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CHAPTER 7 Upper gastrointestinal surgery
282
Oesophageal tumours
Key facts and pathological features
There are several types of oesophageal tumours.
Adenocarcinoma
• Rapidly increasing incidence in western world; ♂:♀, 5:1.
• Commonest in Western Europe.
• Associated with dietary nitrosamines, GORD, and Barrett’s metaplasia.
• Most commonly occurs in the lower third of the oesophagus.
Squamous carcinoma
• Incidence slightly reducing in western world. Commonest in Japan,
northern China, and South Africa; ♂:♀, 3:1.
• Associated with smoking, alcohol intake, diet poor in fresh fruit and
vegetables, chronic achalasia, chronic caustic strictures.
• May occur anywhere in the oesophagus.
Rhabdomyo(sarco)ma Malignant tumour of skeletal muscle wall of the
oesophagus; very rare.
Lipoma and gastrointestinal stromal tumours (GIST, see b p. 292) Rare.
Clinical features
• Dysphagia. Any new symptoms of dysphagia, especially over the age
of 45, should be assumed to be due to tumour until proven otherwise.
• Haematemesis. Rarely the presenting symptom.
• Incidental/screening. Occasionally identifi ed as a result of follow-up/
screening for Barrett’s metaplasia, achalasia, or refl ux disease. Presence
of high grade dysplasia in Barrett’s is associated with the presence of
an occult adenocarcinoma in 30%.
• Features of disseminated disease. Cervical lymphadenopathy,
hepatomegaly due to metastases, epigastric mass due to para-aortic
lymphadenopathy.
• Symptoms of local invasion. Dysphonia in recurrent laryngeal nerve
palsy, cough and haemoptysis in tracheal invasion, neck swelling
in superior vena cava (SVC) obstruction, Horner’s syndrome in
sympathetic chain invasion.
Diagnosis and investigations
• Diagnosis usually by fl exible oesophagoscopy and biopsy.
• Barium swallow only indicated for failed intubation or suspected post-
cricoid carcinoma (often missed by endoscopy).
Staging investigations
• Local staging. Endoluminal ultrasound scan to assess depth of invasion.
• Regional staging. CT scanning to evaluate local invasion, locoregional
lymphadenopathy, liver disease; laparoscopy to assess for peritoneal
disease in junctional tumours.
• Disseminated disease. PET scanning may be used to exclude occult
disseminated disease in patients otherwise considered for potentially
curative treatment.
OESOPHAGEAL TUMOURS
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Treatment
Palliative
Most patients present with incurable disease and require palliation.
• Dysphagia can be treated by endoluminal self-expanding metal stenting
(SEMS), external beam radiotherapy; surgery is very rarely indicated
for palliation.
• Metastases. Systemic chemotherapy if symptomatic.
Potentially curative
• Squamous carcinoma. Radical external beam chemoradiotherapy or
neoadjuvant chemotherapy followed by surgery (radical resection).
• Adenocarcinoma (large). Neoadjuvant chemotherapy followed by
surgery (radical resection).
• Adenocarcinoma (small) or high grade dysplasia in Barrett’s. Surgical
resection/EMR/ablation.
283
CHAPTER 7 Upper gastrointestinal surgery
284
Peptic ulcer disease
Key facts
• Peptic ulceration develops when a breakdown in the mucosal defence
of the stomach or duodenum leads to a mucosal breach.
• May be acute and transient (e.g. stress ulceration after surgery, in
acutely unwell ITU patients).
• If the repair system fails to deal with the breakdown of the mucosa, it
may become chronic.
• The term ‘peptic’ refers to ulcers in columnar mucosa in the lower
oesophagus, stomach, duodenum, or small bowel, usually due to the
action of acid.
Classifi cation
Peptic ulcers can be broadly classifi ed into:
• Gastric ulcers (type I, body and fundal).
• Duodenal and gastric ulcers (type II, prepyloric).
• Atypical ulceration.
Gastric ulceration
• ♂:♀, 3:1; peak age of incidence 50y.
• Associated with Helicobacter (H.) pylori in 45% of cases and with high
alcohol intake, smoking, NSAID use, normal or low acid secretion.
Duodenal and type II gastric ulceration
• ♂:♀, 5:1; peak age of incidence 25–30y.
• Associated with H. pylori in 85% of cases and with high acid secretion,
smoking, NSAID use.
