past but is attended by higher levels of perioperative mortality even if the incidence of recurrent bleeding is less.

Much argument still remains about the use of definitive acid-lowering operations versus haemostatic surgery alone. Bearing in mind that most patients nowadays are elderly and unfit, the minimum surgery that stops the bleeding is probably optimal. Acid can be inhibited by pharmacological means and appropriate eradication therapy will prevent ulcer recurrence. Patients on long-term NSAIDs can be managed as outlined earlier.

Stress ulceration

This commonly occurs in patients with major injury or ill­ness, who have undergone major surgery or who have major comorbidity. Previously, many such patients were to be found in intensive care units. There seems little doubt that the incidence of this problem has reduced in recent years owing to the widespread use of prophylaxis. Ranitidine has been shown to reduce the incidence of stress ulceration, as has the nasogastric administration of sulcrafate. There is no doubt that the prevention of this condition is far better than trying to treat it once it occurs. Endoscopic means of treating stress ulceration may be ineffective and operation required. The principles of management are the same as for the chronic ulcer.

Gastric erosions

Erosive gastritis has a variety of causes, especially NSAIDs. Fortunately, most such bleeding settles spontaneously but when it does not it can be a major problem to treat. In gen­eral terms, although there is a diffuse erosive gastritis, there is one (or more) specific lesion which has a significant sized vessel within it. This should be dealt with appropriately, pre­ferably endoscopically, but sometimes surgery is necessary.

Mallory—Weiss tear

This is a longitudinal tear below the gastro-oesophageal junc­tion, which is induced by repetitive and strenuous vomiting. Doubtless, many such lesions occur and do not cause bleed­ing. When it is a cause of haematemesis the lesion may often be missed as it can be difficult to see as it is just below the gastro-oesophageal junction, a position that can be difficult for the inexperienced endoscopist. Occasionally these lesions continue to bleed and require surgical treatment. Often the situation arises that the surgeon does not have guidance from the endoscopists as regards the site of bleeding, and a high index of suspicion in such circumstances is important. The stomach is opened by longitudinal gastrotomy and carefully inspected high up. It is normally possible to palpate the longitudinal mucosal tear with a little induration at the edges which gives a clue to the lesion’s location. Under-running is all that is required.

Dieulafoy’s disease

This is essentially a gastric arterial venous malformation that has a characteristic histological appearance. Bleeding due to this malformation is one of the most difficult causes of upper gastrointestinal bleeding to treat. The lesion itself is covered by normal mucosa and, when not bleeding, it may be invisible. If it can be seen whilst bleeding all that may be visible is profuse bleeding coming from an area of apparently normal mucosa. If this occurs cause is instantly recognisable. If the lesion can be identified endoscopically there are various means of dealing with it, including injection of sclerosant. If it is identified at operation then only a local excision is necessary. Occasionally a lesion is only recognised after gastrectomy and sometimes not even then. The pathologist, as well as the endoscopist, may have difficulty in finding it.

Tumours

All of the gastric tumours described below may present with chronic or acute upper gastrointestinal bleeding. Bleeding is not normally torrential but can be unremitting. Gastric smooth muscle tumours commonly present with bleeding and have a characteristic appearance, as the mucosa breaks down over the tumour in the gastric wall (Fig. 51.26). Whatever the nature, the tumours should be dealt with as appropriate.

Portal hypertension and portal gastropathy

The management of bleeding gastric varices is very challenging. Fortunately, most bleeding from varices is oesophageal and this is much more amenable to sclerotherapy, banding and balloon tamponade. Gastric varices may also be injected, although this is technically more difficult. Banding can also be used, again with difficulty. The gastric balloon of the Sengastaken—Blakemore tube can be used to arrest the haemorrhage if it is occurring from the fundus of the stomach. Octreotide is a somatostatin analogue which reduces portal pressure in patients with varices and trials suggest that it is of value in arresting haemorrhage in these patients, although its overall effect on mortality remains in doubt. Glypressin is also said to be of use.

Most surgeons prefer to avoid acute surgery on bleeding varices as, by contrast with elective operations for portal hypertension, acute shunts are attended by considerable operative mortality. For this reason the acute TIPSS pro­cedure (transjugular intrahepatic portosystemic shunt) which is described in Chapter 52 can be an extremely useful, although technically demanding, procedure.

Portal gastropathy

Portal gastropathy is essentially the same disease process as described above. The mucosa is affected by the increased portal pressure and may exude blood even in the absence of well-developed visible varices. The treatment is as above.

Aortic enteric fistula

This diagnosis should be considered in any patient with haematemesis and melaena which cannot be otherwise explained. Contrary to expectation, the bleeding from such patients is not always massive, although it can be. Very often there is nothing much to distinguish the bleeding from the aortic enteric fistula from any other recurrent upper gastrointestinal bleeding. The vast majority of patients will have had an aortic graft and in the absence of this the diagnosis is unlikely. However, it is occasionally seen in patients with an untreated aortic aneurysm. A well-performed CT scan will commonly allow the diagnosis to be made with certainty. The condition should be managed by an expert vascular surgeon as, whether secondary or primary, the morbidity and mortality are high.