Chapter 47: Dyspepsia (indigestion)

Dyspepsia or indigestion is a difficult, sometimes vague, symptom to define or evaluate and requires very careful questioning to clarify the exact nature of the complaint.

Dyspepsia embraces the following:

• nausea

• heartburn/regurgitation

• upper abdominal discomfort

• lower chest discomfort

• acidity

• epigastric fullness, bloating or unease

• abdominal distension

The discomfort can sometimes amount to pain. Diagnoses to consider in dyspeptic patients are summarised in TABLE 47.1.

Excessive belching

• Usually functional

• Organic disease uncommon

• Due to air swallowing (aerophagy)

• Common in anxious people who gulp food and drink

• Associated hypersalivation

Management tips

• Make patient aware of excessive swallowing

• Avoid fizzy (carbonated) soft drinks

• Avoid chewing gum

• Don’t drink with meals

• Don’t mix proteins and starches

• Eat slowly and chew food thoroughly before swallowing

• Eat and chew with the mouth closed

If persistent: simethicone preparation (e.g. Mylanta II, Phazyme).

If desperate: place one small cork between the back teeth after meals for 30 minutes.

Excessive flatus

Flatus arises from two main sources:

• swallowed air

• bacterial fermentation of undigested carbohydrate

  Exclude:

• malabsorption

• irritable bowel syndrome

• anxiety → aerophagy

• drugs, especially lipid-lowering agents

• lactose intolerance

Management

• Assess diet (e.g. high fibre, beans and legumes, cabbage, onions, grapes and raisins)

• Avoid drinking with eating, especially with leafy vegetables

• Cook vegetables thoroughly

• Trial a lactose-free diet

• Consider simethicone preparations (e.g. No Gas)

A summary of the diagnostic strategy model is presented in TABLE 47.2.

It is best to consider dyspepsia as:

• ulcer-like—localised pain

• dysmotility-like—diffuse discomfort, feeling full after meals (early satiety), nausea, bloating

• acid-reflux-like—indigestion or heartburn with acid reflux or regurgitation

The ulcer-like category may be due to an ulcer and if not is termed functional (non-ulcer) dyspepsia.

Pitfalls

Perhaps the commonest mistake is to attribute the discomfort of myocardial ischaemia to a disorder of the GIT. A sense of fullness or pressure in the epigastrium can certainly accompany ischaemia.

General pitfalls

• Reflux oesophagitis and PU can mimic ischaemic heart disease.

• Overlooking gastric cancer as a cause of dyspepsia.

• Failing to stress that weight reduction to ideal level will generally alleviate gastro-oesophageal reflux.

• Overlooking drugs as a cause (see TABLE 47.3).

History

It is worthwhile spending some time clarifying the exact nature of the presenting complaint: what the patient means by ‘indigestion’ or ‘heartburn’.¹ The relationship of the symptom to eating is very important, and whether it occurs after each meal or after specific meals.

In particular, care should be taken to consider and perhaps exclude ischaemic heart disease.

Key questions

• How would you describe the discomfort?

• Can you show me exactly where it is and where it radiates?

• What makes your discomfort worse?

• What relieves your discomfort?

• What effect do food, milk and antacids have?

• What effect do coffee, onions or garlic have?

• What effect does a big meal have?

• What about drinking alcohol? Wine?

• What effect does exercise have?

• Do fried or fatty foods make it worse?

• Do hot spicy foods affect it?

• Does the problem come on at night soon after you go to bed?

• Does it wake you up at night?

• Does bending over (e.g. gardening) make it worse?

• Do you have periods of freedom from the problem?

• Are you under a lot of stress or have a lot of worry?

• Do you go flat out all day?

• Do you rush your meals?

• Do you chew your food properly?

• What drugs or medicines do you take?

• How much alcohol do you have? Do you smoke?

• Have you noticed anything else when you have the problem?

• Do you get constipated or have diarrhoea?

• Have you lost weight recently?

• Do you feel the discomfort between your shoulder blades, or in your shoulders or throat?

• Do you experience shortness of breath, syncope or dizziness?

Symptoms analysis

Site and radiation

The site and radiation of pain or discomfort can provide a lead to the diagnosis. Refer to FIGURE 40.9 in CHAPTER 40. If it is felt in the interscapular area, consider oesophageal spasm, gall bladder disease or a DU. Retrosternal discomfort indicates oesophageal disorders or angina, while epigastric discomfort suggests disorders of the biliary system, stomach and duodenum.

