MRCS Applied Basic Science and Clinical Topics

Abdominal emergencies 137

Investigation Diagnostic laparoscopy may be considered
particularly in young women.
Appendicitis is essentially a clinical diagnosis.
Investigations are primarily used to exclude Appendicectomy
an alternative diagnosis. Urinalysis may
exclude a urinary tract infection. A pregnancy Early appendicectomy for non-perforated
test may be necessary to exclude an ectopic appendicitis was first performed in the 1880s.
pregnancy. The serum white cell count and Open appendicectomy is usually performed
CRP may be increased. A normal white cell via a Lanz incision with a muscle splitting
count does not exclude a diagnosis of acute approach. Any pus found should be sent for
appendicitis. A plain abdominal x-ray is of microbiological assessment. Vessels in the
little value. An ultrasound may be helpful mesoappendix should be ligated. The base
in the assessment of an appendix mass or of the appendix should then be ligated and
abscess. An abdominal CT scan should the appendix excised. There is no evidence
be considered in adults if the diagnosis is that burying the stump reduces the infection
unclear or if there is clinical suspicion of an rate. A drain is not necessary unless there has
appendix mass. Laparoscopy may be used as been an appendicular abscess. Consideration
a diagnostic procedure as well as offering the should be given to a midline incision in
opportunity to proceed to treatment. elderly patients, particularly if the diagnosis
is uncertain. Laparoscopic appendicectomy
Scoring systems may be associated with reduced hospital stay
and more rapid return to normal activity.
Scoring systems and computer-aided
diagnosis have been developed and may be Appendix mass
helpful. The Alvarado Scoring system is based
on eight variables: An appendix mass, usually presents with
a several day history of right iliac fossa
• Migration of pain to right iliac fossa pain. Inflammation is localised to the right
• Anorexia iliac fossa by the omentum. The patient is
• Nausea/vomiting usually pyrexial with a palpable mass. Initial
• Tenderness in the right iliac fossa treatment should be conservative with
• Rebound pain fluids, analgesia and antibiotics. The general
• Elevated temperature (more than 37.3°C) condition of the patient and the size of the
• Leukocytosis (more than 10,000/µL) mass should be observed. Conservative
• Left shift management can continue whilst there is
evidence of clinical improvement.
A score of more than seven has both a
sensitivity and specificity of 80% for the Appendix abscess
diagnosis of acute appendicitis. Meta-analysis
has suggested that raised inflammatory An appendix abscess results from localised
markers, clinical signs of peritoneal irritation perforation. The abscess should be surgically
and migration of abdominal pain may be the or percutaneously drained. Appendicectomy
most useful predictors of a diagnosis of acute at initial operation can be difficult. The need
appendicitis in patients with abdominal pain. for interval appendicectomy after an appendix
abscess drainage is unclear. Often the
Management appendix is destroyed when the abscess forms.

In cases of diagnostic doubt, a period Perforated peptic ulcer
of ‘active observation’ is useful. Active
observation reduces the negative Several decades ago, perforated peptic
appendicectomy rate without increasing ulcer was a common disease of young
the risk of perforation. Intravenous fluids men but today it is mainly seen in elderly
and analgesia should be given. Opiate women. Overall, the number of admissions
analgesia does not mask the signs of with peptic ulceration is falling. However,
peritonism. Antibiotics should not be given the number of perforated ulcers remains
until a decision to operate has been made. unchanged. The sustained incidence of

138 Chapter 10  General surgery

perforation is possibly due to increased anti- have no demonstrable gas on a chest x-ray.
inflammatory use in the elderly. About 80% of If diagnostic doubt exists, then a CT scan
perforated duodenal ulcers are Helicobacter will confirm a perforation even if it can
pylori positive. not always show the site. Perforated peptic
ulceration can be associated with elevated
Clinical features serum amylase but not to same level as in
Most perforated peptic ulcers occur in pancreatitis.
patients with pre-existing dyspepsia. Only
about 10% of patients have no previous Management
symptoms. The classic presentation is
with sudden onset of epigastric pain with Most patients require surgery after
rapid generalisation. Examination shows appropriate resuscitation. Conservative
generalised peritonitis with absent bowel management may be considered if there is
sounds. About 10% patients have an significant co-morbidity but this is more likely
associated episode of melaena. to fail if perforation is of a gastric ulcer. Fluid
resuscitation with monitoring of the urine
Investigation output is required. Analgesia and antibiotics
Free gas under the diaphragm on an erect should be administered and a nasogastric
chest x-ray is a classical radiological sign tube placed.
(Figure 10.1). However, 10% of patients
Following adequate resuscitation, the
perforation should be oversewn with an

Erect chest x-ray showing free gas under the diaphragm Figure 10.1  Erect chest x-ray
showing free gas under the
diaphragm.

Abdominal emergencies 139

omental patch. If the surgeon is unable to having ischaemic heart, cerebrovascular and
find the perforation, it is important to open peripheral vascular disease respectively.
the lesser sac. It should also be remembered
that multiple perforations can occur. If Investigation
closure is secure and adequate peritoneal
lavage has been performed then a drain is No single investigation provides pathognomic
not required. evidence of mesenteric ischaemia. The serum
white cell count is often raised. Arterial blood
Pre-pyloric gastric ulcers behave as gases may show a metabolic acidosis. The
duodenal ulcers. All gastric ulcers require serum amylase is raised in 50% of patients.
biopsy to exclude malignancy. Definitive An abdominal x-ray may be normal early in
ulcer surgery is probably not required as the disease process. Late radiological features
50% patients develop no ulcer recurrence. include dilated small bowel and ‘thumb
Postoperatively, patients should receive printing’ of the bowel wall due to mucosal
Helicobacter pylori eradication therapy. oedema. Mesenteric angiography may
Surgery is increasingly performed confirm the diagnosis.
laparoscopically and is associated with no
increased morbidity and reduced hospital Management
stay. The operative mortality depends on the
time from perforation to admission, age, co- Following angiography, a papaverine infusion
morbidity and the presence of hypovolaemia into the superior mesenteric artery (SMA)
on admission. may be beneficial. If this fails to rapidly
improve symptoms, then laparotomy may
Acute mesenteric ischaemia be indicated. Surgery allows confirmation
of diagnosis and assessment of the extent of
Acute mesenteric ischaemia was first ischaemia, the opportunity to revascularise
recognised by Virchow in 1852. It occurs the SMA if appropriate and to resect necrotic
as result of either superior mesenteric bowel. Revascularisation may be achieved
arterial or venous occlusion and can affect by embolectomy, bypass or endarterectomy.
the bowel from the 2nd part of duodenum Resection and primary anastomosis may
to the transverse colon. Embolic arterial be possible. If doubt exists over the bowel
occlusion, atheromatous arterial occlusion viability then a ‘second-look’ laparotomy may
and venous thrombosis account for 50%, 25% be considered. If there is extensive necrosis in
and 10% of cases, respectively. Whatever the an elderly patient, then palliative care may be
underlining aetiology, reduced capillary flow the preferred option.
causes intestinal necrosis. Overall mortality is
approximately 90%. Upper gastrointestinal
haemorrhage
Clinical features
Clinical features
No single clinical feature provides conclusive
evidence of the diagnosis. As a result, the The presentation of an upper gastrointestinal
diagnosis is difficult and often delayed. haemorrhage depends on the amount and
Early diagnosis requires a high index of location of bleeding but invariably it causes
suspicion. Severe central abdominal pain is a haematemesis, coffee ground vomiting or
common presentation. The pain is often out melaena. Patients may also present with
of proportion to the apparent clinical signs. complications of anaemia, including chest
Vomiting and rectal bleeding may also occur. pain, syncope, fatigue and shortness of
Features of chronic mesenteric ischaemia breath. Examination should assess the vital
such a postprandial abdominal pain and signs in order to determine the severity of
weight loss may also be present. There may the bleeding and the timing of intervention.
be evidence of an embolic source (e.g. recent Abdominal examination may be normal
myocardial infarct, cardiac arrhythmia) and but there may be stigmata of chronic liver
there may be features of atherosclerotic disease. Causes of upper gastrointestinal
disease with 75%, 25% and 10% of patients haemorrhage include:

140 Chapter 10  General surgery

• Peptic ulcer (50%) • Continued bleeding that fails to respond to
• Gastric erosions endoscopic measures
• Oesophageal or gastric varices
• Mallory–Weiss tear • Recurrent bleeding
• Angiodysplasia • Patients more than 60 years
• Dieulafoy malformation • Gastric ulcer bleeding
• Gastric neoplasia • Cardiovascular disease with predictive

Initial management poor response to hypotension
Patients should be managed according
to agreed multidisciplinary protocols. For a bleeding duodenal ulcer, the surgical
Close collaboration is required between approach should involve the creation of a
physicians and surgeons. Aggressive fluid gastroduodenotomy between stay sutures.
resuscitation is important. Circulating blood Bleeding is usually from the gastroduodenal
volume should be restored with colloid or artery which should be underun with a
crystalloid. Cross-matched blood should be nonabsorbable suture on round-bodied needle.
given when available. All patients require It is essential to avoid picking up common bile
closed monitoring, possibly in an intensive duct in the suture. The gastroduodenotomy can
care environment with central and arterial then be closed as a pyloroplasty. All patients
pressure monitoring. should be given Helicobacter pylori eradication
therapy postoperatively. If a pyloroplasty will be
Bleeding peptic ulcer difficult because of large ulcer, consideration
should be given to a Polya gastrectomy. For a
Of all patients with a bleeding peptic ulcer, in bleeding gastric ulcer, either local resection
about 80% the bleeding stops spontaneously. of the ulcer or a partial gastrectomy may be
However, about 25% will require intervention appropriate.
for recurrent bleeding within 48 hours. It is
difficult to predict those that will continue to Variceal upper gastrointestinal
bleed. haemorrhage

Management Approximately 90% of patients with portal
All patients require early endoscopy to hypertension have oesophageal varices
determine the site of bleeding and any and 30% of patients with varices will have
continuing blood loss. Features of recent an upper gastrointestinal bleed at some
bleeding include: time. About 80% of upper gastrointestinal
bleeds in patients with portal hypertension
• Ooze from ulcer base are from varices but other causes do occur.
• Clot covering ulcer base The mortality following a variceal bleed is
• Black spot in ulcer base approximately 50% and of those who survive,
• Visible vessel 70% patients will have a rebleed. Survival
is dependent on the degree of hepatic
Proton pump inhibitors may improve impairment.
the outcome in acute non-variceal upper
gastrointestinal haemorrhage. Endoscopic Primary prevention
techniques to stop bleeding include:
Bleeding from oesophageal varices is more
• Laser photocoagulation using the Nd-YAG likely if there is poor hepatic function or large
laser varices. Primary prevention of bleeding is
possible with β blockers which reduce the
• Bipolar diathermy risk of haemorrhage by 40–50%. Band ligation
• Heat probes may also be considered. Sclerotherapy or
• Adrenaline or sclerosant injection shunting is ineffective.

No technique is superior. Active bleeding

Surgery In patients with presumed bleeding
Indications for surgical intervention include: from oesophageal varices, resuscitation

Abdominal emergencies 141

should be as for any other cause of upper Lower gastrointestinal
gastrointestinal haemorrhage. Endoscopy haemorrhage
should be performed to confirm the site of
haemorrhage. Vasopressin and octreotide Lower gastrointestinal haemorrhage accounts
can be used to decrease both the splanchnic for 20% cases of acute gastrointestinal
blood flow and portal pressure. Lactulose bleeding. Most patients are elderly. Most
may also be used to decrease gastrointestinal cases settle spontaneously without the
transit and reduce ammonia absorption. need for emergency surgery. Following
Metronidazole and neomycin may be used to investigation a cause of bleeding is often
reduce gut flora. not found. Causes of lower gastrointestinal
haemorrhage include:
Temporary tamponade can be achieved
with a Sengstaken–Blakemore tube. It has • Diverticular disease
three channels: • Angiodysplasia
• Inflammatory bowel disease
• One to inflate the gastric balloon • Ischaemic colitis
• One to inflate the oesophageal balloon • Infective colitis
• One to aspirate the stomach • Colorectal carcinoma

The use of a Sengstaken–Blakemore tube Angiodysplasia
should be considered as a salvage procedure.
Tamponade is 90% successful at stopping Angiodysplasia is an acquired malformation
haemorrhage. Unfortunately, 50% patients of intestinal blood vessels seen in up to 25%
rebleed within 24 hours of removal of the of asymptomatic patients over the age of 75
balloon. years. It is an incidental finding during 5%
of colonoscopies. About 80% lesions occur
Emergency endoscopic therapy is by in the right side of the colon and are often
either endoscopic banding of varices or associated with cardiac valvular disease.
intravariceal or paravariceal sclerotherapy. Dilated vessels or a ‘cherry red’ areas may
The sclerosants used include ethanolamine be seen at colonoscopy. Early filling of the
and sodium tetradecyl sulphate. If vessels is seen at angiography. Bleeding may
endoscopic methods fail, consideration be visible during the capillary phase of an
needs to be given to oesophageal transection, angiogram.
devascularisation or porto-caval or
mesenterico-caval shunting. Emergency Investigation
shunting is associated with a 20% operative
mortality and 50% risk of encephalopathy. Most patients with lower gastrointestinal
Shunting can also be performed non- haemorrhage are cardiovascularly stable
surgically by transjugular intrahepatic and can be investigated once the bleeding
portosystemic shunting (TIPPS). It has a has stopped. In the actively bleeding patient,
reduced risk of rebleeding but increases the colonoscopy can be difficult and often
risk of encephalopathy. incomplete examinations are performed.
Selective mesenteric angiography may be
Secondary prevention helpful but to see active bleeding it requires
continued blood loss of more than 1 mL/
About 70% of patients with a variceal minute. It may show angiodysplastic
haemorrhage will rebleed. The following have lesions even once the bleeding has ceased.
been shown to be effective in the prevention Radionuclide scanning can be considered
of rebleeding: using technetium-99m labelled red blood
cells.
• b-blockers possibly combined with
isosorbide mononitrate Management

• Endoscopic ligation Acute bleeding tends to be self-limiting
• Sclerotherapy and most patients can be managed
• TIPSS
• Surgical shunting

142 Chapter 10  General surgery

conservatively with intravenous fluids and distension depends on the level of the
blood transfusion, if required. If bleeding obstruction. Distension may be minimal in
persists, an upper gastrointestinal endoscopy high obstruction. Absolute constipation is
should be performed to exclude an upper a late feature of small bowel obstruction.
gastrointestinal cause. In those patients with Dehydration is associated with tachycardia,
significant or ongoing bleeding, consideration hypotension and oliguria. Features of
should be given to a laparotomy and on- peritonism indicate strangulation or
table lavage and panendoscopy. If right- perforation. Auscultation may show high-
sided angiodysplasia is confirmed, a right pitched or tinkling bowel sounds.
hemicolectomy is the operation of choice.
If bleeding diverticular disease is likely, a Investigation
sigmoid colectomy is the operation of choice.
If the source of colonic bleeding is unclear a A supine abdominal x-ray may show dilated
subtotal colectomy and end-ileostomy may small bowel. The valvulae coniventes
be required. differentiate the small from large intestine.
An x-ray may be normal if there is no air–fluid
Small bowel obstruction interface. An erect abdominal film rarely
provides additional information. A CT scan
Aetiology will confirm the diagnosis and may show the
level and cause of the obstruction.
Small bowel obstruction accounts for 5%
of all acute surgical admissions. In the Management
UK, the commonest causes of small bowel
obstruction are: Adequate resuscitation prior to surgery is
vital. Patients may have severe dehydration
• Adhesions (60%) and may require several litres of intravenous
• Strangulated hernia (20%) crystalloid. Adequacy of resuscitation should
• Malignancy (5%) be judged by measurement of the urine
• Volvulus (5%) output or assessment of the central venous
pressure. Surgery in under-resuscitated
Pathophysiology patients is associated with increased
mortality. If the cause of obstruction is
Dilatation of the bowel occurs above the presumed to be due to adhesions and
level of the obstructing lesion. This results there are no features of peritonism, then
in the accumulation of gas and fluid and conservative management for up to 48
reduced fluid reabsorption. Dilation of hours is often safe. Patients undergoing
the gut wall produces mucosal oedema. conservative management requires regular
This initially impairs the venous and clinical review and the willingness to
subsequently the arterial blood flow. consider surgical intervention if conservative
Intestinal ischaemia eventually results in management fails. If there are features of
infarction and perforation of that segment peritonism or systemic toxicity present, then
of bowel. Ischaemia also results in bacterial it is necessary to consider early operation.
and endotoxin translocation. The overall The exact procedure will depend on the
effect is progressive dehydration, electrolyte underlying cause. Absolute indications for
imbalance and systemic toxicity. surgery include generalised or localised
peritonitis, visceral perforation or the
Clinical features presence of an irreducible hernia. Relative
indications include a palpable mass lesion, a
The cardinal clinical features of intestinal ‘virgin’ abdomen or failure to improve with
obstruction are: conservative management.