Atypical ulceration
• Usually due to either atypical sites of gastric acid secretion (e.g.
ectopic gastric mucosa in a Meckel’s diverticulum) or abnormally high
levels of acid secretion (e.g. Zollinger–Ellison syndrome; see b p. 285).
• Associated with ulceration that fails to respond to maximal medical
therapy, multiple ulcers, ulcers in abnormal locations (e.g. distal
duodenum or small bowel).
Clinical features
• Nausea and epigastric pain.
• Duodenal ulceration typifi ed by hunger pains with central back pain
relieved by food; pain is often cyclical and occurs in the early hours of
the morning.
• Gastric ulceration typifi ed by pain precipitated by food with associated
weight loss and anorexia; pain less cyclical.
• Vomiting and upper abdominal distension suggest gastric outlet
obstruction.
Diagnosis and investigations
• Gastroscopy. Commonest diagnostic test.
• Barium meal. May be used if gastroscopy contraindicated.
PEPTIC ULCER DISEASE
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285
• Urease testing. To assess for presence of H. pylori can be performed on
antral biopsies from gastroscopy or as a CO
• Fasting serum gastrin levels. If hypergastrinaemia suspected.
breath test.
2
Complications
• Acute upper GI bleeding (see b p. 294).
• Iron defi ciency anaemia due to chronic low level bleeding.
• Perforation (see b p. 296).
• Gastric outlet obstruction due to chronic scarring at or around the
pylorus.
Treatment
Medical
• Advice to reduce alcohol intake, stop smoking, avoidance of NSAIDs.
• PPIs (e.g. omeprazole 20mg PO od, lansoprazole) or H
ranitidine 150mg PO bd, cimetidine 400mg PO bd) if intolerant to PPI.
• Topical antacids (e.g. Gaviscon
®
, sucralfate, colloidal bismuth),
blockers (e.g.
2
especially for acute ulceration post-operatively or in ITU patients.
• H. pylori eradication therapy (usually triple therapy of metronidazole,
PPI, and clarithromycin).
Surgical
Rarely necessary with the very highly effective acid-reducing drugs and
eradication therapy. Indications include the following.
• Gastric outlet obstruction not responsive or suitable for endoscopic
dilatation. Usual procedure is pyloroplasty (with or without highly
selective vagotomy) or type II partial gastrectomy (Bilroth II or polya).
• Failure to respond to maximal medical treatment with severe
symptoms or due to habitual recidivism. Procedure is type I partial
gastrectomy for type I gastric ulcer or type II partial gastrectomy for
duodenal ulcer.
• Emergency indications include:
Perforation (see • b p. 296);
Bleeding (see • b p. 294).
Zollinger–Ellison syndrome
• Due to hypergastrinaemia causing extensive, persistent, or typical
ulceration.
• Commonest cause is benign secretory gastrinoma (usually
intrapancreatic); occasionally cause is malignant gastrinoma (associated
with MEN syndromes).
• Diagnosed by raised serum gastrin level, tumour located by CT
scanning, angiography, selective pancreatic venous cannulation at
surgery.
• Treatment. Resection of pancreatic tissue containing tumour.
CHAPTER 7 Upper gastrointestinal surgery
286
Gastric tumours
May arise from the tissues of the mucosa (adenocarcinoma), connective
tissue of the stomach wall (previously known as leiomyoma or leiomyosarcoma, but part of the spectrum of disease called gastrointestinal stromal
tumours (GISTs); see b p. 292), the neuroendocrine tissue (carcinoid
tumours; see b p. 292), or the lymphoid tissue (lymphomas).
Key facts
Adenocarcinoma; commonest age of incidence >50y; ♂:♀, 3:1. Predisposing factors include:
• Diet rich in nitrosamines (smoked or fresh fi sh, pickled fruit);
• Chronic atrophic gastritis;
• Blood group A;
• Chronic gastric ulceration related to H. pylori.
Clinical features
Symptoms
• Dyspepsia (any new onset of dyspepsia over the age of 45 should be
considered to be due to adenocarcinoma until proven otherwise).
• Weight loss, anorexia, and lethargy.
• Anaemia (iron defi ciency due to chronic blood loss).
• Occasionally presents as acute upper GI bleeding (see b p. 294).
