Dyspepsia

Dyspepsia describes pain or discomfort in the upper abdomen. It has been defined variously by a number of
expert groups:
Prior to 1991, dyspepsia included patients with symptoms of heartburn and acid reflux.
[1]
The Rome I definition defined patients with sole reflux symptoms as having gastro-oesophageal reflux
disease (GORD) - also seen as 'GERD'.
More recently, these criteria have been extended to exclude patients with predominant reflux
symptoms and symptoms suggestive of irritable bowel syndrome (IBS).
[2]
Incidence
The costs of managing dyspepsia outstrip all other conditions in the NHS. Expenditure on ulcer healing drugs
increases year on year.
[3]
The prevalence of dyspepsia is estimated to be 23-41% of the population. Approximately 25% will
consult their GP.
[4]
There is evidence of inappropriate (not per guidelines) proton pump inhibitor (PPI) prescribing in the
community.
[5] [6]
Presentation
[7]
Epigastric discomfort
Fullness or bloating
Excessive flatus
Nausea
Fatty food intolerance
Always ask about family history and medication use.
Ask about 'red flag' symptoms such as:
Unintentional weight loss.
Recurrent vomiting.
Dysphagia.
Evidence of gastrointestinal (GI) bleeding.
If investigated, patients with dyspeptic symptoms will prove to have either:
[8]
Peptic ulcer disease (10%).
Oesophagitis (15%).
No significant abnormality (non-ulcer dyspepsia or functional dyspepsia - 75%).
Older patients are more likely to have serious disease.
Investigations
[4]
Always check for abdominal mass.
Consider taking FBC to demonstrate another alarm feature, eg iron-deficiency anaemia.
Testing for Helicobacter pylori may be worthwhile. The evidence is equivocal but there seems to be a
subset of H. pylori-related dyspepsia patients who do improve on eradication therapy.
[9]
Eradication of
H. pylori in patients who are about to start non-steroidal anti-inflammatory drugs (NSAIDs)
substantially reduces the risk of endoscopic and complicated ulcers.
[10]
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Differential diagnosis
[4]
Peptic ulcer.
Functional (non-ulcer) dyspepsia.
IBS.
Atypical gastro-oesophageal reflux disease (GORD).
Biliary pain, eg gallstones.
Achalasia.
Medication-induced dyspepsia.
Aerophagia.
Oesophageal spasm.
Carcinoma of oesophagus or stomach.
Exclude abdominal mass and other causes of abdominal pain.
Evidence-based management
Urgent specialist referral - two-week rule
If the patient has dyspepsia at any age with any of the following alarm symptoms:
[11]
Chronic GI bleeding
Progressive unintentional weight loss
Progressive dysphagia
Persistent vomiting
Iron-deficiency anaemia
Epigastric mass
Suspicious barium meal
NB: patients aged 55 years or older with unexplained and persistent recent-onset dyspepsia should be referred
urgently for endoscopy.
[12]
For patients without alarm features and with previous investigations for dyspepsia
It is possible to treat on the basis that a similar pathology has recurred, although refer to a specialist if the patient
is unresponsive to treatment or the diagnosis is in doubt.
If there has been a peptic ulcer previously and no evidence of H. pylori eradication, prescribe H. pylori
eradication therapy if the test is positive. See separate article Helicobacter Pylori for details.
If there has been oesophagitis previously, prescribe a proton pump inhibitor (PPI):
[4]
The National Institute for Health and Clinical Excellence (NICE) suggests full-dose PPI for 1-
2 months and then titrating down to a low dose or as required dosage if symptoms allow
(and there is no underlying condition or co-medication requiring ongoing treatment).
[11]
Where there is no initial response (and recent endoscopy has shown gastro-oesophageal
reflux disease (GORD)), a further month of double dose may be tried, followed by a month
of H
2
-receptor antagonist (H
2
RA).
Prokinetic agents are not recommended. NICE says that cisapride is no longer licensed,
whilst the evidence for metoclopramide and domperidone is limited.