• Colicky central abdominal pain Paralytic ileus
• Vomiting
• Abdominal distension Paralytic ileus is a functional obstruction
• Absolute constipation most commonly seen after abdominal

Vomiting is an early feature of high
obstruction. The degree of abdominal

Abdominal emergencies 143

surgery. It is also associated with trauma, • Colicky central abdominal pain
intestinal ischaemia and sepsis. The small • Early vomiting
bowel is distended throughout its length. • Late absolute constipation
Absorption of fluid, electrolytes and nutrients • Variable extent of distension
is impaired. Significant amounts of fluid may
be lost from the extracellular compartment. Left-sided tumours present with large bowel
obstruction
Clinical features
There is usually a history of recent operation • Change in bowel habit
or trauma. Abdominal distension is often • Absolute constipation
apparent. Pain is often not a prominent • Abdominal distension
feature. If no nasogastric tube is in situ, • Late vomiting
vomiting may occur. Large volume aspirates
my occur via a nasogastric tube. Flatus will Investigation
not be passed until resolution of the ileus.
Auscultation will reveal absence of bowel A plain supine abdominal x-ray may show
sounds. dilated large bowel. The small bowel may also
be dilated depending on the competence of
Investigation the ileocaecal valve. The additional value of
A plain abdominal x-ray may show dilated erect film is debatable. If doubt exists over
loops of small bowel. Gas may be present in either the diagnosis or the site of obstruction,
the colon. If doubt exists as to whether there then an abdominal CT scan or a water soluble
is a mechanical or functional obstruction, contrast enema may provide additional
then an abdominal CT scan or water soluble information.
contrast study may be helpful.
Management
Management
Prevention is better than cure. The bowel All patients with large bowel obstruction
should be handled as little as possible at the require adequate resuscitation and
time of surgery. Sources of sepsis should be prophylactic antibiotics. They should be
eradicated. For an established ileus, then a consented and marked for a potential stoma.
nasogastric tube and fluid and electrolyte At operation, a full laparotomy should be
replacement are required. No drugs are performed. The liver should be palpated for
available to reverse the condition. Paralytic metastases and the colon should be inspected
ileus usually resolves spontaneously after 4 or for synchronous tumours. The appropriate
5 days. operation depends on the level of the
obstruction. For right-sided lesions, a right
Large bowel obstruction hemicolectomy is the procedure of choice.
For transverse colonic lesion, an extended
In the UK, about of 15% colorectal cancers right hemicolectomy is often the most
present with intestinal obstruction. Most appropriate operation. In both cases a stoma
patients are over 70 years of age. The risk of can be avoided. For left-sided lesions, there
obstruction is greatest with left-sided colonic are various options depending on the age and
lesions. Obstructing tumours usually present fitness of the patient, the pathology and the
at a more advanced stage and 25% have experience of the surgeon.
distant metastases at presentation. Intestinal
perforation can occur at the site of the tumour A ‘three-staged’ procedure involves an
or in a dilated caecum if there is closed-loop initial defunctioning colostomy, followed by a
obstruction. resection and anastomosis and finally closure
of colostomy. A ‘two-staged’ procedure
Clinical features involves an initial sigmoid resection and end
Caecal tumours present with small bowel colostomy (Hartmann’s procedure) followed
obstruction by closure of colostomy. A ‘single-staged’
procedure involves resection, on-table lavage
and primary anastomosis. With a two-staged
procedure, only 60% of stomas are ever

144 Chapter 10  General surgery

reversed. With a single stage procedure, a the scope is advanced beyond this point there
stoma is avoided. Anastomotic leak rates of is often a dramatic release of flatus and liquid
less than 4% have been reported following stool. A flatus tube can be inserted and left in
on-table lavage and primary anastomosis. situ for 2 or 3 days. Overall, 80% of patients
Despite this, the total perioperative mortality will settle with conservative management
of malignant large bowel obstruction remains and if adequate decompression is achieved,
at about 20%. no emergency surgical treatment is required.
Unfortunately, about 50% patients will have
Sigmoid and caecal volvulus a further episode of volvulus within 2 years.
If decompression fails or there are clinical
A volvulus is defined as rotation of the gut features of peritonitis, the various surgical
on its own mesenteric axis. It produces options are:
partial or complete intestinal obstruction.
The blood supply to the segment of intestine • Sigmoid colectomy and primary
is compromised resulting in intestinal anastomosis
ischaemia. Venous congestion leading to
infarction can occur. The arterial supply is • Hartmann’s procedure
rarely compromised. A long narrow-based • Paul Mikulicz colostomy
mesentery predisposes to a volvulus.
Caecal volvulus
Sigmoid volvulus
The incidence of caecal volvulus is less than
The sigmoid colon is the commonest site of a that of sigmoid volvulus. It accounts for about
colonic volvulus. A sigmoid volvulus accounts 25% cases of colonic volvulus. Incomplete
for 5% of cases of large bowel obstruction in midgut rotation is a predisposing factor.
the UK. It is usually seen in the elderly or in Incomplete rotation results in inadequate
those with psychiatric disorders. It is a more fixation of the caecum to the posterior
common cause of obstruction in Africa or abdominal wall and the volvulus usually
Asia. The incidence is 10 times higher than in occurs clockwise around the ileocolic vessels.
Europe or USA. It usually also involves the terminal ileum
ileum and ascending colon.
Clinical features and investigation
Clinical features and investigation
The clinical presentation is that of
large bowel obstruction. Pain may be A caecal volvulus usually presents with
minimal and the abdominal distension clinical features of proximal large bowel
disproportionate. About 50% patients have obstruction. Colicky abdominal pain and
had a previous episode. Severe pain and vomiting are common and abdominal
abdominal tenderness suggests ischaemia. distension may occur. A plain abdominal
A plain abdominal x-ray may show large x-ray shows a ‘comma-shaped’ caecal
‘bean’ shaped loop of large bowel arising shadow in the mid-abdomen. Small bowel
from pelvis. If diagnostic doubt exists, loops may lie to the right of the caecum.
consideration should be given to a CT scan If diagnostic doubt exists, consideration
or water-soluble contrast enema. Either should be given to a CT scan or water-soluble
investigation should demonstrate the site of contrast enema. A contrast enema will show
obstruction. a ‘beaked’ appearance in the ascending
colon.
Management
Management
Resuscitation with intravenous fluids is
essential. Conservative management can be Colonoscopic decompression may be
attempted if there are no clinical features of appropriate if the patient is unfit for surgery.
ischaemia or perforation. A rigid or flexible It is successful in only about 30% of patients.
sigmoidoscopy can be both diagnostic and A laparotomy is normally required. If
therapeutic. The obstruction is encountered colonic ischaemia is present, then a right
at about 15 cm from the anal margin. When hemicolectomy should be performed though

Abdominal emergencies 145

a primary anastomosis may be inappropriate. • Chest infection
Exteriorisation of both ends of the bowel may • Myocardial infarction
be the safest option. If the caecum is viable • Cerebrovascular accident
and the volvulus reduced, the following can • Renal failure
be considered: • Puerperium
• Abdominal malignancy
• Right hemicolectomy • Orthopaedic trauma
• Caecostomy • Myxoedema
• Caecopexy • Electrolyte disturbances

Reduction alone is often associated with a Management
high recurrence rate.
The management of colonic pseudo-
Colonic pseudo-obstruction obstruction involves removing the precipitating
causes and decompressing the colon. Drugs
Colonic pseudo-obstruction is often referred with anticholinergic side effects should be
to as Ogilvie’s syndrome. It is a condition stopped, electrolyte disturbances corrected
characterised by reduced colonic mobility and the use of opiates limited. The colon can be
and dilatation. It presents with symptoms decompressed with a flexible sigmoidoscope
and signs of large bowel obstruction but in or a flatus tube. The cautious use of enemas or
the absence of a mechanical obstructing intravenous neostigmine may be considered.
lesion. The diagnosis is confirmed by CT Surgery is rarely required but should be
scan or single contrast enema. Either considered if there is failure of conservative
investigation will exclude an obstructing management. The surgical options include
lesion. Several medical or surgical tube caecostomy or resection with end
predisposing conditions have been ileostomy and mucus fistula formation.
identified including:



Chapter 11 The abdominal
wall

Applied basic sciences Rectus sheath
Anatomy of the anterior
abdominal wall The rectus sheath encloses the rectus
abdominis and pyramidalis muscles. It
The anterior abdominal wall has several contains the anterior rami of the lower
layers including skin, superficial fascia and six thoracic nerves and the superior and
muscles. inferior epigastric vessels. It is formed by the
aponeurosis of the three lateral abdominal
Skin muscles. Between the costal margin and
anterior superior iliac spine the aponeurosis of
The cutaneous nerve supply to the skin of the the internal oblique splits to enclose the rectus
anterior abdominal wall is from the anterior muscle, the external oblique aponeurosis
rami of the lower six thoracic and the first passes in front of muscle and the transversus
lumbar nerves. The dermatomes supplied are aponeurosis passes behind muscle. Between
as follows: the anterior superior iliac spine and the pubis,
the aponeurosis of all three muscles form the
• T7 – epigastrium anterior wall and the posterior wall is absent.
• T10 – umbilicus The curved lower posterior border of the rectus
• L1 – inguinal ligament sheath is known as the arcuate line. At this level
the inferior epigastric vessels enter the rectus
Cutaneous arteries are branches of the sheath. The rectus sheath is separated from its
superior and inferior epigastric arteries fellow on the opposite side by the linea alba.
and the intercostal and lumbar arteries.
The venous drainage is into the axillary and The inguinal canal
femoral veins. A few small paraumbilical
veins drain into the portal vein. The lymphatic Boundaries of the inguinal canal
drainage is into the axillary and superficial
inguinal nodes. The deep inguinal ring is the lateral boundary
of the inguinal canal. It is an opening in the
Superficial fascia fascia transversalis about 1 cm above the
inguinal ligament, midway between the
The superficial fascia is divided into two anterior superior iliac spine and the symphysis
layers. The superficial fatty layer is known as pubis. It lies just lateral to the inferior
Camper’s fascia and the deep membranous epigastric vessels. The medial boundary is
layer is known as Scarpa’s fascia. The fatty the superficial inguinal ring. This a triangular
layer is continuous with superficial fat of the defect in the external oblique aponeurosis
rest of the body. The deep fascia is continuous which overlies the pubic crest which forms the
with deep fascia of the thigh. The deep layer base of the opening. The anterior wall is the
also invests the perineum and is known as external oblique aponeurosis, reinforced in the
Colles fascia. lateral third by the internal oblique muscle.
The posterior wall is the fascia transversalis,
Muscles reinforced in medial third by the conjoint
tendon. The floor of the inguinal canal is the
The muscles of the anterior and lateral inguinal ligament which is the lower border of
abdominal walls are the: the external oblique aponeurosis. Medially it is
continuous with lacunar ligament which gives
• External oblique attachment to fascia lata of the thigh on the
• Internal oblique inferior border. The roof of the inguinal canal
• Transversus abdominis
• Rectus abdominis
• Pyramidalis

148 Chapter 11  The abdominal wall

is formed by the arched fibres of the conjoint Boundaries of the femoral canal
tendon.
The anatomical boundaries of the femoral
Contents of the inguinal canal canal are:

The inguinal canal contains the spermatic • Anterior – inguinal ligament
cord in males and the round ligament of • Posterior – pectineal ligament
the uterus in females. In both, the inguinal • Medial – lacunar ligament
canal contains the ilioinguinal nerve. Each • Lateral – femoral vein
anterior abdominal wall layer gives rise to
a layer of the spermatic cord. From within Incisions and
outwards the coverings are derived as laparoscopic access
follows:
Abdominal incisions are based on anatomical
• Internal spermatic fascia from fascia principles. They must allow adequate assess
transversalis to the abdomen and should be capable of
being extended if required. Ideally muscle
• Cremaster fascia from internal oblique fibres should be split rather than cut and
muscle nerves should not be divided. The rectus
muscle has a segmental nerve supply and,
• External spermatic fascia from external as a result, it can be cut transversely without
oblique muscle weakening a denervated segment of muscle.
Above the umbilicus, tendinous intersections
The spermatic cord contains the: prevent retraction of the muscles. Commonly
used incisions are shown in Figure 11.1.
• Vas deferens
• Artery to vas deferens (branch of the Figure midline incision

inferior vesical artery) A midline incision (Figure 11.2) is the
• Testicular artery (branch of the abdominal commonest approach to the abdomen and
the following structures are divided:
aorta)
• Testicular vein • Skin
• Testicular lymphatics • Linea alba
• Testicular nerve fibres • Transversalis fascia
• Processus vaginalis • Extraperitoneal fat
• Cremasteric artery (branch of the inferior • Peritoneum

epigastric artery)
• Nerve to cremaster (genital branch of

genitofemoral nerve)

Commonly used abdominal incisions Figure 11.1  Commonly used
abdominal incisions. 1 = Kocher;
12 6 2 = Thoracoabdominal; 3 =
7 Midline; 4 = Muscle splitting
43 89 loin; 5 = Pfannenstiel; 6 = Gable;
5 7 = Transverse muscle splitting;
10 8 = Lanz; 9 = Paramedian; 10 =
McEvedy

A midline incision Abdominal hernias 149
A paramedian incision

Figure 11.2  A midline incision Figure 11.3  A paramedian incision

The incision can be extended by cutting of the general surgical workload. A hernia
through or around the umbilicus. Above the consists of a sac, its coverings and contents.
umbilicus, the falciform ligament should be Hernias can be:
avoided. The bladder can be accessed via an
extraperitoneal approach through the space • Reducible
of Retzius. The wound can be closed using a • Irreducible
mass closure technique. • Obstructed or incarcerated
• Strangulated
Paramedian incision
A paramedian incision (Figure 11.3) is made Irreducible hernias have either a narrow neck
parallel to and approximately 3 cm from the or the contents of the hernia are adherent
midline. The incision transverses the: to the sac wall. Obstructed or incarcerated
hernias contain compromised but viable
• Skin intestine. Strangulation occurs when the
• Anterior rectus sheath venous drainage from the contents of the sac
• Rectus – retracted laterally is compromised.
• Posterior rectus sheath – above the arcuate
Inguinal hernias
line
• Transversalis fascia About 3% of adults will require an operation
• Extraperitoneal fat for inguinal hernia at some stage in their lives
• Peritoneum and 80,000 operations are performed each
year in UK. The male:female ratio is 12:1 and
The potential advantages of this incision are the ratio of elective to emergency operation is
that the rectus muscle is not divided and the also about 12:1. The peak incidence is in the
incisions in the anterior and posterior rectus 6th decade.
sheath are separated by muscle. The incision
is closed in layers and takes longer to make Direct inguinal hernia
and close. In the past, it was reported that
paramedian incisions has a lower incidence A direct inguinal hernia is due to weakness
of incisional hernias. in the abdominal wall musculature. It is
more common in older patients. The sac is
Abdominal hernias found medial to inferior epigastric artery.
Complications are unlikely due to the wide
A hernia is a protrusion of an organ through neck of the hernial sac. In adult males, 35% of
the wall that normally contains it. The wall inguinal hernias are direct. Predisposing factors
can be the abdomen, muscle fascia or the include smoking, ilioinguinal nerve damage
diaphragm. Hernias can be congenital and abdominal straining. A pantaloon hernia
or acquired. Abdominal wall hernias are is a special type of direct inguinal hernia. The
common and account for approximately 10% sac has two parts, one is medial and the other is
lateral to inferior epigastric artery.

