This patient had no major signs of chronic liver disease but did admit to recurrent episodes of upper abdominal pain radiating through to his back. These tended to occur on Monday, following his weekend binges. This suggests pancreatic disease resulting from his heavy alcohol intake.

What initial investigations are appropriate?

• FBC, LFTs, calcium, blood alcohol

• Plain X-ray of the abdomen for pancreatic calcification

• Abdominal ultrasound to assess the pancreas for cysts and potential masses.

This patient was admitted in a malnourished, hyperdynamic state due to acute alcohol withdrawal (see p. 72). Treat this initially and further investigate the pancreas later.

Further investigations

• CT scan of the pancreas:

• MRCP: this is non-invasive and of value in assessment of the pancreas and biliary tree

• ERCP to delineate the biliary and pancreatic ducts (if MRCP is unavailable)

• Endoscopic ultrasound: can help define pancreatic cysts and masses

Progress.

This man was treated initially with benzodiazepine and IV thiamine (p. 527) and made a good recovery from his acute withdrawal state. Further investigations showed chronic pancreatitis; he was referred to the Gastroenterology Clinic.

Dysphagia

Dysphagia is difficulty in swallowing. It is an immediate, obstructive sensation during the passage of liquid or solid through the pharynx or oesophagus.

Case history

A 55-year-old patient has been referred urgently because of acute dysphagia. She gave a history of reflux for years and increasing dysphagia for 6 months. She had been eating an orange, which became lodged in her gullet and all efforts to dislodge it were unsuccessful. The underlying diagnosis is likely to be food bolus obstruction on an already present oesophageal stricture.

What should you do?

Refer for an urgent endoscopy. The endoscopy findings were of a stricture in the mid-oesophagus with no obvious malignant lesion. Biopsies were taken and the stricture dilated.

Remember

Submucosal cancer can look like a benign lesion.

Unfortunately, this woman developed severe chest pain immediately after the dilatation and surgical emphysema could be felt in her neck. Clinically, an oesophageal tear is suspected.

A CXR with a water soluble contrast agent orally, confirms an oesophageal rupture.

Diagnosis.

The underlying cause is more likely to be oesophageal cancer because careful dilatation of benign lesions rarely causes a tear.

Initial management

• Nil by mouth

• IV line for fluids

• Antibiotic prophylaxis

• Surgical referral.

Small tears in a peptic stricture can resolve in a few days on conservative management. Large tears generally need surgery in a dedicated thoracic unit. Endoscopic stenting is used initially for tears in malignant lesions but again surgery may be required.

Biopsies later confirmed a squamous carcinoma.

Management will include assessment for surgery with:

• Blood count, liver biochemistry

• CXR

• ECG

• Respiratory function tests

• Abdominal US, CT scan to assess operability

• Endoscopic ultrasound is an accurate way of staging lesion and any local lymph nodes

• PET scan to look for distant metastases.

Discussion should take place at an MDT to decide on the patient’s treatment.

As investigations showed no distant metastases, surgery with neo-adjuvant (preoperative) and adjuvant (postoperative) chemoradiation treatment was given.

Constipation

This is the infrequent passage of stools, < 3 per week + straining and the passage of hard stools.

Case history

Your house officer asks you what she should prescribe for an elderly man who hasn’t opened his bowels for 5 days. The patient, who was previously well and active, had been admitted a week ago with a chest infection. Rectal examination revealed a loaded colon with no local lesion.

Should this patient be investigated?

Not initially because it seems likely that constipation is due to immobility. A barium enema may be necessary if there is no improvement.

Diarrhoea

Increased frequency of defecation can, even in a previously fit patient, produce dehydration and severe electrolyte depletion. Diarrhoea can also be a recurrent problem in patients with established gastrointestinal disease.

What should you do in a case of diarrhoea presenting in A&E?

In the history, ascertain whether the patient has eaten suspect food or travelled overseas. Check for drug history, e.g. antibiotics. Ask about accompanying symptoms, e.g. abdominal pain, weight loss. It is essential to:

• Establish history of onset.

• Determine frequency, consistency, content of stool, presence of blood.

• Determine the state of hydration and electrolyte balance.

• Send stool for culture, parasites (ova or cysts) and C. difficile toxin (if the patient has previously been hospitalised or been on antibiotics).

• Perform a rectal examination; sigmoidoscopy (if bloody diarrhoea) should be done by the gastroenterology team.