[11]
However, several
new-generation prokinetics such as acotiamide are emerging which look promising and are
currently being evaluated.
[13]
The H
2
RAs provide a swift and effective means of acid suppression and can be used
intermittently to achieve control of symptoms. The PPIs are more prolonged in action,
produce more profound acid suppression and are more expensive. Their greater efficacy
may still provide value for money.
Some patients may require prolonged high doses of PPI and may ultimately be candidates
for anti-reflux surgery.
Where patients have reflux, but endoscopy failed to show oesophagitis, try full-dose PPI for a month,
followed by a month of H
2
RA.
If none of the above (non-ulcer dyspepsia), H. pylori eradication (after a positive test) may relieve
symptoms in 1 in 20 patients (NNT = 20).
[14]
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If none of the above and predominant heartburn symptoms (endoscopy-negative reflux disease),
prescribe H
2
RA, or PPI if not controlled.
[15]
If none of the above and predominantly epigastric pain, an H
2
RA is the least costly.
[16]
For the uninvestigated patient without alarm features
The NICE guideline suggests the following steps:
Review medications: possible drug causes of dyspepsia include NSAIDs, steroids, calcium
antagonists, nitrates, theophyllines and bisphosphonates. Reduce or stop if possible.
Offer lifestyle advice, ie stopping smoking, more regular meals, ceasing excessive alcohol
consumption.
Antacids are cheap, simple and may be all that is required for relief of occasional symptoms. Most
antacids contain a mixture of aluminium hydroxide that tends to cause constipation and magnesium
hydroxide that tends to cause diarrhoea. The balance between the two cannot be assured and there
may be disturbance of bowel function. If a large amount of antacid is being consumed, consider acid
suppression.
Try either of the following. The alternative choice can be tried if symptoms persist or return:
Test for H. pylori (carbon-13 urea breath test, stool antigen or laboratory serology) and
eradicate if positive.
Empirical acid suppression (with PPI) - full dose for one month.
Where there has been a satisfactory response at any of the steps above, reassure and return to self-care.
If the patient responds to PPI but then relapses, consider low-dose or intermittent treatment.
If there is no response, consider a prokinetic, eg metoclopramide or H
2
RA, eg ranitidine for one month.
Where patients show an inadequate response to treatment, consider other diagnoses, eg gallstones and/or
referral to a specialist.
Pharmacological issues
[17]
Adverse reactions to PPIs and H
2
RAs are usually rare and mild but severe problems can arise:
Rare but not serious problems may include taste disturbance, peripheral oedema,
photosensitivity, fever, arthralgia, myalgia and sweating.
Serious problems include liver dysfunction, hypersensitivity reactions (including urticaria,
angio-oedema, bronchospasm, anaphylaxis), depression, interstitial nephritis, blood
disorders (including leukopenia, leukocytosis, pancytopenia, thrombocytopenia) and skin
reactions (including Stevens-Johnson syndrome, toxic epidermal necrolysis, bullous
eruption).
Many of the drugs used in the management of peptic ulcer disease carry a warning that they should
not be used in pregnancy or whilst breast-feeding:
This is usually because of lack of information about safety in pregnancy rather than
evidence of adverse effects in pregnancy.
However, misoprostol - a prostaglandin analogue - should be avoided in pregnancy as it
may cause abortion.
PPIs are metabolised mostly in the liver. In liver disease, dose adjustment may be required for
omeprazole, pantoprazole and esomeprazole. There are no data on the use of rabeprazole in people
with severe hepatic impairment, so the manufacturer advises caution.
Omeprazole and esomeprazole may interfere with warfarin monitoring.
Monitoring
[18]
Patients should be reviewed at the end of a course of treatment, especially H. pylori eradication, to confirm a
satisfactory outcome. The criteria to be used to measure satisfactory patient outcome are subject to controversy
and instruments to determine clinical endpoints are evolving.