• Dysphagia uncommon unless involving the proximal fundus and
gastro-oesophageal junction.
Signs
• Weight loss.
• Palpable epigastric mass.
• Palpable supraclavicular lymph node (Troisier’s sign) suggests
disseminated disease.
Diagnosis and investigation
• Diagnosis usually by gastroscopy (barium meal may be required if
gastroscopy contraindicated).
• Staging (see Table 7.1) investigations include:
Thoraco-abdominal CT scan to assess for distant metastases and •
local lymphadenopathy.
Endoluminal ultrasound to assess for local disease.•
Laparoscopy (for patients considered for potential resection) to •
exclude small volume peritoneal metastases.
Treatment
Unfortunately, in the UK, the majority of tumours are metastatic or unresectable due to local extension and so not suitable for consideration of
surgical treatment for cure. The majority of treatment is directed at symptoms and palliation. When a tumour is considered potentially curable, the
treatment offered is based on the extent of disease at staging.
GASTRIC TUMOURS
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Table 7.1 TNM staging of gastric cancers
T (tumour) N (nodes) M (metastases)
Tis, in situ within
mucosa
T1, confi ned to
submucosa
T2, confi ned to
muscle wall
T3, involvement of
serosal surface
T4, involvement of
other organs
H1/2/3, hepatic metastases
N0, no lymph nodes P (peritoneal metastases)
N1, involved nodes
within 3cm of primary
N2, involved nodes
more than 3cm from
primary
H (hepatic metastases)
H0, no hepatic metastases
P0, no peritoneal
metastases
P1/2/3, peritoneal
metastases in increasing
extent
in increasing extent
Early gastric cancer (T1 or 2, N0/1, P0, H0)
• Suitable for attempted curative resection if patient medically fi t enough.
• Surgery. Radical gastrectomy usually preceded by neoadjuvant
chemotherapy in patients fi t.
• Patients now frequently offered preoperative and post-operative
chemotherapy.
• Local resection or ablation has an uncertain place in treatment.
Advanced gastric cancer (T3 or more or any of N2/P1+/H1+)
• Patients will be offered pre- and post-operative chemotherapy.
• Surgical intervention unlikely to be curative.
• May be undertaken for palliative treatment.
• Local ablation for symptom control occasionally possible.
• Palliative chemotherapy occasionally effective for disseminated disease.
287
Key revision points—anatomy and physiology of the
stomach
• The fundus is predominantly a storage zone with few active cells.
• The body contains mostly chief cells (secrete pepsinogen; stimulated
by gastrin and local ACh release) and oxyntic cells (secrete H
stimulated by gastrin, histamine, and ACh; inhibited by H
and GIP).
• The antrum contains G cells (secrete gastrin; stimulated by ACh
from vagus, stretch; inhibited by VIP, secretin, H
+
).
• The pyloric sphincter is a functional sphincter of circular muscle.
• Arterial supply is profuse (gastric ischaemia is rare) via coeliac
axis—left gastric, splenic, and common hepatic arteries.
• Lymphatic drainage follows arteries and is profuse (signifi cant lymph
node metastases are usually fatal).
+
;
+
, secretin,
CHAPTER 7 Upper gastrointestinal surgery
288
Chronic intestinal ischaemia
Caused by chronic reduction in blood supply to the intestine without
acute threat to the viability of the bowel.
Key facts
Chronic intestinal ischaemia is uncommon. Usually presents with vague
symptoms and diagnosis is often prolonged. Causes include:
• Progressive atherosclerosis affecting the visceral vessels; usually
requires more than one vessel to be affected (e.g. superior mesenteric
artery occlusion and coeliac artery stenosis).
• Obliterative small vessel disease (e.g. thromboangiitis obliterans,
systemic sclerosis, severe diabetic vasculopathy).
Clinical features
Symptoms
• Commonest symptom is mesenteric angina, chronic central abdominal
pain brought on by eating; associated with nausea and vomiting.
• May present with weight loss, general anorexia, and malnutrition.
• Often associated with other features of extensive vascular disease such
as renal impairment, coronary disease, claudication.
Signs
Weight loss, central abdominal tenderness.