150 Chapter 11  The abdominal wall

Indirect inguinal hernia The hernia may be tense tender and
irreducible. If strangulation occurs, the lump
Indirect hernias pass through the inguinal will become red and tender and the patient
canal. They can occur in children. The sac may be systemically unwell.
is found lateral to inferior epigastric artery.
Complications are more common than Investigation
with direct hernias. In adult males, 65% of
inguinal hernias are indirect. They are more The diagnosis is usually based on clinical
common on the right side, especially in features alone. The differential diagnosis is
children shown in Table 11.1. A herniogram may help
Clinical features in the investigation of chronic groin pain.
A reducible hernia usually present with a Ultrasound, CT or MRI may be useful if a
lump at the appropriate anatomical site clinically occult hernia is suspected.
(Figure 11.4). It increases in size on coughing
or straining and reduces in size or disappears Management
when relaxed or supine. With an inguinal
hernia, the lump is often above and medial to Herniotomy involves removal of the
the public tubercle. Examination may show sac and closure of the neck. This is the
it to have a cough impulse. Irreducible but treatment of choice in children and
non-obstructed hernias may cause little pain. adolescents. Herniorrhaphy involves a form
If obstruction occurs, colicky abdominal pain, of reconstruction to restore the disturbed
distension and vomiting may occur. anatomy, increase the strength of the
abdominal wall and construct a barrier to
An indirect inguinal hernia recurrence. Herniorrhaphy can be achieved
with the following techniques:
Figure 11.4  An indirect inguinal hernia
• Bassini +/– Tanner Slide
• Nylon darn
• Shouldice
• Lichtenstein
• Other mesh – Stoppa
• Laparoscopic

A Liechtenstein mesh repair is now regarded
as the ‘gold standard’ technique for inguinal
hernia repair as judged by the low-risk of
recurrence. Reducible asymptomatic direct
hernias in adults do not require surgical
intervention. Laparoscopic hernia repair
should be reserved for bilateral or recurrent
hernia. Complications of hernia repairs
include:

• Urinary retention
• Scrotal haematoma
• Damage to the ileoinguinal nerve
• Ischaemic orchitis
• Recurrent hernia

Trusses

About 40,000 trusses are sold annually in UK
of which 20% are purchased prior to seeing
a doctor. About 45% of patients have had
no instruction on correct fitting and 75%
of trusses are reported to be fitted whilst
the patient is standing and the hernia still
apparent.

Abdominal hernias 151

The differential diagnosis of an inguinal and femoral hernia

Inguinal hernia Femoral hernia

Femoral hernia Inguinal hernia
Vaginal hydrocele Lymphadenopathy
Hydrocele of cord Saphena varix
Undescended testis Ectopic testis
Lipoma of cord Psoas abscess
Psoas bursa
Lipoma

Table 11.1  The differential diagnosis of an inguinal and femoral hernia

Surgery for strangulated hernias Femoral hernias

The peak incidence of inguinal hernia Femoral hernias account for 7% of all
strangulation is approximately 80 years abdominal wall hernias. The female:male
of age. About 10% of patients presenting ratio is 4:1. They are more commonly seen in
with a strangulated hernia give no previous middle-aged and elderly women and are rare in
history of a reducible lump. In those with children. They are less common than inguinal
the acute onset of a hernia, the greatest hernias but as common as inguinal hernias in
risk of strangulation is in the first 3 months. older women.
The risk of strangulation depends on the
type of hernia and is more common with Clinical features
indirect hernias. The mortality of surgery Femoral hernias present with a groin lump
for strangulated hernias has changed below and lateral to the public tubercle.
little over the past 50 years and remains Unlike inguinal hernias, the lump is often
at approximately 10%. The mortality is ten irreducible. The differential diagnosis is
times greater than that following an elective shown in Table 11.1. Femoral hernias are
repair. more likely than inguinal hernias to present
with complications such as obstruction and
Recurrent inguinal hernia strangulation. All patients presenting with
small bowel obstruction should be examined
The recurrence rate following primary for a possible femoral hernia.
inguinal hernia repair varies with the
herniorrhaphy technique and duration of Management
follow-up. With Bassini and darn repairs, All uncomplicated femoral hernias should
the recurrence rate may be as high as 20%. be repaired as an urgent elective procedure.
With Shouldice and Lichtenstein repairs, Three classical approaches to the femoral
recurrence rates less than 1% have been canal have been described:
reported. Factors important in recurrence
include the type of hernia, type of operation • Low (Lockwood)
and postoperative wound infection. • Transinguinal (Lotheissen)
Recurrent hernias should be repaired using a • High (McEvedy)
mesh technique and this can be performed as
either an open or a laparoscopic procedure. Irrespective of the approach, surgery
Patients should be consented for a possible involves dissection of the sac, reduction
orchidectomy. of the contents, ligation of the sac and
approximation of the inguinal and

152 Chapter 11  The abdominal wall

pectineal ligaments. It is important to avoid performed through a infra-umbilical
compromising the femoral vein which forms incision. Occasionally the umbilicus needs
the lateral border of the femoral canal. to be excised. The contents of the hernia are
reduced. The defect in the linea alba can be
Special types of hernia repaired with an overlapping Mayo repair or
with the use of a prosthetic mesh.
Some hernia types have eponymous names
(Figure 11.5) attached to them. A Richter Epigastric hernia
hernia is a partial enterocele. It may present
with strangulation and obstruction but no Epigastric hernias arise through a congenital
clinically apparent hernia. A Maydl hernia weakness if the linea alba. The hernia usually
contains a ‘W-loop’ of bowel. Obstruction consists of extra-peritoneal fat from near
with the strangulated bowel within the to the falciform ligament. They are more
abdominal cavity occurs. A Littre hernia is a common in men. Many are asymptomatic or
strangulated Meckel diverticulum and may produce only local symptoms. Strangulation
present as a small bowel fistula. is rare. They can be repaired with either
sutures or the use of a prosthetic mesh.
Other abdominal wall hernias
Incisional hernia
Umbilical hernias
Incisional hernias occur through the scar
Clinical features from a previous operation. Approximately
Two types of umbilical hernia occur in adults. 1% of all abdominal incisions result in an
True umbilical hernias are rare. They occur incisional hernia. They account for 10%
with abdominal distension (e.g. ascites). of all abdominal wall hernias. They arise
Para-umbilical hernias are more common. when there is partial dehiscence of the deep
These occur through the superior aspect of fascial layers but the overlying skin remains
the umbilical scar. They are more common in intact. Most develop within a year of surgery.
women. They usually contain omentum and Symptoms are often minimal with the
only rarely contain bowel. The neck is often cosmetic appearance often the main concern.
tight and the hernia is often irreducible. The Most are wide-necked but strangulation
differential diagnosis of an umbilical hernia can occur. Preoperative, operative or
includes: postoperative factors may be important in the
aetiology.
• Cyst of the vitello-intestinal duct
• Urachal cyst Preoperative factors include:
• Metastatic tumour deposit (Sister Joseph
• Increasing age
nodule) • Malnutrition
• Sepsis
Management • Uraemia
The management of true and para-umbilical • Jaundice
hernias is similar. Surgery is usually • Obesity

Richter and Maydl hernias Figure 11.5  (a) Richter and
(b) Maydl hernias

ab

Intestinal fistulas 153

• Diabetes Intestinal fistulas
• Steroids Enterocutaneous fistulas

Operative factors include: A fistula is an abnormal connection between
a hollow viscus and an adjacent organ or the
• Type of incision skin. A simple fistula is a direct communication
• Technique and materials used between the gut and skin. A complex fistula
• Type of operations has multiple tracks and is usually associated
• Use of abdominal drains an abscess cavity. Fistulae, particularly if high
output (more than 500 mL/day), can result
Postoperative factors include: in dehydration, electrolyte and acid–base
imbalance, malnutrition and sepsis. Fistulae
• Wound infection can arise as a result of:
• Abdominal distension
• Chest infection or cough • Anastomotic leaks
• Trauma – often iatrogenic post surgery
Management • Inflammatory bowel disease
A CT or ultrasound may help clarify the site • Malignancy
of the muscular defect, the hernial sac and its • Radiotherapy
contents. Surgical repair can be challenging
and may not always be appropriate. The In the investigation of a fistula it is important
elderly or infirm may be helped by an to determine the anatomy of the tract.
abdominal wall support. If surgery is Fistulography will define the tract. A small
required, the following should be considered: bowel or barium enema will define the state
of the intestine or the presence of distal
• Fascial closure or mayo-type repair using obstruction. A CT or MRI can define abscess
sutures cavities.

• A ‘keel repair’ using sutures Management
• A mesh repair using polypropylene or
The management of a fistula, at least initially,
PTFE is conservative. This involves skin protection
• Laparoscopic mesh repair from corrosive gastrointestinal contents. It
is also necessary to maintain careful fluid
The results of surgery for incisional hernias balance, restore blood volume and correct
are variable. Re-recurrence rate of 20% have any acid–base imbalance. A proton pump
been reported. The results with mesh are inhibitor may be used to reduce gastric
superior to suture repairs. Composite meshes secretions. Somatostatin analogues (e.g.
may offer a reduced risk of complications. octreotide) may be considered to reduce
A sublay technique, with the mesh placed gastrointestinal and pancreatic secretions.
deep to the abdominal muscles, may have the Nutritional support is important. There
lowest recurrence rate. may be the need to restrict oral intake. A
nasogastric tube should be the considered.
Spigelian hernia Malnutrition can be corrected by either
parenteral or enteral nutrition. Enteral
A Spigelian hernia occurs at the lateral edge nutrition can be given distal to fistula. Any
of the rectus sheath. It is an interparietal associated abscess cavities should be drained.
hernia in the line of the linea semilunaris. It
usually occurs at the level of the arcuate line. Surgery

Obturator hernia An enterocutaneous fistula will not close if:

An obturator hernia occurs in the obturator • There is total discontinuity of bowel ends
canal. It is usually asymptomatic until • There is distal obstruction
strangulation occurs. Patients present with • Chronic abscess cavity exists around the
small bowel obstruction and may complain
of pain on the medial aspect of the thigh. A site of the leak
vaginal examination may allow identification
of a lump in the region of the obturator
foramen.

154 Chapter 11  The abdominal wall

• Mucocutaneous continuity has occurred spine. Positioning should be compatible
with the clothing normally worn by the
Fistulas are less likely to close if: patient. A loop stoma is usually required
to divert bowel contents away from a distal
• They arise from disease intestine (e.g. anastomosis or to rest distal bowel affected
Crohn’s disease) by disease.

• They are end fistulae Ileostomy output is small bowel contents
• The patient is malnourished and is normally between 500–1000 mL per day.
• They are internal fistulas Output greater than this can result in electrolyte
imbalance. The high bile content can damage
Large bowel fistulas are more likely than the skin, hence the need for fashioning a spout
small bowel fistulas to close spontaneously. on an ileostomy. If the output from an ileostomy
About 60% of small bowel fistulas will close is excessive consideration should be given to
with conservative treatment in 1 month once the presence of inflammatory bowel disease,
sepsis has been controlled. Surgery should be para-intestinal sepsis or subacute obstruction.
considered if fistula does not close by 30–40 Colostomy output is normal stool and is usually
days. The mortality associated with fistula is less than 500 mL per day. It is not corrosive to
still at least 10%. the skin. Complications of stomas can be either
physical or functional.
Gastrointestinal stomas
Physical complications include:
Abdominal stomas
• Necrosis
A stoma is a surgically created • Detachment
communication between a hole viscus and • Recession
the skin. Types of stomas includes a: • Stenosis
• Prolapse
• Colostomy • Ulceration
• Ileostomy • Parastomal herniation
• Urostomy • Fistula formation
• Caecostomy
• Jejunostomy Functional disorders include:
• Gastrostomy
• Excess action
Functionally they can be an end, loop or • Reduced action
continent stoma. They should be positioned
away from the umbilicus, scars, costal
margin and the anterior superior iliac

Chapter 12 Upper
gastrointestinal
surgery

Applied basic sciences • Mucosa
Embryology of the • Submucosa
gastrointestinal tract • Muscularis mucosa
• Serosa
Embryologically, the gastrointestinal tract
is divided into three sections. The foregut The mucosa is the innermost layer, which
extends from the oesophagus to the Ampulla lines the lumen. Its functions include:
of Vater in the second part of the duodenum.
The midgut starts at the Ampulla of Vater and • The secretion of mucus and enzymes
continues to the junction of mid and distal • The release of hormones into the plasma
transverse colon. The hindgut consists of the • Protection against infectious disease
distal colon and upper rectum. The blood • Absorption of digestive end products
supply of the three sections arise form the
coeliac axis, superior mesenteric artery and The mucosa consists of three layers. The
inferior mesenteric artery, respectively. epithelium lines the lumen and is typically
simple columnar in type. The lamina
Anatomy of propria is loose connective tissue under
gastrointestinal tract the epithelium and contains capillaries and
lymphoid tissue. A thin layer of smooth
From the oesophagus to the anal canal the muscle underlies the lamina propria. The
wall of the tract has the same basic four layers submucosa lies deep to the mucosa. It is
(Figure 12.1): made up of connective tissue containing
blood and lymphatic vessels and nerve
fibres. The muscularis mucosa lies deep to

The anatomical layers of gastrointestinal tract Figure 12.1  The anatomical layers
of gastrointestinal tract
Serosa
Longitudinal muscle
Circular muscle
Submucosa
Muscularis mucosa
Mucosa
Epithelial lining

Mesentery

156 Chapter 12  Upper gastrointestinal surgery

the submucosa. It is the smooth muscle layer of the left gastric vein and the tributaries of the
responsible for peristalsis and segmentation. azygos vein. Although no anatomical sphincter
It is divided into two layers, an inner circular can be demonstrated, at the lower end of the
layer and an outer longitudinal layer. In oesophagus, a multifactorial ‘physiological’
several sites the circular layer is thickened to sphincter mechanism is present. The lower
form a sphincter. These regulate the passage oesophageal sphincter functions by:
of materials through the gut. The serosa is the
outermost layer of the intraperitoneal organs. • Basal tone
It is also known as the visceral peritoneum. • Adaptive pressure changes
It consists of a simple squamous epithelium • Transient lower oesophageal sphincter
overlying thin areolar connective tissue. The
oesophagus has an adventitia rather than a relaxation
serosa. This is a layer of fibrous connective
tissue that firmly supports the organ. External mechanical factors in preventing
Retroperitoneal digestive organs have both a gastro-oesophageal reflux include:
serosa and an adventitia.
• Flap valve mechanism
Anatomy of the oesophagus • Cardio-oesophageal angle
• Diaphragmatic pinchcock
The oesophagus is approximately 25 cm in • Mucosal rosette
length and is divided into cervical, thoracic • Distal oesophageal compression
and intra-abdominal parts. It extends from • Phreno-oesophageal ligament
the pharynx, at the level of C6 vertebra, to • Transmitted abdominal pressure
the cardia of the stomach in the abdomen.
It traverses the diaphragm at the level of Anatomy of the stomach
T10 vertebra. It is lined throughout by a
stratified squamous mucosa. It has a rich For descriptive purposes the stomach has two
blood supply from the inferior thyroid artery, curvatures and is divided into various regions
branches directly from the aorta and from the (Figure 12.2) as follows:
oesophageal branch of the left gastric artery.
At the lower end there is a porto-systemic • Lesser curve
anastomosis between the oesophageal branch • Greater curve
• Fundus
• Incisura angularis
• Body
• Pylorus

The anatomical regions of the stomach Figure 12.2  The anatomical
regions of the stomach

Applied basic sciences 157

The lesser omentum connects the lesser known as gastric pits. The gastric pits lead
curve of the stomach to the liver. The greater into gastric glands which secrete gastric
omentum is connected to the greater curve of juice. Mucous cells secrete acidic mucus
the stomach. and function as stem cells for the surface
mucosa. Parietal cells secrete hydrochloric
Blood supply acid and intrinsic factor. The chief cells secrete
pepsinogen, an inactive form of pepsin. This is
The five main arteries that supply the stomach activated to pepsin initially by hydrogen ions
(Figure 12.3) are as follows: and by pepsin itself. Neuroendocrine cells
secrete multiple hormones into the plasma.
• Left gastric The most important of these is gastrin.
• Right gastric
• Right gastro-epiploic The vagus nerve
• Left gastro-epiploic
• Short gastric Both of the vagi enter the abdomen through
the oesophageal hiatus. The left vagus nerve
The left gastric artery arises from the passes on to the anterior and the right vagus
coeliac access. The right gastric artery nerve passes on to the posterior walls of the
arises from the common hepatic artery. stomach. The anterior vagus runs along the
The right gastro-epiploic artery arises from lesser curve. The nerve of Latarjet supplies
the gastroduodenal artery. The left gastro- the pylorus. The posterior vagus supplies the
epiploic artery arises from the splenic artery. coeliac ganglion.
The short gastric arteries are branches of the
splenic artery. Anatomy of the small intestine

Lymphatic drainage The small intestine is the longest part of the
alimentary canal. It is divided into three regions
The stomach drains into four groups of nodes
as follows: • Duodenum
• Jejunum
• Hepatic group • Ileum
• Sub-pyloric group
• Gastric group Duodenum
• Pancreatico-lienal group
The duodenum is approximately 25 cm long
Histology and is ‘C’ shaped. Except for the first part it is
retroperitoneal and is divided into four parts:
The gastric mucosa is simple columnar
epithelium with numerous invaginations

Arterial blood supply of the stomach Figure 12.3  Arterial blood supply
of the stomach. 1 = Splenic; 2 =
Short gastrics Left gastric; 3 = Right gastric; 4 =
Left gastro-epiploic Coeliac axis; 5 = Common hepatic.

