Liver infections

Viral hepatitis is a major world health problem. In addition to the well-recognised acute and chronic liver diseases produced by hepatitis A, B and C, other hepatitis viruses have been isolated including hepatitis D, which is usually detected only in patients with hepatitis B virus (HBV) infection, and hepatitis E, which produces a self-limiting hepatitis due to faecal—oral spread similar to hepatitis A.

Hepatitis A presents with anorexia, weakness and general malaise for several weeks prior to the development of clinical jaundice, often accompanied by tenderness on palpation of an enlarged liver. The condition is spread by the faecal—oral route and often spreads rapidly in closed communities. Liver function tests will be compatible with an acute hepatitis with elevation of bilirubin and transaminases. Diagnosis is confirmed by the antibody titre to hepatitis A. The condition is virtually always self-resolving, although rarely the viral hepatitis can lead to fulminant liver failure. Once the clinical condition resolves the liver tends to recover fully with no functional deficit and no long-term sequelae.

Hepatitis B is a more serious condition in most respects than hepatitis A. Although it can also produce an acute self-resolving hepatitis, the virus is often not cleared and pro­duces long-term liver damage with the development of liver cirrhosis and primary liver cancers. Patients may therefore present acutely with malaise, anorexia, abdominal pain and clinical jaundice due to active hepatitis or may present at a late stage owing to the complications of cirrhosis, most com­monly ascites or variceal bleeding. Treatment for acute hepatitis is supportive. In patients with cirrhosis, treatment is initially dictated by the specific complication at presentation (see subsections on the treatment of ascites and variceal bleeding earlier in this chapter). In established cirrhosis, liver transplantation may be considered if viral eradication or suppression can be achieved with antiviral agents (e.g. lamivudine). Without viral suppression death from reinfection of the transplanted liver is common. The hepatitis virus greatly increases the risk of primary liver cancers which usually appear at the stage when the liver parenchyma has become cirrhotic. The assessment and management of HBV cirrhosis with hepatocellular carcinoma (HCC) is discussed in the section on ‘Liver turnouts.

Hepatitis C has become one of the commonest causes of chronic liver disease world-wide and in many countries a large percentage of the population has been exposed. One per cent of blood donors world-wide are hepatitis C virus (HCV) positive. Transmission is often related back to blood transfusion and routine screening of blood for HCV has only recently been introduced in many countries. As with hepatitis B, it may present as an acute hepatitis or remain hidden until the development of cirrhosis and the complications of portal hypertension. Acute hepatitis C proceeds to cirrhosis in about 20 per cent of cases. Deterioration in liver function, encephalopathy, ascites or bleeding in a patient with known HCV cirrhosis necessitates an urgent assessment for liver transplantation, if available. Although reinfection of the graft is common it generally results in a mild hepatitis from which the graft and patient fully recover and is associated with a good long-term outcome.

Ascending cholangitis

Ascending bacterial infection of the biliary tract is usually associated with obstruction, and presents with clinical jaun­dice, rigors and a tender hepatomegaly. The diagnosis is confirmed by the finding of dilated bile ducts on ultrasound, an obstructive picture of liver function tests and the isolation of an organism from the blood on culture. The condition is a medical emergency and delay in appropriate treatment results in organ failure secondary to septicaemia. Once the diagnosis has been confirmed the patient should be com­menced on a first-line antibiotic (e.g. third-generation cephalosporin), rehydrated and arrangements made for endoscopic or percutaneous transhepatic drainage of the biliary tree. Biliary stone disease is a common predisposing factor and the causative ductal stones may be removed at the time of endoscopic cholangiography by endoscopic sphincterotomy.

 Pyogenic liver abscess

The aetiology of a pyogenic liver abscess is unexplained in the majority of patients. It has an increased incidence in the elderly, diabetics and the immunosuppressed, who usually present with anorexia, fevers and malaise accompanied by right upper quadrant discomfort. The diagnosis is suggested by the finding of a multiloculated cystic mass on ultrasound or CT scan (Fig. 52.17) and is confirmed by aspiration for culture and sensitivity. The most common organisms are Streptococcus milleri and Escherichia coil but other enteric organisms such as Streptococcus faecalis, Klebsiella and Proteus vulgaris also occur and mixed growths are common. Opportunistic pathogens include Staphylococci. First-line antibiotics would be a penicillin, aminoglycoside and metronidazole or a cephalosporin and metronidazole. Treat­ment is with antibiotics and ultrasound-guided aspiration. Percutaneous drainage without ultrasound guidance should be avoided as an empyema may follow drainage through the pleural space. A source for the liver abscess should be sought, particularly from the colon. Atypical clinical or radiological findings should raise the possibility of a necrotic neoplasm.

 Amoebic liver abscess

Entamoeba histolytica is endemic in many parts of the world. It exists in vegetative form outside the body and is spread by the faecal—oral route. The most common presentation is with dysentery but it may also present with an amoebic abscess, the common sites being paracaecal and in the liver. The amoebic cyst is ingested and develops into the trophozoite form in the colon which passes through the bowel wall and to the liver via the portal blood. Diagnosis is by isolation of the parasite from the liver lesion or the stool and confirming its nature by microscopy. Often patients with clinical signs of an amoebic abscess will be treated empirically with metronidazole (750 mg t.d.s. for 5—10 days) and investigated further only if they do not respond.

 Hydatid liver disease

This is a very common condition in countries around the Mediterranean. The causative tapeworm, Echinococcus granulosus, is present in the dog intestine and ova are ingested by humans and pass in the portal blood to the liver. Liver abscesses are often large by the time of presentation with upper abdominal discomfort or may present after minor abdominal trauma as an acute abdomen due to rupture of the cyst into the peritoneal cavity. Diagnosis is suggested by the finding of a multiloculated cyst on ultrasound and is further supported by the finding of a floating membrane within the cysts on CT scan (Fig. 52.18). Active cysts contain a large number of smaller daughter cysts (Fig. 52.19) and rupture can result in these implanting and growing within the peritoneal cavity. Liver cysts can also rupture through the diaphragm producing an empyema, into the biliary tract producing obstructive jaundice or into the stomach. Clinical and radiological diagnosis can be supported by serology for antibodies to hydatid antigen in the form of an enzyme-linked immunosorbent assay (ELISA). Treatment is indicated to prevent progressive enlargement and rupture of the cysts. In the first instance a course of albendazole or mebendazole may be tried. Failure to respond to medical treatment usually requires surgical intervention, although percutaneous treatments with hypertonic saline and alcohol have been attempted. The surgical options range from liver resection or local excision of the cysts to deroofing with evacuation of the contents. Contamination of the peritoneal cavity at the time of surgery with active hydatid daughters should be avoided by continuing drug therapy with albendazole and adding perioperative praziquantel. This should be combined with packing of the peritoneal cavity with 2 N saline-soaked packs and instilling hypertonic (2 N) saline into the cyst before it is opened. A biliary communication should be actively sought and sutured. The residual cavity may become infected and this may be reduced, as may bile leakage, by packing the space with pedicled greater omentum (an omentoplasty). Calcified cysts may well be dead. If doubt exists as to whether a suspected cyst is active it can be followed on ultrasound, active cysts gradually becoming larger and more superficial in the liver. Rupture of daughter hydatids into the biliary tract may result in obstructive jaundice or acute cholangitis. This may be treated by endoscopic clearance of the daughter cysts prior to cyst removal from the liver.