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CHAPTER12 Gastrointestinalmedicine
Dyspepsia and
In any year, up to 40% of the adult population suer from dyspepsia— 1:10
seek their GP’s advice; ~10% of these are referred for endoscopy.
H.pylori
Causes
• Gastro- oesophageal reux disease (GORD)— 15– 25% E p. 358
• Peptic ulcer (PU)— 15– 25% E p. 360
• Stomach cancer— 2% E p. 362
• 60% are classied as non- ulcer dyspepsia (NUD, ‘functional’ dyspepsia)—
manage as for uninvestigated dyspepsia (Figure 12.2)
• Rarer causes— oesophagitis from swallowed corrosives, oesophageal
infection (especially in the immunocompromised)
Dierential diagnosis Cardiac pain (dicult to distinguish), gallstone
pain, pancreatitis, bile reux.
Presentation Common symptoms include retrosternal or epigastric
pain, fullness, bloating, wind, heartburn, nausea, and vomiting. Examination
is usually normal though there may be epigastric tenderness. Check for clinical anaemia, epigastric mass/ hepatomegaly, and LNs in the neck.
Management Figure 12.2
Lifestyle advice Give advice on healthy eating, weight d, and smoking
cessation. Avoid precipitating factors, e.g. alcohol, coee, chocolate, fatty
foods. Raising the head of the bed and having a main meal well before going
to bed may help. Promote continued use of antacids/ alginates.
Helicobacter pylori Infection is associated with:
• GI disease— peptic ulcer disease; gastric cancer; non- ulcer dyspepsia;
oesophagitis
• Non- GI disease— ranging from cardiovascular disease and
haematological malignancy to cot death
Testing forH.pyloriN ‘Test and treat’ all patients with dyspepsia who do not
meet referral criteria (Figure 12.2). Choice of test is limited by availability,
ease of access, and cost. Community options are:serology, urea breath
test, and faecal antigen test. A2wk washout period following proton pump
inhibitor (PPI) use is necessary before testing for H.pylori with a breath test
or a stool antigen test.
EradicationN Clears 80– 85% H.pylori infections. First- line options:
• PAC
regimen Full- dose PPI (e.g. omeprazole 20mg bd) + amoxicillin
500
1g bd + clarithromycin 500mg bd for 1wk or
• PMC
For more rst- line options and second- line options see NICE guidelines.
0 Do not retest even if dyspepsia remains unless there is a strong clinical
need. Retest if needed using a urea breath test.
regimen Full- dose PPI (e.g. omeprazole 20mg bd) +
250
metronidazole 400mg bd + clarithromycin 250mg bd for 1wk
Further information
NICE (2014) Gastro- oesophageal reux disease and dyspepsia in adults:
investigation and management. M www.nice.org.uk/ Guidance/ CG184
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DYSPEPSIA AND H.PYLORI
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Response
Figure12.2 Algorithm for management of uninvestigated dyspepsia in general
practice
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CHAPTER12 Gastrointestinalmedicine
Oesophagealconditions
Oesophagitis Common condition. Reux of acid from the stomach
to the oesophagus causes mucosal damage resulting in inammation and
ulceration. Other causes: drugs (e.g. NSAIDs); infection (e.g. CMV, HSV,
candida— especially in the immunocompromised); ingestion of caustic
substances.
Management Treat reux- induced oesophagitis as for GORD— E p. 358.
Otherwise treat the cause.
Barrett’s oesophagus E p. 359.
Chronic benign stricture Recurrent oesophagitis (e.g. 2° to GORD,
NSAIDs, K+ preparations) scars the oesophagus resulting in stricture formation. Most common in elderly .
Presentation Long history of reux with more recent dysphagia. If obstruction is severe undigested food may be regurgitated immediately after
swallowing. May be associated with night- time coughing paroxysms due to
aspiration of gastric contents into the chest. Examination is usually normal.
Management Refer for urgent endoscopy to conrm diagnosis and exclude
carcinoma. Treatment is by endoscopic dilatation of the stricture.
