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The gallbladder and bileducts 345
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Box 33.1 Abdominal colic
Colicky pain is the result of smooth muscle
contraction against a resistance. The common
causes of colic occur in the uterus and fallopian
tubes, renal tract, intestinal tract and biliary tract.
Biliary tract
•
Stone in Hartmann’s pouch.
•
Stone in cystic duct.
•
Stone in sphincter of Oddi.
Renal tract
•
Ureteric colic due to stone, blood clot or tumour.
•
Bladder colic in acute retention owing to enlarged
prostate.
Intestinal tract
•
Mechanical obstruction.
•
Appendicular colic as appendix lumen occludes.
Uterus and Fallopian tubes
•
Parturition.
•
Menstruation.
•
Ectopic pregnancy in a fallopian tube.
intensifies. There is a fever in the range of 38–39 °C with
marked toxaemia and leucocytosis. The upper abdomen is extremely tender, and a palpable mass may
develop in the region of the gallbladder. This represents
the distended, inflamed gallbladder wrapped in inflammatory adhesions to adjacent organs, especially the
omentum. Occasionally, an empyema of the gallbladder develops or, rarely, gallbladder perforation into the
liver or general peritoneal cavity takes place. The swollen gallbladder may press against the adjacent common bile duct and produce a tinge of jaundice, even
though stones may be absent from the duct system.
five per cent of cases of acute cholecystitis
Ninetyare associated with gallstones. Occasionally, fulminating acalculous cholecystitis may occur and this may be
associated with typhoid fever or gas gangrene.
The differential diagnosis is from acute appendicitis, perforated duodenal ulcer, acute pancreatitis,
right basal pneumonia and coronary thrombosis.
Chronic cholecystitis
This is almost invariably associated with the presence
of gallstones. Repeated episodes of inflammation
result in chronic fibrosis and thickening of the entire
gallbladder wall, which may contain thick, sometimes
infected bile.
There are recurrent bouts of abdominal pain owing
to mild cholecystitis, which may or may not be accompanied by fever. Discomfort is experienced after fatty
meals as the gallbladder contracts onto the stones;
there is often flatulence. The picture may be complicated by episodes of acute cholecystitis or symptoms
produced by stones passing into the common bile duct.
The differential diagnosis is from other causes of
chronic dyspepsia, including peptic ulceration and hiatus hernia. Occasionally, the symptoms closely resemble those of angina pectoris. It is as well to remain
clinically suspicious – any or all of these common diseases may well occur in association with gallstones.
Stones inthe common bile duct
(choledocholithiasis)
This may be symptomless. More often, there are attacks
of biliary colic accompanied by obstructive jaundice
with claylasting for hours or several days. The attack ceases
either when a small stone is passed through the sphincter of Oddi or when it disimpacts and falls back into the
dilated common duct. Above the impacted stone, other
stones or biliary sludge may deposit. Occasionally, the
jaundice is progressive and, rarely, it is painless.
or by ERCP or surgery, superimposed infection develops,
or the chronic back- pressure in the biliary system may
result in secondary biliary cirrhosis and liver failure.
bile duct is as follows.
1 With jaundice (75% of cases):
2 Without jaundice (25% of cases):
coloured stools and dark urine, the attacks
If the obstruction is not relieved either spontaneously
The differential diagnosis of stones in the common
a Carcinoma of the pancreas or other malignant
obstructions of the common bile duct.
b Acute hepatitis.
c Other causes of jaundice (see Chapter32).
a Renal colic.
b Intestinal obstruction.
c Angina pectoris.
Ascending cholangitis
Infection of the common bile duct can occur in the
presence of an obstruction to the normal biliary
drainage, usually as a complication of stones in the
duct. This is characterized by jaundice, right upper
quadrant pain and raised temperatures (known as
346 The gallbladder and bileducts
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The rule
(a)
The exceptions to the rule
(c)
(b)
(d)
Charcot’s3 triad). In these instances, the duct system
is severely inflamed and filled with pus, and the liver
may be dotted with multiple small abscesses.
Treatment is with appropriate antibiotics and urgent
biliary drainage (e.g. endoscopic sphincterotomy).