• Do blood cultures in severe cases with a temperature.

• Do a plain abdominal X-ray.

Management

This will depend on the case scenario (see below) but most diarrhoeal illnesses are self-limiting and short lived; 1–10% might persist for a month. Identification of the pathogen will determine specific therapy (see Chapter 1).

Case history (1)

A 24-year-old returned from travelling for 3 months, during which he passed through several countries. He was fairly well on his return but after 3 days he developed severe diarrhoea which has now been present for 2 weeks.

On admission to MAU he is dehydrated and has lost over 5 kg in weight.

What immediate action would you take?

• FBC, U&Es, LFTs.

• Send stools for ova, cysts and culture.

• Rehydration with oral glucose/electrolyte solutions initially. IV fluids are usually not necessary.

• Vomiting might need to be treated with an anti-emetic (metoclopramide 10 mg × 3/day).

Diagnosis

This is not acute diarrhoea due to a viral/bacterial cause as the patient did not have diarrhoea when he returned to the UK. Viral/bacterial diarrhoea usually starts in the country where the infection occurred and generally clears up within 7 days. Possible causes are shown in the Information box.

Information

Causes of non-acute diarrhoea in a returning traveller:

• Giardiasis

• Cryptosporidiosis

• Amoebiasis

• Tropical sprue (SE Asia, Caribbean)

• Schistosomiasis

• Strongyloidiasis

Stool samples showed no abnormal findings.

Progress.

Giardiasis is very likely in this patient and treatment with metronidazole 2 g a day for 3 successive days was given, with dramatic improvement.

Case history (2)

A 30-year-old, white, Caucasian, female patient presented with a 2-week history of passing six to ten motions a day. The stools were loose and contained blood. She felt tired and had lost about 5 kg in weight.

On admission to MAU she was not dehydrated but had a fever and was very lethargic.

What is the differential diagnosis?

• Infective diarrhoea. Send specimens for microbiological testing.

• First presentation of inflammatory bowel disease (most likely in this woman).

Inflammatory bowel disease (IBD)

In any case of persistent diarrhoea presenting in A&E in developed countries, IBD is a possible cause. A previous history of intermittent diarrhoea or recurrent abdominal pain is often present. In developing countries, infective causes are more likely and must be excluded.

What should you do?

General

• Take blood for FBC, ESR, CRP, urea and electrolytes, liver biochemistry.

• Check plain abdominal X-ray for presence of stool, mucosal oedema, bowel dilatation or perforation.

• Sigmoidoscopy: the presence of an inflamed, friable mucosa with loss of vascular pattern or a patchy inflammation indicates inflammatory bowel disease. Take a rectal biopsy.

• Stool cultures (NB: Infective gastroenteritis must always be ruled out). C. difficile toxin assay – 4 stool specimens (90% sensitivity).

In this patient you have ruled out infective gastroenteritis as three stool cultures were negative. Taking into account the history and the sigmoidoscopic finding, you presume this must be inflammatory bowel disease. Her Hb was 100 g/L and CRP 84 mg/L.

Acute colitis is associated with diarrhoea, abdominal pain, fever and systemic disturbance. There is blood in the stools in ulcerative colitis but Crohn’s disease patients only have bloody diarrhoea with Crohn’s colitis. To assess severity, check the factors shown in Table 4.2.

Table 4.2 Findings in severe attack of ulcerative colitis

Haemoglobin	↓	< 100 g/L
Albumin	↓	< 30 g/L
Fever	↑	> 37.5°C
Stool frequency	↑	> 6/day
Erythrocyte sedimentation rate	↑	> 30 mm per hour
Pulse rate	↑	> 90 bpm
Platelets	↑
White blood cells	↑

Always look for the presence of:

• Toxic dilatation: colon > 5 cm diameter and mucosal islands on plain abdominal X-ray (Fig. 4.2).

• Perforation (on abdominal X-ray).

Figure 4.2 (a) Toxic dilatation of the colon; (b) plain abdominal X-ray showing toxic dilatation in ulcerative colitis.

How would you manage this acute situation?

• IV fluids with glucose/saline.

• IV therapy with steroids (IV hydrocortisone 100 mg × 4/day) followed by oral therapy (enteric coated prednisolone 40 mg per day) if patient improves.

• IV antibiotics (metronidazole/cephalosporin).