Carcinoma ofthe oesophagus E p. 362
Presbyoesophagus Common among the elderly. Intermittent sensation
that food is getting stuck— usually at the back of the throat. Examination is
normal as is endoscopy. Barium swallow or oesophageal motility studies
may reveal oesophageal spasm. Reassure.
Globus pharyngis (or hystericus) Sensation of a lump in the throat
without diculty swallowing is common. It may indicate anxiety. Reassure if
no organic signs and treat any dyspepsia. If not responding refer to ENT for
exclusion of an organic cause.
Eosinophilic oesophagitis Chronic, allergic oesophagitis. > .
More common if history of atopy. FH in 7%. Most present aged <40y with
oesophageal dysfunction (dysphagia, food impaction, vomiting, regurgitation, heartburn, abdominal pain). In children may present with failure to
thrive or feeding intolerance. If suspected, refer for endoscopy. Oesophageal
biopsy shows characteristic eosinophilic inltration. Treatment is with a PPI
for 8wk to exclude GORD; if endoscopic changes persist, treatment is with
an exclusion or elemental diet and/ or topical glucocorticoids. Oesophageal
dilatation may be needed in severe cases.
Oesophageal achalasia Failure of relaxation of the circular muscles at
the distal oesophagus. Peak incidence:30– 40y; slightly > .
Presentation Gradual onset of dysphagia over years accompanied by regurgitation of stagnant food and foul belching. Night- time coughing ts are due
to aspiration which can result in recurrent chest infections. Examination is
usually normal although there may be signs of aspiration pneumonia.
Management CXR to exclude aspiration pneumonia; endoscopy conrms
diagnosis. Refer for surgery.
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OESOPHAGEALCONDITIONS
Plummer– Vinson syndrome Iron deciency anaemia + dysphagia
due to a post- cricoid web in the oesophagus. > . Peak incidence:40–
50y. Presents with high dysphagia with food sticking in the back of the throat
± retching/ choking sensation. This is a premalignant condition so refer for
biopsy and dilatation of pharyngeal web; replace iron.
Pharyngeal pouch Pulsion diverticulum of the pharyngeal mucosa
through Killian's dehiscence (area of weakness between the 2 parts of the
inferior pharyngeal constrictor). > ; i with age. Usually develops posteriorly then protrudes to 1 side— L > R. As the pouch gets larger, the
oesophagus is displaced laterally.
Presentation Dysphagia— the rst mouthful is swallowed easily then lls
the pouch which makes further swallowing dicult. Accompanied by regurgitation of food from the pouch ± symptoms of aspiration (night- time
coughing, recurrent chest infection). Aswelling is palpable in the neck in ⅔
of cases.
Management Refer for further investigation. Diagnosis is conrmed with
endoscopy/ barium swallow. Treatment is surgical.
Oesophageal varices Result from portal hypertension (E p. 397) and
can bleed massively— admit as a ‘blue light’ emergency if bleeding.
Impacted oesophageal foreign body Usually the patient notices
something has stuck resulting in pain, diculty swallowing ± retching. If suspected refer immediately to A&E for further investigation ± removal of the
foreign body.
Oesophageal perforation Rare— usually a complication of endos-
copy. Less commonly due to violent vomiting. The patient becomes very
distressed with pain relating to the site of perforation which is worse on
swallowing. Examination reveals tachycardia, shock ± pyrexia ± breathlessness ± surgical emphysema in neck. Admit as a surgical emergency.
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Oesophageal atresia and/ or tracheo- oesophageal
stula
1:2500 live births. 5% have oesophageal atresia alone; 5%
tracheo- oesophageal stula (TOF) alone; the remainder have
both. Risk factors for sudden infant death syndrome.
Presentation
• Antenatal:at routine USS or following investigation of polyhydramnios
• Postnatal:cough or breathing diculties in a newborn infant, choking
on the rst feed, inability to swallow saliva l bubbling of uid from
the mouth developing soon after birth
• Later in childhood:‘H- type’ stulas where there is no atresia but just a
stula may present late with recurrent chest infections
Management Diagnosis is conrmed with X- ray. Treatment is surgical.
