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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
The Stomach and Duodenum 83
Helicobacter pylori infection
Helicobacter pylori is a Gram-negative urease-producing spiral-shaped
bacterium found predominantly in the gastric antrum and in areas of gastric
metaplasia in the duodenum. It is closely associated with chronic active
gastritis, peptic ulcer disease (gastric and duodenal ulcers), gastric cancer
and gastric B cell lymphoma.
Epidemiology
Infection is acquired in childhood and persists for life unless treated. Infection
is associated with lower socioeconomic status and is commoner in developing
countries. Transmission is most likely via the oral–oral or faecal–oral routes.
Clinicopathological features
H. pylori infection produces gastritis mainly in the antrum of the stomach.
In some individuals gastritis can involve the body of the stomach, leading
to atrophic gastritis and in some cases intestinal metaplasia, which is a
pre-malignant condition.
Diagnosis of infection
Diagnosis can be made via non-invasive (serology, breath test or stool antigen) or invasive (antral biopsy for patients undergoing an endoscopy) tests
(Table 3.3).
Management
Eradication of H. pylori is indicated for all patients with peptic ulcer disease,
atrophic gastritis, gastric B cell lymphoma, after gastric cancer resection and
in patients with dyspepsia (‘test and treat’ strategy). It is also indicated for
individuals who have a first-degree relative with gastric cancer. Recurrence
is rare after successful eradication. Several treatment regimens are available, although PPI-based triple therapy regimens for 14 days are favoured
(e.g. omeprazole 20 mg twice daily, metronidazole 400 mg twice daily and
clarithromycin 500 mg twice daily).
Peptic ulcer disease
A peptic ulcer (PU) is a break in the superficial epithelial cells penetrating
down to the muscularis mucosa of either the stomach or the duodenum;
there is a fibrous base and an increase in inflammatory cells. Erosions, by
contrast, are superficial breaks in the mucosa alone. Most PUs occur in the
stomach or proximal duodenum.
Epidemiology
Duodenal ulcers (DUs) are two to three times more common than gastric
ulcers (GUs) and occur in 15% of the population at some time. They are more
84 Gastroenterology and nutrition
Table 3.3 Diagnosis of Helicobacter pylori infection
Method Main use Comments
Non-invasive tests
13
C-urea
breath test
Stool antigen
test
Serology
Invasive tests (endoscopic gastric mucosal biopsy)
Rapid urease
(CLO) test
Histology
PPIs, Proton pump inhibitors.
Hydrolysis of
ingested 13C-urea
by H. pylori to
produce 13C in
expired air
Immunoassay
using monoclonal
antibodies
Serum antibody
detection
Urease from
H.pylori breaks
down urea to
produce ammonia
causing a pHdependent colour
change in the
indicator present
Direct visualization
of the organism
Diagnosis of
infection
Monitoring for
infection after
eradication
Diagnosis of
infection
Epidemiological
studies
Diagnosis of
infection in
patients already
undergoing
endoscopy
Highly sensitive
and specific
False-negative
results after recent
use of PPIs or
antibiotics
Inaccuracy limits
use
Antibodies remain
positive after
infection cleared
Highly sensitive
and specific
False-negative
results after recent
upper gastrointestinal bleeding and
recent use of PPIs
or antibiotics
Subject to
sampling error and
observer variability
common in the elderly and there is a geographical variation with peptic ulcer
disease being more prevalent in developing countries related to high H. pylori
infection. In the developed world the proportion of peptic ulcers secondary to
non-steroidal anti-inflammatory drugs (NSAIDs) is increasing as the prevalence of H. pylori declines.
Aetiology
H. pylori and drugs such as NSAIDs or aspirin are the cause of most PUs.
Co-administration of corticosteroids and NSAIDs further increases the risk of an
ulcer. Reduction of gastric mucosal resistance is thought to be the main factor
in causation of GUs as, in contrast to DUs, gastric acid secretion is reduced.
Aspirin and NSAIDs cause ulcers, at least in part, by reduced production of
The Stomach and Duodenum 85
prostaglandins (through inhibition of cyclooxygenase-1) which provide mucosal
protection in the upper gastrointestinal tract. Less common causes of PUs
are hyperparathyroidism, Zollinger–Ellison syndrome, vascular insufficiency,
sarcoidosis and Crohn’s disease.
Clinical features
The most common presenting symptom is burning epigastric pain, typically relieved by antacids, with a variable relationship to food. DU pain
often occurs when the patient is hungry and classically occurs at night.
Other symptoms, such as nausea, heartburn and flatulence, may occur.
Occasionally ulcers may present as a result of the complications of perforation or haemorrhage.
Investigations
Patients less than 55 years old with ulcer-type symptoms should undergo
non-invasive testing for H. pylori infection (see Table 3.3); upper gastroin-
testinal endoscopy is not usually necessary (see Management of dyspepsia
section).