• Further management: refer to gastroenterologists; consult GI surgeons.

Remember

In acute severe ulcerative colitis, at 3 days post treatment and CRP > 45 mg/L or stool frequency > 8/day gives an 85% chance of needing a colectomy.

Progress and management

There was no response to treatment at 3 days (see Information box). She was started on infliximab 5 mg/kg as ‘rescue therapy’ to avoid immediate colectomy. Ciclosporin 2 mg/kg/day is an alternative.

This patient responded to infliximab and is being followed closely in the Colitis Clinic, continuing on infliximab therapy on a protocol, lasting up to 46 weeks.

Has this patient got Crohn’s disease or ulcerative colitis?

Both can produce an acute colitis. The differentiation is by colonoscopy and histological appearance (see Table 4.3).

Table 4.3 Differentiating between Crohn’s disease and ulcerative colitis

Histological findings	Crohn’s disease	Ulcerative colitis
Inflammation	Deep (transmural), patchy	Superficial (mucosal) continuous
Granulomas	+ +	Rare
Goblet cells	Present	Depleted
Crypt abscesses	+	+ +

Information

Eyes	Uveitis
	Episcleritis, conjunctivitis
Joints	Type I (pauci-articular) arthropathy
	Type II (polyarticular) arthropathy
	Arthralgia
	Ankylosing spondylitis
	Inflammatory back pain
Skin	Erythema nodosum
	Pyoderma gangrenosum (see Fig. 4.3)
Liver and biliary tree	Sclerosing cholangitis
	Fatty liver
	Chronic hepatitis
	Cirrhosis
	Gallstones
Nephrolithiasis
Venous thrombosis

Figure 4.3 Pyoderma gangrenosum (courtesy of David Paige).

Immediate investigations

• Haematological: Hb, WCC, ESR

• Biochemical: U&Es, liver biochemistry, amylase

• Radiological: initial AXR for obstruction. CXR in acute pain for intestinal perforation.

Management

Develop the management plan to include:

• Symptomatic relief.

• Information for patient and relatives.

• Further investigations (endoscopy, ultrasound, CT and MRI as necessary to exclude perforation, obstruction, stones, calcification, cancer and ascites).

• Consultation with surgical colleagues.

In this case, abdominal pain situated in the epigastrium and central abdomen, and of the severity described, is always due to organic disease. Your differential diagnosis should include the following:

Symptom relief

Symptom relief depends on diagnosis. Use anti-spasmodics (hyoscine 20–40 mg × 4/day). Minor analgesics (paracetamol) can help and NSAIDs are useful in some cases. When prescribing opiates (morphine, codeine) remember they can increase constipation and cause spasm in the sphincter of Oddi. Anti-emetics (metoclopramide 10 mg × 2/day or prochlorperazine 5 mg × 2/day) as necessary.

Patient information

This depends on diagnosis but should be delivered to both patients and relatives sensitively and with an understanding of underlying pathology.

Diagnosis and progress.

In this case, the 40-year-old patient turned out to have acute pancreatitis, with a serum amylase of 1000 units. He quickly settled by being nil by mouth and having IV fluids. The aetiology was never established but was thought to have perhaps been viral.

Gastro-oesophageal reflux disease (GORD)

Gastro-oesophageal reflux occurs normally. GORD occurs when the anti-reflux mechanism fails, allowing acidic gastric contents to make prolonged contact with the oesophageal mucosa.

Case history

A 48-year-old man was admitted with severe epigastric pain radiating up into his chest. He thought he had had a heart attack (see p. 284).

What investigations would you do on admission?

It is critical to exclude life-threatening conditions, such as myocardial infarction, pulmonary embolism and pneumothorax before labelling such pain as due to reflux.

Investigations

• FBC, liver biochemistry, serum amylase

• ECG, repeated after 1 hour

• CXR

• Cardiac markers, e.g. troponins and CPK

In this patient, two ECGs, CXR and cardiac markers (e.g. CPK, troponins) were normal. Additional features in the history included:

• Long history of reflux (GORD)

• Burning nature of the pain

• Flatulence

• A relationship of the present pain to previous similar pain

• A food-related element

• Exacerbation of pain with drinking hot liquids.

Features of gastro-oesophageal reflux

• Burning pain produced by bending, stooping or lying down

• Pain seldom radiates to the arms

• Pain precipitated by drinking hot liquids or alcohol

• Pain relieved by antacids.