Postoperatively children may have a barking cough (‘TOF cough’) and/ or
dysphagia— both settle before 2y.
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CHAPTER12 Gastrointestinalmedicine
Gastro- oesophageal reflux andgastritis
Gastro- oesophageal reux disease (GORD) Caused by retro-
grade ow of gastric contents through an incompetent gastro- oesophageal
junction. It aects ~5% of the adult population.
Riskfactors
• Smoking
• Alcohol
• Coee
• Fatty food
• Big meals
Conditions caused byGORD
• Oesophagitis (dened by mucosal breaks) ± oesophageal ulcer
• Benign oesophageal stricture— E p. 356
• Intestinal metaplasia:Barrett's oesophagus
• Oesophageal haemorrhage
• Anaemia
Presentation
• Heartburn:most common symptom. Burning retrosternal or epigastric
pain which worsens on bending, stooping or lying, and with hot drinks.
Relieved by antacids
• Other symptoms:
•
Waterbrash— mouth lls with saliva
• Reux of acid into the mouth— especially on lying at
• Nausea and vomiting
• Nocturnal cough/ wheeze due to aspiration of reuxed stomach contents
• Examination:usually normal. Check for clinical anaemia, epigastric
mass/ hepatomegaly and LNs in the neck
Investigation Endoscopy if indicated— see Figure 12.2, E p. 355
0 Symptoms are poorly correlated with endoscopic ndings. Reux may
remain silent in patients with Barrett's oesophagus but heartburn can severely aect quality of life of patients with −ve endoscopy results.
Initial management
• In all cases give lifestyle advice (E p. 354)
• If diagnosis is clinical (i.e. patient presents with ‘reux- like’ symptoms),
treat as for uninvestigated dyspepsia (Figure 12.2, E p. 355)
• If reux conrmed on endoscopy, oer treatment with a PPI (e.g.
omeprazole 20mg od) for 1– 2mo
• If oesophagitis at endoscopy and still symptomatic on standard dose PPI,
double the PPI dose (e.g. omeprazole 20mg bd) for a further 1mo
• If inadequate response to PPI, try an H2 receptor antagonist (e.g.
ranitidine 150mg bd) and/ or add a prokinetic (e.g. metoclopramide
10mg tds) for 1mo
Long- term management of endoscopic/ barium- conrmed GORD
• Patients who have had dilatation of an oesophageal stricture should
remain on long- term full- dose PPI therapy
• Obesity
• Hiatus hernia
• Tight clothes
• Pregnancy
• Systemic sclerosis
N
• Drugs (NSAIDs, TCAs,
SSRIs, iron supplements,
anticholinergics, nitrates,
alendronic acid)
• Surgery for achalasia
N
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GASTRO-OESOPHAGEAL REFLUX ANDGASTRITIS
• For all other patients, if symptoms recur following initial treatment, oer
a PPI at the lowest dose possible to control symptoms, with a limited
number of repeat prescriptions. Discuss using the treatment on an asrequired basis to manage symptoms
• Refer for consideration of surgery if quality of life remains signicantly
impaired despite optimal treatment or if patient does not wish to
continue PPI/ H2 receptor antagonist therapy long term. Surgery of any
type is >90% successful although results may deteriorate with time
Hiatus hernia Common (30% of over 50s); 50% have GORD. Obesity
is a risk factor. The proximal stomach herniates through the diaphragmatic
hiatus into the thorax.
• 80% have a ‘sliding’ hiatus hernia where the gastro- oesophageal junction
slides into the chest
• 20% have a ‘rolling’ hernia where a bulge of stomach herniates into
the chest alongside the oesophagus. The gastro- oesophageal junction
remains in the abdomen
Management Treat as for GORD.
Barrett’s oesophagus Usually found incidentally at endoscopy for
symptoms of GORD and caused by chronic GORD. The squamous mucosa
of the oesophagus undergoes metaplastic change and the squamocolumnar
junction appears to migrate away from the stomach. The length aected
varies. Associated with i risk of adenocarcinoma of the oesophagus.
