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CHAPTER 8 Liver, pancreatic, and biliary surgery
312
Jaundice—causes and diagnosis
Key facts
Jaundice is clinically apparent at serum bilirubin levels above 40mmol.
Key revision points—physiology of bile
• Unconjugated bilirubin formed mainly in spleen by the breakdown
of haemoglobin.
• It is insoluble and is transported in the plasma bound to albumin.
• Taken up by the liver by active transport, it is converted in the
hepatocytes into conjugated bilirubin (water-soluble).
• It is excreted into the bile canaliculi and via the main bile ducts into
the duodenum.
• Ten per cent of the unconjugated bilirubin is reduced to
urobilinogen by small intestinal bacteria, reabsorbed in the terminal
ileum, and then excreted in the urine (enterohepatic circulation).
• Ninety per cent is converted by colonic bacteria to stercobilinogen
which is excreted in faeces.
Causes and features
Pre-hepatic jaundice (haemolytic)
• Congenital abnormalities of red cell structure or content (e.g.
hereditary spherocytosis, sickle cell disease).
• Autoimmune haemolytic anaemia.
• Transfusion reactions.
• Drug toxicity.
Hepatic jaundice (hepatocellular)
• Hepatic unconjugated hyperbilirubinaemia.
Gilbert’s syndrome. Defi ciency or abnormalities of unconjugated •
bilirubin uptake system.
Crigler–Najjar syndrome. Abnormality of conjugation process •
enzymes.
• Hepatic conjugated hyperbilirubinaemia.
Infection. Viral (e.g. hepatitis A, B, C, EBV, CMV); bacterial (e.g. liver •
abscess, leptospirosis); parasitic (e.g. amoebic).
Drugs, e.g. paracetamol overdose, antipsychotics, antibiotics.•
Non-infective hepatitis, e.g. chronic active hepatitis, alcohol-related.•
Post-hepatic jaundice (obstructive)
• Intraluminal abnormalities of bile ducts.
Gallstones.•
Blood clot.•
Parasites (e.g. fl ukes).•
• Mural abnormalities of bile ducts.
Cholangiocarcinoma.•
Congenital atresia.•
Sclerosing cholangitis.•
JAUNDICE—CAUSES AND DIAGNOSIS
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Biliary cirrhosis (primary (autoimmune) or secondary to sepsis).•
Traumatic/post-surgical stricture.•
• Extrinsic compression of bile ducts.
Pancreatitis.•
Tumours, e.g. head of pancreas, ampulla of Vater.•
Lymphadenopathy of porta hepatis nodes.•
Diagnosis and investigations
History
Common aspects overlooked in the clinical history of jaundiced patients.
• Family history of blood disorders.
• Recent foreign travel and work (exposure to infective agents).
• Recent drugs or changes in medications.
• Recent surgery or anaesthesia.
• History of gallstones.
• Alcohol intake, cholangitis (pain, fever, rigors), and carcinoma,
especially the head of the pancreas.
Basic tests
• Reticulocytosis, abnormal blood fi lm (haemolysis).
• i Prothrombin time.
• ‘Hepatitis screen’ (viral titres for hepatitis A, B, C, CMV, EBV).
• Immunology (anti-smooth muscle antibodies (chronic active hepatitis)
and anti-mitochondrial antibodies (primary biliary cirrhosis)).
• LFTs (see Table 8.1).
Advanced tests
• Ultrasound scan (liver, gall bladder, bile ducts, and pancreas).
Excludes the presence of extrahepatic obstruction (dilated •
common bile duct).
May locate cause and site of obstruction.•
Examines hepatic parenchyma in possible hepatitis.•
• Magnetic resonance cholangiopancreatography (MRCP) for suspected
extrahepatic obstruction with no cause seen on ultrasound.
• Liver biopsy (ultrasound-guided) for suspected hepatitis.
