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Gastrointestinal Bleeding 93
Specific management Varices are treated with banding or glue
sclerotherapy. Ulcers with high-risk stigmata for continued or re-bleeding (active
bleeding, visible vessel, overlying clot) should undergo endoscopic haemostasis
by injection of dilute adrenaline (epinephrine) together with coagulation of the
vessel with thermal therapy (heater or bipolar probe), or application of mechanical
clips (endoclips) to the vessel. Antral biopsies should be taken to look for
H.pylori. A positive biopsy urease test is valid, but a negative test is not reliable.
If the urease test is negative, gastric histology should always be performed. After
diagnosis at endoscopy, an intravenous PPI infusion should be administered to
all patients for 72 hours in the presence of actively bleeding ulcers or ulcers
with a visible vessel, as it reduces re-bleeding rates and the need for surgery.
Surgery is rarely required for persistent or recurrent bleeding from ulcers.
Post-endoscopy
In general, young patients with PU bleeding who are otherwise fit and haemodynamically stable and who have no stigmata of recent bleeding can be
discharged from hospital within 24 hours (post-endoscopy Rockall score ≤1).
H. pylori eradication treatment is given and eradication confirmed by urea
breath test or faecal antigen testing. Assessment of ongoing need for antiplatelet therapy is made and essential treatment is co-prescribed with a PPI.
Lower gastrointestinal bleeding
Bright red or altered blood per rectum suggests bleeding from the colon or
small intestine. Massive bleeding is rare and usually from diverticular disease
or ischaemic colitis (Table 3.5). Minor bleeds from haemorrhoids and anal
fissure are common.
Table 3.5 Causes of lower gastrointestinal bleeding
Colonic
Haemorrhoids
Anal fissure
Neoplasms: benign and malignant
Colitis: ulcerative colitis, Crohn’s, infective, ischaemic
Angiodysplasia (abnormal collections of blood vessels)
Diverticular disease
Small intestine
Neoplasms
Ulcerative disease: Crohn’s disease, vasculitis, NSAIDs
Angiodysplasia
Meckel’s diverticulum
NB: acute massive upper gastrointestinal bleeding may present with fresh rectal bleeding
usually with haemodynamic instability.
NSAIDs, Non-steroidal anti-inflammatory drugs.
94 Gastroenterology and nutrition
Management
Resuscitation with intravenous fluids or blood is necessary with large bleeds.
The site of bleeding is determined from the history and physical examination
including a rectal examination and the following investigations as appropriate:
• Proctoscopy to look for anorectal disease, e.g. haemorrhoids.
• Sigmoidoscopy or colonoscopy for inflammatory bowel disease, polyps,
colon cancer, diverticular disease, ischaemic colitis, vascular lesions.
• Angiography for vascular abnormality, e.g. angiodysplasia.
In the non-emergency setting, bright red fresh rectal bleeding is likely to
originate from a source distal to the splenic flexure and can be investigated
with a flexible sigmoidoscopy rather than full colonoscopy.
Chronic gastrointestinal bleeding
Chronic gastrointestinal bleeding presents with iron deficiency anaemia.
All patients require investigation of the gastrointestinal tract to exclude a
malignancy. The exception is menstruating women less than 50 years of age
without gastrointestinal symptoms, in whom anaemia is assumed to be due
to menstrual blood loss, and frail elderly, when the risks of the investigation
may outweigh the benefits of making a definitive diagnosis. The causes of
chronic blood loss are the same as those that cause acute bleeding (see Fig.
3.3, p. 89 and Table 3.5), although oesophageal varices, duodenal ulcers and
diverticular disease rarely bleed chronically. Malabsorption (most frequently
from coeliac disease), previous gastrectomy and, rarely, poor dietary intake
are causes of iron deficiency and will also present with anaemia.
Investigations
Investigation of iron deficiency anaemia is conducted with an OGD and colonoscopy (‘top and tail’), often performed at the same endoscopic session; a
distal duodenal biopsy is taken to look for coeliac disease. An unprepared
CT scan may be used to investigate colon cancer in frail patients and CT
colonography can be used as an alternative to colonoscopy. Further investigations may be warranted in anaemia not responding to iron treatment and
investigation of the small bowel is warranted:
• Small bowel barium follow-through or MRI (usually only helpful if there
are symptoms to suggest Crohn’s disease)
• Video capsule endoscopy
• Enteroscopy (push and/or balloon-assisted) is particularly useful for
endoscopic therapy of vascular lesions seen at capsule endoscopy
• Coeliac axis and mesenteric angiography
• Technetium-labelled red cell scan.
