an Approach to Dyspepsia
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quoted from NICE, Dyspepsia
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an Approach to Dyspepsia
- 1. An approach to Dyspepsia Al-Momtan, Ahmed Tahir C-2
- 11. INTRODUCTION • Dyspepsia • 40% of adult population / year, 2% consult their GPs • Substantial health care cost: - - - Medication Diagnostic evaluation Time cost from work • Out of 100 pts. 90% will be pain free after 2-3 wks without Rx • Definitive established guideline (NICE) • H.pylori & PUD – well accepted & confirmed
- 12. 5 common causes of dyspepsia 1- NUD. 2- GORD 3- Gastritis 4- Gastric Ulcer. 5- Doudenal Ulcer Rare causes Gastic and oesophageal CA.
- 18. NICE flowchart (functional dyspepsia)
- 21. GORD, Cont.
- 25. ALARM Symptoms! ALARM! • A norexia • L oss of weight (progressive & unintentional) • A naemia due to iron deficiency • R ecent onset of persistent symptoms :vomiting • M elaena, haematemesis • Dysphagia (progressive) • Epigastric mass or • Suspicious barium meal.
- 30. Flowcharts, DU and GU
- 31. Endoscopy • Age < 55 years, presenting with dyspepsia and without alarm S/S, is not necessary. • Age > 55 years presenting with dyspepsia and without alarm S/S do not require routine endoscopy. Considered if : 1.ALARM signals and signs are the major determinant of the need for endoscopy, not age on its own. 2. No response to medication7-10days. 3. Symptoms persist after 6-8wks 4. Signs of systemic illness 5. Recurrence after treatment 6. Long standing G0RD 7. Unexplained weight loss, progressive dysphagia, IDA, abdominal mass on plapation
Editor's Notes
- Epigastric pain – most common Burning pain Aggrav by eating Alleviated by antacids belching/bloating
- Prior hx PUD Ibuprofen Tobacco ETOH Caffeine Poss stress
- Dys=
- The following are some theories as to possible causes:Sensation in the stomach or duodenum may be altered in some way - an 'irritable stomach'. About 1 in 3 people with non-ulcer dyspepsia also have 'irritable bowel syndrome' and have additional symptoms of lower abdominal pains, erratic bowel movements, etc. The cause of irritable bowel syndrome is not known.A delay in emptying the stomach contents into the duodenum may be a factor in some cases. The muscles in the stomach wall may not work as well as they should.Infection with a bacterium (germ) called H. pylori may cause some cases. This bacterium is found in the stomach in some people with non-ulcer dyspepsia. However, many people are 'carriers' of this bacterium, and it causes no symptoms in most people. The role of H. pylori is controversial in non-ulcer dyspepsia (although it is the main cause of duodenal and stomach ulcers). However, getting rid of H. pylori infection helps in some cases.Some people feel that certain foods and drinks may cause the symptoms or make them worse. It is difficult to prove this. Foods and drinks that have been suspected of causing symptoms or making symptoms worse in some people include: peppermint, tomatoes, chocolate, spicy foods, hot drinks, coffee, and alcoholic drinks. However, food is not thought to be a major factor in most cases.Anxiety, depression, or stress are thought to make symptoms worse in some cases.A side-effect of some drugs can cause dyspepsia. The most common culprits are anti-inflammatory drugs such as ibuprofen and aspirin. Various other drugs which sometimes cause dyspepsia, or make dyspepsia worse, include: antibiotics, steroids, iron, calcium antagonists, nitrates, theophyllines, bisphosphonates. (Note: this is not an exhaustive list. Check with the leaflet that comes with your medication for a list of possible side-effects.) If you suspect a prescribed drug is causing the symptoms, or making them worse, then see your doctor to discuss possible alternatives.