Courvoisier’s law4 (Figure33.4)
‘If in the presence of jaundice the gallbladder is palpable, then the jaundice is unlikely to be due to stone.’ This
is an extremely useful rule provided it is quoted correctly. The principle on which it is based is that, if the
obstruction is due to stone, the gallbladder is usually
thickened and fibrotic and, therefore, does not distend.
Moreover, unlike obstruction due to malignant disease,
calculus obstruction is not usually complete. There is
3
Jean Martin Charcot (1825–1893), First Professor of
Neurology, Salpêtrière Hospital, Paris, France.
4
Ludwig Courvoisier (1843–1918), Professor of Surgery,
Basle, Switzerland.
Figure33.4 Obstructive jaundice due
to stone is usually associated with
a small, contracted gallbladder (a).
Therefore, in the presence of jaundice,
a palpable gallbladder indicates that
the obstruction is probably due to
some other cause, the most common
being carcinoma of the pancreas (b).
Exceptions are a palpable gallbladder
produced by one stone impacted
in Hartmann’s pouch resulting in a
mucocele, another in the common
duct causing obstruction (c), which
is very rare or, more commonly, the
gallbladder is indeed distended but is
clinically impalpable (d).
usually some escape of bile into the duodenum, with
decompression of the gallbladder. Obstruction of the
common bile duct due to other causes (e.g. carcinoma
of the head of the pancreas) is usually painless, and
associated with a normal gallbladder, which can dilate.
However, in carcinoma of the bile ducts arising above
the origin of the cystic duct, the gallbladder, distal to the
obstruction, will be collapsed and empty.
Note that the law is not phrased the other way round–
‘If the gallbladder is not palpable, the jaundice is due
tostone’– as 50% of dilated gallbladders cannot be palpated on clinical examination, owing to either the
patient’s obesity or overlap by the liver, which itself is
usually enlarged as a result of bile engorgement.
Only rarely is the gallbladder dilated when jaundice
is due to stone. These circumstances occur when a
stone impacts in Hartmann’s pouch to produce a
mucocele while at the same time jaundice is produced
by a second stone in the common duct, or when a stone
forms in situ in the common bile duct, the gallbladder
itself being normal and, therefore, distensible.
Special investigations
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• Ultrasound: this non- invasive technique gives
three pieces of information:
– The presence of gallstones within the gallblad-
der, revealed as intensely echogenic foci, which
cast a clear acoustic shadow beyond them.
– The thickened wall of the gallbladder in acute
or chronic inflammation.
– The diameter of the common bile duct which,
if over 7mm, is suggestive of the presence of
stones within.
Unfortunately, ultrasound, like CT, is unreliable in
detecting stones in the bile ducts, especially at the
lower end where they are obscured by the overlying duodenal gas.
• Plain abdominal X- ray, though rarely done these
days, reveals radio- opaque gallstones in only 10%
of cases. These usually appear as rings due to calcium deposited on a central translucent organic
core. Occasionally, the gallbladder may be seen to
be calcified (‘porcelain gallbladder’).
• Upper gastrointestinal endoscopy may be advisa-
ble to exclude an associated peptic ulcer or hiatus
hernia when there is any degree of uncertainty in
the clinical picture, even though gallstones have
been noted on ultrasound.
• Liver function tests are performed whenever jaundice, present or past, is a feature. Raised alkaline
phosphatase or alanine transaminase, even in the
absence of a raised bilirubin, is suspicious for
choledocholithiasis. Prothrombin time should
also be checked in the presence of jaundice lest
any invasive procedure be required.
•
Computed tomography (CT) is often performed
for investigation of abdominal pain which may
arise as a consequence of gallstone- related complications, and is useful in detecting cholecystitis,
obstructive jaundice, pancreatitis and rarer complications such as gallstone ileus. The radiolucency of most gallstones means it cannot be used
to exclude or confirm the presence of gallstones in
the gallbladder.
• Magnetic resonance cholangiopancreatography
(MRCP) permits visualization of the biliary tree
and any contained calculi. This non- invasive procedure provides the same diagnostic information
as can be obtained with ERCP but without the
small but important risk of complications (perforation, bleeding, pancreatitis) associated with
ERCP.