Consider referral for endoscopic surveillanceN if:
• Dysplasia
• Other risk factors— , older ager, i length of Barrett’s segment,
Treatment is with long- term PPIs (e.g. omeprazole 20– 40mg od) ± laser
therapy ± resection.
Acute gastritis Mucosal inammation of the stomach with no ulcer.
• Type A— aects the entire stomach; associated with pernicious
anaemia; premalignant
• Type B— aects antrum ± duodenum; associated with H.pylori
• Type C— due to irritants e.g. NSAIDs, alcohol, bile reux
Presentation and investigation Dyspepsia— see E p. 354
Management
• Treat the cause if possible (e.g. H.pylori eradication; d alcohol)
• Acid suppression— H2 receptor antagonist (e.g. ranitidine, nizatidine) or
PPI for 4– 8wk
• Re- endoscope to conrm healing
Complications Haemorrhage, gastric atrophy ± gastric cancer (type Aonly).
Further information
NICE (2014) Gastro- oesophageal reux disease and dyspepsia in
adults:investigation and management. M www.nice.org.uk/ Guidance/
CG184
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CHAPTER12 Gastrointestinalmedicine
Pepticulceration
Peptic ulceration (PU) is a term which includes both gastric and duodenal ulceration. Most patients present with dyspepsia (E p. 354). Specic features
of gastric and duodenal ulcers are listed in Table 12.6.
Management
For patients not takingNSAIDs
• Eradicate H.pylori if present— E p. 354— speeds ulcer healing and d
relapse; conrm eradication with a urea breath test (duodenal ulcer) or
repeat endoscopy (gastric ulcer), and retreat if still present
• If H.pylori negative Treat with full- dose PPI (e.g. omeprazole 20mg od)
for 1– 2mo. If gastric ulcer, re- endoscope to check ulcer is healed
For patients takingNSAIDs
• Stop NSAIDs where possible. If not possible, consider changing to a
safer alternative (e.g. paracetamol, d dose of NSAID, COX2 selective
NSAID) and adding gastric protection with a PPI or misoprostol
• Oer full- dose PPI or H2 receptor antagonist (H2RA) therapy for 2mo
and, if H.pylori is present, subsequently oer eradication therapy
• Check eradication with repeat endoscopy (gastric ulcer) or urea breath
test (duodenal ulcer)
For allpatients
• Lifestyle measures Avoid foods (or alcohol) which exacerbate
symptoms; eat little and often; avoid eating <3h before bed. Stop
smoking
• If symptoms recur following initial treatment Oer a PPI at lowest dose
to control symptoms, with a limited number of repeat prescriptions.
Discuss using the treatment on a prn basis
• Oer H2RA therapy If there is an inadequate response to a PPI
• In patients with unhealed ulcer or continuing symptoms despite
adequate treatment Exclude non- adherence, malignancy, failure
to detect H.pylori, inadvertent NSAID use, other ulcer- inducing
medication, and rare causes, e.g. Zollinger– Ellison syndrome, Crohn’s
disease
• Once symptoms are controlled Review at least annually to discuss
symptom control, lifestyle advice, and medication
• Refer If gastric ulcer fails to heal or if symptoms do not respond to
medical treatment. Possible surgical procedures include:gastrectomy,
vagotomy and drainage procedure; highly selective vagotomy
Zollinger– Ellison syndrome Association of peptic ulcer with a
gastrin- secreting pancreatic (rarely duodenal) adenoma— 50– 60% are malignant, 10% are multiple, and 30% are associated with multiple endocrine
neoplasia (MEN I). Incidence:0.1% of patients with duodenal ulcer disease.
Suspect in those with multiple peptic ulcers resistant to drugs, particularly
if associated with diarrhoea ± steatorrhoea or a family history of peptic
ulcers (or islet cell, pituitary, or parathyroid adenomas). Refer for further
investigation. Treatment is with PPIs (e.g. omeprazole 10– 60mg bd) ±
surgery.