Management
The cause of the bleeding is treated and oral iron is given to treat the anaemia.
The Small Intestine 95
Table 3.6 Disorders of the small intestine causing malabsorption
Coeliac disease
Crohn’s disease
Dermatitis herpetiformis
Tropical sprue
Bacterial overgrowth
Intestinal resection
Whipple’s disease
Radiation enteritis
Parasite infection, e.g. Giardia intestinalis
THE SMALL INTESTINE
The principal role of the small intestine is the digestion and absorption of
nutrients. Vitamin B12 and bile salts have specific receptors in the terminal
ileum but other nutrients are absorbed throughout the small intestine.
Presenting symptoms of small bowel disease are diarrhoea, steatorrhoea,
abdominal pain or discomfort, and anorexia causing weight loss. Small
bowel disease may also be found after investigation for specific deficiencies
such as vitamin B12. The two most common causes of small bowel disease
in developed countries are coeliac disease and Crohn’s disease. Disorders
of the small intestine causing malabsorption are shown in Table 3.6.
Investigation of suspected small bowel disease (e.g. in a symptomatic patient
and/or folate/vitamin B12 deficiency) is initially with coeliac serology, small
bowel barium follow through or MRI and endoscopic small bowel biopsy.
Coeliac disease (gluten-sensitive enteropathy)
This is an autoimmune condition characterized by an abnormal jejunal
mucosa that improves when gluten (contained in wheat, rye and barley) is
withdrawn from the diet and relapses when gluten is reintroduced. About 1 in
100 individuals in European-derived populations have coeliac disease, most
of whom are undiagnosed.
Aetiology
A strong association exists between coeliac disease and two human
leucocyte antigen (HLA) class II molecules, HLA DQ2 and DQ8. The
peptide α-gliadin is the toxic portion of gluten. Gliadin is resistant to
proteases in the small intestinal lumen and passes through a damaged (as a result of an infection or possibly gliadin itself) epithelial
barrier of the small intestine where it is deaminated by tissue transglutaminase so increasing its immunogenicity. Gliadin then interacts
96 Gastroenterology and nutrition
with antigen-presenting cells in the lamina propria via HLA DQ2 and
DQ8 and activates gluten-sensitive T cells. The resultant inflammatory
cascade and release of mediators contribute to the villous atrophy and
crypt hyperplasia that are typical histological features of coeliac disease.
There is an increase in intraepithelial lymphocytes but the pathogenic
role of these lymphocytes, compared with lamina propria lymphocytes,
is controversial.
Environmental factors are also thought to be important, with breastfeeding and the age of introduction of gluten into the diet being significant.
Rotavirus infection in infancy also increases the risk; adenovirus-12, which
has sequence homology with α-gliadin, was suspected as a causative agent,
but this is now thought to be unlikely.
Clinical features
Presentation is at any age but there are two peaks in incidence: infancy
(after weaning on to gluten-containing foods) and in adults in the fifth
decade. There may be non-specific symptoms of tiredness and malaise, or
symptoms of small intestinal disease (see above). Diarrhoea or steatorrhoea,
abdominal pain and weight loss suggest more severe disease. Mouth ulcers
and angular stomatitis are frequent and can be intermittent. Infertility and
neuropsychiatric symptoms of anxiety and depression can occur. Physical
signs are usually few and non-specific, and related to anaemia and nutritional
deficiency. Rare complications include tetany, osteomalacia or malnutrition
with peripheral oedema. Long-term problems include osteoporosis and
polyneuropathy. There is an increased incidence of atopy and autoimmune
diseases (Table 3.7).
Investigations
Serum antibodies Immunoglobulin (Ig) A tissue transglutaminase (tTG)
antibodies have a very high sensitivity and specificity for coeliac disease.
False negatives occur in IgA deficiency (2% of coeliacs) when IgG-based
tests should be used. IgA endomysial (EMA) antibodies are less sensitive.