- Non-ulcer dyspepsia (NUD), sometimes called ‘functional’ dyspepsia, refers to patients whose endoscopic investigation has excluded gastric or duodenal ulcer, malignancy or oesophagitis. Simple gastritis or duodenitis found by endoscopy are not considered significant abnormalities, but erosive duodenitis and gastric erosions are considered part of the spectrum of ulcer disease. The Rome II definition [4] further excludes patients with predominant heartburn and without oesophagitis as ‘endoscopy negative reflux disease’ (ENRD) and those with pain relieved by defecation as irritable bowel syndrome. Non-ulcer dyspepsia (including ENRD) accounts for the majority of dyspeptic patients at endoscopy. Trials indicate that, untreated, at least 70% of these patients will have persistent symptoms a year after diagnosis: unlike peptic ulcer disease there is no ‘one off’ cure and treatment may often be needed on a long-term basis. A Swedish study followed 1,059 individuals for a year and found that only 12% of those originally with dyspeptic symptoms were asymptomatic and 16% were classed as having irritable bowel syndrome, one year later [390]. There is uncertainty about the definition and cause of non-ulcer dyspepsia. The long term value of available symptomatic treatments rests upon extrapolation from short term trials. There is considerable uncertainty about the appropriate long term management of patients with persistent symptoms. In the light of this uncertainty, patients should be offered periodic review of their condition and medication, with a trial of reduced use if appropriate. Previously published reviews of H. pylori and pharmacological therapies have been updated to evaluate specific treatments for NUD include antacids, H2RAs, PPIs, prokinetic agents, H. pylori eradication and psychological interventions. Available evidence from trials indicates that eradication of H. pylori (if present) is an effective and cost-ffective option. Benefit is obtained by a short course of therapy, whilst acid suppression requires long term treatment. Thus eradication therapy is more likely to be cost-effective in spite of its small treatment effect on symptoms. Long term acid suppression is appropriate for H. pylori negative patients and those failing to respond to eradication. Short term evidence from trials shows that both PPIs and H2RAs can reduce the symptoms of dyspepsia, but there are methodological concerns about the interpretation of these trials. On balance PPIs are recommended over H2RAs on pharmacological grounds and the quality of available trials, while the cost of maintenance dose PPIs and H2RAs is similar. It is possible that different therapies are working selectively on particular kinds of patient, in which case available treatments should not be regarded as mutually exclusive options
- There are a variety of non-invasive tests for H. pylori [397]. Serology has been widely used in clinical practice and two meta-analyses [398,399] indicate that sensitivity and specificity are usually greater than 85% (Table 19). Laboratory-based testing is relatively inexpensive (at a total cost of about £10) and medication does not interfere with the accuracy of the test [400]. The sensitivity and specificity of serology varies in different populations. The reason for this is uncertain but may relate to different strains of H. pylori or genetic differences in the population causing diverse immune responses. The appropriate cut-off for a commercial kit being used should therefore be locally validated [401]. Near patient serology tests have been developed, where the result is obtained in situ rather than from a laboratory [402], but the accuracy of these kits varies widely in different communities [403]. Detecting antibodies to H. pylori antigens in the saliva is another non-invasive method of diagnosing the infection, but again the accuracy of this method is inconsistent across different populations [404]. Urea breath tests are consistently accurate with about 95% sensitivity and specificity reported in studies but have reduced accuracy in patients taking antibiotics or PPIs [405]. 14 C-urea breath tests are not appropriate for primary care as they involve a small dose of radiation. 13 C-urea breath tests do not involve ionising radiation and are simple to perform although they are relatively expensive at about £19 per test. Faecal antigen tests appear to perform as well as urea breath tests may be cheaper at about £11 per test, although patient acceptability with this form of testing may be a problem [406]. The Health Protection Agency Helicobacter Working Group does not recommend the routine use of serology because of the poor positive predictive value in populations with low prevalence [407]. Serology fails to diagnose patients with active disease, it merely indicates if an individual has ever encountered the antigen. This means that significant numbers of patients will be falsely diagnosed as positive and thus be inappropriately treated, possibly have their true diagnosis missed or delayed. They also note that all serological kits are unhelpful in children and less reliable in older patients. Realistically it is very difficult to undertake local validation of kits and laboratories tend to accept commercial companies’ assurances of kits. The guideline group did not consider that serology performs adequately when compared to the laboratory based stool antigen tests and Urea Breath Tests that are now available.
- 1 If NSAID continuation is necessary, after ulcer healing offer long term gastric protection or consider substitution to a newer COX-selective NSAID. 2 Use a carbon-13 urea breath test, stool antigen test or, when performance has been validated, laboratory-based serology. 3 Use a PPI, amoxicillin, clarithromycin 500 mg (PAC 500 ) regimen or a PPI, metronidazole, clarithromycin 250 mg (PMC 250 ) regimen. Follow guidance found in the British National Formulary for selecting 2 nd line therapies. After two attempts at eradication manage as H. pylori negative. 4 Perform endoscopy 6-8 weeks after treatment. If retesting for H. pylori use a carbon-13 urea breath test. 5 Offer low dose treatment, possibly used on an as required basis, with a limited number of repeat prescriptions. 6 Review care annually to discuss symptoms, promote stepwise withdrawal of therapy when appropriate and provide lifestyle advice. In some patients with an inadequate response to therapy it may become appropriate to refer to a specialist. ------------- If NSAID continuation is necessary, after ulcer healing offer long term gastric protection or consider substitution to a newer COX-selective NSAID. Use a carbon-13 urea breath test, stool antigen test or, when performance has been validated, laboratory-based serology. Use a PPI, amoxicillin, clarithromycin 500 mg (PAC 500 ) regimen or a PPI, metronidazole, clarithromycin 250 mg (PMC 250 ) regimen. Use a carbon-13 urea breath test. Follow guidance found in the British National Formulary for selecting 2 nd line therapies. Offer low dose treatment, possibly on an as required basis, with a limited number of repeat prescriptions. Consider: non-compliance with treatment, possible malignancy, failure to detect H. pylori infection due to recent PPI or antibiotic ingestion, inadequate testing, or simple misclassification; surreptitious or inadvertent NSAID or aspirin use; ulceration due to ingestion of other drugs; Zollinger-Ellison syndrome; Crohn’s disease. A small number of patients with chronic, refractory peptic ulceration may require maintenance acid suppression. In some patients with an inadequate response to therapy it may become appropriate to refer to a specialist for a second opinion.
- Dyspepsia with acute Upper GI bleeding?