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PEPTICULCERATION
Table12.6 Features ofgastric and duodenal ulcers
Gastric ulcer (GU) Duodenal ulcer (DU)
Population Typically aects middle aged/
Risk factors H.pylori (70– 90%)
Presentation May be asymptomatic
Examination In uncomplicated gastric
Investigation As for dyspepsia (E p. 355)
Complications Bleeding:acute GI bleeding— E p. 1061; iron deciency
elderly
NSAID use (i risk ×3– 4)
Delayed gastric emptying
Reux from the duodenum (i
by smoking)
Epigastric pain worsened by
food and helped by antacids
or lying at ± weight loss
With complications (see
below)
ulceration, examination is
usually normal though there
may be epigastric/ left upper
quadrant tenderness
anaemia— E p. 638
Perforated peptic ulcer:DU > GU; GUs may perforate
posteriorly into the lesser sac; DUs usually perforate
anteriorly into the peritoneal cavity. There may not be a past
history of indigestion. Presents with sudden- onset severe
epigastric pain which rapidly becomes generalized. When
a GU perforates into the lesser sac symptoms may remain
localized or be conned to the right side of the abdomen.
Examination:generalized peritonism with ‘board- like rigidity’.
Management:acute surgical admission
Pyloric stenosis in adults:duodenal stenosis 2° to scarring from
a chronic DU. Characterized by copious vomiting of food
1– 2days old. There may not be a past history of indigestion.
Examination:if prolonged vomiting may be evidence of
dehydration ± weight d.Succussion splash may be audible.
Management:surgical referral for conrmation of diagnosis and
surgical relief
Typically aects young– middleaged although can aect any
adult. >
H.pylori (>90%)
NSAID use
Gastric hyperacidity
Rapid gastric emptying
Smoking
Stress ()
May be asymptomatic or
spontaneously relapse
and remit
Epigastric pain typically relieved
by food and worse at night ±
weight i ± waterbrash (saliva
lls the mouth)
With complications (see
below)
In uncomplicated duodenal
ulceration, examination is
usually normal though there
may be epigastric tenderness
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Further information
NICE (2014) Gastro- oesophageal reux disease and dyspepsia in
adults:investigation and management. M www.nice.org.uk/ Guidance/
CG184
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CHAPTER12 Gastrointestinalmedicine
Gastro- oesophagealmalignancy
Carcinoma of the oesophagus Common cancer accounting for
7500 deaths/ y in the UK. Most common in patients >60y. Overall :
85:1. Usually presents late when prognosis is poor. 2 types:
• Squamous cell carcinoma (50%)— predominant form in upper ⅔ of the
oesophagus
• Adenocarcinoma (50%)— predominant in lower ⅓ of the oesophagus.
Incidence is i. : 85:1
Common riskfactors
Squamous cell carcinoma: Adenocarcinoma:
• Smoking*
• Alcohol
• Low fruit/ vegetable
intake
* Risk d to that of a non- smoker 10y after giving up.
Other riskfactors
• Previous mediastinal radiotherapy (i ×2 for patients treated for breast
cancer; i × 20 for patients treated for Hodgkin’s lymphoma)
• Plummer– Vinson (or Patterson– Kelly) syndrome— oesophageal web
and iron deciency anaemia
• Tylosis— rare, inherited disorder with hyperkeratosis of the palms—
40% develop oesophageal cancer
Presentation Short history of rapidly progressive dysphagia aecting solids
initially then solids and liquids ± weight loss ± regurgitation of food and
uids (may be bloodstained). Retrosternal pain is a late feature. Other
symptoms include hoarseness and/ or cough (due to aspiration or stula
formation). Examination may be normal. Look for evidence of recent
weight loss, hepatomegaly, and cervical lymphadenopathy.