The gallbladder and bileducts 347
•
Endoscopic ultrasound (EUS) involves an endo-
scopic procedure with an ultrasound probe at the
tip of an endoscope. This is more sensitive than an
MRCP in detecting common bile duct stones or
sludge, but also more invasive, carrying a small
risk of bleeding and perforation. This procedure
may be useful in patients where the differential
diagnosis includes a mass lesion (as tissue samples can be taken via this route) or in patients with
contraindications to MRI. Unlike ERCP, this
investigation does not allow clearance of any
ductal stones.
Endoscopic retrograde cholangiopancreatography
•
(ERCP): endoscopic intubation of the bile ducts
through the ampulla of Vater is more invasive than
MRCP or EUS, but in addition to visualizing the
ducts and contained stones it also permits their
extraction, often after first carrying out a diathermy
sphincterotomy/balloon sphincteroplasty opening
up the sphincter of Oddi
tion of the bile duct. ERCP has been largely replaced
by MRCP for diagnosis but remains an essential
part of hepatobiliary management in offering
endoscopic therapeutic options and removing the
reliance on open surgical procedures.
5
to facilitate instrumenta-
Treatment
Biliary colic
Most patients with biliary colic are managed in the
outpatient setting, but consideration should be
given to elective laparoscopic cholecystectomy to
control their symptoms and avoid other complications of gallstones.
Acute cholecystitis
At least 90% resolve on bed rest with antibiotics and
pain relief. Early cholecystectomy during the same
admission is advocated where possible to prevent
further attacks; however, the operation may be
more technically challenging due to increasing
inflammation after the first 48 to 72 hours.
Cholecystectomy is routinely performed laparoscopically, with the advantages of minimal scarring
of the abdominal wall and rapid convalescence
5
Ruggero Oddi (1864–1913), Surgeon, Genoa, Italy. e
sphincter was rst described in 1654 by Francis Glisson
(1597–1677), Regius Professor of Physic, Cambridge, UK.
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compared with an open procedure. Nevertheless,
operative difficulties and anatomical aberrations
may necessitate conversion to an open operation in
approximately 2–5% of cases.
Perforation of the acutely inflamed gallbladder can
occur, either into the adjacent liver parenchyma with
a resultant liver abscess, or into the peritoneal cavity
with biliary peritonitis. The latter is rare and requires
urgent surgery, and carries a high mortality.
In patients unfit for surgery, a cholecystostomy
(drainage of the gallbladder under ultrasound guidance) may be performed to control symptoms of sepsis and pain. This may also be a temporizing measure
in some patients with gallbladder empyema or localized perforation, with a subsequent cholecystectomy
once the inflammation has subsided.
Chronic cholecystitis
Cholecystectomy is performed, usually laparoscopically.
Intraoperative cholangiography may help ascertain
the presence of any stones within the common bile
duct, particularly if associated with deranged liver
function tests. The cystic duct is intubated and radioopaque contrast medium is injected into the common
duct. If stones are convincingly demonstrated at intraoperative cholangiography, the surgeon may choose
between postoperative evacuation of the stones via
ERCP, or laparoscopic or open clearance. The stones
can be removed either via the cystic duct, or directly
through the common bile duct. If the stones are
removed through the bile duct, the incision on the bile
duct can be either closed primarily (if wide enough to
avoid postoperative stricturing) or drained using a
latex T-
tube inserted into the common duct. The
T- tube is removed 10days postoperatively, provided a
check cholangiogram taken through the tube confirms that the ducts are clear and that there is free flow
of contrast into the duodenum. If there is any doubt
about the presence of ductal stones at the time of surgery, an MRCP can be performed following recovery.
Any stones still present can then be removed at ERCP.
