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CHAPTER 8 Liver, pancreatic, and biliary surgery
322
Portal hypertension
Key facts Normal portal vein pressure is 5–10mmHg. Portal hyperten-
sion (PH) develops when the portal pressure is greater than 12mmHg.
Causes and pathological features
Causes
• Prehepatic. Congenital portal vein atresia or portal vein thrombosis
due to neonatal umbilical sepsis, phlebitis of the portal vein from
abdominal infection (e.g. acute appendicitis or diverticulitis), trauma, or
a thrombosed portocaval shunt.
• Hepatic. Cirrhosis (e.g. alcoholic most frequently in the UK), chronic
active hepatitis, and parasitic diseases (e.g. schistosomiasis).
• Post-hepatic. Budd–Chiari syndrome (hepatic vein thrombosis),
constrictive pericarditis, or tricuspid valve incompetence (rare).
Features and complications
• Decreased or reversed portal blood fl ow to the liver promotes the
development of portosystemic anastomosis between the portal system
and systemic circulation:
Left gastric vein into the oesophageal veins at the gastro-•
oesophageal junction—oesophageal and gastric varices.
Superior rectal into inferior rectal veins at the lower rectum—•
rectal varices.
Obliterated umbilical vein into the epigastric veins—‘caput •
medusae’.
• Oesophageal or gastric varices may bleed torrentially.
• Liver cell dysfunction/liver failure occurs in hepatic and post-hepatic
causes.
• Ascites. In part due to portal hypertension, but may be due to
associated liver dysfunction.
• Splenomegaly (hypersplenism may result).
• The Child–Pugh classifi cation is used to assess the severity of portal
hypertension (see Table 8.2).
Diagnosis and investigations
Many investigations may be used at different times in PH.
• FBC, U&Es, LFTs, and clotting.
• Screening tests for causes of cirrhosis (see b p. 324).
• CT and ultrasound scan to assess liver morphology, diagnose PH, and
assess cause.
• Transabdominal Doppler ultrasound to assess blood fl ow in the portal
vein and hepatic artery.
• Gastroscopy in acute variceal bleeding (see b p. 272).
Treatment
Cause
• Anticoagulation for Budd–Chiari syndrome.
• Treatment for hepatic causes.
PORTAL HYPERTENSION
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Table 8.2 The Child–Pugh classifi cation of portal hypertension
1 point 2 points 3 points
Bilirubin (μmol/L) <34 34–51 >51
Albumin (g/L) >35 28–35 <28
PT (s) <3 3–10 >10
Ascites None Moderate Moderate–severe
Encephalopathy None Moderate Moderate–severe
Grade A: 5–6 points; Grade B: 7–9 points; Grade C: 10–15 points.
Chronic complications
• Oesphago-gastric varices.
Beta-blockers (e.g. propranolol or nadolol) reduce portal venous •
pressure.
Repeated injection sclerotherapy or variceal ligation.•
Elective portosystemic shunts (e.g. splenorenal anastomosis).•
Liver transplant may be considered for treatment if associated with •
severe liver disease.
• Rectal varices. Injection sclerotherapy.
• Symptomatic splenomegaly or hypersplenism. Splenectomy (laparoscopic
or open).
• Ascites. Oral spironolactone; in cases of tense ascites, paracentesis may
be required with IV albumin replacement.
Acute complications Bleeding oesophago-gastric varices.
Key revision points—anatomy of portal circulation
• The hepatic portal circulation carries blood from the GI tract (from
the distal oesophagus to the anorectal junction) to the liver.
• Portosystemic anastomoses occur in ‘junctional’ areas of venous
drainage.
Left gastric veins (portal) and oesophageal veins (hemi/azygous •
veins) at the gastro-oesophageal junction.
Superior rectal veins (portal) and inferior rectal veins (pudendal •
veins) in the lower rectum.
Pancreatic and duodenal veins (portal) and retroperitoneal (hemi/•
azygous) veins in the upper retroperitoneum.
Umbilical vein (portal) into the epigastric veins at the umbilicus.•
• Portal venous blood drains into liver venous sinusoids and hence
into the hepatic veins.
