Liver infections are classified according to the category of the infecting agent as viral, bacterial or parasitic. Viral infections include both primary hepatitis viruses or secondary causes where the liver is involved during systemic viral infections such as cytomegalovirus, HIV and herpes simplex. This chapter will not discuss viral infections of the liver.
Pyogenic or bacterial abscess may be caused by several factors and is classified by the route of entry of the organisms. Infections may arise from the biliary tract, portal vein and hepatic artery or by direct extension.
- Infections arising from the biliary tract are the most common and result in 30% to 50% of the total number of pyogenic abscesses. The resultant cholangitis leads to liver abscesses, which are frequently multiple. Biliary obstruction is commonly present from causes such as choledocholithiasis and benign or malignant strictures. Other causes of cholangitis include iatrogenic intervention from endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic procedures.
- Another common route of entry of infection is the portal vein. Conditions such as complicated diverticular disease, appendicitis, peritonitis and pancreatitis may cause portal vein pyaemia, resulting in pyogenic liver abscesses.
- Septicemia from any cause may also give rise to multiple liver abscesses via dissemination from the hepatic artery. These account for 5 to 15% of pyogenic liver abscesses. Common causes include bacterial endocarditis, pneumonia and intravenous drug abuse.
- Other causes of liver abscesses include complicated liver trauma from blunt or penetrating causes, or by direct extension from other conditions such as empyema of the gall bladder. In a number of cases, the cause is not obvious.
The infecting organism varies according to the site of entry. In biliary or portal vein sepsis, the organisms are enteric and usually polymicrobial. Staphylococcus aureus is evident in 20% of cases and is confirmed predominantly from haematogenous spread.
Clinical presentation and diagnosis
The most common presenting symptoms include pyrexia and rigours associated with right upper quadrant pain, general malaise and anorexia. Examination may reveal tender hepatomegaly. A pleural effusion may be present. Occasionally, hypotension and cardiovascular collapse may be the presenting symptoms.
Liver function tests may show hyperbilirubinemia and raised alkaline phosphatase and transaminase levels. Blood cultures are frequently positive. A leucocytosis is usually evident.
Radiological investigations include ultrasound orCT scan of the abdomen to determine the size, characteristics, number and anatomical location of the liver abscesses. A chest X-ray may show an elevated hemidiaphragm or a pleural effusion. Further tests such as an ERCP or a colonoscopy may be required to determine the cause of pyogenic liver abscesses.
Therapeutic principles include symptomatic measures, appropriate antibiotic therapy and drainage of the liver abscess. In addition the diagnosis and eradication of the underlying cause is essential.
- Symptomatic measures include a regimen of analgesics and attention to adequate nutrition and hydration.
- Antimicrobial therapy is dependent on the underlying cause. Biliary or enteric causes involve microbial cover against Gram-negative and anaerobic organisms. Haematogenous causes usually include antibiotic cover against the staphylococcus organisms. Administration of antibiotics is usually prolonged over several weeks to eradicate infection and avoid recurrence.
- Drainage of the abscess may be achieved by percutaneous drainage under ultrasound control or by repeated percutaneous aspiration. Open surgical drainage is now rarely indicated.
- Frequent clinical, biochemical, microbial and radiological follow-up is required to assess progress and detect relapses.
Amoebic liver abscesses
Amoebic infestation is caused by the organism Entamoeba histolytica. It is rare in Australia but endemic in many areas of the tropics such as India and other parts of Asia. Transmission is by passage of cysts in the stool, the cysts then being ingested orally as a result of poor hygienic practices. The organism penetrates the mucosa of the gastrointestinal tract to gain access to the liver by the portal venous system. The resultant abscess has an ‘anchovy paste’ appearance and may be secondarily infected, usually by enteric organisms. Risk factors include malnutrition, depressed immunity and low socioeconomic status.
Complications of amoebic abscess include rupture into the peritoneal cavity or hollow viscus such as colon or stomach. Rarely there may be pleuropulmonary involvement.
The onset of the disease may be sudden or gradual. Right upper quadrant pain associated with general malaise and weight loss are the most common symptoms on presentation. Pyrexia and sweating occurs in about 60% of patients. Approximately 30% of patients have diarrhoea. Signs may include tender hepatomegaly and, occasionally, jaundice.
Full blood examination may show leukocytosis and eosinophilia. Liver function tests are frequently deranged and show a hepatocellular pattern of injury. Amoebic serology and stool cultures are usually positive. Ultrasound with needle aspiration and culture confirm the diagnosis.
Symptomatic measures include analgesics and attention to nutrition and hydration. Antimicrobial therapy is the mainstay of treatment. This may be associated with percutaneous drainage or repeated aspiration if necessary. The antibiotic of choice is metronidazole.
There are two forms of hydatid disease, the most common being Echinococcus granulosus, which causes cystic hydatid disease. Echinococcus alveolaris is a much rarer form and is characterised by an infiltrative pattern of liver involvement.
In this disease, the human is an intermediate host. The ova are ingested by humans from the faeces of tapeworm-infected dogs. Dogs are usually infected by feeding of offal of infected sheep. The ova reach the stomach of the human, where they hatch, penetrate the wall of the intestine and pass to the liver by the portal vein. Others may pass from the liver into the lung, brain, or other organs. Development of the cyst in liver then occurs. These cysts exhibit a slow growth pattern and infection usually occurs in childhood.