Obstructive jaundice dueto stones
Impacted stones are removed using a balloon or
6
Dormia
tomy is performed as soon as possible lest new stones
6
Italy.
basket at ERCP. Subsequent cholecystec-
Enrico Dormia (1928–2009), Professor of Urology, Milan,
pass into the ducts. The presence of high fever makes
removal of the impacted stones and drainage of the
obstructed common bile duct imperative as an emergency procedure. Any intervention is preceded by
giving intravenous vitamin K, since a lack of bile salts
in the gut reduces absorption of this fat vitamin; hence, serum prothrombin is lowered with
consequent bleeding tendency. Rarely ERCP may be
unsuccessful, and biliary drainage may require a percutaneous transhepatic external biliary drain to alleviate the sepsis.
Acute or chronic pancreatitis
Gallstones are one of the commonest causes of acute
pancreatitis, a condition which can sometimes prove
threatening particularly for patients with other
lifecomorbidities. The diagnosis and management of
acute and chronic pancreatitis are discussed in
Chapter34.
Non- surgical treatment
ofgallstones
There is no satisfactory or effective non- surgical
treatment for gallstones. Gallstone dissolution via oral
bile salts such as chenodeoxycholic or ursodeoxycholic acid, or lithotripsy (ultrasonic destruction of
gallstones) are options that have been previously
employed to avoid surgical intervention. However, the
high risk of stone migration or recurrence within the
gallbladder, and the potential for pancreatitis or biliary obstruction from lithotripsy, are such that these
are no longer recommended forms of treatment.
The symptomless gallstone
The incidental diagnosis of gallstones is becoming
increasingly common during routine ultrasound
examination of the abdomen for a variety of nonbiliary reasons. Given the risks of cholecystectomy,
there is no evidence at present to support surgery for
patients with asymptomatic gallstones, unless conditions associated with an increased risk of gallbladder
cancer, such as porcelain gallbladder or large gallbladder polyps, are also present.
Complications
ofcholecystectomy
There are two special dangers after cholecystectomy,
whether performed by laparotomy or laparoscopy.
soluble
The gallbladder and bileducts 349
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1 Leakage of bile. This may result from:
Injury to bile canaliculi in the gallbladder bed
a
of the liver.
b
Injury to the common hepatic or common bile
duct, or aberrant low inserting rightducts.
c
Slipping of the ligature or clip from the cystic
duct.
Leakage from the common bile duct after
d
exploration.
ERCP may identify the site of the leak, and temporary stenting
thus allowing the bile fistula to close spontaneously;
if this does not occur, further exploration may be
required. A percutaneous drain is usually placed to
prevent generalized biliary peritonitis.
2
Jaundice. This may be due to:
a
Missed stones in the common bile duct.
b Inadvertent injury to the common bile duct.
Cholangitis or associated pancreatitis.
c
Residual stones in the common duct can usually be removed by ERCP; if a T- tube is still present
in the common duct, the stone can be removed by
means of a Burhenne basket
track formed by the tube under X- ray control.
7
will ensure adequate biliary drainage,
8
passed along the
sided bile
Clinical features
Gallbladder polyps may be entirely asymptomatic
and simply represent an incidental finding on an
ultrasound examination performed for reasons other
than biliary symptoms; if they are situated distally in
the gallbladder close to Hartmann’s pouch, they may
produce symptoms identical to those of gallstones.
Treatment
Cholecystectomy is recommended for polyps associated with gallbladder symptoms or those of greater
than 10 mm in diameter. Patients with polyps measuring 6 mm in diameter or greater, and with additional risk factors (over the age of 50, sessile polyps
and those with primary sclerosing cholangitis) should
also be counselled for cholecystectomy. Patients
without additional risk factors or with smaller
(<6mm) asymptomatic polyps should undergo surveillance via annual ultrasound, with surgery advocated if polyps increase in size on imaging.
Carcinoma ofthe
gallbladder
Gallbladder polyps
Pathology
Gallbladder polyps may be single or multiple and are
increasingly being detected by ultrasound examination. They appear as lesions within the gallbladder
which do not cast an acoustic shadow (as stones do)
and which do not move when the patient rolls onto
one side, indicating that they are attached to the gallbladder wall. Polyps may represent a premalignant
lesion, the risk of malignancy rising with increasing
size of polyp, and becoming significant when the size
reaches 1 cm and probable when the size reaches
1.5cm. Sessile morphology, corosing cholangitis and age over 50 years are additional
risk factors for malignancy within a polyp.