Older patients require endoscopic diagnosis and exclusion of cancer. All
gastric ulcers must be biopsied to exclude an underlying malignancy and
should be followed up endoscopically until healing has taken place.
All patients with ‘alarm symptoms’ should undergo endoscopy:
• iron deficiency anaemia
• weight loss
• anorexia
• haematemesis/melaena
• persistent vomiting
• epigastric mass.
Management
Ulcers associated with H. pylori Treatment regimens (p. 83) that successfully
eradicate H. pylori result in ulcer healing rates of over 90% and prevent ulcer
recurrence. There is usually no need to continue antisecretory treatment (with a
PPI or H2-receptor antagonist) unless the ulcer is complicated by haemorrhage
or perforation. This approach to treatment is indicated in all patients with
H.pylori-associated peptic ulcer disease. Eradication is confirmed by either a
urea breath test or faecal antigen testing in patients who remain symptomatic
or who have had an ulcer complication.
H pylori-negative peptic ulcers are usually associated with aspirin or
NSAID ingestion. Treatment is with PPIs (p. 130) and stopping the offending
drug if at all possible.
Follow-up endoscopy plus biopsy is performed for all GUs to demonstrate
healing and exclude malignancy (initial biopsies may be false negatives).
Surgery is now rarely necessary for PU but is reserved for the treatment
of complications.
86 Gastroenterology and nutrition
Complications
Perforation This is an uncommon complication of PU disease. DUs perforate
more commonly than GUs, usually into the peritoneal cavity. Treatment is
surgical closure of the perforation and drainage of the abdomen. H. pylori
should subsequently be eradicated. Conservative treatment with intravenous
fluids and antibiotics may be indicated in elderly or very ill patients.
Gastric outlet obstruction Ulcer disease causing obstruction is now rare
and carcinoma is the commonest cause of obstruction. Outflow obstruction
occurs because of surrounding oedema or scarring following healing.
Patients present with copious projectile vomiting and a succussion splash
may be detectable clinically. Metabolic alkalosis may develop as a result of
loss of acid. In patients with PU disease the oedema will usually settle with
conservative management with nasogastric suction, fluid resuscitation and
PPIs. Surgery is rarely required.
Haemorrhage See page 89.
Management of dyspepsia
Significant gastrointestinal pathology is uncommon in most young people
with dyspepsia (p. 66). Furthermore, the close association of H. pylori with
peptic ulcer disease and the ability to detect H. pylori by non-invasive
methods means that investigation with endoscopy is unnecessary in most
patients. An approach to the management of dyspepsia is outlined in Fig. 3.2.
Gastropathy
The commonest cause of gastropathy is mucosal damage associated
with the use of aspirin or NSAIDs. These drugs deplete mucosal
prostaglandins by inhibiting the cyclo-oxygenase pathway, which leads
to mucosal damage. Other causes include alcohol misuse and infections,
e.g. cytomegalovirus and herpes simplex virus. Gastric erosions can
also be seen after severe stress (stress ulcer), burns (Curling’s ulcer),
and in renal and liver disease. Symptoms include indigestion, vomiting
and haemorrhage, although these correlate poorly with endoscopic and
pathological findings. Erosions (superficial breaks in the mucosa <3 mm)
and subepithelial haemorrhage are most commonly seen at endoscopy.
Treatment is with a PPI and removal of the offending cause, if possible.
Prophylactic PPI therapy is also given to prevent future damage in patients
who continue to take aspirin or NSAIDs.
Gastritis
The commonest cause of gastritis is H. pylori infection. Other causes
are autoimmune gastritis (the cause of pernicious anaemia associated
with antibodies to gastric parietal cells and intrinsic factor), viruses and
duodenogastric reflux. Gastritis is a histological diagnosis and is usually discovered incidentally when a gastric mucosal biopsy is taken for histology at
The Stomach and Duodenum 87
Dyspepsia
Notes:
A
T
patient needs US or CT scan.
Predominant
epigastric
pain
Alarm symptoms
or signs, or age
55 years
OGD + CLO
Abnormal
Appropriate
management
larm symptoms or signs: dysphagia, weight loss, vomiting, gastrointestinal bleeding,
epigastric mass.
hink if pain could be originating from biliary tract (page 141) or pancreas (page 189) and
Normal
All others
Review medication and
lifestyle factors
Assess H. pylori status by
non-invasive method (page 85)
Positive
Eradicate
H. pylori
Symptomatic treatment:
antacids, PPI
Negative
Predominant
heartburn
Manage as
GORD
(page 76)
Fig. 3.2 Approach to the investigation of patients with dyspepsia. CLO, Rapid
urease test; CT, computed tomography; GORD, gastro-oesophageal reflux disease;
OGD, oesophagogastroduodenoscopy; PPI, proton pump inhibitor; US, ultrasound.
endoscopy. Gastritis is usually asymptomatic; whether H. pylori gastritis itself
produces functional dyspepsia is controversial. At endoscopy the mucosa
may appear reddened or normal. No specific treatment is required although
eradication treatment for H. pylori is often given.