Serological testing is offered to patients with signs or symptoms or in
conditions where there is an increased risk of disease (see Table 3.7).
Distal duodenal biopsies Small bowel biopsy is considered the ‘gold
standard’ for positive diagnosis and is therefore desirable in all but the
most clear-cut cases, because treatment involves a lifelong diet that is
both expensive and socially limiting. However, with the increasing accuracy
of serological tests, it is no longer necessary to take duodenal biopsies
for suspected coeliac disease in patients without antibodies. Histological
changes are of variable severity and show an increase in the number of
intraepithelial lymphocytes, crypt hyperplasia with chronic inflammatory cells
in the lamina propria and villous atrophy. The latter is seen in other conditions
(e.g. tropical sprue, Whipple’s disease), but coeliac disease is the commonest
cause of subtotal villous atrophy.
The Small Intestine 97
Table 3.7 Individuals who should be offered serological testing
for coeliac disease
Autoimmune disease
Type 1 diabetes mellitus
Thyroid disease
Autoimmune liver disease
Addison’s disease
Irritable bowel syndrome with diarrhoea (symptoms may be similar to coeliac
disease)
Unexplained osteoporosis
Those with a first-degree relative (10-fold increase compared with general
population)
Down’s syndrome (20-fold increase)
Turner’s syndrome
Infertility and recurrent miscarriage
Other investigations
A mild anaemia is present in 50% of cases. There is almost always folate
deficiency, commonly iron deficiency and, rarely, vitamin B12 deficiency. In
severe cases biochemical evidence of osteomalacia may be seen (low calcium and high phosphate) and there is hypoalbuminaemia.
Small bowel radiology or capsule endoscopy is usually only performed
when a complication such as lymphoma is suspected.
Bone densitometry (dual-energy X-ray absorptiometry (DXA) scan) is
performed at diagnosis because of the increased risk of osteoporosis.
Management
Treatment is with a lifelong gluten-free diet and correction of any vitamin
deficiencies. Pneumococcal vaccine is given as coeliac disease is associated
with hyposplenism. Symptoms and serological testing (undetectable antibodies indicate a response) are used to monitor recovery and compliance with
the diet; re-biopsy is reserved for patients who do not respond or in whom
there is diagnostic uncertainty.
Complications
There is an increased incidence of malignancy, particularly intestinal T cell
lymphoma, small bowel and oesophageal cancer. The incidence may be
reduced by a gluten-free diet.
Dermatitis herpetiformis
Dermatitis herpetiformis is an itchy, symmetrical eruption of vesicles and
crusts over the extensor surfaces of the body, with deposition of granular IgA
98 Gastroenterology and nutrition
at the dermoepidermal junction of the skin including areas not involved with
the rash. Patients also have a gluten-sensitive enteropathy, which is usually
asymptomatic. The skin condition responds to dapsone, but both the gut and
the skin will improve on a gluten-free diet.
Tropical sprue
This is a progressive small intestinal disorder presenting with diarrhoea,
steatorrhoea and megaloblastic anaemia. It occurs in residents or visitors
to endemic areas in the tropics (Asia, some Caribbean islands, Puerto Rico,
parts of South America). The aetiology is unknown but likely to be infective.
Diagnosis is based on demonstrating evidence of malabsorption (particularly
of fat and vitamin B12) together with a small bowel mucosal biopsy showing features similar, but not identical, to those in untreated coeliac disease.
Infective causes of diarrhoea, particularly Giardia intestinalis, should be
excluded. Treatment is with folic acid and tetracycline for 3–6 months and
correction of nutritional deficiencies.
Bacterial overgrowth
The upper small intestine is almost sterile. Bacterial overgrowth occurs when
there is stasis of intestinal contents as a result of abnormal motility, e.g. systemic sclerosis, or a structural abnormality, e.g. previous small bowel surgery
or a diverticulum. E. coli and/or Bacteroides are found as part of a mixed flora.
Clinical features
The bacteria deconjugate bile salts, causing diarrhoea and steatorrhoea.
Some bacteria can metabolize vitamin B12 and interfere with its binding to
intrinsic factor, leading to mild vitamin B12 deficiency.
Diagnosis
A therapeutic trial of antibiotics is given when clinical suspicion is high.