323
CHAPTER 8 Liver, pancreatic, and biliary surgery
324
Cirrhosis of the liver
Key facts
• Commonest cause of liver failure in the UK.
• Commonest cause is alcohol-related.
Causes
• Congenital.
Haemochromatosis.•
Wilson’s disease.•
Other metabolic disorders (e.g. • α1-anti-trypsin defi ciency).
• Acquired.
Alcohol intake.•
Chronic hepatitis (autoimmune, infective types B, C, and D, •
drug-induced).
Primary biliary cirrhosis.•
Secondary biliary cirrhosis (gallstones, strictures, cholangitis).•
Hepatic vein obstruction, e.g. Budd–Chiari syndrome.•
Idiopathic.•
Pathological features
Cirrhosis is characterized by fi brosis of the liver parenchyma, nodular
regeneration, and hepatocellular necrosis.
• Micronodular form. Small and uniform nodules (<4mm in diameter),
separated by thin fi brous septa uniformly throughout the liver.
• Macronodular form. Larger nodules separated by wider scars and
irregularly distributed throughout the liver.
• Mixed.
Clinical features
• One-third of cirrhosis patients are compensated, i.e. do not produce
any clinical symptoms, and are incidentally discovered during a medical
examination, at operation, or at autopsy.
• Two-thirds are decompensated, i.e. have features of liver cell
dysfunction or complications.
Features fall into three broad groups.
Portal hypertension See b p. 322.
Hepatocellular failure
• Jaundice.
• Spider naevi.
• Ascites.
• Hypoalbuminaemia.
• Clotting disorders.
• Encephalopathy.
• Gynaecomastia and testicular atrophy.
• Hepatorenal syndrome (renal failure in the setting of hepatic failure
due to renal vasoconstriction of unknown aetiology).
CIRRHOSIS OF THE LIVER
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Malignant change
• Hepatatocellular carcinoma (particularly chronic hepatitis B infection).
• Often indicated by sudden rapid decrease in hepatocellular function.
Diagnosis and investigation
Diagnosis of cause
• Metabolic screen (e.g. serum copper).
• Hepatitis screen (A, B, C, D, E; EBV, CMV).
• Autoimmune screen (anti-mitochondrial antibodies, anti-smooth
muscle antibodies).
• Abdominal ultrasound and CT may show type of cirrhosis, intra- or
extra-hepatic biliary dilatation, extrahepatic obstructive causes.
• Liver biopsy to confi rm diagnosis and establish type, activity, evolution,
and cause.
Investigation of severity or complications
• LFTs (transaminases, γGT, albumin, bilirubin).
• Clotting studies (PT).
• Transabdominal ultrasound or CT scan (splenomegaly and ascites).
Treatment
Removal of the cause/prevent progression
• Abstinence from alcohol.
• Interferon α. Chronic hepatitis B, response rate <50%.
• Combination therapy (interferon A and ribavirin for 6 months.
Moderate to severe hepatitis C.
• Immunosuppression for autoimmune causes.
Treatment of complications
• PH (see b p. 322).
• Encephalopathy. Treatment aims to lower the amount of nitrogen
absorbed from the gut.
Administration of oral lactulose.•
Oral, non-absorbable antibiotics.•
Careful IV fl uid replacement to prevent sodium overload.•
Diet of high carbohydrate, low salt, moderate protein.•
• Ascites. Oral spironolactone; in cases of tense ascites, paracentesis may
be required with IV albumin replacement.
• Decompensated hepatocellular failure. Consider liver transplant.
325
CHAPTER 8 Liver, pancreatic, and biliary surgery
326
Pancreatic cancer
Key facts
• Fourth commonest solid organ cancer in the UK.
• Incidence is increasing rapidly.
• Eighty per cent of cases occur between the sixth and seventh decades.
• Risk factors include cigarette smoking, increasing age, high fat diet,
diabetes mellitus, excessive alcoholism, and chronic pancreatitis.
• Occupational hazards, e.g. exposure to naphthylene and benzidine.