Gastric cancer
Epidemiology
Gastric cancer is the fourth most common cancer worldwide and the second
leading cause of cancer-related mortality. Incidence increases with age and
is more common in men. The frequency varies throughout the world, being
more common in Japan and Chile, and relatively less common in the USA.
Although the incidence overall is decreasing worldwide, proximal gastric
cancers are increasing in frequency in the West.
88 Gastroenterology and nutrition
Aetiology
The aetiology of gastric cancer is unknown. H. pylori infection is implicated as this causes chronic gastritis which in some individuals leads
to atrophic gastritis and pre-malignant intestinal metaplasia. Other
risk factors include lifestyle factors (tobacco smoking, diets low in
fruits and vegetables or high in salted, smoked or preserved foods),
pernicious anaemia, family history of gastric cancer and after partial
gastrectomy.
Pathology
Tumours most commonly occur in the antrum and are almost always adenocarcinomas. They are localized ulcerated lesions with rolled edges (intestinal,
type 1), or diffuse with extensive submucosal spread, giving the picture of
linitis plastica (diffuse, type 2).
Clinical features
Pain similar to peptic ulcer pain is the most common symptom. With
more advanced disease, nausea, anorexia and weight loss are common.
Tumours near the pylorus may cause outflow obstruction and vomiting,
while dysphagia occurs with lesions in the cardia. Almost 50% of patients
have a palpable epigastric mass, and a lymph node may be palpable in
the supraclavicular fossa (Virchow’s node). Metastases in the peritoneum
and liver cause ascites and hepatomegaly. Skin manifestations of malignancy, such as dermatomyositis (p. 302) and acanthosis nigricans, are
occasionally associated.
Investigations
Gastroscopy and biopsy is the initial investigation of choice. CT, EUS and
laparoscopy are then used to stage the tumour in a similar manner to
oesophageal cancer.
Management
Surgery is the most effective form of treatment if the tumour is operable.
Adjuvant (post-operative) chemoradiotherapy is given for more advanced
tumours. Palliative chemotherapy is sometimes used for unresectable lesions
with a modest improvement in survival.
Prognosis
Overall survival is poor, with a 5-year survival rate of 10%. Five-year survival after ‘curative’ surgery is 50%. In Japan there is an active endoscopic
screening programme, and earlier diagnosis and an aggressive surgical
approach have resulted in a 5-year survival of 90%.
Gastrointestinal Bleeding 89
Other gastric tumours
Gastrointestinal stromal tumours (GISTs) are a subset of gastrointestinal
mesenchymal tumours. They are usually asymptomatic and discovered
incidentally, although they can ulcerate and bleed. They were previously
considered to be benign but are now recognized to have malignant potential.
Treatment is surgical as far as possible. Imatinib, a tyrosine kinase inhibitor,
is used for unresectable or metastatic disease, and additionally as adjunctive
therapy after surgical removal of the primary in the absence of metastatic disease.
Gastric lymphoma arises from mucosal areas and is called mucosa-
associated lymphoid tissue tumour (MALToma). Gastric lymphoma presents
similarly to gastric carcinoma. Most gastric lymphomas are associated with
H. pylori infection and some can be treated by eradication of H. pylori only.
Other patients are treated with surgery or chemotherapy with or without
radiotherapy.
Gastric polyps are uncommon and usually regenerative. Adenomatous
polyps are rare.
GASTROINTESTINAL BLEEDING
Acute upper gastrointestinal bleeding
This is a common emergency admission with an overall mortality rate of
5%–12%. Haematemesis and melaena usually indicate bleeding from a
site proximal to the jejunum. Acute massive upper gastrointestinal bleeding may present with fresh rectal bleeding, almost always in association
with shock.
Aetiology
Peptic ulcers are the most common cause often associated with aspirin
or NSAID ingestion (Fig. 3.3). Relative incidences vary according to patient
population. Anticoagulants do not cause bleeding per se but bleeding from
any cause is greater if the patient is anticoagulated.
Management
This is summarized in Emergency Box 3.1.