Otherwise, diagnosis is usually by a hydrogen breath test in which hydrogen
is measured in exhaled air after oral lactulose. With bacterial overgrowth an
early peak is seen in the breath hydrogen followed by the later colonic peak
(normally present due to metabolism of lactulose by colonic bacteria).
Management
The underlying cause should be corrected if possible. Otherwise, rotating
courses of antibiotics, e.g. tetracycline and metronidazole, are given.
Intestinal resection
The effects of small intestinal resection depend on the extent and the area
involved. Resection of the terminal ileum leads to:
Miscellaneous Small Intestinal Conditions 99
• Steatorrhoea and gallstone formation. Increased bile salt synthesis can
compensate for loss of approximately one-third of the bile salts in the
faeces. Greater loss than this results in decreased micelle formation and
steatorrhoea, and lithogenic bile and gallstone formation
• Vitamin B12 deficiency. In turn this leads to megaloblastic anaemia
• Bile salt induced diarrhoea. Bile salts overflow into the colon causing
secretion of water and electrolytes and diarrhoea.
• Oxaluria and oxalate stones. Bile salts in the colon cause increased oxalate
absorption with oxaluria, leading to urinary stone formation (p. 367).
More extensive resection leaving less than 1 m of small bowel is followed
by the short bowel syndrome. The majority of cases occur after resection
due to Crohn’s disease, mesenteric ischaemia, trauma, volvulus or surgical
complications. Parenteral nutrition is the mainstay of treatment for patients
in whom absorptive function has failed. Intestinal transplantation is used in
a few centres.
The ability of patients to cope without supplemental intravenous fluids or
nutrition depends on:
• Amount of resected bowel – most patients with <100 cm of jejunum and
no colon will require supplements.
• Location of resected bowel (jejunal resection is better tolerated than
ileal).
• Health of the residual intestine, i.e. there are fewer problems after
resection following trauma than in patients with Crohn’s disease.
Whipple’s disease
This is a rare disease caused by the bacterium Tropheryma whipplei.
Steatorrhoea, abdominal pain, fever, lymphadenopathy, arthritis and neurological involvement occur. Small bowel biopsy shows periodic acid-Schiff
(PAS)-positive macrophages which on electron microscopy are seen to
contain the causative bacteria. Treatment is with co-trimoxazole for 1 year.
MISCELLANEOUS SMALL INTESTINAL CONDITIONS
Tuberculosis
This results from reactivation of the primary disease caused by Mycobacterium
tuberculosis. In developed countries it is most commonly seen in ethnic
minority groups or patients who are immunocompromised due to human
immunodeficiency virus (HIV) infection or drugs. The ileocaecal valve is the
most common site affected.
Clinical features
There is abdominal pain, diarrhoea, anorexia, weight loss and fever. A mass
may be palpable. Presentation can be similar to Crohn’s disease.
100 Gastroenterology and nutrition
Diagnosis
Imaging Chest X-ray shows evidence of pulmonary tuberculosis in 50%
of cases. A small bowel follow-through may show features similar to those
of Crohn’s disease (p. 102). US or CT shows mesenteric thickening and
lymphadenopathy.
Pathology and culture of tissue is desirable but not always possible.
Treatment is started if there is a high degree of suspicion. Specimens can be
obtained at laparoscopy; laparotomy is rarely required.
Management
Treatment is similar to that for pulmonary tuberculosis but given for 1 year.
Protein-losing enteropathy
Increased protein loss across an abnormal intestinal mucosa occasionally
leads to hypoalbuminaemia and oedema. Causes include Crohn’s disease,
Ménétrier’s disease (thickening and enlargement of gastric folds), coeliac
disease and lymphatic disorders, e.g. lymphangiectasia.
Meckel’s diverticulum
A diverticulum projects from the wall of the ileum approximately 60 cm
from the ileocaecal valve. About 50% contain gastric mucosa which
secretes acid, and peptic ulceration may occur. Presentation is with lower
gastrointestinal bleeding, perforation, inflammation (presents similarly to
appendicitis) or with obstruction (due to an associated band). Treatment is
surgical removal.