The cyst has a characteristic appearance (see Hydatid cyst of the liver.). There is a capsule or exocyst, which is really the compressed host tissue. The endocyst includes the laminated membrane from the parasite, which contains the germinal layer and scolices. The cyst is fluid-filled and also contains brood capsules. The natural history of hydatid cysts is that of continued growth. Apart from local compressive effects, rupture may occur into the biliary tree causing obstructive jaundice. Rupture into the peritoneal or thoracic cavity may also occur in addition to hematogenous spread to other organs such as lung, bone, brain and spleen. The cysts may become secondarily infected.
Hydatids may be symptomless and are detected as incidental findings on radiological investigations for other conditions. The most common symptoms are right upper quadrant pain, jaundice, pruritus and pyrexia. A persistent cough may indicate pulmonary involvement.
Liver function tests may show either an obstructive or hepatocellular pattern. Full blood examination may reveal a leukocytosis or eosinophilia. There are numerous serological tests available. The most sensitive and specific test is immunoelectrophoresis, which is not only diagnostic but is an indicator of the response to treatment. Radiological tests to assess the size and location of the cyst include ultrasound and CT scan. ERCP or magnetic resonance cholangiopancreatography (MRCP) may be indicated to detect biliary connections or bronchobiliary fistulas.
- ConservativeSmall (<2–3 cm) asymptomatic cysts, which are deep in the parenchyma, require no treatment. Complications in this group are rare. These patients however need regular follow–up.
- MedicalDrug therapy may be used alone or in conjunction with surgical procedures. Mebendazole or albendazole may be used in patients with hydatid disease who are regarded as poor risk for surgery or with widely disseminated disease. It may be also be used by percutaneous injection under ultrasound localisation directly into the cyst. These drugs may also be administered either before or after definitive surgery to minimise the risk of recurrence. Prolonged courses over 6-12 weeks are usually required. Medical therapy alone is successful in 30 to 50% of cases. These drugs may be toxic to the liver and bone marrow and require careful monitoring.
- SurgeryThe principles of surgical management include (a) complete neutralisation and removal of the parasite components, including the germinal membrane, scolices and brood capsules; (b) prevention of contamination or spillage to prevent anaphylaxis or recurrence and (c) management of the residual cavity.
Procedures may include liver resection, with total excision of the cyst, including the capsule (pericystectomy). This is rarely indicated and is suitable for peripheral or pedunculated cysts.
Scolicidal agents are frequently injected into the cyst prior to manipulation to destroy active components and prevent recurrence if spillage occurs. Commonly used agents include cetrimide or hypertonic saline. The contents of the cyst are then evacuated. The residual cavity may be filled with saline and closed (capittonage) or obliterated by an omental pedicle, especially in infected cysts.
Biliary communications may need to be closed and bile duct explored to remove hydatids causing biliary obstruction.
Liver fluke disease
Infestations of clinical importance include those by Fasciola hepatica, Clonorchis sinensis and Ascaris lumbricoides. These parasites are trematodes and undergo both sexual (definitive host) and asexual (intermediate host) reproduction.
This condition exists all over the world but is commonly seen in Middle and Western Europe, South America and the Caribbean. It is known as the common sheep fluke and is found in sheep- and cattle-rearing countries.
The parasite inhabits the gall bladder and bile ducts and passes ova in the stool. The human is an incidental host, especially those eating raw vegetables. Cysts are ingested from vegetables and subsequently penetrate the intestinal wall. They then migrate by the transperitoneal route and invade the liver capsule and enter the biliary system, where they are sometimes confused as stones.
Patients may be asymptomatic or present with acute or chronic symptoms. Acute symptoms include a sudden onset of right upper quadrant pain, pyrexia or cholangitis and symptoms of allergic reactions. Hepatosplenomegaly may be present. Chronic symptoms include intermittent biliary colic, cholecystitis, jaundice anaemia and hypoproteinaemia.
Full blood examination may show eosinophilia. Liver function tests show features consistent with cholestasis. Stools are examined for the presence of ova. Specific serological testing usually confirms the diagnosis.
The condition is treated by albendazole, praziquantel or bithional. Cholecystectomy and exploration of the common bile duct by ERCP may also be necessary.
Chlonorchis sinensis is a flat worm which inhabits the biliary tree. Cysts from infected fish are ingested and migrate from the duodenum into the bile ducts. Ova are excreted from the stools. The intermediate host is a snail, which completes the life cycle by infecting fish. Humans are infected by eating raw fish.
The biliary epithelium becomes inflamed from constant irritation, leading to cholangitis, ductal fibrosis, stricturing and stone formation. There is a high incidence of cholangiocarcinoma.
The classic symptoms associated with clonorchis infestation are recurrent pyogenic cholangitis. There are recurrent attacks of right upper quadrant pain, jaundice and pyrexia. Examination may reveal tender hepatomegaly and splenomegaly if portal hypertension exists.
Imaging of the biliary tree by MRI or ERCP is essential to delineate the distribution of stones and strictures. Ova are demonstrated in faeces or duodenal aspirate.
The drug of choice is Praziquantel. Surgery is indicated if stones or strictures are present.
The roundworm Ascaris lumbricoides is endemic in tropical and subtropical areas. The worms inhabit the small intestine and enter the common bile duct by the duodenal ampulla of Vater.
They induce mechanical obstruction of the biliary tree. Cholangitis, empyema of the gall bladder and multiple liver abscesses may occur as a result of secondary infection.
Stool examination commonly demonstrates the presence of worms. Ultrasound is highly accurate in delineating the worms in the biliary tree.