Published on 24/06/2015 by admin

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Last modified 24/06/2015

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Case vignette

A 56-year-old man presents with severe nocturnal epigastric pain. The pain was initially relieved by food ingestion and antacids. However, lately the pain has been recalcitrant and progressive. He also complains of fatigue and exertional retrosternal discomfort. He is a heavy smoker and consumes alcoholic spirits on a regular basis. He is on aspirin. On examination there was tenderness to deep palpation in the epigastric region. He also had conjunctival pallor. His pulse rate was 110 bpm and irregularly irregular.

Approach to the patient

Peptic ulcer disease is a common associated morbidity in the long case.


Enquire about the initial presentation—the symptoms of epigastric pain, dyspepsia, reflux and anorexia. It is important to obtain details about any previous or current gastrointestinal bleeding. A medication history should be obtained, to exclude causative agents, such as aspirin or NSAIDs. Ask when and how the diagnosis was made and whether the patient has had a gastroscopy. Ask how the patient has been treated in the past and whether they have ever been tested for Helicobacter pylori. A history of gastrointestinal bleeding becomes an issue if the patient has a comorbid condition that would require anticoagulation or antiplatelet therapy, such as coronary stenting or AF. Be alert to features that may indicate the possibility of gastric carcinoma, such as significant weight loss, persistent vomiting or jaundice in the setting of liver secondaries.


The patient may have epigastric tenderness. A mass lesion in the abdomen should alert to neoplasia. Do not forget to look for signs of anaemia.


Figure 12.1 Scanning electron micrographs of a 48-h culture of H. pylori (A, B), and infection of cultured AGS cells for 24 h (C, D) or 48 h (E, F). A, blebs (→) protrude from the spiral-shaped bacterial body. B, numerous vesicles (→) are visible on the bacterial surface. C, bacteria are tightly embodied in a dense network of extended microvilli. Spirals are attached horizontally (→) or perpendicularly (arrowhead). D, H. pylori displays various shapes when attached to the cell surface: the spiral (white→), U-shaped (white arrowhead), doughnut (black→), or coccoid form (black arrowhead)

(reprinted from Heczko U, Smith V C, Mark Meloche R et al 2000 Characteristics of Helicobacter pylori attachment to human primary antral epithelial cell. Microbes and Infection 2:8)


Figure 12.2 Foveolar cells with ‘cobblestoning’. The changes are patchy and often mild. When the cells bulge out, resembling cobblestones, the appearance is almost always diagnostic of H. pylori infection

(reprinted from Robin W J 2000 Gastric pathology associated with Helicobacter pylori. Gastroenterology Clinics of North America 29:47)


Figure 12.3 Duodenal ulcer

(courtesy of Dr George Ostapowicz)


All patients who present with symptoms suggestive of peptic ulcer disease or a diagnosis of peptic ulcer disease should be tested for H. pylori infection. This is achieved by performing the rapid urease test in those undergoing endoscopy and by serology. However, in individuals under age 50 without alarm symptoms, it is reasonable to treat without investigation and assess response (in both H. pylori positive and H. pylori negative individuals).
Negative tests can be confirmed with non-endoscopic tests, such as the urea breath test or the stool antigen test. The urea breath test can be accurately interpreted only if antisecretory therapy has been withheld for a minimum of 2 weeks prior to the test.
However, negative tests do not necessarily need confirmation (realising that serology may only be 70–80% accurate). In such situations it would be reasonable to treat with a proton pump inhibitor (PPI) initially. If there is no response or symptoms return, further investigation with gastroscopy is indicated.
If the patient has had an acute event, check the full blood count (looking for anaemia) and electrolyte profile (looking for an elevation in blood urea level that is disproportionate to the creatinine level). In this situation gastroscopy is definitely indicated.


Case vignette

A 33-year-old female presents to hospital with high fevers and severe abdominal pain in the background of anorexia and weight loss. She was diagnosed with Crohn’s disease 3 years ago upon investigation for chronic fevers, diarrhoea, weight loss, abdominal pain, nausea and vomiting. Her Crohn’s disease is managed with long-term mesalazine therapy. She is also on cipramil for depression.
On examination she has tenderness with guarding in the left lower quadrant and aphthous ulceration in the oral mucosa. She is cushingoid. Investigations reveal a mild anaemia, leucocytosis, thrombocytosis and significantly elevated CRP. Abdominal CT reveals an abscess in the sigmoid region. She is commenced on high-dose antibiotics and steroids. The abscess is drained percutaneously under CT guidance.
While in hospital her symptoms improve. However, on the third day in hospital she develops severe retrosternal chest pain that radiates to the neck and jaw. ECG reveals ST segment elevation in the septal leads. She also complains of severe left calf pain and tenderness. She is commenced on a heparin infusion and subsequently taken to the cardiac catheterisation laboratory. Angiography shows evidence of slow coronary flow in the left anterior descending artery. Otherwise the coronary anatomy is normal with no evidence of any occlusive disease in any artery. She has a peak troponin I level of 20 and echocardiography shows significant hypokinesis of the anteroseptal region of the left ventricle, suggesting significant myocardial damage or stunning. Lower limb Doppler studies reveal DVT of the left leg.

Approach to the patient (ulcerative colitis and Crohn’s disease)

Knowledge of the basic principles of management of ulcerative colitis and Crohn’s disease will be very useful because inflammatory bowel disease can make patients ideal long cases with multifaceted issues.


Ask when and how the initial presentation was made and what investigations led to the diagnosis. Take a detailed history of gastrointestinal symptoms, such as abdominal pain, diarrhoea, tenesmus, per rectum bleeding, rectal mucous discharge, anorexia, nausea and vomiting. Ask about constitutional symptoms and weight loss. The combination of symptoms such as per rectal bleeding and mucus together with tenesmus and constipation with the absence of systemic symptoms is very suggestive of ulcerative proctitis. Episodes of abdominal pain and bloating, together with vomiting a few hours after food ingestion are symptoms suggestive of small bowel involvement, especially terminal ileal Crohn’s disease.
Ask about systemic features such as oral ulcers, arthritis, biliary colic (uncommon), pyoderma gangrenosum and erythema nodosum. Ask how often acute exacerbations happen and how they are treated. It is very important to obtain a detailed medication history, enquiring about current therapy as well as agents tried previously. Ask about adverse effects associated with medications, especially corticosteroids. Take a detailed smoking history, as smoking prevents exacerbation of ulcerative colitis but precipitates Crohn’s disease. Check the family history, as Crohn’s disease especially tends to be familial. The clinical features alone often may not differentiate between Crohn’s disease and ulcerative colitis.
Once the precise disease entity is identified, it is important to localise the possible areas of involvement in the gastrointestinal tract. Ask about any diagnosis of gastrointestinal malignancy. Risk of malignancy, especially colorectal cancer, is increased in individuals with inflammatory bowel disease, especially ulcerative colitis.
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