Intestinal ischaemia
Ischaemia is usually due to reduced arterial inflow as a result of atheroma,
embolism (e.g. in atrial fibrillation), vasculitis or profound and prolonged
shock. It presents acutely with severe abdominal pain but there is often
little to find on abdominal examination. Surgery is necessary to resect the
gangrenous bowel and the mortality is high. It may also present chronically
with post-prandial abdominal pain and weight loss. Diagnosis is made by
angiography.
Tumours of the small intestine
These are rare and present with abdominal pain, diarrhoea, anorexia and
anaemia. Carcinoid tumours have additional clinical features as described
below.
Miscellaneous Small Intestinal Conditions 101
Malignant tumours
Adenocarcinoma accounts for 50% of malignant small bowel tumours; there
is an increased incidence in patients with coeliac disease and Crohn’s disease. Non-Hodgkin’s lymphoma constitutes 15% of malignant small bowel
tumours and they may be B cell or T cell in origin. The latter occur with
increased frequency in coeliac disease. Treatment is surgical excision with or
without chemotherapy and radiotherapy.
Benign small bowel tumours
• Peutz–Jeghers syndrome is an autosomal dominant condition with
mucocutaneous pigmentation (circumoral, hands and feet) and
hamartomatous gastrointestinal polyps. Polyps may occur anywhere
in the gastrointestinal tract, but are most common in the small bowel.
They may bleed or cause intussusception, and may undergo malignant
change.
• Adenomas, leiomyomas and lipomas are rare. They are usually
asymptomatic and discovered incidentally.
• Familial adenomatous polyposis (p. 113).
Carcinoid tumours
Pathology
Carcinoid tumours originate from (serotonin-producing) enterochromaffin
cells of the intestine. Carcinoid syndrome is the term applied to the symptoms that arise as a result of serotonin (5-hydroxytryptamine, 5-HT), kinins,
histamine and prostaglandins, released into the circulation from secondaries
in the liver.
Clinical features
Patients with gastrointestinal carcinoid tumours have the carcinoid syndrome
only if they have liver metastases. Tumour products are then able to drain
directly into the hepatic vein (without being metabolized by the liver) and into
the systemic circulation, where they cause flushing, wheezing, diarrhoea,
abdominal pain, and right-sided cardiac valvular fibrosis causing stenosis
and regurgitation.
Investigations
A high level of 5-hydroxyindoleacetic acid (5-HIAA), the breakdown product of
serotonin, is found in the urine in the carcinoid syndrome. A liver ultrasound
confirms the presence of metastases.
102 Gastroenterology and nutrition
Management
Treatment of the carcinoid syndrome is symptomatic and aimed at:
• Inhibition of tumour products with the somatostatin analogue octreotide,
or with 5-HT antagonists, e.g. cyproheptadine
• Reducing tumour mass through surgical resection, hepatic artery
embolization, radiofrequency ablation or chemotherapy.
INFLAMMATORY BOWEL DISEASE
Inflammatory bowel diseases (IBD) refers to chronic systemic diseases
involving inflammation of the intestine. Two major forms of IBD are
recognized:
• Crohn's disease (CD), which can affect any part of the gastrointestinal
tract
• Ulcerative colitis (UC), which affects only the colon.
In 10% of cases of IBD causing colitis, a definitive diagnosis of either UC
or CD is not possible and the diagnosis is termed colitis of undetermined type
(indeterminate colitis).
Epidemiology
IBD occurs worldwide but is most common in Northern Europe, the UK and
North America. Presentation is usually in the teens and twenties. In the UK,
there are about 400 IBD patients per 100 000 population.
Aetiology
IBD represents the outcome of three essential interacting cofactors: genetic
susceptibility, the environment and host immune response.
Genetic susceptibility
• Genetic association is stronger for CD than UC.
• There is familial aggregation of disease.
• Concordance rates are higher in monozygotic (58% for CD) than dizygotic
twins (4%).
• Disease susceptibility genes, e.g. mutations in the CARD15 (NOD2) gene
on chromosome 16, confer susceptibility to stricturing small bowel CD.
• Increased incidence of HLA-B27 in IBD with ankylosing spondylitis.
Environment
• Smoking is associated with a twofold increased risk for CD. In contrast,
current smoking is associated with a reduced risk for developing UC
compared with non-smokers.
• Stress and depression may precipitate relapses in IBD.
• Enteric microflora is altered and the intestinal wall is contaminated by
adherent and invading bacteria.