313
Table 8.1 Liver function tests in jaundice
Haemolytic Hepatocellular Obstructive
Unconjugated
bilirubin
Alkaline
phosphatase
γ glutamyl
transferase
Transaminases Normal Increased Normal
Lactate
dehydrogenase
Increased Increased Normal
Normal Normal Much increased
Normal Increased Much increased
Normal Increased Normal
CHAPTER 8 Liver, pancreatic, and biliary surgery
314
Jaundice—management
Complications of jaundice
• Renal failure (hepatorenal syndrome). Caused by a combination of
infection, dehydration, and a direct effect of high levels of bilirubin and
other toxic products of metabolism on the kidney; mortality is highest
when the patient is over 65 with an elevated blood urea.
• Biliary infection (cholangitis). Commonest in obstructive jaundice or
with previously damaged biliary tree; commonly due to Gram –ve
bacteria (e.g. Escherichia coli, Pseudomonas).
• Deranged coagulation. Due to decreased synthesis of vitamin K
dependent clotting factors (III, VII, IX, X) and impaired platelet
function.
• Relative immunosuppression. Predisposes to systemic infections (e.g.
chest infection) and reduces wound healing due to combinations of
jaundice, infection, and reduced proteosynthesis.
Acute presentation—general treatment
Fluid balance
• Correct dehydration. Give up to 1000mL IV crystalloid if there is no
pre-existing liver disease; sodium input should be carefully monitored
in pre-exisisting liver disease—ask for senior advice.
• Monitor hourly urine output—urethral catheter.
• Treat infection. Take blood cultures if the patient is pyrexial. Give IV
antibiotics according to local protocol (e.g. cefuroxime 750mg IV tds,
IV gentamicin, PO or IV ciprofl oxacin (500mg IV)); treatment of bile
duct obstruction may be required urgently (e.g. radiologically-guided
drainage, ERCP, or rarely, surgery); consider prophylactic antibiotics.
• Check clotting times (APTT, PT). Give vitamin K 10mg IV stat if PT is
prolonged.
• Ensure adequate nutrition. Ensure the patient has a dietetic review;
enteral feeding is optimum, but may require a fi ne bore NGT or, very
occasionally, a surgical gastrostomy or jejunostomy.
• Preoperative biliary decompression has not been proven to reduce
post-operative complications.
Acute presentation—specifi c treatments
• Endoscopic procedures (ERCP).
Sphincterotomy. Used for common bile duct stone extraction, •
treatment of ampullary strictures due to tumours or infl ammation.
Stent insertion (plastic or expanding metal). Used for bile duct •
stones that cannot be removed easily, post-operative or benign
strictures, malignant strictures, external compression of bile duct.
• Percutaneous transhepatic cholangiogram (PTC). Used for stent
insertion (often in combination with ERCP), temporary external
drainage of obstructed biliary system.
• Surgical drainage (e.g. choledochoduodenostomy). Very rarely used
if other interventions failed due to very high morbidity and mortality.
JAUNDICE—MANAGEMENT
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Elective presentation—specifi c treatments
• Haemolytic jaundice.
Steroids for autoimmune case.•
Splenectomy (laparoscopic). Rarely used for hereditary causes and •
failed medical treatment.
• Obstructive jaundice.
ERCP and PTC may be used as above for stones, strictures, •
compression.
Surgical drainage (e.g. choledochoduodenostomy or •
cholecystojejunostomy) used for failed interventional treatments.
Surgical resection, e.g. Whipple’s pancreaticoduodenectomy. Used •
for very selected cases where pancreatic or distal bile duct tumours
are benign or malignant, but potentially curable on staging; staging
of potentially suitable patients may include endoscopic ultrasound,
CT scan, ERCP or MRCP, visceral arteriography, laparoscopy.
• Hepatocellular jaundice.
Remove causative agent and support liver function.•
Consider transplantation in specifi c circumstances.•
• Selective arteriography of the hepatic, coeliac, and superior mesenteric
arteries gives information about anatomical variants, vessel invasion,
tumour operability.
Prognosis in acute jaundice
Adverse risk factors include:
• Age >65y.
• Elevated plasma urea.
• Elevated plasma bilirubin (>200g/L).
• Uncontrolled sepsis and multiple organ dysfunction (typically acute
tubular necrosis).