Immediate resuscitation Two large-bore (16-gauge) intravenous
cannulas should be inserted and blood taken for full blood count, liver
biochemistry, urea and electrolytes (U/E), coagulation screen and ‘group and
save’; cross-match at least 4 units of blood if there is evidence of a large
bleed. Intravenous fluids are started while the patient is assessed further,
including a history and physical examination. In many patients no specific
90 Gastroenterology and nutrition
Reflux
oesophagitis (2%–5%)
Drugs (NSAIDs)
)
Other uncommon causes
Gastric antral vascular ectasia (GA
Hereditary telangiectasia
(Osler–W
Pseudoxanthoma elasticum
Blood dyscrasias
Dieulafoy gastric vascular abnormality
Portal gastropathy
A
ortic graft surgery with fistula
Mallory–Weiss
syndrome (5%–10%)
50%
Gastric ulcer
Duodenal ulcer
eber–Rendu syndrome)
Alcohol
VE)
Varices (10%–20%
Gastric varices
Gastric carcinoma
(uncommon)
Haemorrhagic gastropathy
and erosions (15%–20%)
Fig. 3.3 Causes of upper gastrointestinal haemorrhage. The approximate
frequency is also given.
treatment is required, bleeding stops spontaneously and the patient remains
well compensated. In patients with large bleeds or clinical signs of shock,
urgent blood transfusion is required. The principle is to restore the blood
volume rapidly to normal; plasma expanders or sodium chloride 0.9% are
given until the blood becomes available. Transfusion must be monitored to
avoid overload leading to heart failure, particularly in the elderly. Monitoring
pulse rate and central venous pressure will guide transfusion requirements.
Drugs such as aspirin, NSAIDs and anticoagulants are stopped and the
international normalized ratio (INR) reversed if necessary. Cardiology advice
should be sought before stopping aspirin and clopidogrel in patients with
low-risk bleeds.
Gastrointestinal Bleeding 91
Emergency Box 3.1 Approach to the management of
upper gastrointestinal bleeding
Immediate assessment +
resuscitation
Risk assessment
(Rockall score)
Pre-endoscopy
drug therapy
Endoscopy
Mallory–Weiss tear
Usually stop
spontaneously,
may need
endoscopic
haemostasis
Gastric
cancer
Usually small
bleeds. Large
bleeds may need
emergency
surgery
haemostasis
Cessation
of bleeding
Peptic
ulceration
Endoscopic
Surgery after
two re-bleeds*
Varices
Page 169
Re-bleed
*NB: less common causes of upper gastrointestinal bleeding are not indicated on this
figure.
Consider angiography with transcatheter embolization of bleeding lesions if high-risk
surgical patient.
Risk assessment Scoring systems have been developed to assess the
risk of re-bleeding or death. The ‘Rockall’ score (Table 3.4) helps to identify
those at high risk of recurrent or life-threatening haemorrhage and those at
low risk who may be suitable for early hospital discharge (pre-endoscopy
score 0, post-endoscopy ≤1). The Glasgow-Blatchford score uses the level of
plasma urea, haemoglobin and clinical markers, but not endoscopic findings.
Endoscopy
Endoscopy will usually diagnose, stratify risk and enable therapy to be
performed if needed. It should be carried out as soon as possible after
resuscitation. In patients with Rockall scores of 0 or 1 pre-endoscopy, it may
92 Gastroenterology and nutrition
Table 3.4 Rockall score for upper gastrointestinal haemorrhage
Score 0 Score 1 Score 2 Score 3
Age (years)
Shock
Comorbidity
Endoscopic
stigmata
Diagnosis
<60
None
None Cardiac failure,
None or dark
spot seen
M–W tear: no
lesion seen
and no SRH
Parameters indicated in bold calculate a pre-endoscopy Rockall score — maximum 7.
Final Rockall score — maximum 11.
M–W tear, Mallory–Weiss tear; SRH, stigmata of recent haemorrhage; IHD, ischaemic
heart disease.
Low-risk patients (post-endoscopy score ≤1) 5% risk of re-bleeding, 0% risk of death.
High-risk patients (post-endoscopy score 5–11), 11%–41% risk of death.
Death and re-bleeding are particularly common in inpatients and patients with varices.
60–79
>80
Pulse >100 Pulse >100
Systolic BP
Systolic BP
>100
IHD, comorbidity
Blood in upper
gastrointestinal
tract
Adherent clot
Visible or
spurting vessel
All other
diagnoses
Malignancy of
upper
gastrointestinal
tract
Renal/
liver failure,
any other
disseminated
malignancy
be possible to discharge the patient and arrange an outpatient endoscopy,
depending on local policy.
Endoscopy can detect the cause of the haemorrhage in 80% or more
of cases. In patients with a peptic ulcer, if the stigmata of a recent bleed
are seen (i.e. a spurting vessel, active oozing, fresh or organized blood clot
or black spots), the patient is more likely to re-bleed. Calculation of the
post-endoscopy Rockall score (Table 3.4) gives an indication of the risk of
re-bleeding and death.
Balloon tamponade may be performed as a temporizing measure for
patients with uncontrollable haemorrhage likely due to varices using a device
such as a Sengstaken–Blakemore tube. Tracheal intubation is necessary
if such a device is to be placed; ensure proper device placement prior to
inflation to avoid oesophageal rupture.