Management Refer for urgent endoscopy if suspected. Rapid- access dysphagia clinics are run in many areas. Specialist management involves resection (treatment of choice but only 1:3 patients are suitable), chemotherapy,
radiotherapy, and/ or palliation with a stenting tube. Tubes commonly become blocked. Good palliative care is essential— refer early (E p. 1011).
Overall 8% 5y survival.
Stomach cancer Stomach cancer causes ~5000 deaths/ y in the UK;
95% are adenocarcinomas. Disease aecting older people with 92% diagnosed >55y; > (5:3). Incidence has more than halved over the past
30y in the UK probably due to improved diet.
Other risk factors Include:
• Geography— common in Japan
• Blood group A
• H.pylori infection (not clear if
eradication d risk)
• Atrophic gastritis
• Smoking*
• Obesity
• Low fruit/ vegetable intake
• GORD— particularly Barrett’s oesophagus
(risk i >30×— the longer the aected
segment, the higher the risk)
• Pernicious anaemia
• Smoking
• Adenomatous polyps
• Social class
• Previous partial gastrectomy
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GASTRO-OESOPHAGEALMALIGNANCY
Presentation Often non- specic. Presents with dyspepsia, weight d, an-
orexia or early satiety, vomiting, dysphagia, anaemia, and/ or GI bleeding.
Suspect in any patient >55y with recent- onset dyspepsia (within 1y) and/
or other risk factors. Examination is usually normal until incurable. Look for
epigastric mass, hepatomegaly, jaundice, ascites, enlarged supraclavicular
LN (Virchow’s node), acanthosis nigricans.
Management If suspected refer for urgent endoscopy. In early stages total/
partial gastrectomy may be curative. Most present at later stage. Overall 5y
survival is 15%.
Post- gastrectomysyndromes
Abdominal fullness A feeling of early satiety ± weight loss. Advise to take
small, frequent meals.
Bilious vomiting Aects 710% patients post- gastrectomy. Intermittent sudden
attacks of bilious vomiting 15– 30min after eating ± epigastric cramping pain
relieved by vomiting. Usually settles spontaneously. Metoclopramide may
be helpful in the interim. If symptoms are severe or fail to settle, request
surgical review. Surgical bile diversion or stomach reconstruction may alleviate symptoms.
Dumping Abdominal distension, colic, and vasomotor disturbance (e.g.
sweating, fainting) after meals. Aects 1– 2% of gastrectomy patients (more
common early after surgery— most settle within 6mo). 2 types:
• Early dumping Due to rapid gastric emptying. Starts immediately after a
meal. Consists of:sweating, ushing, tachycardia, palpitations, epigastric
fullness, and nausea. Occasionally there may be vomiting, diarrhoea,
± colicky abdominal pain. Advise:small, dry meals with restricted
carbohydrate. Take drinks between meals. If severe, re- refer
• Late dumping Due to rapid gastric emptying l hyperglycaemia. The
resultant hyperinsulinaemia causes a rebound hypoglycaemia. Starts
1– 2h after meals. Consists of:faintness, sweating, tremor, and nausea.
Advise patients to d the sugar content of meals, rest for 1h after each
meal, and take glucose if symptoms occur. If severe, re- refer
Diarrhoea post- gastrectomy 50% of patients who have had a truncal vagotomy or gastrectomy suer some frequency of defecation; 5% require
treatment. The diarrhoea is typically episodic and unpredictable. The exact
mechanism is not clear. Treatment is with codeine phosphate or loperamide
prn. Antibiotic treatment is occasionally successful— seek expert advice.
Surgical measures are rarely necessary.
Anaemia Gastrectomy can result in both vitamin B12 deciency and iron de-
ciency anaemia. Prophylactic vitamin B12 injections may be advised by the
operating surgeon. Many advise iron supplements for life. An annual FBC to
monitor for anaemia is advisable. Treat with iron/ vitamin B12 supplements.
Stomach cancer Risk of stomach cancer is i after partial gastrectomy (2×
after 20y and 7× after 45y).
Advice and support forpatients
Cancer Research UK F 0808 800 4040 M www.cancerresearchuk.org/
about- cancer/ stomach- cancer
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