Character of the pain

There tends to be considerable overlap in the character of the pain from the various disorders but some general characteristics apply:

• burning pain → gastro-oesophageal reflux (GORD)

• constricting pain → ischaemic heart disease or oesophageal spasm

• deep gnawing pain → PU

• heavy ache or ‘killing’ pain → psychogenic pain

Aggravating and relieving factors

Examples of these factors include:

• eating food may aggravate a GU but relieve a DU

• eating fried or fatty foods will aggravate biliary disease, functional dyspepsia and oesophageal disorders

• bending will aggravate GORD

• alcohol may aggravate GORD, oesophagitis, gastritis, PU, pancreatitis

Associated symptoms

Relevant examples:

• difficulty in swallowing → oesophageal disorders

• lump or constriction in throat → psychogenic

• acid regurgitation → GORD, oesophagitis

• anorexia, weight loss → stomach cancer

• water brash → GORD, hiatus hernia, PU

• symptoms of anaemia → chronic oesophagitis or gastritis, PU, cancer (stomach, colon)

• flatulence, belching, abnormal bowel habits → irritable bowel syndrome

• diarrhoea 30 minutes after meal → mesenteric ischaemia

Examination

The physical examination does not often provide the key to the diagnosis but it is important to perform very careful palpation and inspection. Look for evidence of clinical anaemia and jaundice. Diffuse mild abdominal tenderness and a pulsatable abdominal aorta are common findings but do not necessarily discriminate between organic and functional problems. Specific epigastric tenderness suggests peptic ulceration while tenderness over the gall bladder area (Murphy sign) indicates gall bladder disease. An epigastric mass indicates stomach cancer.

Investigations

Do not overinvestigate. Investigations tend to be unrewarding in most instances of dyspepsia and could be postponed if the history is suggestive of a functional cause and the symptoms are not severe.¹ A trial of treatment such as changing adverse lifestyle factors, dietary modification and antacids could be the initial approach. Age is important in determining the extent of investigations, which are more relevant in those over 40 years.

The investigation of choice is endoscopy, which is superior to barium studies in investigation of the upper GIT. Gastroscopy is indicated for the alarm symptoms:

• abnormal symptoms of reflux/dyspepsia

• change of symptoms

• dysphagia

• unexplained weight loss

• GIT bleeding

• pain radiating to back

• pain waking at night

• abnormal signs on examination

• other tests: fasting serum gastrin (? hypersecretion)

Helicobacter pylori tests³

Helicobacter pylori has been proved to cause ulcers. Most DUs and about two-thirds of GUs have been attributed to H. pylori infection.

Non-invasive tests:

• serological—IgG antibodies (sensitivity 85–90%, specificity 90–99%); excellent for diagnosis, not for follow-up

• urea breath test (high sensitivity 97% and specificity 96%), good for follow-up

• stool antigen test (sensitivity 96%, specificity 97%)

  Invasive tests:

• gastric mucosal biopsy during endoscopy can detect H. pylori through histology or rapid urease testing or H. pylori culture

An organic disorder is more likely in the older patient, in whom it is important to consider stomach cancer. Symptoms such as anorexia, vomiting and weight loss point to such a problem.

Other conditions causing dyspepsia that are more prevalent in this age group are:

• constipation

• mesenteric artery ischaemia

• congestive cardiac failure

Dyspepsia is an uncommon problem in children but can be caused by drugs, oesophageal disorders and gastro-oesophageal reflux in particular.⁴ Reflux can be considered to be physiological or pathological.

Gastro-oesophageal reflux

Regurgitation of feeds because of gastro-oesophageal reflux is a common physiological event in newborn infants. A mild degree of reflux is normal in babies, especially after they burp; this condition is called posseting.

Symptoms

Milk will flow freely from the mouth soon after feeding, even after the baby has been put down for a sleep. Sometimes the flow will be forceful and may even be out of the nose.

Despite this vomiting or regurgitation, the babies are usually comfortable and thrive. Some infants will cry, presumably because of heartburn.⁴

In a small number the reflux may be severe enough (pathological) to cause serious problems such as oesophagitis with haematemesis or anaemia, stricture formation, failure to thrive, apnoea and aspiration.

Prognosis

Reflux gradually improves with time and usually ceases soon after solids are introduced into the diet. Most cases clear up completely by the age of 9 or 10 months, when the baby is sitting. Severe cases tend to persist until 18 months of age.

Investigations

These are not necessary in most cases but in those with persistent problems or complications referral to a paediatrician is recommended. The specialist investigations include barium meal with cine scanning, oesophageal pH monitoring or endoscopy and biopsy.

Management

Appropriate reassurance with parental education is important. It should be pointed out that changes in feeding practice and positioning will control most reflux.