• Underlying malignant disease.
315
CHAPTER 8 Liver, pancreatic, and biliary surgery
316
Gall bladder stones
Key facts Present in 10% of people >50y in the UK.
Pathological features
Bile has three major constituents:
• Bile salts (primary—cholic and chenodeoxycholic acids; secondary—
deoxycholic and lithocholic acids).
• Phospholipids (90% lecithin).
• Cholesterol.
Bile containing excess cholesterol relative to bile salts and lecithin predisposes to gallstone formation.
Types of gallstones
• Pure cholesterol (10%). Often solitary, large (>2.5cm), round.
• Pure pigment (bile salts 10%). Pigment stones are of two types:
Black (associated with haemolytic disease).•
Brown (associated with chronic cholangitis and biliary parasites).•
• Mixed (80%). Most common; usually multiple.
Predisposing conditions
• Increasing age.
• Female (pregnancy and use of the oral contraceptive).
• Obesity.
• Multiparity.
• Chronic haemolytic disorders (only for pigment stones).
• Long-term parenteral nutrition (alteration of bile constituents).
• Previous surgery (e.g. vagotomy or resection of the terminal ileum)
or disease involving the distal small bowel (e.g. Crohn’s disease)—
alteration of bile constituents.
Clinical features (common presentations)
Biliary colic Intermittent severe epigastric and right upper quadrant pain;
usually associated with nausea and vomiting. Resolves after few hours;
tenderness over gall bladder during acute episodes.
Acute cholecystitis
Severe continuous right upper quadrant pain; often radiates to right fl ank
and back associated with anorexia and pyrexia. Tenderness over gall bladder during inspiration (Murphy’s sign).
Complications of acute cholecystitis include:
• Formation of an empyema or abscess of the gall bladder (rare).
Indicated by high swinging fever and severe localized pain;
• Perforation with biliary peritonitis (very rare).
• Cholecystoenteric fi stula formation (may lead to a gallstone entering
and obstructing the distal ileum (‘gallstone ileus’; see b p. 302);
• Jaundice due to compression of the adjacent common bile duct by
pressure (‘Mirizzi syndrome’).
Chronic cholecystitis Repeated episode of infection causes thickening and
fi brosis of gall bladder.
GALL BLADDER STONES
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Mucocele Stone in neck of gall bladder; bile is absorbed, but mucus secretion continues, producing a large, tense globular mass in right upper
quadrant.
Empyema Abscess of gall bladder.
Diagnosis and investigations
• FBC, U&E, LFTs, blood culture, serum amylase—in acute
presentations
• Abdominal X-ray. Only 10% of calculi are radio-opaque.
• Oral cholecystogram (Graham–Cole test). Rarely used.
• Ultrasound. Procedure of choice; identifi es stones, determines wall
thickness, and assesses ductal dilatation.
• Hepatobiliary iminodiacetic acid (HIDA) scan. Useful when ultrasound
fi ndings are equivocal.
Surgical treatment
Cholecystectomy
Majority done laparoscopically; often done as a day case. This is the treatment of choice for all patients fi t for GA. Indicated for:
• Patients with symptoms deemed to be due to gall bladder stones.
• Asymptomatic patients with gall bladder stones at risk of complications
(diabetics, porcelain gall bladder (15–20% associated with carcinoma),
history of pancreatitis, long-term immunosuppressed).
Risks of laparoscopic cholecystectomy
• Conversion to open operation, 5–10%.
• Bile duct injury, <1%.
• Bleeding, 2%.
• Bile leak, 1%.
Non-surgical treatments
Percutaneous drainage of gall bladder
• Done under ultrasound or CT guidance.
• Used for empyema of the gall bladder in patients unsuitable for
emergency cholecystectomy.
• After resolution of the infection, the calculi may be removed
percutaneously.
Dissolution therapy
• Rarely used. Requires a functioning gall bladder, small stones.
• Problems—requires prolonged treatment, <70% response, high rate of
recurrence of stones, side effects of medication (diarrhoea, pruritus).