7
Charles Stent (1845–1901), English dentist.
8
H. Joachim Burhenne (1925–1996), Radiologist, Vancouver,
Canada.
existing primary scle-
Pathology
This is a relatively uncommon tumour in most countries but shows particularly high prevalence in certain
areas including parts of northern India, Chile, China
and Korea. The aetiology behind this is unclear and
has been proposed to include salmonella infections,
dietary factors and other environmental exposures.
Gallbladder cancer is strongly associated with the
presence of gallstones, pancreatobiliary malfunction
and ‘porcelain’ gallbladders; however, the exact role
of these conditions as a cause for cancer development
remains uncertain, and may be related to chronic irritation or the carcinogenic effect of cholic acid derivatives. It is 2–3 times more common in women, and
90% of gallbladder cancers are adenocarcinoma with
the remaining 10% consisting of squamous carcinoma or neuroendocrine tumours.
This aggressive tumour often invades the adjacent
liver parenchyma and bile ducts, and disseminates
both via lymphatic spread to nodes in the porta hepatis and beyond, as well as haematogenous spread via
the portal vein to the liver.
350 The gallbladder and bileducts
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Clinical features
Carcinoma of the gallbladder may be silent, but can
also present with a picture closely resembling chronic
cholecystitis, with right upper quadrant pain, nausea
and vomiting, in addition to weight loss and, later, progressing to obstructive jaundice. At this stage, a palpable mass may be present in the gallbladder region.
Treatment
Occasionally, cholecystectomy performed for stones
reveals the presence of an unexpected early tumour.
Under these circumstances, longfollow depending on the histopathological stage of
the tumour. Patients with very early tumours may
have good longtomy alone. Those with tumours invading the muscle layer of the gallbladder and beyond would
generally benefit from a radical cholecystectomy
incorporating resection of the adjacent liver and
removal of local lymph nodes. Surgery yields much
more limited survival in patients with involvement of
adjacent organs or invasion of the rightinflow, and is contraindicated in the presence of
metastatic disease, where chemotherapy is the more
appropriate treatment option.
term survival with a cholecystec-
term survival may
sided liver
Cholangiocarcinoma
Pathology
The incidence of cholangiocarcinoma (carcinoma of
the bile ducts) is increasing. The disease commonly
occurs after 50 years of age and is more common in
men. It is associated with primary sclerosing cholangitis, and to a lesser extent, congenital hepatic fibrosis, choledochal cysts and polycystic liver.
Macroscopically, cholangiocarcinomas may occur
within the liver substance, or in the larger extrahepatic bile ducts. The confluence of the left and right
hepatic ducts, or the common hepatic duct with the
cystic duct, are common sites. Microscopically, these
are mucin-
secreting adenocarcinomas.
Clinical features
The usual presentation is with painless progressive
jaundice, with dark urine and pale stools. Epigastric
pain, steatorrhoea and weight loss are common.
There may be hepatomegaly, usually without a palpable gallbladder because the tumour is proximal to, or
at, the cystic duct confluence. Hilar cholangiocarcinoma (Klatskin tumour
is intrahepatic biliary dilation without common bile
duct dilation. Confirmation is often by MRCP, or percutaneous transhepatic cholangiography and brush
cytology (poor sensitivity), and EUS biopsy if possible. ERCP examination alone often fails to visualize
the intrahepatic biliary tracts, however, when combined with cholangioscopy may be successful in
obtaining images of concerning lesions or strictures
as well as histological confirmation of malignancy.
9
) should be suspected if there
Treatment
The tumours are slow growing. Palliation of distal strictures is often achieved by endoluminal stenting at
ERCP, and percutaneous transhepatic cholangiography
for more proximal strictures, or, less frequently, surgical
bypass. The prognosis is poor, and curative resection is
only possible in a small percentage of cases with early
presentation of hilar tumours (Klatskin tumour
Good results have been reported with extended right
hepatectomy (to include the caudate lobe) together
with excision of the adjacent portal vein and venous
reconstruction. In the rarer cases in which the tumour
is located distally in the common bile duct, a Whipple’s
resection (see Figure34.2) may be possible.
