Page 198 - Medicine and Surgery

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194 Chapter 5: Hepatic, biliary and pancreatic systems

preceding the onset of jaundice. On examination there foratleast6months.However,itissometimesdiagnosed
may be an enlarged, tender liver, pale stools and dark earlier than this.
urine. Stigmata of chronic liver disease should be looked
for to exclude acute on chronic liver disease.
Aetiology
The main causes of chronic hepatitis:
Microscopy
Viral hepatitis: Hepatitis B virus (+/− hepatitis D),
Acute viral hepatitis has a histological appearance which
hepatitis C virus.
can be mimicked by drug reactions. Hepatocytes un-
Autoimmune: Autoimmune chronic hepatitis, pri-
dergo ballooning degeneration appearing swollen and
mary biliary cirrhosis (PBC).
vacuolated. There is a lymphocytic infiltration. Cell
Toxic:Alcohol-inducedhepatitis(rare),drug-induced
death is by apoptosis and results in the formation of
hepatitis (methyldopa, isoniazid, ketoconazole, anti-
Councilman bodies. As regeneration occurs the normal
retroviral drugs).
architectureisdisrupted.Inseverecases,necrosisspreads
Nonalcoholic hepatosteatosis (NASH).
from one portal tract to the central vein or from central
Inherited: Wilson’s disease, α 1 antitrypsin deficiency,
vein to central vein, so that confluent areas of necrosis
haemochromatosis.
form termed bridging necrosis.
Complications Clinical features
Fulminant liver failure, chronic hepatitis, and cirrhosis. Patients may present with non-specific symptoms
(malaise, anorexia and weight loss) or with the compli-
Investigations
cations of cirrhosis such as portal hypertension (bleed-
Serum bilirubin and transaminases (aspartate

ing oesophageal varices, ascites, encephalopathy). Fol-
transaminase (AST) and alanine aminotransferase
lowing acute viral hepatitis persistently raised serum
(ALT)) are raised in acute liver injury.
transaminases (aspartate transaminase, alanine amino-
Prothrombin time and albumin should be measured.

transferase) may be detected during follow-up. Asymp-
Ultrasound may be needed to exclude obstructive

tomatic patients with chronic viral hepatitis may be de-
jaundice, if applicable.
tected during screening at blood donation.
Serological testing will identify viral infections.

Specific tests depend on suspected causes, e.g. parac-

etamol levels. A liver biopsy may be required if the Microscopy
cause is not identified. Features include lymphocyte infiltration, fibrosis and fat
deposition. Histologically three patterns of chronic hep-
Management atitis are seen.
In most cases supportive management is the only avail- Chronic active hepatitis (CAH). A severe pattern
able treatment. This includes careful fluid balance, which is likely to progress rapidly to cirrhosis with
adequate nutrition and anti-emetics. Where possible re- chronic inflammatory cells infiltrating the portal
moval of the causative agent, e.g. alcohol or specific ther- tracts and extending into the lobule with ‘piecemeal
apies should be given (see Wilson’s Disease page 211 and necrosis’. Fibrous tissue formation links portal tracts
Paracetamol poisoning page 527). Patients require se- to central veins or central veins to each other (bridging
rial liver function tests (including clotting) to follow the necrosis).
course of the hepatitis. Chronic persistent hepatitis (CPH) has a more
favourable prognosis unless caused by hepatitis C
virus. CPH may also develop into CAH in some
Chronic hepatitis
e-antigen positive hepatitis B infected patients. In-
Definition flammation is confined to the portal tracts.
Chronic hepatitis is a clinical and pathological syn- Chronic lobular hepatitis (CLH) is most com-
drome characterised by a variable degree of hepatocel- monly associated with viral hepatitis. Hepatitis B pa-
lular necrosis and inflammation, without improvement tients who are e-antigen positive may develop CAH.