Diagnosis and investigations
• Usually diagnosed by imaging of the visceral arteries in combination
with clinical symptoms. Methods of imaging visceral vessels include:
CT angiogram.•
MR angiogram.•
Transfemoral digital subtraction angiogram/aortogram.•
• Other investigations should include:
Assessment of renal function.•
Assessment of coronary circulation.•
Exclusion of aneurysmal disease.•
• Small vessel disease may require autoimmune screen.
Complications
• Acute intestinal ischaemia is less common due to the development of
collaterals although, if undiagnosed, loss of all visceral vessels results in
eventual pan-intestinal infarction.
• Chronic ischaemic strictures due to focally severe ischaemia.
Treatment
Medical
• Stop smoking.
• Control of hypertension; treatment of any hyperlipidaemia.
• Aspirin 75mg od to prevent thromboembolic events.
• Control diabetes if present.
• Treatment of autoimmune disease if present.
CHRONIC INTESTINAL ISCHAEMIA
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Interventional
Commonest treatment for large vessel stenosis is radiologically guided
stenting. Risks converting stenosis to acute occlusion with the risk of precipitating emergency surgery. Not possible if the stenosis is at the aortic
ostium of the vessel affected.
Surgical
• Rarely indicated. Commonest procedure is external iliac to ileocolic
artery side-to-side bypass.
• Overall prognosis is poor as the underlying disease process is often
widespread and progressive.
Key revision points—anatomy and physiology of the
small intestine
• Duodenum is a secretory and digestive organ; described in four parts
(second part admits the common bile and pancreatic ducts via the
ampulla of Vater on the medial wall).
• Jejunum is a secretory and digestive organ. Typical features include:
thick, red-purple wall; prominent plicae circulares; single arterial
arcades with long mesenteric vessels.
• Ileum is predominantly an absorptive organ. Typical features include:
thin blue-purple wall; prominent lymphoid aggregates; multilayered
mesenteric arterial arcades.
• Terminal ileum is a specialized area of ileum, particularly concerned
with absorption of bile salts, vitamin B12/IF complex.
289
CHAPTER 7 Upper gastrointestinal surgery
290
Surgery for morbid obesity
Key facts
• Approximately 25% of UK adult population are classifi ed as obese, a
body mass index (BMI) of greater than 30kg/m
• Admissions to hospital due to obesity-related disease have increased
eightfold in the last 10y.
• Obese patients are exposed to an increased risk of chronic diseases,
particularly type 2 diabetes, hypertension, hyperlipidaemia, and
arthritis.
• Increased risk of some forms of cancer (colon and endometrial).
Clinical features
Symptoms
• The symptoms of obesity are generally related to the underlying
condition that develops in association with it.
• Commonly, patients fi nd their physical capacity is reduced and they
become short of breath more easily on exertion
Signs
• Examination of obese patients can be challenging as their size can
reduce the ability to elicit clinical signs.
• Assess for signs of respiratory disease, dyspnoea at rest.
• Investigation of possible biliary disease (common bile duct stones,
biliary strictures, biliary tumours, biliary injuries, intrahepatic biliary
disease).
• Investigation of pancreatic disease (pancreatic duct strictures,
pancreatic duct abnormalities).
• Therapeutic interventions for pancreatico-biliary disease:
Stenting for common bile duct stones, strictures, tumours.•
Sphincterotomy for the extraction of biliary stones.•
Diagnosis and investigations
Exclude underlying endocrine disorders—Cushing’s disease, hypothyroidism, polycystic ovarian syndrome.
Treatment
Medical
• Diabetic control. Oral hypoglycaemics and insulin, if necessary.
• Medication for anti-hypertensive and cardiovascular disease.
• Psychological and dietetic support for weight loss programme.
• Anti-obesity medication. Orlistat (reduces fat absorption) is the
commonest.
Surgical
• Should only be considered after non-surgical treatments have failed
and patient has been through a preoperative assessment to ensure
they are able to make the necessary post-operative dietary and
lifestyle changes.
• Procedures have either a restrictive or malabsorptive effect.
2
.
SURGERY FOR MORBID OBESITY
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• Adjustable gastric banding is the commonest restrictive operation
(the band is placed around the cardia of the stomach and restricts the
volume of food, but not liquid that can be ingested at one time).
• Gastric bypass involves a restrictive element (division of the stomach
to create a small remnant) and a malabsorptive element (division and
re-anastomosis of small bowel to reduce its ability to absorb food).
• These procedures are most commonly performed laparoscopically.
291
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