2
5

4

1
3

Gastroduodenal

Right gastro-epiploic

158 Chapter 12  Upper gastrointestinal surgery

• First part is continuation of the pylorus intestinal glands (crypts of Lieberkuhn). They
and runs transversely contain absorptive cells and neuroendocrine
cells. The submucosa is unremarkable except
• Second part runs vertically in front of the in the proximal duodenum and terminal
hilum of the right kidney ileum. The proximal duodenal submucosa
contains alkaline mucus glands (Brunner’s
• Third part runs horizontally below the glands) and the terminal ileal submucosa
pancreas contains aggregates of lymphoid tissue know
as Peyer’s patches.
• Fourth part runs upward to the
duodenojejunal junction Gastric physiology

The ligament of Treitz connects the The motility of the stomach is increased by
duodenojejunal flexure to the right crus both distension and parasympathetic activity,
of the diaphragm. The duodenal papilla via acetylcholine and gastrin. It is decreased
is found on the medial wall of the second by low pH stomach contents which inhibits
part. It is the site of entry of the common gastrin release. Fats stimulate the release of
bile duct and pancreatic duct. The blood cholecystokinin. Acid stimulates the release
supply of the duodenum is from the superior of secretin. Hyperosmolality of duodenal
pancreaticoduodenal artery, a branch of contents reduces gastric emptying. The rate
the gastroduodenal artery and the inferior of emptying also depends on the type of food.
pancreaticoduodenal artery, a branch of Carbohydrate-rich content is faster than
the superior mesenteric artery. The venous protein-rich and fatty food. The stomach
drainage is into the portal and superior produces about 2500 mL of secretion per
mesenteric vein. The lymphatic drainage is to day. The pH is acidic and can be close to
the coeliac and superior mesenteric nodes. one. Gastric secretions are rich in potassium,
hydrogen ions, chloride and bicarbonate. It
Jejunum and ileum also contains intrinsic factor and pepsin.

The jejunum and ileum are about 6 m Secretion of gastric acid
long. The proximal 40% is the jejunum.
The jejunum begins at the duodenojejunal A H+/K+ ATPase is present in the apical
junction. The ileum ends at the ileocaecal membrane of the parietal cells. It pumps H+
valve. The ileum is connected to the ions into the gastric gland lumen against their
posterior abdominal wall by the small bowel concentration gradient. Potassium is actively
mesentery. The blood supply is from the pumped into the parietal cell in exchange.
superior mesenteric artery and branches Potassium then diffuses back into the lumen
form arcades within the mesentery. The of the gastric glands. Chloride diffuses from
lower part of the ileum is supplied by the the parietal cell into the lumen passively
ileocolic artery. The venous drainage is into down its electrochemical gradient. High
the superior mesenteric vein. The lymphatic concentrations of potassium and chloride
drainage is into the superior mesenteric are maintained within the parietal cell and
nodes. chloride and bicarbonate exchanged on the
basolateral membrane.
Histology
Control of gastric acid
The small intestine is highly modified for
absorption of fluid and nutrients. Structures Gastrin acts in two ways. It stimulates
that maximise the surface area include the: gastrin receptors on the parietal cells and
stimulates the release of histamine from
• Plicae circulares – deep permanent folds of enterochromaffin-like cells. Gastrin leads to
the mucosa and submucosa an increase in intracellular Ca2+. Histamine
then acts on H2 on the parietal cells. These are
• Villi – finger-like extensions of the mucosa G protein mediated receptors. They lead to
• Microvilli – projections of the plasma

membrane of each absorptive epithelial cell

The epithelium of the small intestine is a
simple columnar layer with goblet cells.
Epithelial invaginations are known as the

Oesophageal disease 159

an increase in intracellular cAMP and hence • Grade 1 – Erythaema isolated to one
in protein kinases which leads to activation mucosal fold
of H+/K+ ATPase. Acetylcholine activates
M3 muscarinic receptors. This increases • Grade 2 – Linear erosions on more than
intracellular Ca2+. Its release is stimulated one fold
by vagal action. Prostaglandin E activates an
inhibitory G protein. It thus blocks the action • Grade 3 – Circumferential erosions
of histamine and gastrin by inhibiting protein • Grade 4 – Ulceration, shortening or
kinase synthesis. Gastric inhibitory peptide
and vasoactive intestinal peptide and secretin stricture formation
act by inhibiting gastrin release. • Grade 5 – Barrett epithelium formation

Oesophageal disease The Los Angeles classification of GORD is as
Gastro-oesophageal follows:
reflux disease
• Grade A – Erosions <5 mm on one fold
Gastro-oesophageal reflux disease (GORD) • Grade B – Erosions >5 mm on one fold
can be defined as excessive amounts of • Grade C – Erosions on two more folds
reflux of gastric secretions associated with
significant symptoms or complications. It <75% of circumference
affects 40% of the adult population. It is • Grade D – Erosions >75% of circumference
due to either acid or bile reflux but delayed
oesophageal clearance may also be an In those in whom surgery is being considered,
important aetiological factor. Gastric acid 24-hour pH monitoring and oesophageal
hypersecretion is rarely implicated. Failure manometry are important. During 24-hour
of the function of the lower oesophageal pH monitoring a probe is placed 5 cm above
sphincter mechanism is a common finding. lower oesophageal sphincter. A pH of less than
Reflux exposes the lower oesophagus to acid 4 for over 1% of the time when erect or 6% of
or bile, increasing the risk of mucosal injury. the time when supine is suggestive of GORD.

Clinical features Management

About 20% patients with oesophagitis are Most patients gain symptomatic relief
symptom free. The commonest symptom with conservative treatment. Lifestyle
is heartburn. This is usually short-lived, modifications are important and patients
intermittent, retrosternal chest pain often should stop smoking, reduce their alcohol
associated with an acid taste in the mouth. intake and lose weight. Drug treatment
Symptoms are often worse when supine or at involves the use of proton pump inhibitors
night. Dysphagia may develop if complications and prokinetic agents. Proton pump
occur. There is a poor correlation between inhibitors will allow 80% of patients to
symptoms and endoscopic evidence of have mucosal healing at 8 weeks. However,
oesophagitis. A symptom diary may help in the about 20% will relapse despite maintenance
assessment of the patient. therapy. Life-long therapy is often required.

Investigation Surgical options

Endoscopy may provide histological The indications for surgery are:
confirmation of oesophagitis and allow
assessment of severity. However, about 30% • Failure of conservative management
of patients with symptoms of GORD have no • Recurrent symptomatic relapse
endoscopic evidence of mucosal injury. • Bile reflux
• Documented evidence of deficient lower
The Savary Miller grading of GORD is as
follows: oesophageal sphincter
• Complications of GORD

Fundoplication is the operation of choice,
usually performed as a laparoscopic
procedure. Important features are:

• Mobilisation of the gastric fundus
• A tension free wrap possibly around a 50 Fr

oesophageal bougie
• A wrap suture line of less than 3 cm

160 Chapter 12  Upper gastrointestinal surgery

Several types of fundoplication have epithelium extending more than 3 cm above
been described (Figure 12.4). Following gastro-oesophageal junction. The significance
fundoplication about 3% of patients of ‘short segment’ Barrett’s, less than 3 cm
develop dysphagia and 11% develop gastric long, is unclear.
bloat. A partial fundoplication, is associated
with less dysphagia and fewer gas-related Management
symptoms.
If recognised at endoscopy, most patients with
Oesophageal carcinoma Barrett’s oesophagus are started on life-long
acid suppression. There is little evidence that
Barrett’s oesophagus it causes regression of metaplasia. Anti-reflux
surgery may reduce progression to dysplasia
Barrett’s oesophagus was first described and cancer. Recent interest has been shown in
by Norman Barrett in 1950. It consists of endoscopic mucosal ablation and this is usually
a columnar cell-lined distal oesophagus achieved with photosensitisers and laser
due intestinal metaplasia of the distal therapy. The role of endoscopic surveillance
oesophageal mucosa. It is a pre-malignant of Barrett’s oesophagus is controversial. The
condition and can progress to dysplasia aim of surveillance is to detect dysplasia before
and adenocarcinoma. Barrett’s oesophagus progression to carcinoma. However, about
increases the risk of malignancy by 30-fold. 40% of patients with dysplasia already have a
It is an acquired condition due to gastro- focus of adenocarcinoma. Oesophagectomy
oesophageal reflux. Bile reflux appears to be for oesophageal dysplasia has an 80% 5-year
an important aetiological factor. About 10% survival.
of patients with gastro-oesophageal reflux
develop Barrett’s oesophagus. Approximately Oesophageal carcinoma
1% of patients with Barrett’s oesophagus per
year progress to oesophageal carcinoma. Oesophageal cancer is the sixth leading cause
of cancer death worldwide. It accounts for
Clinical features about 7000 deaths per year in the UK. Of all
oesophageal carcinomas, 90% are squamous
Barrett’s oesophagus per se is usually cell carcinomas. They usually occur in the
asymptomatic, recognised as an incidental upper or middle third of the oesophagus.
finding at endoscopy. It appears as ‘velvety’

Types of fundoplication

Figure 12.4  Types of fundoplication

Oesophageal disease 161

Only 5–10% are adenocarcinomas and operation regularly. The operative mortality
these usually occur in the lower third of the should be less than 5%. Preoperative
oesophagus. Wide variation in incidence has chemotherapy may improve survival. The
been reported both between countries and operative approach needs to ensure 10 cm
in different ethnic groups and populations proximal clearance to avoid submucosal
within a country. There is a clear positive spread. The approach depends on the site and
association with social deprivation. type of tumour and can involve:

Risk factors for squamous cell carcinoma are: • Total gastrectomy via a thoracoabdominal
approach
• Alcohol/tobacco
• Diet high in nitrosamines • Subtotal two-stage oesophagectomy (Ivor–
• Aflatoxins Lewis)
• Trace element deficiency – molybdenum
• Vitamin deficiencies – vitamins A and C • Subtotal three-stage oesophagectomy
• Achalasia (McKeown)
• Coeliac disease
• Genetic – tylosis • Transhiatal oesophagectomy
• High incidence in Transkei, areas of
Complications of surgery include:
Northern China and the Caspian littoral
region • Chest infection/pleural effusion
• Anastomotic leak
Clinical features • Chylothorax
The classical clinical presentation of • Recurrent laryngeal nerve damage
oesophageal carcinoma is progressive • Benign anastomotic stricture
dysphagia, first with solids and then with
liquids. Respiratory symptoms may occur Of those undergoing ‘curative’ treatment
due to overspill of fluid or solids into the less than 40% survive 1 year. Overall, 5-year
respiratory tract or occasionally because of the survival is very poor and is at best 20%.
formation of a trachea-oesophageal fistula.
Weight loss is usually a prominent feature. Palliative treatment

Investigation In those with inoperable disease, the
The diagnosis can be confirmed by aim of palliative treatment is to relieve
endoscopy plus biopsy. Most tumours are obstruction and dysphagia with minimal
irresectable and incurable at presentation. morbidity. This may be achieved with
The resectability and fitness for surgery can oesophageal intubation or stenting.
be assessed by: Open surgical intubation (Celestin or
Mousseau–Barbin tubes) is now obsolete.
• CT scanning Endoscopic or radiological placement is
• Lung function tests now most commonly practiced. An Atkinson
• Endoscopic ultrasound tube can be placed endoscopically but
• Bronchoscopy requires dilatation with risk of oesophageal
• Laparoscopy perforation. There has been a recent
increased use of self-expanding stents that
Management require no pre-dilatation. Complications
Adenocarcinomas are not radiosensitive of stents and tubes include oesophageal
and surgery is the mainstay of treatment. perforation, tube displacement or migration
Squamous cell carcinomas can be treated and tube blockage due to ingrowth or
with either surgery or radiotherapy. overgrowth of tumour. Endoscopic laser
ablation produces good palliation in over
Surgery 60% of cases buy may need to be repeated
Less than 50% of patients are suitable for every 4 to 6 weeks. It is associated with
potentially curative treatment. Treatment the risk of oesophageal perforation in
should be in centres that perform the about 5% cases. Squamous carcinomas are
radiosensitive and its use may produce some
palliation but at the risk of forming a tracheo-
oesophageal fistula.

162 Chapter 12  Upper gastrointestinal surgery

Oesophageal perforation systemic upset or those with a small
contained thoracic leak. It requires the
Oesophageal perforation is a rare patient to be ‘nil by mouth’ and to receive
condition associated with a high mortality. antibiotics and intravenous fluids. Failure of
Management and outcome depends on the conservative management will need surgery.
time from injury to diagnosis. ‘Early’ injuries The surgical management principals for
are those identified within 24 hours. ‘Late’ thoracic perforations include:
injuries are those identified later than 24
hours. The causes of oesophageal perforation • To control the oesophageal leak
are multiple and include: • Eradicate mediastinal/pleural sepsis
• Re-expand lung
• Endoscopic intubation • Prevent gastric reflux
• Sclerotherapy of oesophageal varices • Nutritional and pulmonary support
• Endoscopic prostheses • Antibiotics
• Traumatic intubation • Postoperative drainage of residual septic foci
• Perioesophageal surgery
• Trauma The methods of treatment include:
• Caustic ingestion
• Barotrauma • Primary closure with a buttress or patch
• Tumours • Exclusion and diversion
• Infections • T-tube fistula
• Thoracic drainage and irrigation
Boerhaave’s syndrome • Resection
• Decompression gastrostomy and feeding
Boerhaave’s syndrome is post-emetic rupture
of the oesophagus. It was first described by jejunostomy
Herman Boerhaave in 1723. His patient was
Baron Jan von Wassenaer, Grand Admiral of If operated on within 24 hours the mortality is
the Dutch Fleet who vomited after a meal and 5 to10%. If the operation is delayed more than
developed left-sided chest pain. He died 18 48 hours, the mortality is more than 50%.
hours later. At post mortem, he was shown
to have a tear of the left posterior wall of the Achalasia
oesophagus, 5 cm above the diaphragm,
surgical emphysema and food in the left Dysphagia can result from either extrinsic
pleural space. or intrinsic mechanical oesophageal
compression or primary or secondary
Clinical features neuromuscular problems. The causes
include:
Oesophageal rupture occurs after 0.1% of
standard endoscopies and 2% of endoscopies • Carcinoma of the bronchus
at which an oesophageal dilatation is • Thoracic aortic aneurysm
performed. The diagnosis requires a high • Goitre
index of suspicion. Typical symptoms include • Benign stricture
chest pain and dyspnoea. Signs include • Oesophageal carcinoma
pyrexia, tachycardia, hypotension and • Bolus obstruction
tachypnoea. Subcutaneous emphysema may • Achalasia
be present. Undiagnosed, systemic sepsis • Diffuse oesophageal spasm
rapidly develops and death often occurs with • Nutcracker oesophagus
48 hours. A chest x-ray may show a pleural • Multiple sclerosis
air/fluid level and mediastinal emphysema. • Systemic sclerosis
The diagnosis can be confirmed by water- • Chagas disease
soluble contrast swallow or CT scan. • Autonomic neuropathy

Management Achalasia is due to a reduced number of
ganglion cells in the oesophageal myenteric
Conservative management may be plexus. The vagus nerves show axonal
appropriate for small perforations without degeneration of the dorsal motor nucleus
and nucleus ambiguous. The aetiology is
unknown but a neurotropic virus may be

Gastric disease 163

important. The pathological features are oesophageal reflux and 3% a peptic stricture.
similar to Chagas disease which is due to Some centres combine a cardiomyotomy with
Trypanosoma cruzi infection. an antireflux operation.