Extracorporeal shock wave lithotripsy Hardly ever used; risk of visceral
injury and high risk of stone recurrence.
317
CHAPTER 8 Liver, pancreatic, and biliary surgery
318
Common bile duct stones
Key facts
• Types of stones as per gall bladder stones (see b p. 316).
• Common bile duct (CBD) stones present in 10% of patients with
gallstones.
• Most pass from the gall bladder into the CBD (secondary duct stones).
• Rarely form within the CBD (primary duct stones); almost always
associated with partial duct obstruction.
Clinicopathological features
Asymptomatic Usually found incidentally on ultrasound for gall bladder
stones.
Obstructive jaundice
• Usually due to CBD stone causing obstruction; rarely due to stone-
induced CBD stricture.
• Anorexia, nausea, itching.
• Dark urine and pale stools.
• Epigastric pain and fever more common with CBD stones than other
cause; due to associated low grade bile infection.
• A palpable, distended gall bladder is rare with CBD stones.
Courvoisier’s law
‘If in the presence of jaundice, the gall bladder is palpable, then the cause
of the jaundice is unlikely to be due to stone.’
This is due to the fact that CBD stones originate in the gall bladder
which is usually scarred and fi brotic, preventing distension.
Ascending cholangitis Constant severe right upper quadrant pain, obstructive jaundice, and high swinging fever (‘Charcot’s triad’).
Acute pancreatitis Sixty per cent of acute pancreatitis in adults in the UK
is due to gallstones (see b p. 316).
Diagnosis and investigations
Basic tests
FBC (i WCC in cholangitis and pancreatitis), U&E, creatinine, LFTs
(i conjugated bilirubin and alkaline phosphatase), serum amylase
(i in pancreatitis), clotting studies.
Advanced tests
Ultrasound (transabdominal)
• Best fi rst-line investigation.
• Accuracy low for distal CBD stones, in acute presentations, obesity,
with extensive overlying bowel gas.
COMMON BILE DUCT STONES
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MRCP
• Investigation of choice for inconclusive ultrasound result.
• Non-invasive, avoids radiation exposure, highly accurate.
ERCP
• Used diagnostically for patients unable to tolerate MRCP
(claustrophobia).
• Mainly reserved for therapeutic interventions:
Endoscopic sphincterotomy (ES) and stone extraction or •
destruction (lithotrypsy).
Stent insertion for unextractable stones.•
• Risks of ERCP (i with ES):
Haemorrhage.•
Acute pancreatitis.•
Ascending infection.•
Perforation (usually retroduodenal, may cause peritonitis).•
PTC
• Used for failure of ERCP as therapeutic procedure (often in
combination with ERCP).
• Risks include sepsis, tube movement, leakage around the tube, and
dehydration.
Treatment
Principles of treatment of CBD stones are as follows.
Emergency treatment of CBD stones
• Indicated in unresolving gallstone pancreatitis, unresolving ascending
cholangitis.
• Usually ERCP with stone extraction or stent insertion.
• Occasionally PTC required.
Elective treatment of CBD stones
• Indicated for:
All patients having had complications (pancreatitis, cholangitis, •
obstructive jaundice).
All patients with gall bladder stones due for cholecystectomy.•
• Usually by ERCP or combined ERCP/PTC.
• Common bile duct exploration required at time of cholecystectomy
(laparoscopic or open) if ERCP/PTC fail or impossible or as surgeon’s
preference. Open CBD exploration may require a T-tube to be left in
the CBD.
Treatment of persistent CBD stones after cholecystectomy
• Rarely necessary with more accurate preoperative diagnosis and more
effective preoperative treatments.
• Stones can be extracted via a T-tube track if present (6 weeks after
surgery with radiologically guided basket extraction).
• Post-operative ERCP is rarely required.
319
CHAPTER 8 Liver, pancreatic, and biliary surgery
320
Chronic pancreatitis
Key facts
• Characterized by recurrent or persistent abdominal pain arising from
the pancreas.
• Often associated with exocrine or endocrine pancreatic insuffi ciency.