• There may be hereditary factors involved as 1 in 20 patients with
pancreatic cancer have a family history of pancreatic cancer.
Pathological features
• Ninety per cent ductal adenocarcinoma.
• Seven per cent mucinous cystic neoplasms (mucinous cystadenoma/
cystadenocarcinoma), serous cystadenoma, and papillary cystic tumour.
• Three per cent islet cell tumours.
Clinical features
Carcinoma of the head of pancreas (65%)
• Obstructive jaundice (90%). Due to compression or invasion of the
CBD. Gall bladder is typically palpable.
• Pain (70%). Epigastric or left upper quadrant, often vague and radiates
to the back.
• Hepatomegaly. Due to metastases.
• Anorexia, nausea and vomiting, fatigue, malaise, dyspepsia, and pruritus.
• Acute pancreatitis. Occasionally the fi rst presenting feature.
• Thrombophlebitis migrans (10%). Presents as emboli; splenic vein
thrombosis may lead to splenomegaly in 10% of patients.
Carcinoma of the body (25%) and tail (10%)
• Usually asymptomatic in the early stages.
• Weight loss and back pain (60%).
• Epigastric mass.
• Jaundice suggests spread to hepatic hilar lymph nodes or metastases.
• Thrombophlebitis migrans (7%).
• Diabetes mellitus (15%).
Diagnosis and investigations
• FBC, LFTs, blood sugar.
• Elevated serum CA 19–9 (sensitivity 90%; specifi city 70% for diagnosis).
Level correlates with the tumour volume.
• Transabdominal ultrasound scan (sensitivity 70%; 30% in lesions <2cm).
• Doppler ultrasound images blood fl ow in the portal vein and superior
mesenteric vessels.
• Helical CT scan of pancreas with dual phase IV contrast assesses size
of the primary lesion, vascular invasion, and distant metastasis.
PANCREATIC CANCER
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• FNAC. Usually CT or ultrasound-guided (specifi city 99%; sensitivity
50–70%).
• EUS more accurate than CT in detecting pancreatic lesions <3cm in
diameter and peripancreatic lymph node involvement.
• PET may help differentiate neoplastic from non-neoplastic lesions and
may be used to exclude extra-pancreatic spread that would preclude
surgical resection.
• ERCP is 85% accurate; can provide cytology as well as achieving biliary
drainage via insertion of a stent.
• Selective angiography or CT angiography used to assess resectability
based on encasement of the major vessels.
• Laparoscopy used to rule out peritoneal disease and liver metastasis
<2cm prior to offering surgical resection.
Treatment
Palliative treatment
The majority of tumours (95%) are not suitable for surgical resection due
to presence of metastases, local invasion, involved lymph glands, age, or
comorbidity of patient.
Relief of jaundice
Obstructive jaundice is associated with pruritus, coagulopathy, immunological and nutritional derangement, deterioration in liver function, risk of
acute renal failure (hepatorenal syndrome), and increased susceptibility to
infection. Relief of jaundice is achieved by:
• Endoscopic biliary stenting by ERCP.
• Percutaneous biliary drainage by PTC and internal stenting or insertion
of an internal-external drainage catheter.
• Surgical biliary drainage by cholecystojejunostomy or choledoco-
jejunostomy.
Relief of duodenal obstruction Surgical gastric bypass (gastrojeju nostomy).
Relief of pain
• Oral morphine (oramorph or MST).
• Chemical ablation of the coeliac ganglia (percutaneous coeliac
nerve block or thoracoscopic division of the splanchnic nerves are
alternatives).
Curative treatment Radical surgical resection is the only hope of cure if
patient is suitable.
• Pancreatoduodenectomy (Whipple’s operation) for periampullary
tumours and cancer of the pancreas confi ned to the head.
• Total pancreatectomy for extensive tumour.
• Distal pancreatectomy for tumours in the tail.
Adjuvant therapy For advanced disease, adjuvant chemotherapy (e.g. 5-fl uorouracil) improves prognosis.
Prognosis Poor; even in patients with resectable disease, the 5y survival
is 12%.