9
Additional resources
Case 89: A schoolmistress with attacks of abdominal pain
Case 90: A collection of calculi
9
Gerald Klatskin (1910–1986), liver Physician, Yale,
New Haven, CT, USA. Pioneered the liver biopsy and is
considered to be one of the fathers of hepatology.
).
The pancreas
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Raaj Kumar Praseedom
Learning objectives
✓ To know the causes and management of acute pancreatitis, and the
factors that predict its severity.
✓ To have knowledge of pancreatic cancer, its presentation and the
surgical approach to treatment of carcinoma of the head of the
pancreas.
34
Congenital anomalies
The pancreas develops as a dorsal and a ventral bud from
the duodenum (Figure 34.1). The ventral bud rotates
posteriorly, thus enclosing the superior mesenteric vessels; it forms the major part of the head of the pancreas,
and its duct becomes the main duct of Wirsung,
in the great majority of cases has a shared opening with
the common bile duct in the ampulla of Vater.
dorsal bud becomes the body and tail and its duct
becomes the accessory duct of Santorini.
3
1
which
2
The larger
Annular pancreas
The two developmental buds may envelop the second
part of the duodenum, producing this rare form of
extrinsic duodenal obstruction.
1
Johann Georg Wirsung (1589–1643), Professor of Anatomy,
University of Padua, Italy, where he was murdered.
2
Abraham Vater (1684–1751), Professor of Anatomy,
Wittenberg, Germany.
3
Giovanni Domenico Santorini (1681–1737), Professor of
Anatomy and Medicine, Venice, Italy.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Heterotopic pancreas
This is produced occasionally by an accessory
budding from the primitive foregut. A nodule of pancreatic tissue may be found in the stomach, duodenum, jejunum or, rarely, a Meckel’s diverticulum. This
may produce obstructive or dyspeptic symptoms.
Acute pancreatitis
Acute inflammation of the pancreas is a common
cause of acute abdominal pain, with significant morbidity and mortality.
Aetiology
Most cases of acute pancreatitis are associated with
either gallstones or alcohol, although a number of
less common causes have been identified.
Gallstones are present in half of the cases in the UK.
•
• Alcohol: the majority of cases of non- gallstone
pancreatitis are alcohol related. This is particularly
common in France and North America. Alcohol is
also the most common cause of recurrent pancreatitis. The mechanism is unclear, and it may follow
either chronic alcohol abuse or binge drinking.
352 The pancreas
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Foregut
Hepatic
diverticulum
Gallbladder
Ventral
pancreatic
bud
Dorsal
pancreatic bud
Midgut
(a) (b)
Gallbladder
and bile duct
Dorsal and
ventral pancreatic buds
(c)
Common
bile duct
Duodenum
Head of
pancreas
Ampulla
Figure34.1 (a–d) The development of the pancreas and biliary tree. Reproduced from Ellis H, Mahadevan V (2010)
Clinical Anatomy, 12th edn. Oxford: Wiley-
Other less common causes of pancreatitis include
the following:
Postoperative: particularly after cardiopulmonary
•
bypass or damage to the pancreas during mobilization of the duodenum at partial gastrectomy or
splenectomy.
• Endoscopic retrograde cholangiopancreatography
(ERCP): particularly if pancreatic duct injection was
Accessory pancreatic
duct (Santorini)
(d)
Blackwell.
Tail of pancreas
Main pancreatic
duct (Wirsung)
Uncinate process
pancreas
Superior mesenteric artery
Superior mesenteric vein
performed or there was difficulty cannulating the
papilla with subsequent oedema and obstruction.
• Autoimmune (often characterized by raised serum
IgG4 levels) and associated with other autoimmune conditions (e.g. Sjøgren’s syndrome).
• Infection, for example mumps, cytomegalovirus or
coxsackie infection.
• Tra uma, particularly blunt trauma or crush injury.
The pancreas 353
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• Drugs, for example corticosteroids, sodium valproate, azathioprine.