The infant should be placed on the left side for sleeping with the head of the cot elevated about 20–30 degrees. The old bucket method, in which the child is placed in a bucket, is not necessary.

Smaller, more frequent feeds and thickening agents are appropriate.

Giving the baby thicker feeds usually helps those with more severe reflux. The old-fashioned remedy of using cornflour blended in bottles is still useful.

Bottle-fed babies (powdered milk formula):

• Carobel: Add slightly less than 1 full scoop per bottle.

• Gaviscon: Mix slightly less than ½ teaspoon of Infant Gaviscon Powder with 120 mL of formula in the bottle.

• Cornflour (maize based): Mix 1 teaspoon with each 120 mL of formula. Check with your doctor or nurse for the proper method.

• Prethickened formulas include Karicare and S26 AR: Very simple to use but more expensive.

Breastfed babies:

• Carobel: Add slightly less than 1 full scoop to 20 mL cool boiled water or 20 mL expressed breast milk and give just before the feed.

• Gaviscon: Mix slightly less than ½ teaspoon of Infant Gaviscon Powder with 20 mL cool boiled water or expressed breast milk and give just after the feed.

For persistent or complicated reflux, including painful oesophagitis, specialist-monitored treatment will include the use of antacids and H₂-receptor blocking agents (e.g. ranitidine).⁵

Gastro-oesophageal reflux disease (GORD)^6,7 in adults

Clinical features

• Nausea

• Bloating and belching

• Heartburn

• Acid regurgitation, especially lying down at night

• Water brash (mouth fills with saliva)

• Nocturnal cough with possible asthma-like symptoms

• Diagnosis usually made on history

• Investigation usually not needed (reserve for alarm features as described in the red flag box and non-responsive treatment)

Complications

• Oesophagitis ± oesophageal ulcer

• Iron-deficiency anaemia

• Oesophageal stricture

• Respiratory: chronic cough, asthma, hoarseness

• Barrett oesophagus (from prolonged reflux)

Barrett oesophagus

• Usually a metaplastic response to prolonged reflux

• A premalignant condition (adenocarcinoma)

• Lower oesophagus lined with gastric mucosa (at least 3 cm) of metaplastic columnar epithelium

• Prone to ulceration

• Needs careful management, which includes PPIs for symptoms of oesophagitis + reflux

• Consider 2 yearly endoscopies with biopsies

• Diagnosed by endoscopy and biopsy

Investigations⁶

• Endoscopy (see Red flag pointers)—perform prior to empirical therapy. Limited role—about one third negative

• Barium swallow and meal

• 24-hour ambulatory oesophageal pH monitoring

Management of GORD^6,7,8,9

• Patient education/appropriate reassurance

• Consider acid suppression or neutralisation

• Attend to lifestyle:

  • – reduce weight if overweight (this alone may abolish symptoms)

  • – reduce or cease smoking

  • – reduce or cease alcohol (especially with dinner)

  • – avoid fatty foods (e.g. pastries, french fries)

  • – reduce or cease coffee, tea and chocolate

  • – avoid coffee and alcohol late at night

  • – avoid gaseous drinks

  • – leave at least 3 hours between the evening meal and retiring

  • – increase fibre intake (e.g. high fibre cereals, fruit and vegetables)

  • – small regular meals and snacks

  • – eat slowly and chew food well

  • – sleep on the left side

  • – main meal at midday; light evening meal

  • – avoid spicy foods and tomato products

• Drugs to avoid: anticholinergics, theophylline, nitrates, calcium-channel blockers, doxycycline. Pill-induced oesophagitis occurs, especially with tetracyclines, slow-release potassium, iron sulphate, corticosteroids, NSAIDs—avoid taking dry; use ample fluids

• Elevation of head of bed or wedge pillow: if GORD occurs in bed, sleep with head of bed elevated 10–20 cm on wooden blocks or use a wedge pillow (preferable)

• Antacids (see TABLES 47.4 and 47.5): best is liquid alginate/antacid mixture, e.g. Gaviscon/Mylanta plus 20 mL on demand or 1–2 hours after meals and at bedtime

Antacids are appropriate for rapid relief of mild intermittent or occasional breakthrough symptoms but are ineffective for long-term management.