Features of myocardial ischaemia

• Gripping or crushing pain

• Pain radiates into neck, shoulders and both arms

• Pain produced by exercise

• Accompanied by breathlessness.

Diagnosis of GORD was made in this patient from the history.

Progress and management

He was given liquid Gaviscon (10 mL) and a proton pump inhibitor (PPI, e.g. omeprazole 20 mg × 2 daily for 6 weeks, reducing to 10 mg) to control the symptoms. Endoscopy will need to be performed in this man in view of his age.

Remember

• Reflux can be difficult to diagnose and although it is often associated with a hiatus hernia, more formal investigation might be necessary, e.g. endoscopy followed by oesophageal pH, impedance and pressure monitoring if necessary

• At endoscopy, assess degree of oesophagitis and check for Barrett’s oesophagus (including biopsies).

Barrett’s oesophagus

This occurs as a result of longstanding reflux. It consists of columnar epithelium with intestinal metaplasia extending upwards into the lower oesophagus and replacing normal squamous epithelium. Barrett’s oesophagus (even short segment < 3 cm) is pre-malignant for adenocarcinoma. Risk factors for progression are male sex, age > 45 years, length of segment > 8 cm, early age of onset and duration of symptoms of GORD, the presence of ulceration and stricture and a family history. Dysplasia is patchy and biopsies from all four quadrants (every 2 cm) of the Barrett’s segment must be performed. There is no evidence that treatment with PPIs or surgery leads to Barrett’s regression. Patients without dysplasia do not require surveillance. Low-grade dysplasia requires regular endoscopic surveillance. High-grade dysplasia is now treated with radiofrequency ablation using the HALO system, but endoscopic ablation therapy with photodynamic therapy or laser is also used.

Peptic ulcer disease

Case history (1)

In the clinic you see a 40-year-old man with epigastric pain that has been present on and off for a number of years. The doctor’s letter indicates that the man has been a regular attender and has received antacids, H₂ receptor antagonists and a PPI at some time over the last 5 years. In 2005 the patient was found to have H. pylori antibodies in his serum and was given eradication therapy.

Treatment of H. pylori infection

Patients with peptic ulcer disease who are H. pylori positive should be given combination eradication therapy:

• Clarithromycin 500 mg twice daily for 1 week

• Amoxicillin 1 g twice daily for 1 week

• Omeprazole 20 mg twice daily for 2 weeks.

With increasing resistance to clarithromycin, quadruple therapy is now being used, as in this patient. He was given omeprazole 20 mg × 2, tri-potassium di-citrato bismuthate 120 mg × 4, tetracycline 500 mg × 4 and metronidazole 500 mg × 3 – all daily for 2 weeks.

Progress.

This patient has had no further problems since his quadruple therapy and a stool antigen test was negative for H. pylori.

Case history (2)

You are asked by the cardiologists to see a man with epigastric pain. He has been admitted for urgent percutaneous coronary intervention (PCI). He is already on aspirin 75 mg daily. He has had many similar episodes of pain over the years. In 1988 he had an endoscopy and was told that he had an ulcer and was given Zantac. He points with one finger to his epigastrium as the site of his pain.

This is a classic history of duodenal ulcer disease.

What should you do?

As the PCI is tomorrow you recommend he is given a PPI, e.g. omeprazole 20 mg × 2 daily and referred to gastroenterology outpatients.

The cardiology SpR would like to put the patient on anti-platelet therapy post PCI and is worried that he has an ulcer. This is a problem of balancing the risks. As the coronary stent is urgent they will have to go ahead with anti-platelet therapy with a cytoprotective PPI. The ideal situation for this man would be to perform endoscopy prior to PCI and if an ulcer is present, to heal his ulcer before the intervention.

After reassessment with the Consultant Cardiologist, it is still decided that the PCI is urgent and will go ahead despite its risks, which are fully discussed with the patient.

How do you investigate a patient with a suspected ulcer in the community?

• Less than 45 years: H. pylori serology. If positive, eradication therapy (see p. 48). If negative, treat symptomatically.

• Greater than 45 years: patients with new dyspepsia and those with alarm symptoms (e.g. anorexia, weight loss) should be referred for endoscopy.