Hypothermia.
•
•
Hypercalcaemia.
Hyperlipidaemia.
•
•
Vascular: pancreatitis may occur in malignant
hypertension, cholesterol emboli and vasculitis
such as polyarteritis nodosa, probably as a result
of local infarction causing enzyme liberation.
Carcinoma of the pancreas (very uncommon).
•
•
Idiopathic: the cause of some cases of pancreatitis
cannot be determined.
Pathology
Acute pancreatitis differs from other inflammatory
conditions because of the autodigestion that may
result from liberation of digestive enzymes. The pancreas is normally protected from autodigestion by
storing its enzymes in intracellular zymogen granules
before secreting them as proenzymes. Trypsin, for
example, is secreted as trypsinogen and converted to
trypsin by the action of enterokinase in the gut.
Trypsin itself then cleaves other proenzymes, thus
activating them. One such enzyme is phospholipase
A which, in pancreatitis, is involved in cell wall damage and fat necrosis along with pancreatic lipase.
The mechanisms initiating autodigestion are multiple. Duodenopancreatic reflux is an important factor
that may occur as a result of injury to the papilla following endoscopic cannulation, trauma or surgery in
this region, or as a result of damage to the sphincter
owing to the recent passage of a stone (hence the
strong association of pancreatitis and biliary calculi).
Duodenal fluid containing enterokinase then refluxes
into the duct, activating the pancreatic proenzymes.
Duodenal reflux can be shown experimentally to produce pancreatitis and may be a common factor that
underlies many of the aetiological associations mentioned above. As inflammation proceeds, local infarction may occur as arterioles thrombose, and more
proenzymes leak out of the necrotic cells to be activated. Once started, pancreatitis can be rapidly progressive, with widespread autodigestion not only
confined to the pancreas. There follows multifailure secondary to the severe systemic inflammatory
response triggered by the local severe inflammation.
As inflammation and autodigestion progress, liquefying necrotic material and inflammatory exudate
collect in the lesser sac. This fluid, walled off by the
stomach in front and necrotic pancreas behind,
forms the so- called ‘pseudocyst of the pancreas’.
Intra- abdominal fluid collections following acute
system
pancreatitis are classified into the following according
to the Revised Atlanta classification.
•
Acute peripancreatic fluid collection (<4weeks).
•
Acute necrotizing collection (<4weeks).
Pseudocyst (>4weeks).
•
•
Walled- off necrosis (>4weeks).
Macroscopic pathology
It is not desirable to operate on patients with acute pancreatitis due to the very high mortality and morbidity
associated with it. If surgery has occurred, pancreatitis
should be suspected when blood-
stained peritoneal
effusion and white spots of fat necrosis are seen scattered throughout the peritoneal cavity; these are produced by lipase released from the pancreas, which
liberates fatty acids and glycerol from fat; these acids
combine with calcium to produce insoluble calcium
soaps (saponification). The pancreas is swollen,
haemorrhagic or, in severe cases, actually necrotic.
Superadded infection of the necrotic tissue is often fatal.
Clinical features
The condition can present at any age but is uncommon
in childhood. The patient presenting with gallstone
pancreatitis is commonly middlecontrast, the alcohol- related form commonly first presents in patients who are younger than 40. Pain is of
rapid onset, is severe, constant, usually epigastric and
often radiates into the back. The patient typically sits
forward, and repeated retching is common. Vomiting is
early and profuse. The patient may be shocked with a
rapid pulse, cyanosis (indicating circulatory collapse)
and a temperature that may be either subnormal or
raised up to 39.5 °C (103°F). Abdominal examination
reveals generalized tenderness and guarding.
On rare occasions, a few days after a severe attack,
the patient may develop a bluish discoloration in the
loins from extravasation of blood- stained pancreatic
juice into the retroperitoneal tissues (Grey Turner’s
4
sign
). The tracking of fluid that results in this sign can
often be seen on computed tomography (CT) imaging
of patients with acute pancreatitis even when it is not
clinically apparent. A bluish discolouration around
the umbilicus may also be observed (Cullen’s sign
4
George Grey Turner (1877–1951), Professor of Surgery,
University of Durham, then Foundation Professor of Surgery
at the Royal Postgraduate Medical School, London, UK.