327
CHAPTER 8 Liver, pancreatic, and biliary surgery
328
Cancer of the liver, gall bladder,
and biliary tree
Key facts
• Commonest tumours of the liver are metastatic (pancreas, colon,
stomach, oesophagus, and breast).
• Thirty-fi ve per cent of patients who die of malignant disease have
hepatic metastases.
Clinicopathological features
Hepatocellular carcinoma (HCC)
• Ninety per cent of primary liver tumours, but <1% of all new cancers
in UK.
• Common in Africa and Asia; commoner in men than women.
• Risk factors:
Cirrhosis, especially due to chronic viral hepatitis (HBV/HCV) or •
alcohol.
Afl atoxin exposure, contraceptives, and androgens.•
• Arises from liver parenchymal cells, spreads via local invasion, via
portal vein invasion to other sites in the liver, or via hepatic vein
invasion to distant metastases (e.g. lung).
• Commonest presentation—rapid deterioration in pre-existing
cirrhosis.
Cholangiocarcinoma
• Usually arises in the extrahepatic biliary tree, but may be intrahepatic.
• Typical sites are distal CBD, common hepatic duct, confl uence of
hepatic ducts (‘Klatskin tumour’).
Adenocarcinoma of the gall bladder
• Gallstones are found in 70% of cases.
• Associated with ulcerative colitis and primary sclerosing cholangitis.
• Often diagnosed incidentally as unexpected fi nding during or after
cholecystectomy for ‘benign’ disease causing right upper quadrant pain.
• May present as a gall bladder mass or obstructive jaundice due to local
invasion of the common hepatic duct.
• Spread is direct into liver tissue (possibly resectable), to hilar lymph
nodes, or blood-borne (incurable).
Ampullary carcinoma
• Typically small and presents relatively early due to the early onset of
painless obstructive jaundice.
• Best prognosis of all hepatobiliary cancers due to early presentation
before local or lymphatic spread.
Other primary liver cancers
• Fibrolamellar carcinoma (FLC).
Usually affects younger patients (3rd and 4th decades).•
Does not occur on a background of liver disease.•
Presents as a large vascular mass.•
CANCER OF THE LIVER, GALL BLADDER, AND BILIARY TREE
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• Angiosarcoma.
Less than 1% of liver tumours (most common sarcoma of the liver).•
Associated with exposure to arsenicals, vinyl chloride, anabolic •
steroids, and contraceptives.
Diagnosis and investigations
• AFP >500ng/mL highly suggestive of HCC, even in cirrhosis.
• Ultrasound scan often identifi es site and cause of biliary obstruction;
good assessment of liver parenchyma.
• Needle biopsy to confi rm diagnosis of HCC.
• ERCP. Diagnosis of ampullary and bile duct carcinoma; allows biopsy
or brush cytology of distal tumours; allows therapeutic stenting.
• MRCP. Diagnosis of proximal tumours or where ERCP not possible.
• PTC. Diagnosis of intrahepatic biliary tumours, therapeutic stenting, or
external drainage of proximal biliary tumours.
• CT scan. Assessment of local spread (including blood vessels), lymph
nodes, metastases.
Treatment
Curative
• Surgery offers the only cure for primary liver or biliary cancers.
• Patients suitable for resection must:
Be fi t for major surgery.•
No evidence of metastases or involved lymph nodes (rare).•
Tumours technically suitable for complete resection (rare).•
• Surgical options for resection include:
Partial hepatectomy (HCC).•
Liver transplantation (HCC associated with chronic hepatitis).•
Radical cholecystectomy (adenocarcinoma of gall bladder).•
Radical excision of bile duct with reconstruction •
(cholangiocarcinoma).
Pancreaticoduodenectomy (Whipple procedure) (distal •
cholangiocarcinoma or ampullary carcinoma).
Palliative
• Endoscopic or percutaneous stenting for unresectable
cholangiocarcinoma or ampullary carcinoma.
• Chemotherapy is of minimal benefi t in any primary liver or biliary
cancers.
• Embolization. Percutaneous thermal or radiofrequency ablation
(HCC).