Remember

• H. pylori serology can remain positive even after successful eradication of H. pylori

• Current H. pylori infection can be detected by the urea breath test (see Fig. 4.4), endoscopy (urease test, histology or culture) and detection of stool antigen.

Case history (2)

A 40-year-old woman was seen in the A&E department with a sprained ankle. She was sent home with a strapped ankle and given diclofenac to take for the pain. There was no history of indigestion. Ten days later she is brought in by ambulance having vomited blood. The bleeding was thought to be related to the NSAID therapy.

On examination she was not shocked and there are no signs of chronic liver disease. She had stopped bleeding and an endoscopy was performed in the next 24 h.

A bleeding ulcer, with a fresh adherent clot, was seen on endoscopy and was injected with adrenaline (epinephrine) 1:10 000 and a heater probe was also used. A biopsy was taken for H. pylori.

A bleeding ulcer might have certain stigmata that suggest rebleeding is likely to recur (see Remember box).

Gastric cancer does not usually cause an acute GI bleed; it is more likely to produce anaemia from chronic blood loss.

Remember

Stigmata of a recent bleed from an ulcer on endoscopy:

• Spurting vessel

• Prominent vessel

• Fresh adherent clot.

Progress.

The H. pylori test was positive, indicating chronic peptic ulcer disease. The haematemesis was precipitated by the NSAIDs.

Discharge policy

The patient’s age, diagnosis on endoscopy, co-morbidity and the presence or absence of shock should be taken into consideration. In general, patients under the age of 60, as well as older patients who are haemodynamically stable and have no stigmata of recent haemorrhage on endoscopy, can be discharged within 24 h.

Note: All shocked patients need careful observation in hospital. Check your own hospital’s guidelines.

What do you do?

• Exclude all obvious causes of bleeding:

• Heavy periods

• Rectal bleeding

• Recurrent nose bleeds.

• If there is no obvious menorrhagia, you can assume the anaemia is due to gastrointestinal disease. Malabsorption: coeliac disease is still very underdiagnosed.

• The patient travels a lot abroad and could have a bowel infestation. Remember hookworm is the most common cause of iron deficiency anaemia world-wide.

• Occult bleeding from the GI tract is common and can be confirmed by haemoccult testing. This, however, is totally unnecessary in a patient with iron deficiency because if there is no history of blood loss, blood can then only be lost from the GI tract.

Information

Faecal occult bloods:

• Of no use in males or post-menopausal females with iron deficiency anaemia and no other cause for bleeding

• Useful for screening populations for colonic cancer

What additional investigations are appropriate?

• Rectal examination is mandatory to exclude rectal cancer. Proctoscopy to exclude piles.

• Gastroscopy: peptic ulcer, gastric cancer and GORD can certainly occur in this age group. Also do a duodenal biopsy for coeliac disease (see Fig. 4.5).

Figure 4.5 Small intestinal mucosa showing normal villi with normal columnar cells compared to coeliac mucosa showing subtotal villus atrophy, crypt hyperplasia, lamina propria inflammation and an increase in intra-epithelial lymphocytes.

Remember

Coeliac disease:

• Is increasingly recognised world-wide and has an incidence of less than 1:100 in many countries. Certain areas of the world are said to have a higher incidence, e.g. Ireland and Italy

• Malabsorption of iron as well as increased iron loss can occur. There might be other deficiencies as well, e.g. calcium and folic acid

• A history of steatorrhoea can be missed unless a detailed stool history is taken (Note: many patients do not have steatorrhoea or any gastrointestinal symptoms)

• Coeliac serology with anti-endomysial and anti-tissue transglutaminase (the target antigen for the endomysial antibody) antibodies. A serum IgA must be performed as these are IgA in vitro tests. Deaminated gluten peptide (DGP) testing is now becoming available. These tests have a high sensitivity and specificity.

• Diagnosis is confirmed by biopsy of duodenal/jejunal mucosa

• Treatment is with a gluten-free diet.

If gastroscopy is unhelpful, full colonic assessment is necessary. The best investigation is colonoscopy, which will allow full assessment of the colon when biopsy, polypectomy, laser treatment of angiodysplasia can be performed as appropriate.

If the above investigations are negative you have a problem. A small minority of patients fall into this category and the host of further investigations, performed with advice from the GI unit, will include:

• Small bowel follow-through

• Capsule endoscopy

• Enteroscopy

• Meckel’s scan

• Angiography: preferably performed when a patient is bleeding and in this patient unlikely to be helpful

• Laparotomy with possibly simultaneous on-table endoscopy at the time.