5
omas Stephen Cullen (1869–1953), Canadian Professor
of Gynaecology, Johns Hopkins, Baltimore. He described
the sign in ectopic pregnancy, but it may also occur in acute
pancreatitis and with a ruptured abdominal aortic aneurysm.
aged or elderly. By
5
).
354 The pancreas
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Differential diagnosis
The less severe episode of acute pancreatitis simulates acute cholecystitis; the more severe attack, with
a marked degree of shock, is usually mistaken for a
perforated peptic ulcer, leaking abdominal aortic
aneurysm or coronary thrombosis. Differentiation
must also be made from high intestinal obstruction
and from other causes of peritonitis.
Special investigations
The investigation comprises tests to confirm the diagnosis and tests to assess the severity of the disease (i.e.
diagnostic and prognostic).
•
Serum amylase. Amylase is liberated into the
circulation by the damaged pancreas, and
exceeds the kidney’s ability to excrete it, so the
serum concentration rises. It is usually significantly raised (fivefold or more) in the acute
phase, but returns to normal within 2–3 days;
the urinary amylase is elevated for a longer
period and may be useful in the diagnosis of
cases presenting late. Occasionally, an overwhelming attack of pancreatitis with extensive
destruction of the gland, or an attack occurring
as an acute exacerbation of chronic pancreatitis,
is associated with a normal serum amylase.
Other causes of raised serum amylase need to
be borne in mind before assuming a diagnosis
of pancreatitis (Box34.1).
• Serum lipase: like amylase, serum concentrations
of lipase are raised in pancreatitis.
Full blood count: there is a moderate leucocytosis,
•
and anaemia in severe cases.
• C- reactive protein (CRP) is often raised in severe
cases.
• Blood glucose is often raised, with glycosuria in
15% of cases.
• Arterial blood gases: hypoxia and acidosis occur in
severe cases.
• Serum calcium may be lowered, partly as a result
of fat saponification.
• CT may confirm pancreatitis if the amylase is normal or the diagnosis otherwise is unclear. At a later
stage, necrotic pancreas, abscess or pseudocyst
may be visualized.
• Electrocardiography (ECG) may show diminished
T waves, or arrhythmia, and can cause confusion
with cardiac ischaemia.
Box 34.1 Raised serum amylase
The causes of raised serum amylase are listed
below. Only those marked with an asterisk cause a
marked increase in amylase (fivefold or more).
Impaired renal excretion
•
Renal failure*.
•
Macroamylasaemia (amylase not cleared by
kidneys owing to complexing or protein binding).
Salivary gland disease
•
Salivary calculi.
•
Parotitis.
Metabolic causes
•
Severe diabetic ketoacidosis*.
•
Acute alcoholic intoxication.
•
Morphine administration (causing sphincter of
Oddi spasm
Abdominal causes
•
Acute pancreatitis*.
•
Perforated peptic ulcer.
•
Acute cholecystitis.
•
Intestinal obstruction.
•
Afferent loop obstruction following partial
gastrectomy.
•
Ruptured abdominal aortic aneurysm.
•
Ruptured ectopic pregnancy.
•
Mesenteric infarction.
•
Trauma, open or blunt.
•
Inflammatory bowel disease.
6
).
• Abdominal X- rays often give no direct help. The
absence of free gas or of localized fluid levels
assists in the differential diagnosis of perforated
duodenal ulcer or high intestinal obstruction. In
some cases, a solitary dilated loop of proximal
jejunum may be seen (the ‘sentinel loop sign’).
Radio- opaque pancreatic calculi may be present
in cases of chronic pancreatitis.
Ultrasound should be carried out in all cases to
•
rule out gallstone- related acute pancreatitis.
Patients with acute gallstone pancreatitis should
undergo a cholecystectomy prior to discharge
from the hospital to prevent relapse.
6
Ruggero Oddi (1864–1913), Surgeon, Genoa, Italy; he
identied the sphincter while a medical student in Perugia,
Italy.
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