If no relief after several weeks, the following approaches are recommended by the Gastroenterological Society of Australia (GESA).⁶

Reduce acid secretion. Select from:

• Proton-pump inhibitor (PPI) for 4 weeks (preferred agent) 30–60 minutes before food lansoprazole 30 mg mane

  or

  omeprazole 20 mg mane

  or

  pantoprazole 40 mg mane

  or

  esomeprazole 20 mg mane

  or

  rabeprazole 20 mg mane

• H₂-receptor antagonists (oral use for 8 weeks) famotidine 20 mg bd

  or

  nizatadine 150 mg bd or 300 mg nocte

  or

  ranitidine 150 mg bd pc or 300 mg nocte

• Antacids are useful for daytime symptoms

Although the more traditional step-up approach of 1. Antacids → 2. H₂-receptor antagonists → 3. PPI can be used, there has been a change to favour a high level (more potent) initial therapy with PPIs at standard dose (a step-down approach; see FIG. 47.1). This is based on the grounds of outcomes, speed of response and total cost. May need to eradicate H. pylori if present.

Surgery is usually for young patients with severe reflux. The gold standard is a short, loose 360-degree fundoplication.

Functional (non-ulcer) dyspepsia^{7, 10}

This term applies to the 60% of patients presenting with dyspepsia in which there is discomfort on eating in the absence of demonstrable organic disease. This can be considered in two categories (although there is overlap):

• ulcer-like dyspepsia

  or

• dysmotility-like dyspepsia

Ulcer-like dyspepsia

Treat as for GORD. A practical approach is to commence with a 4-week trial of a PPI or an H₂-receptor antagonist and cease if symptoms resolve.⁷

Dysmotility-like dyspepsia

Clinical features

• Discomfort with early sense of fullness on eating

• Nausea

• Overweight

• Emotional stress

• Poor diet (e.g. fatty foods)

• Similar lifestyle guidelines to GORD

Management

• Treat as for GORD (stage 1).

• Include antacids.

• If not responsive:

  • – Step 1: H₂-receptor antagonists

  • – Step 2: prokinetic agents

  domperidone 10 mg tds

  or

  metoclopramide 10 mg tds

Peptic ulcer disease^10,11

Features (general)

• Common: 10–20% incidence over a lifetime

• Point prevalence of ulcer disease: 3–5%

• DU:GU = 4:1

• DUs common in men 3:1

• Cumulative mortality of 10%

• Risk factors:

  • – male sex

  • – family history

  • – smoking (cause and delayed healing)

  • – stress

  • – common in blood group O

  • – NSAIDs 2–4 times increase in GU and ulcer complications

  • – H. pylori: if absent and no NSAIDS, no ulcer

• Unproven risk factors:

  • – corticosteroids

  • – alcohol (except for gastric erosion)

  • – diet (does reduce recurrence of PU)

• Types of ulcers:

  • – lower oesophageal

  • – gastric

  • – stomal (postgastric surgery)

  • – duodenal

Note: If NSAIDs and H. pylori are not implicated, it is referred to as idiopathic (affects a small population group).

Clinical features

• Episodic burning epigastric pain related to meals (1–2 hours after)

• Relieved by food or antacids (generally)

• Dyspepsia common

• May be ‘silent’ in elderly on NSAIDs

• Physical examination often unhelpful

Investigations

• Endoscopy (investigation of choice):¹² 92% predictive value

• Barium studies: 54% predictive value

• Serum gastrin (consider if multiple ulcers)

• H. pylori test: serology or urea breath test; diagnosis usually based on urease test performed at endoscopy

Complications

• Perforation

• Bleeding → haematemesis and melaena

• Obstruction—pyloric stenosis

• Anaemia (blood loss)

• Cancer (in GU)

• Oesophageal stenosis

Bleeding peptic ulcer

This can be treated with endoscopic haemostasis with heater probe or injection of adrenaline or both. Also IV omeprazole 80 mg bolus, then 8 mg/hr IV infusion for 3 days. Surgery is an option. IV esomeprazole or pantoprazole can also be used.

Management of peptic ulcer disease

Aims of treatment:

• relieve symptoms

• accelerate ulcer healing

• prevent complications

• minimise risk of relapse

The treatment of a GU is similar to that for a DU except that GUs take about 2 weeks longer to heal and the increased risk of malignancy has to be considered.

General measures: (lifestyle and symptom relief)

• same principles as for GORD

• stop smoking

• avoid irritant drugs: NSAIDs, aspirin

• normal diet but avoid foods that upset

• antacids

If H. pylori positive—eradicate with combined therapy. Confirm eradication with a urea breath test (DU) or repeat gastroscopy (GU) and repeat if still present.⁸

If H. pylori negative—treat with full-dose PPI.

Proton-pump inhibitors (PPIs) provide more potent acid suppression and heal GUs and DUs more rapidly than H₂-receptor antagonists.

