Requirements for blood are shown in Table 7.4. When the patient is stable a detailed history and examination may be obtained to establish the cause (Table 7.5). OGD is essential to achieve a diagnosis within 24 hours.

Table 7.4 Guidelines for cross-matching and transfusion of blood in upper GI bleeds

Clinical state	Action
Without haemodynamic problems	None
With haemodynamic problem	4 units
Anaemic (Hb <10 g/dL)	1 unit of blood for every 1 g deficit below 10 g/dL
Continued bleeding	Guided by clinical features but at least 4 units
Re-bleed if under 60 years	No action unless there is haemodynamic instability
Re-bleed if over 60 years	4 units

Table 7.5 Salient historical features in common causes of haematemesis

Cause	Mechanism	Historical features
Mucosal tear at cardia (Mallory–Weiss syndrome)	Forceful attempted vomiting	Acute inebriation Initial clear vomit Bright red haematemesis
Oesophageal varices	Rupture or erosion of mucosa over varix	Past liver disease Absence of peptic ulcer history Dark red haematemesis
NSAID-induced erosions	Breakdown of mucosal barrier to acid	Pain-producing associated disorder (e.g. rheumatoid arthritis) Intake of NSAID, including low-dose aspirin
Peptic ulcer	Peptic digestion of vessel in base of ulcer Fibrinoid necrosis of vessel holding lumen open Exacerbation of ulceration by NSAIDs	Previous episodes of dyspepsia Diagnosed ulcer Recent worsening of symptoms Blood of variable colour with or without clots
Angiodysplaslas	Rupture or mucosal digestion of a surface lesion	No history on initial occurrence
Other causes to consider	Varies with cause	Examples: History of anticoagulant intake Haematological disorders

Treatment depends on cause and may be conservative or operative. Patients with Hb >12 g/dL are unlikely to re-bleed. Increasingly endoscopic interventions are used (e.g. injection of adrenaline (epinephrine) into ulcer base, clipping of the artery, thermocoagulation and banding of varices).

Peptic ulcer

Many bleeds are self-limiting. Withdrawal of NSAIDs and treatment with PPIs or H₂ receptor antagonists is effective. Patients more likely to re-bleed are elderly, with a large ulcer with endoscopic stigmata of visible vessel, adherent clot, black spot in the ulcer crater or actively bleeding vessel (Table 7.6). The decision to operate should be made in a multidisciplinary setting (Table 7.7). Absence of H. pylori is confirmed by ¹³C urea breath test or by stool sample.

Table 7.6 Re-bleeding in peptic ulcer

Class of evidence	Features
Haemodynamic evidence of continued blood loss after resuscitation	Persistent – low or falling CVP; tachycardia; hypotension
Clinical evidence of continued or repeated bleeding	Further fresh haematemesis (not old blood) Melaena
Re-endoscopy	Visible fresh bleeding
Haematological	Progressive haemodilution beyond 24 hours

Table 7.7 Indications for surgery for a bleeding duodenal ulcer

Timing	Age (years)	Basis of decision
Immediate	Any	Uncontrollable spurting vessel at endoscopy Clinical exsanguination
Delayed	Over 60	More than 4 units of blood required for haemodynamic stabilisation or more than 8 units over 48 hours
Delayed	Under 60	More than 8 units necessary for stabilisation or more than 12 units needed over 48 hours
On rebleeding	Over 60	One re-bleed after initial successful control but while still in hospital
On rebleeding	Under 60	Two re-bleeds after initial successful control but while still in hospital

Operatively, for DU the bleeding vessel is under-run with a suture. Definitive operations for peptic ulceration (vagotomy and pyloroplasty) are rarely required, since medical therapy is so effective. Gastric ulcers may be excised locally and sent for pathology to exclude malignancy. If malignancy is confirmed, elective radical surgery may be contemplated.

Oesophageal varices

Oesophageal varices are increasingly common, especially in alcoholic liver disease. Fifty per cent of patients with varices have a bleed and 70% will have another within 1 year. Mortality is higher according to the amount of blood lost, inability to control the bleeding and the severity of the liver damage. Treatment aims to reduce portal pressure (intravenous infusion of vasopressin and betablockade) and to tamponade the oesophageal varices with a Sengstaken-Blakemore tube. Further treatment may include sclerosant injection or rubber band ligation via the endoscope.

Transjugular intrahepatic portosystemic shunting (TIPSS) is replacing gastric transection and surgical portosystemic shunts as a means of reducing variceal pressure. Variceal bleeding has a high mortality and is best treated in a specialist unit.

Gastric erosions

Gastric erosions associated with liver or multi-organ failure as a cause of upper GI bleeding are managed conservatively with proton pump inhibitors and occasionally sucralfate. Operation (gastrectomy) is rarely contemplated.

Mallory–Weiss tear

The Mallory–Weiss syndrome is bleeding from an incomplete lower oesophageal tear due to severe vomiting. The blood loss is usually self-limiting.