Progress.

This patient turned out to have menorrhagia due to fibroids, despite initially denying heavy periods.

Remember

• Iron deficiency anaemia in a post-menopausal female or any male with no obvious cause of blood loss must have a GI cause for the anaemia

• Few patients have an inadequate iron intake in developed countries.

How would you manage the patient initially?

• Establish IV infusion and give 0.9% saline

• Check Hb and U&Es

• Group and cross match blood

• Insert a CVP line

• Transfuse blood.

The patient stabilised and had no further bleeding.

Additional examination

Additional investigations must include a rectal examination, proctoscopy and rigid sigmoidoscopy.

Proctoscopy

This will allow the diagnosis of haemorrhoids and an anal fissure. These are the most common causes of rectal bleeding, but rarely if ever cause torrential blood loss. Features of bleeding from an anorectal lesion:

• Passage of blood after a motion, and not mixed with it

• Blood dripping into the pan

• Blood just on the paper

• Anal pain, particularly with an anal fissure.

Family history of colon cancer

Case history

A doctor phones to discuss a possible referral to the gastroenterology clinic. He has just seen an anxious, 32-year-old woman whose mother has recently died of colonic cancer. The patient has just discovered that her maternal aunt died of a similar complaint. The doctor emphasises that the patient herself has no GI symptoms.

What should you advise?

The patient needs to be seen by a gastroenterologist with a view to a full discussion on the pros and cons of having a colonoscopy.

Family cancer syndromes:

Familial adenomatous polyposis: multiple polyps are found throughout the colon and upper small bowel. All patients should be screened after age 12 years because all patients will develop colon cancer unless the colon is removed.

Hereditary non-polyposis cancer of the colon (HNPCC) (Table 4.5): this accounts for 5–10% of colon cancers; the average age of diagnosis is 45 years. Cancers are mainly in the right-hand side of the colon.

A flexible sigmoidoscope can only reach 60–70 cm up the colon, where approximately 60% of cancers occur (Fig. 4.6).

Table 4.5 Diagnostic criteria for hereditary non-polyposis colon cancer (HNPCC)

Modified Amsterdam criteria

← One individual diagnosed with colorectal cancer (or extra-colonic HNPCC-associated tumours) before age 50 years

← Two affected generations

← Three affected relatives, one a first-degree relative of the other two

← FAP should be excluded

← Tumours should be verified by pathological examination

Bethesda guidelines

← Colorectal cancer diagnosed in patient who is younger than 50 years

← Presence of synchronous, metachronous colorectal, or other HNPCC-associated tumours, irrespective of age

← Colorectal cancer with the MSI-H ↑ histology ↑ diagnosed in a patient who is younger than 60 years

← Colorectal cancer diagnosed in one or more first degree relatives with an HNPCC-related tumour, with one of the cancers being diagnosed under the age 50 years

← CRC diagnosed in two or more first or second degree relatives with HNPCC-related tumours, irrespective of age

MSI-H, microsatellite instability – high.

Figure 4.6 Distribution of colorectal cancer (%).

The gastroenterologist advises a colonoscopy for this patient, which she agrees to have after full discussion.

Remember

Risks for development of colon cancer:

• Normal: 1:50

• With a first-degree relative: 1:17

• With an elderly first-degree relative: 1:30.

Progress.

This patient’s colonoscopy showed a 2 cm polyp which was fully excised. Histologically this was a tubular adenoma and she was asked to return for a surveillance colonoscopy in 3 years’ time. She was told that she would need continuous follow-up in view of the family history.

Functional bowel disease

Case history

A 30-year-old woman is in the A&E department with severe lower abdominal pain. She is rolling around in agony but the surgical registrar has found no evidence of serious disease. He has already fully examined her and investigated her with routine blood tests and an abdominal X-ray, all of which are normal. Her boyfriend is aggressive and insisting that something must be done. The casualty officer is looking for help.

What do you do?

• Re-take the history with the possibility of this being irritable bowel syndrome (IBS).

• Re-examine the abdomen: think of all the causes of an acute abdomen again (see Information box).

• Review the investigations.

The history strongly supports the diagnosis of IBS. Remember that the pain can be very severe and real to the patient even though it is related to life events, i.e. the pain is not just ‘all in the mind’.

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