• 4–8-week oral course

Use with caution in:

• the elderly

• those on drugs, especially warfarin, anticonvulsants, beta blockers

• liver disease

Therapy to eradicate Helicobacter pylori^13,14

This organism has a proven link with PU disease (both DU and benign non-drug induced GU), gastric cancer and maltoma (a gastric lymphoma) because of mucosal infection. This hypothesis is supported by a very low relapse of DU in subjects eradicated of H. pylori. Most infected people are asymptomatic but infection leads to a lifetime risk of peptic ulcer disease in 15–20% and of gastric cancer in up to 2%.¹⁰ Twenty per cent of people have a variety of symptoms including those from gastritis and duodenitis. Treatment is based on combination triple or quadruple therapy, which can achieve a successful eradication rate of 85–90%.

Drug treatment regimens (examples)⁷

First-line therapy:

• PPI (e.g. omeprazole or esomeprazole 20 mg)

  plus

  clarithromycin 500 mg

  plus

  amoxycillin 1 g

  All orally twice daily for 7 days; this is the preferred regimen (available as a combination pack)

  Note: a 10–14-day course improves eradication rate by approx. 5%.¹

  or

  PPI + clarithromycin + metronidazole 400 mg (twice daily for 7 days)—if hypersensitive to penicillin

  or

  PPI + amoxycillin + levofloxacin (for salvage therapy)

  or

  other combinations: quadruple therapy e.g. bismuth + PPI + tetracycline + metronidazole (for failed triple combination)

Note: Resistance to metronidazole is common (>50%) and to clarithromycin is increasing (about 5% plus), but uncommon with tetracycline and amoxycillin.⁶

Antacids are good for daytime relief.

Maintenance anti-secretory therapy is usually unnecessary for H. pylori ulcers after successful eradication.⁷

For children with confirmed H. pylori:

• PPI + amoxycillin + clarithromycin

Indications (now uncommon) include:

• failed medical treatment after 1 year

• complications:

  • – uncontrollable bleeding

  • – perforation

  • – pyloric stenosis

• suspicion of malignancy in GU

• recurrent ulcer after previous surgery

NSAIDs and peptic ulcers^7,15

1. Ulcer identified in NSAID user:

   • stop NSAID (if possible)

   • check smoking and alcohol use

   • try alternative anti-inflammatory analgesic:

     • – paracetamol

     • – COX-2 selective drug

     • – enteric-coated, slow-release aspirin

     • – corticosteroids intra-articular or oral

   • PPI for 4 weeks (gives best results)

   Note: Healing time is doubled if NSAID continued.² About 90% heal within 12 weeks. Check healing by endoscopy at 12 weeks. Do H. pylori test.

2. Prevention of ulcers in NSAID user:¹⁵

   Primary prophylaxis is usually reserved for those at significantly increased risk, e.g. older persons (>75 years) and past history PU.

   Use one of the following PPIs:⁷

   esomeprazole 20 mg bd for 7 days

   or

   omeprazole 20 mg daily

   or

   pantoprazole 40 mg daily

Increased dietary fibre assists DU healing and prevention.

Note: Do H. pylori test and, if present, it should be eradicated with combination therapy after the ulcer has healed, especially in people who continue to take NSAIDs.¹

Autoimmune gastritis⁷

This is an inflammatory condition with antibodies to parietal cells and intrinsic factor. It is asymptomatic and may lead to pernicious anaemia. Diagnosis is confirmed by histology or endoscopy. H. pylori is absent.

Treat with iron and vitamin B12 if they are low.

Stomach cancer

Clinical features

• Male to female ratio = 3:1

• Usually asymptomatic early

• Consider if upper GIT symptoms in patients over 40 years, especially weight loss

• Recent-onset dyspepsia in middle age

• Dyspepsia unresponsive to treatment

• Vague fullness or epigastric distension

• Anorexia, nausea, ± vomiting

• Dysphagia—a late sign

• Onset of anaemia

• Changing dyspepsia in GU

• Changing symptoms in pernicious anaemia

• H. pylori is implicated as a cause and its treatment reduces the risk¹

Risk factors: ↑ age, blood group A, smoking, sugar, atrophic gastritis

Limited physical findings

• Palpable abdominal mass (20%)

• Signs (see FIG. 47.2) in advanced cases

Investigations

• Endoscopy and biopsy is optimal test

• Barium meal—false negatives

Treatment

• Surgical excision: may be curative if diagnosed early but overall survival is poor (22% at 5 years)

• Infants with persistent gastro-oesophageal reflux not responding to simple measures

• Failure to respond to stage 1 therapy for heartburn, when endoscopy is required

• Patients with persistent or recurrent ulcers

• Any patient with a PU complication, such as haemorrhage, obstruction or perforation

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Heartburn

• Hiatus hernia

• Peptic ulcer

• Reflux disease

• Reflux in infants