If simple acid suppression is given, the patient should be reviewed after one or two months to ascertain that the
end is being achieved and there are no warning signs such as weight loss to suggest malignancy.
Page 3 of 5
Referral for endoscopy
Routine endoscopic investigation of dyspeptic patients is not necessary but should be considered in patients over
the age of 55 where symptoms persist despite H. pylori testing and acid suppression.
[11]
Patients with the following risk factors have a higher risk of malignancy and so lower your threshold for
endoscopy referral:
[12]
Family history of upper GI cancer in more than two first-degree relatives.
Barrett's oesophagitis.
Pernicious anaemia.
Peptic ulcer surgery over 20 years ago.
Known dysplasia, atrophic gastritis, intestinal metaplasia.
Further reading & references
Ford AC, Moayyedi P; Dyspepsia. BMJ. 2013 Aug 29;347:f5059. doi: 10.1136/bmj.f5059.
Endoscopy. Asurgeon describes what an endoscopy is , what happens during the procedure, and how you can prepare
yourself for it. Ashort video from NHS Choices. (June 2008)
1. No authors listed; Management of dyspepsia: report of a working party. Lancet. 1988 Mar 12;1(8585):576-9.
2. Drossman DA, Dumitrascu DL; Rome III: New standard for functional gastrointestinal disorders. J Gastrointestin Liver Dis.
2006 Sep;15(3):237-41.
3. Dyspepsia - Data Focused Commentary, National Prescribing Centre, 2007
4. Dyspepsia - unidentified cause, Prodigy (June 2008)
5. Batuwitage BT, Kingham JG, Morgan NE, et al; Inappropriate prescribing of proton pump inhibitors in primary care.
Postgrad Med J. 2007 Jan;83(975):66-8.
6. Hughes JD, Tanpurekul W, Keen NC, et al; Reducing the cost of proton pump inhibitors by adopting best practice. Qual
Prim Care. 2009;17(1):15-21.
7. Dyspepsia, Gastro Training, 2011
8. Talley NJ et al; American Gastroenterological Association Technical Review on the Evaluation of Dyspepsia,
Gastroenterology, 2005;129:17561780.
9. Suzuki H, Nishizawa T, Hibi T; Can Helicobacter pylori-associated dyspepsia be categorized as functional J Gastroenterol
Hepatol. 2011 Apr;26 Suppl 3:42-5. doi:
10. Should You Eradicate Helicobacter Pylori Prior to Chronic NSAID Treatment? - Smith J; Clinical Correlations, 2011
11. Dyspepsia: Managing dyspepsia in adults in primary care; NICE Clinical Guideline (2004)
12. Referral for suspected cancer; NICE Clinical Guideline (2005)
13. Tack J, Janssen P; Emerging drugs for functional dyspepsia. Expert Opin Emerg Drugs. 2011 Jun;16(2):283-92. Epub
2011 Mar 17.
14. Moayyedi P, Soo S, Deeks J, et al; Eradication of Helicobacter pylori for non-ulcer dyspepsia. Cochrane Database Syst Rev.
2005 Jan 25;(1):CD002096.
15. Dyspepsia - proven gastro-oesophageal reflux disease, Prodigy (June 2008)
16. Moayyedi P, Soo S, Deeks J, et al; Pharmacological interventions for non-ulcer dyspepsia. Cochrane Database Syst Rev.
2006 Oct 18;(4):CD001960.
17. British National Formulary
18. Ang D, Talley NJ, Simren M, et al; Review article: endpoints used in functional dyspepsia drug therapy trials. Aliment
Pharmacol Ther. 2011 Mar;33(6):634-49. doi:
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical
conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its
accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions.
For details see our conditions.
Original Author:
Dr Hayley Willacy
Current Version:
Dr Laurence Knott
Peer Reviewer:
Dr Hannah Gronow
Last Checked:
14/12/2011
Document ID:
459 (v6)
EMIS
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