Aortoenteric fistula

This is a rare cause of UGIH unless the patient has had previous aortic surgery (e.g. AAA repair), in which case it must be the presumed diagnosis until proved otherwise. A major bleed may be preceded by a number of minor ones (the ‘herald bleed’) which may lull doctors into a false sense of security. CT scanning should be performed before OGD (look for inflammation between the duodenum and the aortic graft). OGD usually shows bleeding but not the source. Treatment usually requires removal of the aortic graft which is infected and extra-anatomic reconstruction (axillo-bifemoral bypass). This carries a high mortality (over 40%).

Disorders of the small bowel

Meckel’s diverticulum

This is a remnant of the vitello-intestinal duct of the embryo which classically occurs in 2% of patients, is 5 cm long and 60 cm from the ileocaecal junction. It occurs on the antimesenteric border of the terminal ileum (Figure 7.4).

Figure 7.4 Meckel’s diverticulum.

Clinical features

Most Meckel’s diverticula are an incidental finding at laparotomy although, because of the presence of ectopic gastric mucosa, symptoms typical of appendicitis may occur if the mucosa is inflamed. Alternatively, chronic lower GI bleeding from ulceration ulceration can lead to anaemia. Intestinal obstruction due to a volvulus of small bowel around the band from the apex of the diverticulum to the back of the umbilicus may occur. Investigations include a technetium scan for GI bleeding or a red cell scan if bleeding is severe. Excision of the diverticulum is curative.

Tuberculosis

Aetiology

The organism enters the gut via the lymphoid follicles of the ileum. Both human and bovine strains of Mycobacterium tuberculosis may be the cause but the latter is uncommon. In patients with immunodeficiency, unusual strains (e.g. M. avium-intracellulare) may be found. TB infection of the small bowel is uncommon but remains a feature of communities with poor nutrition.

Pathology

Typically, tuberculosis causes ulceration, lymph node enlargement and subsequent caseation and healing with the formation of strictures. Tuberculous peritonitis involving the peritoneum produces characteristic miliary nodules and the development of ascites.

Clinical features

Weight loss, low grade pyrexia, anaemia, diarrhoea, vague abdominal pain and rectal bleeding may all be present. Inflammatory masses and strictures can cause obstructive symptoms. Abdominal TB and Crohn’s disease may be difficult to distinguish one from another.

Investigations

MRI enteroclysis can provide functional pictures. Barium follow-through may show distortion of the caecum and is difficult to distinguish from Crohn’s disease. Laparoscopy may be helpful in this situation. Half of patients with abdominal TB also have an abnormal chest X-ray.

Treatment

The primary treatment of abdominal TB is the same as TB of other organs, i.e. with antibiotics (usually a combination of rifampicin and isoniazid) for up to six months.

Radiation enteritis

Radiotherapy, increasingly used for the treatment of malignancy, can damage small and large bowel. Radiation enteritis may not develop until many years after the treatment. The end effect is an endarteritis in the small blood vessels of the wall of the gut, leading to mucosal atrophy and fibrosis, strictures, ulceration and obstruction. Surgical excision of the damaged loops may be required. Care must be exercised in using healthy un-irradiated bowel for one side of the anastomosis. Poor healing and anastomotic breakdown are common.

Small bowel neoplasms

Primary tumours in the small bowel are uncommon. Small bowel tumours are associated with polyposis coli, Peutz–Jeghers syndrome and Gardner’s syndrome. Immunocompromised patients are prone to small bowel malignancy including Kaposi’s sarcoma and lymphomas. Lymphomas are more common in the Middle East than in Western society. Secondary metastases to the small bowel can occur, especially in malignant melanoma and small-cell carcinoma of the lung.

Carcinoid tumours

See Chapter 11, p. 192.

Typhoid

This is caused by Salmonella typhi. Two hundred cases occur in the UK per year. It may occur in the immigrant population or those who have travelled to endemic countries. The organism enters Peyer’s patch and may result in perforation or bleeding during the third week of the disease. Patients present urgently with signs of peritonitis and perforation. Surgical closure of the perforation is required. Chloramphenicol is given intravenously for 2 weeks postoperatively.

Crohn’s disease

Aetiology

This chronic inflammatory condition may affect any part of the GI tract from the mouth to the anus, though the most commonly affected area is the terminal ileum. The cause of this condition is not known, although tuberculosis-type organisms (mycobacteria) have been implicated.

Pathology

There is transmural inflammation with oedema, fissures and non-caseating foci of epithelioid and giant cells leading to fibrosis. Skip lesions can occur throughout the bowel (i.e. there may be normal segments of bowel between affected areas). Oedema and fibrosis lead to intestinal obstruction and internal fistulae may form between loops of bowel, retroperitoneum or the skin.

Clinical features

Acute

There are three main acute presentations of Crohn’s disease: right iliac fossa (RIF) pain mimicking appendicitis, small bowel obstruction and perianal suppuration in the form of abscess and fistula. All these are common on general surgical takes and Crohn’s disease is always in the differential diagnosis of these problems.

Chronic

Crohn’s colitis resembles ulcerative colitis (p. 149, p. 152); the clinical features are similar. There may be symptoms of ill health, weight loss, abdominal pain and diarrhoea. A mass may be present in the RIF. There may be signs of the ‘Crohn’s anus’: skin tags, fissuring and scarring from previous perianal abscess. Other clinical signs that may suggest the diagnosis include clubbing, erythema nodosum, pyoderma gangrenosum and uveitis.