Clinical features Gastric disease
Gastric cancer
Achalasia is most commonly seen in patients
between 40–70 years. The incidence is Gastric cancer is one of the commonest causes
the same in either sex. Symptoms include of cancer deaths world wide. It accounts for
dysphagia, weight loss, regurgitation and 7000 deaths per year in the UK. The incidence
chest pain. About 5% of patients develop increases with age. The male: female ratio is
squamous carcinoma of the oesophagus. The 2:1. Despite an overall decline in the incidence
differential diagnosis includes: rates of gastric cancer, several countries,
including the UK, have seen an increase in the
• Diffuse oesophageal spasm incidence of adenocarcinomas of the gastric
• Infiltrating carcinoma cardia, sometimes referred to as proximal
• Hypertrophic lower oesophageal sphincter gastric cancer.
• Scleroderma
• Chagas disease Risk factors include:

Investigation • Diet low in Vitamin C
• Blood group A
A chest x-ray may show widening of the • Pernicious anaemia
mediastinum with an air/fluid level and • Hypogammaglobulinaemia
absence of the gastric fundus gas bubble. • Post gastrectomy
A barium swallow may show oesophageal
dilatation, with food residue, small tertiary Precursor states include:
contractions and a ‘rat tail’ appearance of the
distal oesophagus. Oesophageal manometry • Helicobacter pylori infection
will show an absent primary peristaltic wave • Atrophic gastritis
and non-propulsive tertiary contractions. • Intestinal metaplasia
An endoscopy is essential to exclude • Gastric dysplasia
‘pseudoachalasia’ due to a submucosal • Gastric polyps
oesophageal carcinoma. It will also show
a tight lower oesophageal sphincter which Pathology
relaxes with gentle pressure. Macroscopically, the appearance of tumours
vary. Malignant gastric ulcers typically
Management have raised everted edges and sometimes a
necrotic base (Figure 12.5). Colloid tumours
Management of achalasia is by either balloon are large gelatinous growths. Linitis plastica is
dilatation or cardiomyotomy. In balloon a diffusely infiltrating tumour of the mucosa
dilatation, a Rider Moeller balloon is placed and submucosa with marked fibrosis leading
across the lower oesophageal sphincter and to a shrunken thickened stomach that fails to
is inflated to 300 mmHg for 3 minutes. With distend. Most tumours are adenocarcinomas
this approach 60% of patients are dysphagia with varying degrees of differentiation.
free at 5 years. The procedure may need to be Anaplastic signet-ring tumours have a
repeated. The risk of oesophageal perforation poor prognosis. Spread is typically via the
following balloon dilatation is about 3%. lymphatics or portal system. Transcoelomic
spread to the ovaries can occur (Krukenberg
Cardiomyotomy was described by Heller tumours).
(1914) and Grenveldt (1918). It may be
performed laparoscopically. The muscle Clinical features
fibres of the lower oesophagus are incised New onset dyspepsia over the age of 50 years
along an 8–10 cm length down to the mucosa. is suspicious of a gastric carcinoma as is
Following this procedure 85% of patients
are dysphagia free. About 10% develop

164 Chapter 12  Upper gastrointestinal surgery

Macroscopic appearance of a gastric cancer symptoms over the age of 40 years. It will
confirm the diagnosis, site and extent of
Figure 12.5  Macroscopic appearance of a gastric tumour. Staging requires a combination
cancer of preoperative investigations and
intraoperative assessment. Endoscopic
constant or worsening dyspepsia that fails ultrasound may allow assessment of
to respond to treatment. Weight loss and an intramural tumour penetration. Abdominal
epigastric mass are worrying signs. Some CT will allow assessment of nodal spread and
patients will develop an iron-deficiency the extent of metastatic disease. Laparoscopy
anaemia. Dysphagia and early postprandial will show peritoneal seedlings and peritoneal
vomiting occur with proximal obstructing lavage will allow detection of free tumour
tumours. Late postprandial vomiting cells. The Birmingham Staging System is a
especially of altered food and with no bile clinicopathological staging system (Table
suggests gastric outlet obstruction. Most 12.1). It does not require detailed assessment
patients present late and are not amenable to of the lymph node status.
radical surgery.
Investigation Management
Upper gastrointestinal endoscopy should
be considered in patients with dyspeptic Surgery offers the only prospective of
cure. Antral tumours may be suitable for
a partial gastrectomy usually with Polya
reconstruction. Other tumours will need a
total gastrectomy with oesophagojejunal
anastomosis and Roux-en-Y biliary diversion.
A tumour is considered resectable if it is
confined to the stomach or only the N1 or N2
nodes involved. Nodes less than 3 cm from
tumour are N1 nodes. Nodes greater than
3 cm from tumour are N2 nodes.

If the tumour and N1 nodes are resected
it is regarded as a D1 gastrectomy. If the
tumour and N2 nodes are resected then it is
regarded as a D2 gastrectomy. The evidence
to support the use of D2 gastrectomy is
incomplete. A D2 gastrectomy is associated
with increased postoperative mortality but
may have improved long-term survival.
Even in patients with incurable disease,

Stage Birmingham staging of gastric cancer

Stage 1 Description
Stage 2
Stage 3 Disease confined to muscularis propria
Stage 4a Muscularis and serosal involvement
Stage 4b Gastric and nodal involvement
Residual disease
Metastatic disease

Table 12.1  Birmingham staging of gastric cancer

Gastric disease 165

surgery may palliate symptoms. Results Peptic ulcer disease
from adjuvant chemotherapy post surgery
are disappointing. Chemoradiotherapy Peptic ulcer disease is defined as the
may reduce relapse and improve survival. presence of complete, established defects
Prognosis is generally very poor and overall, in the columnar mucosa of the lower
the 5-year survival rate is approximately 5%. oesophagus, stomach or duodenum.
Survival is 70%, 32%, 10% and 3% for Stages Proximal gastric ulcers (type 1) are most
1, 2, 3 and 4 respectively. commonly found on the lesser curve and
antrum of the stomach. Distal gastric and
Other gastric tumours duodenal ulcers (type 2) are found in the pre-
pyloric region or duodenum. Type 2 ulcers
Gastrointestinal stromal tumours are four-times more common. Important
aetiological factors include:
Gastrointestinal stromal tumours (GIST)
is a term that describes all tumours arising • Helicobacter pylori infection
from non-epithelial and non-lymphoid • Drugs – NSAIDS
tissues of the gastrointestinal tract. They • Smoking and alcohol
include tumours of benign, malignant and • Male sex
indeterminate potential. Leiomyosarcomas • High acid production
are a form of GIST and account for 2–3%
of all gastric tumours. They arise from Helicobacter pylori is a urease-producing
the smooth muscle of the stomach wall. Gram-negative spiral flagellated bacterium.
Lymphatic spread is rare. About 75% present It is found in 90%, 70% and 60% of patients
with an upper gastrointestinal bleed and with duodenal ulceration, gastric ulceration
60% patients have a palpable abdominal and gastric cancer respectively.
mass. The diagnosis can be confirmed by
upper GI endoscopy and CT scanning. Partial Clinical features
gastrectomy may allow adequate resection.
The 5-year survival is approximately 50%. The number of hospital admissions for
uncomplicated peptic ulcer disease is falling.
Gastric lymphoma The incidence of complications related
to anti-inflammatory use is increasing.
The stomach is the commonest extranodal Duodenal ulcers usually present with
primary site for non-Hodgkin’s lymphoma. epigastric pain, worse when fasting and
Gastric lymphoma accounts for approximately relieved by food. Symptoms may be worse
1% of gastric malignancies. The clinically at night. The pain often follows a relapsing
presentation is similar to gastric carcinoma. and remitting course. Gastric ulcers often
About 70% of tumours are resectable and the present with epigastric pain that is worse
5-year survival is approximately 25%. Both on eating. Weight loss is a more prominent
adjuvant radiotherapy and chemotherapy may feature. Patients may also present with iron-
be useful. deficiency anaemia.

Sister Mary Joseph’s nodule Investigation

Sister Mary Joseph was head nurse to The diagnosis can be confirmed by upper
William Mayo in Rochester Minnesota, who gastrointestinal endoscopy. The presence of
was the first to notice that a ‘nodule’ in the Helicobacter pylori can be detected by:
umbilicus was often associated with advanced
intra-abdominal malignancy. It usually • Microscopy – silver or Giemsa staining of
presents as firm, red, non-tender nodule antral biopsies
and results from spread of tumour within the
falciform ligament. About 90% of tumours • Rapid urease test – colour changes due to
are adenocarcinomas and the commonest change in pH
primaries are stomach and ovary. The primary
tumour is almost invariably inoperable. • 13C or 14C breath test – ingested radioactive
urea is broken down to carbon dioxide

• Serology – detected immunologically using
an ELISA

166 Chapter 12  Upper gastrointestinal surgery

Medical management and complications. Operations for duodenal
ulceration reduce acid production by
Proton pump inhibitors produce healing the stomach. The cephalic phase of acid
of 90% of peptic ulcers with 2 months of production can be reduced by a vagotomy.
treatment. Recurrence rates are low on long- The antral phase can be reduced by
term maintenance therapy. Helicobacter pylori antrectomy. There may be the need for a
can be eradicated in 80% patients with triple gastric drainage procedure to overcome the
antibiotic therapy. Various drug combinations effects of a vagotomy on gastric emptying.
have been described including amoxycillin,
metronidazole and omeprazole. Short- Open surgical procedures include:
term recurrence rates are low. Long-term
recurrence rates are at present unknown. • Truncal vagotomy and pyloroplasty
• Truncal vagotomy and gastrojejunostomy
Drugs have changed the need for ulcer • Highly selective vagotomy
surgery over last 20 years. Admissions for • Anterior seromyotomy and posterior
elective surgery have significantly reduced.
The number of complications of peptic ulcer truncal vagotomy
disease however remain unchanged due to
increased use of anti-inflammatory use in Laparoscopic peptic ulcer operations include:
elderly. Bleeding and perforation still have a
mortality of more than 10%. • Thoracoscopic truncal vagotomy and
pyloric stretch
Surgery
• Highly selective vagotomy
A Billroth I gastrectomy was originally • Posterior truncal vagotomy and selective
described for the resection of distal gastric
cancers. It is still used in gastric cancers if anterior vagotomy
radical gastrectomy is inappropriate. It was • Posterior truncal vagotomy and anterior
later applied in the treatment of benign gastric
ulcers. It is useful if the ulcer is situated high seromyotomy
on the lesser curve. It is less effective than
Polya gastrectomy for duodenal ulcers. Post gastrectomy complications include:

A Billroth II or Polya gastrectomy • Recurrent ulceration
(Figure 12.6) was initially described for • Diarrhoea
duodenal ulceration but is rarely performed • Dumping
today. It is useful in recurrent ulceration • Bilious vomiting
following previous vagotomy. When • Iron deficient anaemia
constructing the gastrojejunal anastomosis • B12 deficiency
it is necessary to consider whether to form • Folate deficiency
an antecolic or retrocolic anastomosis
and whether the anastomosis should be Post vagotomy complications include:
isoperistaltic or antiperistaltic. A Roux-en-Y
jejunojejunostomy may also be fashioned • Diarrhoea
(Figure 12.6b). • Dumping
• Bilious vomiting
Current surgical options
Pyloric stenosis
Current indications for surgical treatment of
duodenal ulceration are: Gastric outflow obstruction due to pyloric
stenosis is most commonly secondary to
• Intractability chronic prepyloric or proximal duodenal
• Haemorrhage ulceration. It usually presents with vomiting of
• Perforation undigested food, weight loss, epigastric pain
• Obstruction and dehydration. The abdomen is distended
and there may be visible peristalsis and a
The aim of surgery is to cure the ulcer succussion splash. Biochemical assessment
diathesis with the lowest risk of recurrence may show a hypochloraemic, hypokalaemic
metabolic alkalosis. Endoscopy will confirm
the diagnosis and may allow balloon dilatation
of the stricture. If this fails then surgery is by
either gastrojejunostomy or proximal gastric
vagotomy with duodenoplasty.

Gastric disease 167

Billroth II gastrectomy with a Roux-en-Y jejunojejunostomy Figure 12.6  (A) Billroth II
gastrectomy with a Roux-en-Y
jejunojejunostomy (B)

ab

Gastric volvulus Organoaxial and mesentericoaxial
gastric volvulus
A gastric volvulus is an abnormal rotation
of the stomach of more than 180°. It Figure 12.7 Schematic representation of organoaxial
causes closed loop obstruction and can (A) and mesentericoaxial (B) gastric volvulus
result in incarceration and strangulation
of the stomach. Depending on the axis Progressive distension and non-productive
of rotation it is classified as organoaxial retching may develop. Haematemesis is a late
or mesentericoaxial (Figure 12.7). About feature. Borchardt triad describes:
10% cases occur in children and is usually • Epigastric pain
associated with a diaphragmatic hernia. In • Retching
adults, it is associated with laxity of gastric • Inability to pass a nasogastric tube
ligament. Chronic gastric volvulus presents with
intermittent epigastric pain and distension.
Classification Early satiety, dyspepsia and dysphagia may
occur. The symptoms are often minimal and
In organoaxial volvulus, the axis of rotation the diagnosis can be difficult.
extends from gastro-oesophageal junction Investigation
to the pylorus. The gastric antrum rotates A chest x-ray may shows a retrocardiac gas-
in the opposite direction to fundus. This is filled viscus. A plain abdominal x-ray may
commonest type of volvulus and is usually show a distended stomach. The diagnosis
associated with diaphragmatic defect.
Strangulation occurs in about 10% of cases.
In mesentericoaxial volvulus, the axis of
rotation bisects the lesser and greater curves.
The gastric antrum rotates anteriorly and
superiorly and the posterior surface of
stomach lies anteriorly. Rotation is usually
incomplete. The diaphragm is usually intact
and strangulation is rare.

Clinical features

Acute gastric volvulus usually presents with
sudden onset of severe epigastric or left
upper quadrant pain. If part of the stomach
is in the thorax, then chest pain may occur.

168 Chapter 12  Upper gastrointestinal surgery

can be confirmed by a contrast study or abdominal pain and fatigue. There may also
abdominal CT scan. be features of malabsorption. Anaemia can
develop due to iron, folic acid or B12 deficiency.
Management Calcium and vitamin D malabsorption may
cause osteopenia. A mild coagulopathy may
Endoscopic reduction may be attempted in develop due to vitamin K malabsorption.
both acute and chronic cases. However, it
should not be attempted if there is clinical Investigation
suspicion of strangulation. A PEG can be
inserted after reduction to reduce the risk Several investigations can be used to assist in
of recurrence. Surgery is often required the diagnosis but many tests are only useful if
and involves reduction of the volvulus, the patient is still on a normal diet containing
assessment of viability of the stomach and gluten. Endoscopy with duodenal biopsies is
resection if required. An anterior gastropexy the gold standard.
may be considered to prevent recurrence.
Mortality following surgery for acute gastric Multiple biopsies are required. Most
volvulus is about 10%. patients with coeliac disease have a small
bowel that appears normal on endoscopy.
Coeliac disease Endoscopy may show scalloping of the small
bowel folds and a mosaic pattern to the
Coeliac disease is an autoimmune disorder mucosa. Serological tests have a high sensitivity
of the small bowel. It occurs in genetically and specificity. Serological tests include the
predisposed individuals. It affects about detection of IgA antibodies against reticulin
1% of the population and can present in or gliadin. The pathological changes of coeliac
either childhood or adulthood. It is caused disease in the small bowel are categorised by
by a reaction to gliadin, a gluten protein the Marsh classification as follows:
found in wheat. Long term it leads to an
increased risk of both adenocarcinoma and • Stage 0 – Normal mucosa
lymphoma. Coeliac disease has been linked • Stage 1 – Increased number of intra-
with a number of conditions including IgA
deficiency, dermatitis hepatiformis, other epithelial lymphocytes
autoimmune diseases including autoimmune • Stage 2 – Proliferation of the crypts of
thyroiditis and primary biliary cirrhosis
and undefined neurological disorders and Lieberkuhn
epilepsy. • Stage 3 – Partial or complete villous

Pathophysiology atrophy
• Stage 4 – Hypoplasia of the small bowel
The vast majority of coeliac patients have one
of two types of HLA DQ, a gene that is part of architecture
the MHC class II antigen-presenting receptor.
There are seven HLA DQ variants (DQ2 The changes classically improve or reverse
and D4 through 9). Two of these variants – after gluten is removed from the diet. Repeat
DQ2 and DQ8 – are associated with coeliac biopsies should be considered after 6 months
disease. The gene is located on the short arm of gluten exclusion.
of chromosome 6. The receptors formed by
these genes bind to gliadin peptides. Coeliac Management
disease shows incomplete penetrance.
The only effective treatment is a life-long
Clinical features gluten-free diet. No medication exists that
will prevent damage when gluten is present.
Many patients are asymptomatic. In those with Adherence to the diet allows the intestines
symptoms they include, diarrhoea, weight loss, to heal and leads to the resolution of all
symptoms in the vast majority of cases. A tiny
minority of patients suffer from refractory
disease. Steroids or immunosuppressants
may be considered in this situation.