• Characterized by irreversible destruction and fi brosis of pancreatic
parenchyma.
• May arise following one or more episodes of acute pancreatitis or may
be a chronic progressive process de novo.
Pathological features
• The process may affect the whole or part of the gland (focal).
• The head tends to be the most severely involved part in chronic
alcohol disease.
• Features of acute pancreatitis may occur—oedema, acute
infl ammatory infi ltrate, focal necrosis, intraparenchymal haemorrhage.
• Chronic infl ammatory changes cause progressive disorganization of the
pancreas:
Glandular atrophy and duct ectasia.•
Microcalcifi cation and intraductal stone formation with cystic •
changes secondary to duct occlusion.
Causes and clinical features
Causes
• Recurrent acute pancreatitis of any cause, especially alcohol.
• Secondary to pancreatic ductal obstruction:
Pancreatic head cysts, tumours.•
Pancreatic duct strictures—post-surgery, ERCP, parasitic infestation.•
Congenital pancreatic abnormalities (pancreas divisum, annular •
pancreas).
Cystic fi brosis.•
• Associated with autoimmune diseases (primary biliary cirrhosis,
primary sclerosing cholangitis).
• Congenital idiopathic chronic pancreatitis.
Features of chronic infl ammation
• Recurrent or chronic abdominal pain:
Typically epigastric, radiating to the back and requiring opiates.•
Worse with food, alcohol.•
Features of exocrine failure
• Anorexia and weight loss (due to protein malabsorption).
• Steatorrhoea (due to fat malabsorption); soft, greasy, foul-smelling
stools that typically fl oat on water.
Features of endocrine failure Insulin-dependent diabetes mellitus (due to
loss of β islet cells).
CHRONIC PANCREATITIS
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Diagnosis and investigations
Basic tests
• Plain abdominal X-ray may show pancreatic calcifi cation.
• Abdominal ultrasound may show cystic change and duct dilatation
within the pancreas.
Advanced tests
• Pancreatic CT scan.
May identify a cause, e.g. anatomical variants, tumours, cysts.•
May show extent of disease. Pancreatic atrophy, disorganization of •
pancreatic ducts, altered acinar pattern with fi brosis, calcifi cation,
and cystic change.
• MRI scan. May show the same changes as CT.
• ERCP. Demonstrates irregularity of the pancreatic duct strictures,
calculi, dilated segments (‘chain of lakes’), and changes in fi rst and
second order branches and cyst formation; a secondary effect from
involvement of the head is stricture of the bile duct, leading to an
‘obstructive’ pattern of LFTs.
Treatment
• Prevention of cause/progressive damage.
Stop alcohol, deal with gallstones, treat autoimmune disease.•
Encourage a diet rich in antioxidants (vitamins A, C, E, selenium).•
• Control symptoms/complications.
Dietary modifi cations. Adequate carbohydrates and protein, •
reduced fat.
Pancreatic exocrine enzyme supplements (e.g. Creon•
®
).
Analgesia. May require opiates (e.g. MST) or coeliac plexus block.•
Control of diabetes mellitus often requires insulin; control is often •
diffi cult due to variable pancreatic function.
Surgical treatment Indications include the following.
• Treatment of reversible cause (anatomical abnormalities, tumours,
cysts, ductal strictures and stones). Operations used include those to
remove causes and those to drain an obstructed pancreatic duct:
Pancreaticoduodenectomy (Whipple procedure).•
Partial pancreatectomy of the head (Frey procedure) or tail (distal •
pancreatectomy).
Pancreaticojejunostomy (Peustow or Duval procedure).•
• Treatment of severe intractable pain or multiple relapses. Operations
are usually to resect affected portion:
Partial pancreatectomy of the head (Frey procedure) or tail (distal •
pancreatectomy).
Total pancreatectomy.•
• Complications (pseudocyst, obstruction, fi stula, infections, portal
hypertension).
Resectional surgery is associated with increasing risk of exocrine and
endocrine pancreatic failure and high risk of complications. All surgery
is associated with a risk of symptom recurrence due to recurrent or progressive disease.
321
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