Hepatobiliary disease

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8 Hepatobiliary disease

Jaundice

Classification

Jaundice is due to elevated bilirubin in blood (upper limit of normal is 17 µmol/L). Jaundice may be pre-hepatic, hepatic or post-hepatic (Table 8.1).

Table 8.1 Classification and causes of jaundice

image

Investigations

Blood tests

See Table 8.2. Liver function tests (LFTs) comprise:

• bilirubin

• alkaline phosphatase

• alanine transferase and aspartate transferase

• albumin

• PT clotting

• alpha-fetoprotein

• gamma-glutamyl transferase (indicative of cell damage caused by alcohol).

Table 8.2 Liver enzymes in jaundice

  Alkaline phosphatase Aspartate and alanine transferases
Hepatocellular damage ↑ ↑↑↑
Extrahepatic biliary obstruction ↑↑↑ ↑

Serum albumin is a good indicator of hepatic function along with vitamin K dependent clotting factors (prothrombin time). Alpha-fetoprotein is a tumour marker of hepatocellular carcinoma.

Imaging

Ultrasound is most useful and is non-invasive, inexpensive and repeatable. It reliably detects biliary dilatation, gallstones and pancreatic lesions. CT scan provides more precise anatomy. MRI scan (magnetic resonance cholangiopancreatography MRCP) is being increasingly used instead of endoscopic retrograde cholangiopancreatography (ERCP) to delineate common bile duct anatomy/abnormality.

Percutaneous transhepatic cholangiography (PTC) is used when other methods of imaging fail. PTC and ERCP can obtain cytological material for analysis and may proceed to interventions such as biliary stenting. Endoscopic ultrasound (EUS) is increasingly used for diagnosis and obtaining cytology.

Arteriography demonstrates pathological circulation of tumours and helps to determine operability of malignant lesions.

Surgery in jaundice

Jaundiced patients are prone to significant postoperative morbidity. Preoperative correction of as many factors as possible is mandatory prior to surgery. Infective complications are common so antibiotic prophylaxis is essential (also used prior to invasive radiology). Jaundice is also associated with poor wound healing with delayed angiogenesis and reduced collagen synthesis. Clotting is corrected by vitamin K. This takes time and levels should be checked just prior to surgery. Preoperative biliary decompression by stenting the common bile duct endoscopically can be helpful. Hepatorenal syndrome is prevented by adequate preoperative hydration, to avoid hypotension (set up an intravenous infusion (IVI) and urinary catheter 24 hours preoperatively to ensure good hydration and urine output).

Biliary atresia

Mild jaundice is not uncommon in the neonatal period but persistent or worsening jaundice after 2 weeks is abnormal and suggests biliary atresia. The cause is unknown. Without surgery, death from liver failure results within 6 months. Treatment requires hepatic portoenterostomy or liver transplantation.

Liver infections

Pyogenic liver abscess

Liver abscess is rare. Common organisms include Streptococcus milleri, E. coli, Enterococcus faecalis, Staphylococcus aureus and Bacteroides (see Box 8.1 for causes).

Box 8.1 Causes of liver abscess

Cholangitis

Portal pyaemia secondary to abdominal infection, e.g. appendicitis, diverticulitis, peritonitis

Biliary disease

Trauma

Empyema of gallbladder

Septicaemia

Infected liver cyst

Cryptogenic

Symptoms and signs are variable and may reflect underlying disease – fever, rigors, jaundice and upper abdominal pain.

Investigations include WBC, LFTs, blood cultures, ultrasound, CT scan and white cell scan. Differential diagnosis includes tumour and amoebic abscess.

Management requires IV antibiotics. Percutaneous drainage may be used and the collection followed ultrasonically. Sometimes open surgical drainage is required. Morbidity and mortality are high if abscesses are multiple or inadequately drained.

Amoebic liver abscess

Due to infection with Entamoeba histolytica as a complication of parasitic colitis, the amoeba enters the portal circulation through an ulcer in the colonic mucosa. Abscesses due to the parasite may be single (common) or multiple. They may be extensive and are more common in the right lobe of the liver. The pus formed is thick and contains small quantities of blood – the description often used is that it resembles anchovy sauce. Extension of the abscess may lead to pleural effusion, bronchopleural fistula and lung abscess.

Clinical features

There may be a history of colitis. More usually there is progressive, painful right upper quadrant pain with sweating, rigors and pyrexia. Respiratory symptoms may occur. Physical findings include right upper quadrant tenderness, hepatomegaly and jaundice.

Investigation and management

Investigations include ultrasound or CT scan with aspiration and culture of pus, stool examination, serology testing (negative almost excludes abscess).

Metronidazole is specific with or without percutaneous drainage. Open surgery is unusual.

Hydatid disease

This is a common condition in the Mediterranean and Middle East, due to the parasite Echinococcus granulosus (tapeworm). The tapeworm develops in the dog intestine after the dog eats contaminated sheep or cattle offal. The ova are shed in the faeces which contaminate grass or vegetables and are then eaten by sheep, cattle or humans. The ova pass to the liver and develop into hydatid cysts. The cysts usually occupy the upper pole of the right lobe and are slow growing. Many become inactive and calcify.

Clinical features are a symptomless mass, abdominal pain and jaundice.

Investigations include plain X-ray, which may show calcification, ultrasound and CT.

Calcified cysts require no treatment. Drug therapy includes albendazole. Obstructive jaundice due to daughter cysts or cholangitis is managed by endoscopic sphincterotomy. Open surgery is rarely needed.