Chapter 13 Hepatobiliary
and pancreatic
surgery

Applied basic sciences • Right and left hepatic ducts
Anatomy of the liver • Right and left branches of the hepatic artery
and pancreas • Portal vein
• Hepatic lymph nodes
Liver
The blood supply to the liver is from the
The liver is the largest organ in the hepatic artery and portal vein. Blood is mixed
body (Figure 13.1). It occupies the right in the central vein of each liver lobule. The
hypochondrium and extends into the venous drainage is via the hepatic veins into
epigastrium. It is protected by the ribs and the vena cava.
costal cartilages. Its relations include the
abdominal part of the oesophagus, stomach, The falciform ligament ascends from
duodenum, hepatic flexure of the colon umbilicus. Within the falciform ligament runs
and the right kidney and adrenal gland. It the ligamentum teres. This is the remains
is divided into right and left lobes by the of the umbilical vein. On the surface of the
falciform ligament. The right lobe is also liver the falciform ligament splits in two.
divided into the quadrate and caudate The right side forms the upper layer of the
lobes. The quadrate and caudate lobes coronary ligament. The left side forms the
are functionally part of the left lobe. It is upper layer of left triangular ligament. The
surrounded by a fibrous capsule. The porta extremity of the coronary ligament forms the
hepatis is found on the posterior–inferior right triangular ligament. An area devoid of
surface. The free edge of less omentum is peritoneum is known as the bare area.
attached to the margins of the porta hepatis.
The porta hepatis contains the: Extrahepatic biliary apparatus

The extrahepatic biliary apparatus consists of
the:

Gross anatomy of the liver Figure 13.1  Gross anatomy of
the liver
Coronary ligament

Diaphragm

Left lobe

Right lobe Falciform
Gallblader ligament

Inferior Round
border ligament

170 Chapter 13  Hepatobiliary and pancreatic surgery

• Right and left hepatic ducts Pancreas
• Common hepatic duct
• Common bile duct The pancreas is situated retroperitoneally
• Gallbladder and is a combined endocrine and exocrine
• Cystic duct gland. It is divided into the head, neck,
body and tail. It develops from the ventral
The right and left hepatic ducts emerge from and dorsal pancreatic buds. The ventral
right and left lobes in the porta hepatis. They bud produces the head and the uncinate
unite to form the common hepatic duct which process. The dorsal bud gives rise to the
is about 4 cm long. The common hepatic body and tail of the pancreas. The head lies
duct descends in the free edge of the lesser within the curve of the duodenum and the
omentum and is joined by cystic duct to form uncinate process projects from the head.
the common bile duct. The common bile duct The superior mesenteric vessels separate the
is about 8 cm long and also in the free edge of head from the body. The tail extends into the
the lesser omentum. It then extends behind lienorenal ligament along with the splenic
the first part of the duodenum, and lies on the artery. The pancreas is closely related to
posterior aspect of pancreas. It drains into the several other organs (Figure 13.3). Anterior
second part of the duodenum at the ampulla relations include the transverse mesocolon
of Vater. The terminal part is surrounded by and stomach. Posterior relations include
sphincter of Oddi. the inferior vena cava, aorta, portal vein,
common bile duct and left kidney. Superior
Gallbladder relations include the first part of duodenum
and splenic artery.
The gallbladder lies on the viseral surface
of liver. It is divided into the fundus, body The pancreas has two ducts – the main
and neck. The fundus projects from the and accessory pancreatic ducts (Figure
inferior margin of the liver and comes into 13.4). The main pancreatic duct begins in
contact with abdominal wall at level of tip of the tail and drains into the second part of
9th costal cartilage. The neck is continuous the duodenum together with the common
with cystic duct. Relations of the gallbladder bile duct. The main duct is also known as the
include the anterior abdominal wall, visceral duct of Wirsung. The accessory duct begins
surface of liver, transverse colon and the in the head and is also known as the duct of
first and second parts of the duodenum. Santorini. It usually drains into the main duct
The blood supply is from the cystic artery, a but can open separately into the duodenum.
branch of the right hepatic artery. The cystic The blood supply of the pancreas is from the
vein drains directly into the portal vein. The superior and inferior pancreaticoduodenal
cystic duct is about 4 cm long but is subject to arteries. The superior pancreaticoduodenal
anatomical variations (Figure 13.2). artery is an indirect branch of the hepatic

Anatomical variations of the cystic duct

Common Fibrous
hepatic duct connection

Gallbladder Cystic
duct

Common B Low D E
a bile dict
junction
C

Figure 13.2  Anatomical variations of the cystic duct. A = Normal; B = Low insertion of cystic duct; C = No
cystic duct; D = Cystic duct joins right hepatic duct; E = Cystic duct passes in front of common bile duct

Applied basic sciences 171

Important relations of the pancreas Figure 13.3  Important relations
of the pancreas

Inferior Coeliac axis Left gastric
vena cava artery

Portal vein Splenic
Common artery
bile duct
Spleen
Right Pancreas
kidney
Left kidney
Colon Hepatic artery
Superior mesenteric
Duodenum artery

Superior mesenteric vein

Anatomy of the two pancreatic ducts Figure 13.4  Anatomy of the two
pancreatic ducts

artery. The inferior pancreaticoduodenal The remaining 25% is arterial blood from
artery is a branch of the superior mesenteric the hepatic artery. Terminal branches of the
artery. The splenic artery supplies the body hepatic portal vein and hepatic artery enter
and tail. It is a direct branch of the coeliac sinusoids in the liver (Figure 13.5). Sinusoids
trunk. The venous drainage corresponds to are distensible vascular channels lined with
the arterial supply and drains into the portal highly fenestrated endothelial cells and
system. bounded circumferentially by hepatocytes.
As blood flows through the sinusoids,
About 80% of the mass of pancreas is plasma is filtered into the space between the
composed of acinar cells. These form the endothelium and hepatocytes. Blood flows
exocrine portion of the gland. The Islets of through the sinusoids and empties into the
Langerhans are dispersed within the gland central vein of each lobule. Central veins
and are islands of endocrine tissue. The islets coalesce into the hepatic veins which leave
consist of Type A (20%), B (70%) and D (10%) the liver and drain into the vena cava.
cells. Type A, B and D cells produce glucagon,
insulin and somatostatin respectively. The intrahepatic biliary apparatus

Physiology of the liver The biliary system is a series of channels and
ducts that conveys bile from the liver into the
Approximately 75% of the blood entering the lumen of the small intestine. Hepatocytes are
liver is venous blood from the portal vein.

172 Chapter 13  Hepatobiliary and pancreatic surgery

Anatomy of the liver sinusoids Figure 13.5  Anatomy of the liver
sinusoids

arranged in ‘plates’ with their apical surfaces system of the spleen. It is not water soluble
facing and surrounding the sinusoids. The and is transported to the liver bound to
basal surfaces of adjoining hepatocytes are albumin. In the liver it is conjugated with
joined together by junctional complexes glucuronic acid, rendering it water soluble
to form bile canaliculi. A canaliculus is the and allowing its excretion in bile.
dilated intercellular space between adjacent
hepatocytes. Hepatocytes secrete bile into Hepatobiliary and
the canaliculi which flows parallel to the pancreatic disease
sinusoids, but in the opposite direction to Obstructive jaundice
the blood flow. At the ends of the canaliculi,
bile enters into the bile ducts, which are true In healthy individuals, serum bilirubin
ducts lined by epithelial cells. Bile ducts are concentrations are low. When biliary
in close proximity to the terminal branches of obstruction occurs, the serum levels of
the portal vein and hepatic artery, and form conjugated bilirubin are increased, resulting
the portal triad. in its accumulation in tissues and its excretion
in the urine. The causes of obstructive
Bile is a complex fluid containing jaundice are shown in Table 13.1. Obstructive
water, electrolytes, bile acids, cholesterol, jaundice can result in several systemic
phospholipids and bilirubin. Adults produce complications.
approximately 500 mL of bile each day.
Bile acids are derivatives of cholesterol Clinical features
synthesised in the hepatocyte. Cholesterol Accumulation of bilirubin in tissues produces
is converted into the bile acids, cholic and jaundice, characterised by the deposition of
chenodeoxycholic acids, which are then yellow bilirubin pigments in the skin, sclerae,
conjugated to an amino acid (glycine or mucous membranes and other tissues.
taurine) to yield a conjugated form that is Patients often complain of itch and may
actively secreted into canaliculi. Bile acids notice pale stools and dark urine.
are important for digestion and absorption
of fats and fat-soluble vitamins in the small Complications
intestine. Vitamin K is required for the γ-carboxylation
of the clotting factors II, VII, IX, XI. It is a fat
Waste products, including bilirubin, are soluble vitamin that is not absorbed in the
eliminated from the body by secretion into presence of obstructive jaundice. Deranged
bile. Bilirubin is a tetrapyrrole and is a normal production of clotting factors can result in
product of haem catabolism. Unconjugated
bilirubin is formed in the reticuloendothelial

Hepatobiliary and pancreatic disease 173

Causes of obstructive jaundice

Common Infrequent Rare

Common bile duct stones Ampullary carcinoma Benign strictures – iatrogenic,
Pancreatitis trauma
Carcinoma of the head of pancreas Liver secondaries Recurrent cholangitis
Mirrizi syndrome
Malignant porta hepatis lymph Sclerosing cholangitis
nodes Cholangiocarcinoma
Biliary atresia
Choledochal cysts

Table 13.1  Causes of obstructive jaundice

a bleeding tendency. Active bleeding or the bile duct obstruction. Transabdominal
need for urgent surgical intervention requires ultrasound has a high sensitivity and
correction of the clotting disorder with specificity for the detection of CBD dilatation
the use of fresh frozen plasma. Parenteral and it may also allow identification of the
administration of vitamin K should also underlying cause. CT or MRI scanning is
be considered but its actions are more useful in the obese or if there is excessive
prolonged. bowel gas. Both imaging modalities are
better at visualising the lower end of the
Hepatorenal syndrome is poorly common bile duct and the pancreas. In
understood. It is defined as renal failure post those with a obstructive jaundice due to a
intervention in a patient with obstructive pancreatic tumour, they allow staging and
jaundice. It is due to Gram-negative the assessment of operability. ERCP allows
endotoxinaemia from the gut. Preoperative biopsies or brush cytology specimens to
lactulose may improve the outcome. be taken, stone extraction to occur or the
insertion of a biliary stent.
Investigation
Management
Investigation of a jaundiced patient will
allow the differentiation of hepatocellular The management of obstructive jaundice
and obstructive jaundice in about 90% involves correction of any complications,
cases. In obstructive jaundice, the serum decompression the biliary tree and treatment
and urine conjugated bilirubin levels are of the underlying cause. Broad spectrum
increased. Other liver function tests will also antibiotic prophylaxis should be given.
be deranged. The increase in serum ALP Parenteral vitamin K and fresh frozen
and GGT is relatively more than the AST plasma may be needed to correct the clotting
and ALT. The converse is seen in patients disorder. Fluid expansion will reduce the risk
with hepatocellular causes of jaundice. of the hepatorenal syndrome.
The albumin may be reduced and the PTT
prolonged. Gallstones

The normal CBD is less than 8 mm in Gallstones are found in about 12% of adult
diameter. The CBD diameter increases with men and 24% of adult women. The prevalence
age and after previous biliary surgery. Its of gallstones increases with advancing age.
diameter is also increased in patients with Only about 10–20% of gallstones ever become

174 Chapter 13  Hepatobiliary and pancreatic surgery

symptomatic. Over 10% of those with stones Biliary colic and acute cholecystitis
in the gallbladder have stones in the common
bile duct. Biliary colic arises as a result of intermittent
obstruction of the cystic duct due to the
Pathophysiology presence of gallstones within Hartmann’s
Three types of stones are recognised: pouch. Acute cholecystitis results from
• Cholesterol stones (15%) persistent obstruction of the cystic duct.
• Mixed stones (80%) Increased pressure within the gallbladder
• Pigment stones (5%) results in an acute inflammatory response.
Cholesterol stones result from a change in Secondary bacterial infection may occur
the solubility of bile constituents. Bile acids in about 20% of cases. The most common
act as a detergent keeping cholesterol in organisms implicated are Escherichia coli,
solution. Bile acids, lecithin and cholesterol Klebsiella and Strep. faecalis.
result in the formation of micelles. Bile is
often supersaturated with cholesterol and Clinical features
this favours the formation of cholesterol
microcrystals. Biliary infection, stasis Biliary colic typically presents with right
and changes in gallbladder function can upper quadrant abdominal pain precipitated
precipitate stone formation. Bile is infected by food. The pain may radiate to the back and
in 30% of patients with gallstones. Gram- scapula and usually resolves spontaneously
negative organisms are the most common after 30 minutes to a few hours. Systemic
isolated. Mixed stones are probably a variant upset is mild and abdominal signs may be
of cholesterol stones. Pigment stones are minimal. In contrast, acute cholecystitis
small, dark stones made of bilirubin and presents with constant pain of longer
calcium salts. They contain less than 20% of duration. This is often associated with fever,
cholesterol (Figure 13.6). Only about 10% tachycardia and localised tenderness in right
of gallstones are radio-opaque. The clinical upper quadrant. Murphy’s sign, guarding in
presentations of gallstones include: right upper quadrant on deep inspiration,
• Biliary colic may be present. Jaundice is uncommon in
• Acute cholecystitis uncomplicated acute cholecystitis.
• Empyema of the gallbladder
• Mucocele of the gallbladder Complications of acute cholecystitis
• ‘Flatulent dyspepsia’ include:
• Mirizzi’s syndrome
• Obstructive jaundice • Gangrenous cholecystitis
• Pancreatitis • Gallbladder perforation
• Acute cholangitis • Cholecystoenteric fistula
• Gallstone ileus
Multiple pigment stones in a gallbladder
Investigation
Figure 13.6  Multiple pigment stones in a gallbladder
Ultrasound is the initial investigation of
choice. In patients with biliary colic, stones
may be seen within a normal gallbladder.
In acute cholecystitis, the diagnostic
features include the presence of gallstones,
a distended thick-walled gallbladder,
pericholecystic fluid and Murphy’s sign
demonstrated with the ultrasound probe. The
common bile duct should also be visualised
and its diameter assessed. Liver function tests
are often normal but inflammatory markers
may be raised. A dilated common bile duct
and deranged liver function indicate the need
for further assessment for the presence of
common bile duct stones.

Hepatobiliary and pancreatic disease 175

Management is still approximately 0.5%. Complications
include:
The initial management of acute cholecystitis
is usually conservative. The patient is fasted, • Bile duct damage
given intravenous fluids and opiate analgesia. • Retained stones
Intravenous antibiotics should be given to • Bile leak
prevent secondary infection. Overall, about • Wound dehiscence
80% patients improve with conservative • Pulmonary atelectasis
treatment.
The morbidity associated with open
If fit, patients should be considered for a surgery lead to the development firstly of
laparoscopic cholecystectomy. The timing ‘mini’ cholecystectomy through a short
of surgery is controversial. Evidence now transverse incision and then laparoscopic
suggests that early surgery, less than 72 cholecystectomy, introduced in 1988. About
hours after the onset of symptoms, is safe. It 40,000 cholecystectomies are performed
has a lower conversion rate and avoids the annually in the UK. More than 4000 common
complications of conservative treatment bile ducts are cleared of stones.
failure. If patient are unfit for surgery,
percutaneous cholecystotomy may be Laparoscopic cholecystectomy
beneficial. It may be particularly useful in
patients with acalculus cholecystitis. Laparoscopic cholecystectomy has been
shown to be equally as effective as open
Mirizzi’s syndrome cholecystectomy and is associated with
reduced morbidity and a faster postoperative
The Mirizzi’s syndrome refers to common recovery. The conversion rate to an open
hepatic duct obstruction caused by an procedure is about 5%.
extrinsic compression from an impacted
stone in the cystic duct or Hartmann pouch of Preoperative ERCP is indicated if:
the gallbladder. Obstruction occurs because
of either mechanical obstruction or because • Recent jaundice
of inflammation around the common hepatic • Abnormal liver function tests
duct. Patients present with right upper • Significantly dilated common bile duct
quadrant abdominal pain and jaundice. • Ultrasonic suspicion of bile duct stones

Acute cholangitis Technique

Acute cholangitis results from infection in The routine use of a nasogastric tube and
an obstructed biliary tree, usually as a result urinary catheter is controversial and both are
of gallstones. The classical clinical picture usually avoided. A CO2 pneumoperitoneum is
consists of intermittent right upper quadrant induced using either a Veress needle or open
abdominal pain, jaundice and fever – the technique. The open (Hasson) technique
Charcot triad. Patients often have features is believed to be safer. Over half of bowel
of severe sepsis and untreated, it can lead injuries that occur during a laparoscopic
to hepatic abscess formation. Management cholecystectomy are caused by either the
is with parenteral antibiotics and biliary Veress needles or trocars. The abdominal
decompression. Operative mortality in the pressure should be set to 12–15 mmHg.
elderly is up to 20% but early endoscopic Higher intra-abdominal pressure can reduce
drainage has been shown to decrease pulmonary compliance, decrease venous
mortality by up to 30%. return and result in higher end-tidal CO2
levels. Surgery is usually performed using four
Treatment of gallbladder stones standard ports (2 × 10 mm and 2 × 5 mm).
The patient is positioned with head up tilt and
In 1882 the first open cholecystectomy was rolled to the left. Calot triangle is dissected
performed by Langenbuch in Berlin. It was using a retrograde technique. The cystic duct
associated with significant complications. and artery are identified and ligated with
Today mortality for open cholecystectomy clips or endo-loops. About 50% surgeons
routinely use intraoperative cholangiography.

