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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.
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Gastro-oesophageal reflux
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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.
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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.
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Despite this vomiting or regurgitation, the babies are usually comfortable and thrive. Some infants will cry, presumably because of heartburn.4
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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.
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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.
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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.
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Appropriate reassurance with parental education is important. It should be pointed out that changes in feeding practice and positioning will control most reflux.
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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.
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Smaller, more frequent feeds and thickening agents are appropriate.
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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.
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Bottle-fed babies (powdered milk formula):
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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.
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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.
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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
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Gastro-oesophageal reflux disease (GORD)6,7 in adults
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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)
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Red flag pointers for upper GIT endoscopy
Anaemia (new onset)
Dysphagia
Odynophagia (painful swallowing)
Haematemesis or melaena
Unexplained weight loss >10%
Vomiting
Older age >50 years
Chronic NSAID use
Severe frequent symptoms
Family history of upper GIT or colorectal cancer
Short history of symptoms
Unresponsive H. pylori treatment
++
Oesophagitis ± oesophageal ulcer
Iron-deficiency anaemia
Oesophageal stricture
Respiratory: chronic cough, asthma, hoarseness
Barrett oesophagus (from prolonged reflux)
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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
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Management of GORD6,7,8,9
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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
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Antacids are appropriate for rapid relief of mild intermittent or occasional breakthrough symptoms but are ineffective for long-term management.
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If no relief after several weeks, the following approaches are recommended by the Gastroenterological Society of Australia (GESA).6
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Reduce acid secretion. Select from:
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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
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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.
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Surgery is usually for young patients with severe reflux. The gold standard is a short, loose 360-degree fundoplication.
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Functional (non-ulcer) dyspepsia7, 10
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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):
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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
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Dysmotility-like dyspepsia
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Discomfort with early sense of fullness on eating
Nausea
Overweight
Emotional stress
Poor diet (e.g. fatty foods)
Similar lifestyle guidelines to GORD
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Peptic ulcer disease10,11
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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:
Types of ulcers:
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Note: If NSAIDs and H. pylori are not implicated, it is referred to as idiopathic (affects a small population group).
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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
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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
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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.
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Management of peptic ulcer disease
++
++
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
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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
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If H. pylori negative—treat with full-dose PPI.
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Proton-pump inhibitors (PPIs) provide more potent acid suppression and heal GUs and DUs more rapidly than H2-receptor antagonists.
++
++
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Therapy to eradicate Helicobacter pylori13,14
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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%.
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Drug treatment regimens (examples)7
++
++
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)
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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:
++
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Indications (now uncommon) include:
++
failed medical treatment after 1 year
complications:
suspicion of malignancy in GU
recurrent ulcer after previous surgery
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NSAIDs and peptic ulcers7,15
++
Ulcer identified in NSAID user:
stop NSAID (if possible)
check smoking and alcohol use
try alternative anti-inflammatory analgesic:
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.
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
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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
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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.
++
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
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Risk factors: ↑ age, blood group A, smoking, sugar, atrophic gastritis
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Limited physical findings
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DxT malaise + anorexia + dyspepsia + weight loss ➜ stomach cancer
++
DxT triple loss of appetite + weight + colour ➜ stomach cancer
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