Liver tumours

Benign tumours

Benign tumours are common and are usually haemangiomas, focal nodular hyperplasia or hepatic adenomas (occasionally associated with oral contraceptives). CT or MRI scan facilitates diagnosis. Biopsy is contra-indicated for haemangioma and no treatment is needed. Distinguishing between a benign adenoma and a well-differentiated hepatocellular carcinoma may be difficult.

Malignant tumours

Hepatocellular carcinoma

Hepatocellular carcinoma is common in Africa but rare in the UK. Widespread Hep-B vaccination is reducing incidence in the Far East. Predisposing factors include alcoholic cirrhosis and chronic liver disease caused by hepatitis B or C, or haemochromatosis. The disease is frequently multifocal with metastatic spread to the lungs.

Presenting features are vague or superimposed on a background history of previous liver disease. Malaise, weight loss and abdominal discomfort are common. Hepatomegaly and signs of metastatic disease may be obvious.

Investigation includes liver function tests and alpha-fetoprotein. CT scan and angiography confirm the presence of tumour and vascular anatomy.

Surgical resection offers the only hope of cure, with a 45% 5-year survival rate. Palliative treatment includes embolisation of tumour blood supply, chemotherapy, alcohol injection and CT-guided cryotherapy.

Cholangiocarcinoma

Cholangiocarcinoma may be intra- or extrahepatic (Klatskin tumours). There is an association with primary sclerosing cholangitis, liver flukes and anabolic steroids.

Clinical features may include progressive jaundice, weight loss, cholangitis and palpable mass in the right upper quadrant.

A combination of ultrasound, CT or MRI combined with ERCP/PTC demonstrates the site of the lesion. Fine-needle aspiration cytology may confirm the diagnosis.

The prognosis is poor; surgical reconstruction may be possible with up to 40% 5-year survival, dependent upon appropriate selection of patients. Biliary enteric bypass and endoscopic biliary stenting provide other palliative options.

Liver metastases from distant primary cancer

Almost any cancer may metastasise to the liver but the commonest are colon, breast, lung, pancreas and stomach. Most metastases are asymptomatic. Large lesions may cause pain, jaundice and anorexia. CT scan and MRI are used to assess resectability, particularly for colorectal primary lesions with increasing prospects of cure combined with chemotherapy. Most other metastatic lesions are treated with palliative chemotherapy.

Gallstones (cholelithiasis)

Epidemiology and aetiology

Gallstones occur in 10% of the population over 50. They are more common in females but can affect anyone. Cholesterol is the principal constituent of the majority of stones, usually combined with bile pigment, especially bilirubin. Stones composed of pigment alone account for 5% of the total. Eighty per cent of stones are asymptomatic. Gallstones are caused by a combination of excess cholesterol concentration in bile, stasis or increased bilirubin secretion in bile. Bacterial infection may also play a role. Symptoms of gallstones are related to the complications they cause (Box 8.2).

Box 8.2 Complications of gallstones

Gallbladder

Biliary colic (p. 95)

Acute cholecystitis

Empyema

Mucocele

Common bile duct

Obstructive jaundice

Cholangitis

Pancreatitis

Small intestine

Gallstone ileus

Stones in the gallbladder

Biliary colic (see p. 95)

When a gallstone becomes impacted in Hartmann’s pouch or the cystic duct it causes biliary colic. The cycle of the colic is long and the pain may be felt as a constant pain in the epigastrium and right upper quadrant, radiating through to the back. Attacks may be precipitated and exacerbated by eating fatty food. Vomiting is common. The pain spontaneously settles when the stone disimpacts, or passes into the common bile duct. Physical findings may be minimal.

LFTs and WBC are normal. Plain X-ray reveals only 10% of gallstones and is not a useful test. Ultrasound detects 98% of gallbladder stones but is less reliable for bile duct stones.

Management requires analgesics and bed rest (antibiotics are not required for biliary colic), then elective cholecystectomy.

Acute cholecystitis

If a stone impacts in the cystic duct preventing gallbladder drainage, a chemical cholecystitis ensues often with secondary bacterial infection. The pain is more severe and persistent than in biliary colic. Fever is usually present. There is tenderness and guarding in the right upper quadrant (positive Murphy’s sign). Hyperaesthesia of the skin over the ninth to eleventh right ribs posteriorly (Boas’ sign) may be present. Omentum and small bowel adhere to the inflamed gallbladder and may be palpated as a mass in the right upper quadrant.

The WBC is raised and LFTs often mildly deranged due to partial obstruction of the hepatic duct. Ultrasound confirms stones in the gallbladder with a thickened wall, often surrounded by fluid. Initial treatment is nonoperative with analgesics, antibiotics and intravenous fluids. Failure to settle may result in empyema formation or perforation of the gall bladder. Cholecystectomy prevents further attacks, and should either be performed early (within 2–3 days) or after 6 weeks when inflammation has subsided.

Chronic cholecystitis

This is due to recurrent attacks of obstruction and inflammation; a history of intolerance of fatty foods is common. Diagnosis is confirmed on ultrasound, which reveals a shrunken gallbladder with a thick, fibrotic wall. Cholecystectomy results in cure.

Stones in the bile duct (choledocholithiasis)

Common bile duct stones may cause obstructive jaundice, acute cholangitis and acute pancreatitis. The majority of stones originate from the gallbladder but some may form within the duct system de novo. Common bile duct stones are usually removed prior to cholecystectomy at ERCP and sphincterotomy. This is performed using baskets or sweeping the duct with a balloon.

Obstructive (cholestatic) jaundice

A history of preceding biliary colic is common. The main complaints are jaundice, pruritus, dark urine and pale stools. Abdominal signs are minimal (Courvoisier’s law: a palpable gallbladder in the presence of jaundice is NOT due to stones).

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