176 Chapter 13  Hepatobiliary and pancreatic surgery

Cholangiography allows definition of An ERCP showing stones in the
the biliary anatomy and identification of common bile duct
unsuspected common bile duct stones found
in about 10% of patients. Figure 13.7  An ERCP showing stones in the
common bile duct
Bile duct injury About 80% of patients have mild disease with
a low-risk of complications and negligible
Bile duct injury occurs in between mortality. However, a small proportion of
0.1% and 0.5% of patients undergoing patients have severe disease. About 40% of
laparoscopic cholecystectomy. The risk these develop life-threatening complications
is related to surgical inexperience and including infected pancreatic necrosis. The
problems identifying the biliary anatomy. mortality associated with infected pancreatic
The outcome is improved if recognised at necrosis is about 50%.
time of initial surgery. For most injuries
hepaticojejunostomy is the treatment of Aetiology
choice. If the recognition of the injury is Gallstones and alcohol account for 80% of
delayed, then the complication is associated cases of acute pancreatitis. Aetiological factors
with higher morbidity and mortality. include:
Management then requires drainage of
collections and control of sepsis. Long-
term risks include stricture formation and
cirrhosis.

Common bile duct stones

Accurate prediction of the presence of
common bile duct stones can be difficult.
The common bile duct can be imaged by
ultrasound, MRCP and ERCP (Figure 13.7).
The latter is the investigation of choice
as it is both diagnostic and therapeutic.
A sphincterotomy can be performed and
common bile duct stones can be extracted
with either balloons or a Dormia basket. If
necessary, a biliary stent can be inserted.

Stone extraction is about 90% successful
but has a complication rate of approximately
5%. Mortality is less than 1%. If stone
extraction fails, patient will require:

• Open cholecystectomy and exploration of
the common bile duct

• Laparoscopic exploration of common bile
duct

• Mechanical lithotripsy

If stones are retained after exploration of the
common bile duct, then consideration needs
to be given to:

• Early ERCP
• Exploration via T-tube tract at 6 weeks

Acute pancreatitis

Epidemiology

In the UK, the incidence of acute pancreatitis
is about 50 per 100,000 population per year.

Hepatobiliary and pancreatic disease 177

• Idiopathic pancreatitis. A serum amylase of three times
• Obstruction – choledocholithiasis, the upper limit of normal has a sensitivity and
specificity of 60% and 95%, respectively. About
pancreatic tumours 20% of patients with acute pancreatitis have a
• Pancreatic structural anomalies normal serum amylase, particularly if alcohol
• Toxins – alcohol, drugs (e.g. salicylates, is an important aetiological factor. Serum
lipase is more sensitive and may remain
azathioprine, cimetidine) elevated longer but is not routinely measured.
• Trauma – accidental, iatrogenic Other causes of hyperamylasaemia include:
• Metabolic abnormalities
• Infection • Perforated peptic ulcer
• Vascular anomalies • Cholecystitis
• Generalised peritonitis
About 20% of cases of acute pancreatitis are • Intestinal obstruction
idiopathic. Gallstones less than 5 mm in • Mesenteric infarction
diameter are more likely to cause pancreatitis • Ruptured abdominal aortic aneurysm
than larger ones. Less than 5% of patients • Ruptured ectopic pregnancy
with gallstones develop pancreatitis.
CT scanning of the abdomen is the
Clinical features standard imaging modality for evaluating
acute pancreatitis and its complications
The classic presentation of acute pancreatitis (Figure 13.8). Typical CT findings in
is with sudden onset severe epigastric pain. acute pancreatitis include focal or diffuse
The pain is constant in nature and radiates enlargement of the pancreas, heterogeneous
through to the back. Patients are often pyrexial enhancement of the gland, irregular contour
and dehydrated. Tenderness may be localised of the pancreatic margins, blurring of the
to epigastrium or generalised. Eponymous peripancreatic fat planes and the presence
signs of retroperitoneal haemorrhage are of intraperitoneal or retroperitoneal
rare and appear late but include Cullen’s fluid collections. Complications of acute
and Grey Turner’s signs. The differential pancreatitis such as pseudocysts, abscess
diagnosis includes perforated peptic ulcer, formation, pancreatic necrosis, venous
acute cholecystitis and mesenteric ischaemia. thrombosis, pseudoaneurysm development
Complications of acute pancreatitis can be and haemorrhage can also be recognised.
local or systemic (Table 13.2). Pancreatic necrosis is recognised by failure
of the pancreas to enhance after intravenous
Investigation contrast administration.

Serum amylase has a low sensitivity and Abdominal ultrasound is the ‘gold
low specificity for the diagnosis of acute standard’ investigation for the detection
of gallstones. Gallstone may not be visible
Complications of acute pancreatitis on abdominal CT scanning. Clinical and
biochemical that features suggest a gallstone
Local Systemic aetiology include:

Necrosis possibly with Hypovolaemia and • Female sex
infection shock • Age more than 50 years
Coagulopathy • Amylase more than 4000 IU/L
Pancreatic fluid Respiratory failure • Bilirubin more than 35 μmol/L
collections Renal failure • Increased AST
Hyperglycaemia • Increased ALP
Colonic necrosis Hypocalcaemia
Prognostic factors
Gastrointestinal
haemorrhage Half of all deaths from acute pancreatitis
occur within the first week due to multi-organ
Splenic artery failure. This usually occurs in the absence of
aneurysm local complications. Late deaths are often

Table 13.2  Complications of acute pancreatitis

178 Chapter 13  Hepatobiliary and pancreatic surgery

An abdominal CT scan showing acute pancreatitis Figure 13.8  An abdominal CT
scan showing acute pancreatitis

due to local complications. Mortality from Ransom’s criteria are not ideal. They can not
pancreatitis is due to: be applied fully for 48 hours and are also a
poor predictor later in the disease. They have
• Early multiple organ failure been described as a ‘single snapshot in a
• Late infected pancreatic necrosis whole feature length of the film’. APACHE II
• Haemorrhage is a multivariate scoring system. It measures
• Associated co-morbidity objective parameters – vital signs and
biochemical analysis. It takes account of the
Most patients with acute pancreatitis have premorbid state and age and can be used
mild disease which accounts for less than 5% throughout the course of the illness.
of the mortality from the disease. The aim
of prognostic scores is to identify patients Management
with severe disease, allowing them to be
more closely monitored in an intensive care The aims of treatment of acute pancreatitis
environment. The scoring systems need to are to halt the progression of the local disease
have a high sensitivity and specificity and and to prevent remote organ failure. In severe
ideally should be applicable on admission. disease, this requires full supportive therapy
Ranson’s criteria are measured both on often in ITU or HSU environment.
admission and at 48 hours.
All patients should be monitored with a
Ransom’s criteria scored on admission: urinary catheter. A CVP line and arterial line
should be considered in those with significant
• Age more than 55 years physiological derangement. There should
• WCC more than 16,000 be regular assessment of serum electrolytes,
• LDH more than 600 U/L calcium, blood sugar and liver function tests.
• AST more than 120 U/L Patients require fluid resuscitation with both
• Glucose more than 10 mmol/L colloid and crystalloid, correction of hypoxia
with an increased FiO2 and the administration
Ransom’s criteria scored within 48 hours: of adequate analgesia.

• Haematocrit fall more than 10% Antibiotic prophylaxis is useful in those
• Urea rise more than 0.9 mmol/L with severe pancreatitis. ERCP maybe of
• Calcium less than 2 mmol benefit within the first 48 hours in patients
• pO2 less than 60 mmHg with predicted severe gallstone disease.
• Base deficit more than 4
• Fluid sequestration more than 6 L

Hepatobiliary and pancreatic disease 179

Nutritional support is important. Pancreatitis walled peri-pancreatic fluid collection. It has
is associated with a catabolic state. The no epithelial lining and the fluid has a high
benefit of pancreatic ‘rest’ by limiting oral amylase content. Acute fluid collections are
intake is unproven and there is evidence that not pseudocysts and the collection needs to be
early enteral nutrition is safe. Nasojejunal present for at least a month to be regarded as
feeding limits pancreatic secretion and is a pseudocyst. The diagnosis may be suggested
preferable to oral or nasogastric feeding. by continuing abdominal pain and vomiting
and the persistent elevation of the serum
All patients with pancreatitis should amylase. Pseudocysts can be classified as:
undergo an ultrasound within 24 hours
of admission. If it confirms gallstones and • Type 1 – Normal duct anatomy. No fistula
the patient has severe pancreatitis, then between duct and cyst
consideration should be given to early ERCP. If
the patient fails to settle during the first week • Type 2 – Abnormal duct anatomy and no
of admission, a contrast enhanced CT should fistula present
be used to assess for the presence of pancreatic
necrosis. If there is clinical or radiological • Type 3 – Abnormal duct anatomy and
suspicion of pancreatic abscess formation, then fistula present
consideration should be given to CT-guided
aspiration. A pancreatic necrosectomy may Investigation
be required if these is clinical deterioration An abdominal ultrasound will allow
and bacteriological proof of infection. The assessment of changes in the size of the
operative mortality associated with pancreatic cyst and an abdominal CT will allow its
necrosectomy is more than 40%. relationship to adjacent organs to be defined
(Figure 13.9). An ERCP should be considered
Pseudocysts to define the pancreatic duct anatomy.

Peripancreatic fluid collections are common Management
after an episode of pancreatitis. About 35% of The treatment options for a pancreatic
patients with acute pancreatitis will develop a pseudocyst include:
peri-pancreatic fluid collection but more than
50% of these will resolve spontaneously over • Percutaneous drainage
a 3-month period. A pseudocyst is a fibrous • Endoscopic drainage
• Surgical drainage

An abdominal CT scan showing a pancreatic pseudocyst Figure 13.9  An abdominal
CT scan showing a pancreatic
pseudocyst

180 Chapter 13  Hepatobiliary and pancreatic surgery

Percutaneous drainage can be either by Investigation
ultrasound or CT guidance. It is about 80%
successful in those with Type 1 cysts. The Blood tests may show a raised white cell
outcome is less certain if there is a fistula count, increased ESR and deranged liver
to the pancreatic duct or abnormal duct function tests. Chest x-ray often shows a
anatomy (Type 2 and 3 cysts). These patients raised right hemidiaphragm and pleural
require either endoscopic or surgical effusion. An abdominal ultrasound will
drainage. Endoscopic drainage and insertion localise the abscesses and will guide drainage.
of pigtail catheter can be performed by a A CT scan may be useful if the diagnosis is in
transpapillary or transmural route. Surgical doubt or if there are multiple abscesses.
drainage can be by a cystogastrostomy or
a Roux-loop cystojejunostomy. Surgery Management
allows adequate internal drainage and a
biopsy of the cyst wall can taken to exclude a Patients should be started on appropriate
cystadenocarcinoma. Surgery is associated antibiotics. Percutaneous drainage
with a higher risk of complications but a under ultrasound guidance is the initial
lower cyst recurrence rate. treatment of choice. If biliary obstruction is
present, consideration should be given to
Pyogenic liver abscess decompression by either ERCP or the use
of a percutaneous drain. Surgery may be
Pyogenic liver abscesses are usually seen required if there is failure of resolution with
in elderly and infirm patients. They can be percutaneous drainage or intraperitoneal
multiple or solitary and arise as a result of rupture occurs. Both situations are
biliary sepsis. The mortality is high as the associated with a high mortality.
diagnosis is often delayed. The commonest Laparoscopic drainage may succeed after
organisms involved are: failure of the percutaneous route.

• Escherichia coli Amoebic liver abscess
• Klebsiella
• Proteus Amoebic liver abscesses are due to infection
• Bacteroides species with the protozoan parasite, Entamoeba
histolytica. It is found in the stool of carriers
Aetiology in the cystic or trophozoite form. It is
transmitted by the faecal–oral route. The
The causes of pyogenic liver abscess are: liver is the commonest extraintestinal site
of infection. About 10% of affected patients
• Portal pylophlebitis – appendicitis, develop liver abscesses. The abscesses
diverticulitis or pelvic infections can be solitary or multiple. About 80% of
abscesses develop in the right lobe of the
• Biliary disease – cholecystitis, ascending liver. They can present several years after
cholangitis or pancreatitis intestinal infection.

• Trauma – blunt or penetrating Clinical features
• Direct extension – empyema of the gall­
Patients present with malaise, pyrexia and
bladder, subphrenic or perinephric abscess weight loss. The right hypochondrial pain is
• Septicaemia often mild. Less than 20% of patients present
• Infected liver cysts or tumours with diarrhoea. Jaundice is uncommon.
Complications can arise as a result of
Clinical features abscess rupture or extension of infection.
Complications occur in 5% of patients and
Patients are generally systemically unwell. include:
They often have severe abdominal pain
usually localised to the right hypochondrium • Amoebic empyema
accompanied by a swinging pyrexia, • Hepato-bronchial fistula
rigors and weight loss. About 25% present • Lung abscess
with jaundice. Examination may show a
hypochondrial or epigastric mass. About 30%
of patients have a pleural effusion.