Prognosis
• HCC. 5y survival 44% if surgically resectable.
• Cholangiocarcinoma. Median survival 9 months.
• Adenocarcinoma of gall bladder. 5y survival <5%.
About 20% of these tumours are resectable at the time of diagnosis.
329
CHAPTER 8 Liver, pancreatic, and biliary surgery
330330
Acute variceal haemorrhage
Key facts Mortality rate of fi rst variceal bleed with established PH
is 30%.
Causes and features
See b p. 294 for differential diagnosis. Typical variceal bleeding is:
• Rapid onset, copious dark red venous blood with little mixing with
food.
• Features of established PH, e.g. caput medusa.
• Features of developing hepatic encephalopathy (ingested blood
provides an extremely protein-rich ‘meal’).
Emergency management
Resuscitation (see Fig. 8.1)
• Establish large calibre IV access. Give crystalloid fl uid up to 1000mL
if tachycardic or hypotensive. Only use O –ve blood if the patient
is in extremis; otherwise wait for cross-matched blood if transfusion
needed.
• Catheterize and place on a fl uid balance chart.
• Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), cross-
match (at least 3U if haematemesis large), clotting.
• Always consider alerting HDU/ITU; variceal bleeds can deteriorate
extremely rapidly.
• Monitor pulse rate, BP, and urine output (urinary catheter).
• Insertion of a Sengstaken–Blakemore gastro-oesophageal tube may be
a life-saving resuscitation manoeuvre. Usually only inserted without a
prior gastroscopy if the patient is known to have varices and has lifethreatening bleeding. Key points are the following.
If the patient needs a ‘Sengstaken’ tube, they need to be on ITU.•
Most patients need sedation or a GA for the tube to be inserted.•
The tube is inserted and the gastric balloon blown up fi rst and •
traction applied gently until the tube becomes fi xed; this alone may
stop the bleeding if the varices are gastric.
If bleeding continues, the oesophageal balloon is blown up to a •
pressure around 20–30mmHg.
The oesophageal balloon must be defl ated regularly to prevent •
oesophageal necrosis.
Establish a diagnosis
• Urgent OGD is the investigation of choice (at least within 24h).
May require ongoing resuscitation with anaesthetist present.•
Never• biopsy suspected varices.
Therapeutic interventions, including sclerotherapy and banding, are •
up to 90% successful at controlling acute bleeds and preventing
further interventions.
ACUTE VARICEAL HAEMORRHAGE
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Early treatment
• Give IV PPI (e.g. omeprazole 40mg); stop all NSAIDs.
• Give IV vasopression, somatostatin, or octreotide to lower
oesophageal variceal pressure.
• Blood transfusion if large volume haematemesis or drop in Hb.
• Ensure that the appropriate surgical team knows of the patient in case
surgical intervention is required.
• Consider giving FFP to correct clotting abnormalities.
Defi nitive management
Considered for failed endoscopic treatment and ongoing bleeding.
• Transjugular intrahepatic portosystemic shunt formation (TIPS)
(intrahepatic shunt). May be performed to rapidly reduce the portal
pressure, but has the risk of inducing portal encephalopathy.
• Extrahepatic shunt. In portacaval shunts, encephalopathy occurs in 50%
of survivors and the procedure is now seldom performed.
• Oesophageal transaction.
Left gastric vein devascularization.•
Extremely high mortality.•
Low incidence of encephalopathy, but high incidence of recurrent •
bleeding.
Variceal bleed (Dx by Hx & Ex)
If INR > 1.4 give 2U FFP & Vit K 10mg IV
Start IV terilipressin 4mg stat IV bolus & 1mg IV qds
Give ciprofloxacin 1g IV
331331
Active bleeding
Emergency OGD ± endotherapy
Active bleeding
despite endotherapy
Insert Sengstaken tube
Continue terilipressdin IV
Failure to control bleeding
Consider repeated endotherapy
Consider TIPS
Bleeding controlled
by endotherapy
Grossly unstable
Insert CVL
Admit to critical care
Consider Sengstaken tube
Fig. 8.1 Management of acute variceal haemorrhage.
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