Hepatobiliary and pancreatic disease 181

• Pericarditis pain. Only 15% of patients become jaundiced.
• Peritonitis Other features include skin rashes, pruritus
and allergic reactions. Cysts can rupture
Investigation resulting in a bronchobiliary fistula.
Blood tests will show a raised white cell count
and ESR. A latex agglutination assay is positive Investigation
in more than 90% patients. Sigmoidoscopy,
stool microscopy and rectal biopsy may About 30% of patients have an eosinophilia.
identify the organism. A chest x-ray may show The diagnosis can be confirmed by an indirect
a raised right hemidiaphragm, atelectasis or haemagglutinin assay. A plain abdominal
abscess. The abscess can often be identified x-ray may show calcification in the cyst wall.
on ultrasound. Aspiration produces a typical Cysts can be imaged with ultrasound or CT.
‘anchovy sauce’ appearing pus. The pus is Aspiration should not be performed if hydatid
odourless and sterile on routine culture. disease is suspected as this is associated
with risk of dissemination of infection or
Management anaphylaxis.
Metronidazole is the antibiotic of choice.
If it is ineffective, chloroquine and Management
dehydroemetine may be considered.
Ultrasound-guided aspiration may be useful. Pharmacological treatment is not curative but
Surgery is rarely required. The prognosis in is used as an adjunct to surgery to kill spilled
uncomplicated cases is good with a mortality scolices. The drugs of choice are albendazole,
of less than 1%. If pulmonary complications mebendazole and praziquantel. If surgery
occur, mortality can be as high as 20%. is required, a laparotomy is performed to
exclude other cysts. The liver is packed off with
Hydatid disease hypertonic saline-soaked swabs. Cysts are
then decompressed with a trocar and cannula
Hydatid disease is due to infection with the Scolicidal agent (e.g. hypertonic saline or
helminth, Ecchinococcus granulosa. The adult 0.5% silver nitrate) can be injected into the
worm is normally found in the dog and sheep cyst cavity. The cavity is filled with saline and
intestine. Man is an accidental intermediate a suction drain inserted. Alternatively, liver
host. Human infection is most commonly cysts can be excised. Hepatic resection may be
seen in Mediterranean areas, Australia and required for recurrent cysts. The recurrence
South America. The liver is the commonest rate is approximately 5% at 5 years.
organ involved but the lung, brain and bone
can also be infected. Cysts are unilocular, Hepatocellular carcinoma
can be up to 20 cm in diameter and may be
multiple. Daughter cysts may develop. About Hepatocellular carcinoma (HCC) is a
70% of cysts develop in the right lobe of the primary malignant tumour of the liver. It
liver. Pathologically, hydatid liver cysts have is uncommon in northern Europe where
three distinct layers: hepatic secondaries are 30 times more
common than primary liver tumours. The
• Ectocyst – fibrous adventitial layer due to highest incidence is seen in east Africa and
host response south-east Asia. In these areas, it is one of
the commonest malignant tumours. The
• Middle layer – laminated membrane of male:female ratio is 4:1. In Europe, the peak
proteinaceous material age at presentation is 80 years. In Africa
and Asia, the peak age at presentation is 40
• Endocyst – inner germinal layer from years.
which the scolices may be detached
Aetiology
Clinical features
The clinical presentation is often non-specific The incidence of HCC parallels the world-
and patients may be asymptomatic. About wide prevalence of hepatitis. Aetiological
60% have right hypochondrial abdominal factors include:

182 Chapter 13  Hepatobiliary and pancreatic surgery

• Cirrhosis After resection, 5-year survival is typically
• Viral hepatitis – particularly Hepatitis B 30–60%. The 5-year recurrence rate is over 80%.
Only a small proportion of patients are cured.
and C
• Mycotoxins – aflatoxin produced by Liver transplantation may be considered
for irresectable disease confined to the liver.
Aspergillus flavus The operative mortality is often 10–20%.
• Alcohol Metastases after transplantation occur in
• Anabolic steroids 30–40% of patients. After transplantation,
• Primary liver diseases – primary biliary 5-year survival is less than 20%.

cirrhosis, haemochromatosis Most patients are only suitable for
palliative treatment. The median survival in
Clinical features those with irresectable disease is 6 months.
Possible palliative interventions include:
The possibility of a HCC should be suspected in
any patient with cirrhosis who shows evidence • Devascularisation procedures
of clinical deterioration. The commonest • Chemotherapy
clinical features are right hypochondrial pain • Cryotherapy
and an abdominal mass. Malaise, weight • Chemo-embolisation
loss and low grade pyrexia are often present. • Thermotherapy
Jaundice is a late feature. Haemobilia or
haemoperitoneum are often the immediate Chemo-embolisation improves survival
cause of death. As most tumours present compared to conservative treatment alone.
late, screening of high-risk patients has been
advocated in countries with a high prevalence. Cholangiocarcinoma

Investigation Cholangiocarcinoma is a rare tumour of
the biliary tree. It accounts for about 1000
Tumours can be imaged by ultrasound – deaths per year in UK. It arises from the
transabdominal or laparoscopic, CT scanning epithelium of the biliary tract. About 25%
or CT portography. Assessment of serum are intrahepatic. It often presents late with
a-fetoprotein (aFP) may also be useful. aFP irresectable disease. Cure rates are low and
is a normal fetal serum protein produced by the median survival is less than 12 months.
the yolk sac and liver. Progressive increases Neoadjuvant and adjuvant therapies have
in serum levels are seen in 70–90% of not improved survival. Risk factors for
patients with HCC. Slightly increased and cholangiocarcinoma include:
often fluctuating serum levels also seen
in hepatitis and cirrhosis. In patients with • Age
HCC, serum levels correlate with tumour • Primary sclerosing cholangitis
size and the rate of increase in serum levels • Choledocholithiasis
correlates with growth of the tumour. Tumour • Biliary papillomatosis
resection usually results in a fall in serum • Choledochal cysts
concentrations and serial assessment is • Thorotrast
useful in measuring response to treatment. • Liver flukes (Clonorchis sinesis)

Management Clinical features
Most patients present with obstructive
Only about 25% patients with HCC are suitable jaundice. Pain and fever are uncommon.
for surgery. The two surgical options are Late presentation is associated with fatigue,
surgical resection or liver transplantation. malaise and weight loss. Some cases
Surgical resection involves either hemi- are found incidentally when imaging is
hepatectomy or segmental resection. Most performed for other reasons.
tumours are irresectable due to large size,
involvement of major vessels, associated Investigation
advanced cirrhosis or metastatic disease. The Liver function tests usually show an
presence of cirrhosis increases the operative obstructive picture. Serum CA19.9 and
mortality from about 5% to more than 20%.

Hepatobiliary and pancreatic disease 183

CA125 may be raised. The diagnosis can be presence of vascular invasion. Spiral CT has
confirmed by CT or MRI. An ERCP can be improved on the resolution of conventional
both diagnostic and therapeutic. Specimens CT imaging. Contrast-enhanced triple-phase
can be obtained for cytology or histology and imaging is the imaging modality of choice.
a biliary stent can be inserted. It has sensitivity of greater than 95% for
detection of pancreatic tumours and until
Management recently was probably the most useful of
staging investigations. MRI is increasingly
Surgery offers the only chance of cure. been used for imaging of the pancreas.
The tumour is resected and biliary However, both ultrasound and CT often
reconstruction is performed. The aim is fail to detect small hepatic metastases.
for resection with tumour-free margins. Laparoscopy will identify liver or peritoneal
Determinants of resectability are the metastases in 25% of patients deemed
extent of the tumour, vascular invasion, resectable after conventional imaging. The
hepatic lobar atrophy and the absence of use of laparoscopic ultrasound may improve
metastatic disease. Liver transplantation in the predictability of resection.
cholangiocarcinoma is controversial due to
high recurrence rates. Management

Pancreatic carcinoma Pancreatic resection is the only hope of
cure but only 15% of tumours are deemed
Pancreatic carcinoma is the second resectable. Resectability is determined by
commonest tumour of the digestive system. assessment of tumour size (<4 cm), absence
The incidence is increasing in the Western of invasion of the superior mesenteric
world. It is uncommon below 45 years of age. artery or portal vein and the absence of
More than 80% of cases occur between 60 and ascites, nodal, peritoneal or liver metastases.
80 years of age. The male:female ratio is 2:1. Overall, 75% of patients have metastases at
Most tumours are adenocarcinomas. More presentation. Preoperative biliary drainage
than 80% occur in the head of the pancreas. is of unproven benefit and has not been
Overall 5-year survival is less than 5%. The shown to reduce postoperative morbidity or
prognosis of ampullary tumours is much mortality.
better.
Whipple’s operation
Clinical features
A Whipple’s procedure involves a
About 30% of patients present with pancreatico-duodenal resection
obstructive jaundice. This is classically (Figure 13.10). An initial assessment of
described as ‘painless jaundice’. However, resectability is performed by dissection
most patients develop pain at some stage and Kocherisation of the duodenum.
and 50% present with epigastric pain. About The head of the pancreas and duodenum
90% of patients develop anorexia and weight are excised followed by an end-to-side
loss. Abdominal examination may show the pancreaticoduodenostomy, an end-to-
gallbladder to be palpable. Courvoisier’s Law side choledochoduodenostomy and
states that if in the presence of jaundice the gastrojejunostomy. Octreotide can be given
gallbladder is palpable, it is unlikely to be due for 1 week to reduce pancreatic secretion.
to gallstones. Operative mortality in experienced centres is
less than 5%. In those suitable for resectional
Investigation surgery, 5-year survival is still only 30%.
Postoperative morbidity is 30–50%. About
Abdominal ultrasound has sensitivity of 10% of patients develop diabetes and 30%
about 80% for the detection of pancreatic of patients require postoperative exocrine
cancer. It can detect the level of biliary supplements. Postoperative adjuvant
obstruction, excludes gallstones and may chemotherapy may improve survival.
identify the pancreatic mass. Doppler
ultrasound allows assessment of the

184 Chapter 13  Hepatobiliary and pancreatic surgery

Postoperative anatomy following a Whipple’s procedure Figure 13.10  Postoperative
anatomy following a Whipple’s
procedure. A, gastrojejunostomy;
B, pancreaticoduodenostomy; C,
choledochoduodenostomy.

Complications of a Whipple’s procedure Complications include bleeding, perforation,
include: pancreatitis and it has a mortality less than
3%. However, about 20% of patients who
• Delayed gastric emptying undergo palliative stenting will develop
• Gastrointestinal haemorrhage duodenal obstruction. The patency of plastic
• Operative site haemorrhage stents is often only 3 to 4 months but this can
• Intra-abdominal abscess be improved with the use of self-expanding
• Pancreatic fistula metal metal wall stents.

Pylorus-preserving proximal Biliary drainage can also be
pancreaticoduodenectomy achieved by choledochojejunostomy
or cholecystojejunostomy. About 10%
A pylorus-preserving proximal of these patients will develop duodenal
pancreaticoduodenectomy preserves the obstruction. A ‘triple bypass’ involves a
gastric antrum and pylorus. Compared with choledochojejunostomy, gastrojejunostomy
a Whipple’s procedure, it is associated with and entero-enterostomy. This removes the
reduced morbidity, fewer post gastrectomy risk of duodenal obstruction and often avoids
symptoms and less entero-gastric reflux. recurrent jaundice.
There is improved postoperative nutrition but
no difference in mortality. There are concerns Pain occurs in over 80% of patients with
that there may be an associated increased risk advanced malignancy and can be palliated
of local recurrence. with:

Palliative treatment • Slow release morphine
• Coeliac nerve block
About 85% of patients with pancreatic • Thoracoscopic section of the splanchnic
cancer are not suitable for curative resection.
Palliation of symptoms can be achieved nerves
either surgically or endoscopically. Surgical
palliation has initially a higher complication Pancreatic neuroendocrine
rate but produces better long-term symptom tumours
control. Palliative treatment should achieve
relief of jaundice by either endoscopic The pancreas is derived embryologically
stenting or surgery, prevention of duodenal from the foregut. It has both exocrine and
obstruction by gastrojejunostomy and relief endocrine components. The endocrine
of pain possibly by a coeliac plexus block. components are within the Islets of
External biliary drainage is rarely required. Langerhans with various cell types:

Endoscopic stenting of the common bile •  a cells secrete glucagon
duct is achievable in over 95% of patients. •  b cells secrete insulin
•  d cells secrete somatostatin

Hepatobiliary and pancreatic disease 185

Endocrine tumours arise from the Islets of the presence of metastatic disease. Octreotide
Langerhans and may produce hormones. may help control symptoms.
They may be associated with the multiple
endocrine neoplasia (MEN) syndromes. Chronic pancreatitis

Insulinomas Chronic inflammation of the pancreas
results in irreversible destruction of both the
Insulinomas are rare. The annual incidence endocrine and exocrine pancreatic tissue.
in the UK is 1–2 per million population. The male to female ratio is approximately
They are usually solitary and can occur at 4:1. The mean age of onset is 40 years.
any age. They are slightly more common in The incidence is increasing. Chronic
women. Approximately 90% are less than pancreatitis increases the risk of pancreatic
2 cm in diameter, 90% are benign and 10% are carcinoma. Early stages of the disease
associated with MEN Type 1 syndrome. The may be characterised by episodes of acute
symptoms of an insulinoma are non-specific pancreatitis and the pancreas may appear
and variable and may be induced by exercise. macroscopically normal. The late stages
The symptoms are those of hypoglycaemia. of disease are characterised by pancreatic
The diagnosis can be difficult. It is necessary fibrosis and calcification. Pancreatic duct
to demonstrate hypoglycaemia in the dilatation and stricture formation may occur.
presence of symptoms. Insulin levels are Cysts form within the pancreatic tissue.
usually normal or raised. Serum C-peptide Aetiological factors include:
levels are often increased. The diagnosis can
be confirmed by CT. Resection offers the only • Alcohol
chance of cure. The 10-year survival rate is • Tobacco
over 90%. Hepatic artery embolisation and • Pancreatic duct strictures
chemotherapy maybe required in metastatic • Pancreatic trauma
disease. • Hereditary pancreatitis
• Tropical pancreatitis
Gastrinomas
Clinical features
Gastrinomas occur in both the duodenum
and pancreas. Gastrin over-production results Pain is the principal symptom in most
in the Zollinger–Ellison syndrome. Patients patients, usually epigastric and radiating
presents with severe peptic ulcer disease and to the back. The pain may be continuous
diarrhoea. About 20% of patients have MEN or episodic, often interferes with life and
type 1 syndrome. Gastric acid hypersecretion may lead to opiate abuse. Weight lost may
can be controlled by either a proton pump occur. Loss of exocrine function produces
inhibitor or surgery. Historically, total malabsorption and steatorrhoea. Loss of
gastrectomy was performed and the tumour endocrine function results in diabetes.
was left in situ. Today the tumour can be
removed by either distal pancreatectomy, Investigation
enucleation, duodenectomy or a Whipple’s
procedure. Patients with metastatic disease The serum amylase is often normal. A plain
can be managed with chemotherapy or abdominal x-ray may show pancreatic
α-interferon. calcification. CT or MRI is the most useful
investigation for imaging the pancreas and
Glucagonomas may confirm pancreatic enlargement, fibrosis
and calcification. ERCP has a high sensitivity
Glucagonomas are rare and occur as part of for detecting chronic pancreatitis. An MRCP
the MEN type 1 syndrome. Metastatic disease will outline the state of the pancreatic ducts.
is often detected at presentation. Symptoms Pancreatic function test rarely provide useful
are often non-specific but patients may have a information.
characteristic rash and mucositis. The diagnosis
is confirmed by the detection of a raised serum Management
glucagon. Surgery may be beneficial even in
Treatment of the early stages of the disease
is with a low fat diet. Alcohol abstention is

186 Chapter 13 Hepatobiliary and pancreatic surgery
  
essential. Opiate analgesia should be avoided The aetiology of portal hypertension can be

if possible. Pancreatic enzyme supplements prehepatic, intrahepatic or posthepatic

may reduce both the steatorrhoea and the (Table 13.3).

frequency of painful crises. Pathophysiology

Surgery Increased portal pressure reduces portal

Surgery is associated with significant venous flow. It encourages the development

morbidity and mortality. It does not of porto-systemic anastomoses. Theses

arrest the loss of endocrine and exocrine develop at sites of connections between the

function. The aim of surgery is to remove portal and systemic circulation at the:
any mass lesion and relieve pancreatic duct
obstruction. A mass lesion can be removed • Gastro-oesophageal junction
by pancreaticoduodenectomy or a Beger’s • Lower rectum
• Peri-umbilical veins
.ir/procedure – resection of the pancreatic • Retroperitoneal veins of Retzius
• Peri-hepatic veins of Sappey
head with preservation of the duodenum.
Pancreatic duct obstruction can be relieved Clinical features
by pancreaticojejunostomy or a Frey’s
Cirrhosis is the commonest cause of
sprocedure in which the diseased portion of portal hypertension in the UK. Cirrhosis
sthe pancreatic head is excised and a lateral produces features of hepatocellular failure,
portal hypertension, variceal bleeding and
pancreaticojejunostomy is fashioned. Disease ascites. About 90% of patients with cirrhosis
will develop oesophageal varices. Upper
nconfined to pancreatic tail may require distal gastrointestinal bleeding will occur in 30%
iapancreatectomy. Surgery relieves symptoms of these patients. The severity of cirrhosis
can be assessed using the Child–Pugh
in about 75% of patients. classification (Table 13.4) and can be divided
into three groups:
rsPortal hypertension

The normal portal venous pressure is

e5–10 mmHg. Portal hypertension is defined
.pas a portal pressure more than 12 mmHg.
://vipPrehepatic
Aetiology of portal hypertension
Portal vein thrombosis
Splenic vein thrombosis Intrahepatic Posthepatic
Presinusoidal Caval abnormality
ttpTropical splenomegaly Schistosomiasis Constrictive pericarditis
hArterio-venous fistula Primary biliary cirrhosis
Chronic active hepatitis
Sarcoidosis

Sinusoidal

Cirrhosis – post hepatitic, alcohol,
cryptogenic, metabolic

Non-cirrhotic – cytotoxic drugs, Vitamin A
intoxication

Postsinusoidal

Budd–Chiari syndrome

Veno-occlusive disease

Table 13.3 Aetiology of portal hypertension