Fullminant Hepatitis

• Fulminant hepatic failure is the clinical

syndrome associated with massive necrosis of
liver cells or sudden, severe impairment of
hepatic function.
 Etiology
• Fulminant hepatic failure is caused by viral
hepatitis, drug reactions, or poisonings in
more than 90% of cases.

• In Western countries about 80% of cases are

due to hepatitis virus infections; of these,
hepatitis B virus is the most common.
 Manifestation
• progressive jaundice, hepatic coma, and liver
atrophy developing with in 8 weeks of the
onset of the first symptoms of the disease in
individuals with no previous history of hepatic
disease
 Complications
• Hepatic encephalopathy is a universal
complication in fulminant liver failure, as it is
required for the diagnosis.

• Patients with stage I encephalopathy are

generally alert and have mainly
neuropsychiatric disturbances.
 Treatment
• Patients with FH should be managed in an
intensive care unit and transferred as soon as
possible to centres with a liver transplant
program.
• As most patients with acute liver failure
develop dome degree of circulatory
dysfunction, attention must be paid to fluid
management and haemodynamics.
 Treatment
• In addition, surveillance for, and prompt
treatment of infection is also crucial.
• Coagulation parameters, complete blood counts,
metabolic panels (including glucose) and arterial
blood gas should be checked frequently.
• Serum aminotransferases and bilirubin are
generally measured daily to follow the course of
the condition; however, changes in
aminotransferase levels correlate poorly with
prognosis, and a decline should not be
interpreted as a sign of improvement
Post Hepatic Syndrome
Budd Chiari Syndrome
 Definition
• Budd-Chiari syndrome (BCS) is a rare and
potentially life-threatening disorder
characterized by obstruction of the hepatic
outflow tract at any level between the
junction of the inferior vena cava with the
right atrium and the small hepatic veins.
 Etiology

• BCS is further classified as being primary or

secondary
• depending on the exact nature of the hepatic
venous outflow obstruction. When flow is
obstructed by compression or invasion of a lesion
outside the hepatic venous outflow track, it is
regarded as being secondary

• Examples: malignant and cystic extrinsic

obstruction
• By far the most common cause of primary BCS is
thrombosis, although geographical differences
exist with idiopathic membranous obstructions
(webs) being prevalent in Asia

• in China the etiology of BCS is different. Data

show that prothrombotic disorders are not
common in China as a cause of BCS, but
endoluminal aberrancies caused by unknown
factors (but possibly related to environmental
conditions and infection) result in BCS in China.
 epidemiology
• Asian: China
• Amerika
• Europe
 Clinical manifestation

• The classic triad of abdominal pain, ascites and

hepatomegaly is commonly present in patients,
with abdominal pain presenting in 61%, ascites in
83% and hepatomegaly in 67% of patients.
• Other clinical features include fever, pedal edema
and truncal hepatic veins.
• Less common clinical manifestations include
esophageal bleeding (5%) and hepatic
encephalopathy (9%).
 Diagnostic workup

• If non invasive: Doppler ultrasonography,

computed tomography (CT) or magnetic
resonance imaging (MRI).
• If finding a pathologic invasive: sonography
 PATHOGENESIS
• Obstruction of a single hepatic vein is
generally not evident; two veins must be
blocked for clinical disease
• The result of these hemodynamic changes is
sinusoidal dilation and filtration of interstitial
fluid. Filtrated interstitial fluid passes through
the liver capsule when it exceeds the capacity
of lymphatic drainage. Thus, liver congestion,
right upper quadrant pain and ascites occur.
• . The combined effect of these changes in
hepatic circulation on liver parenchyma is
hypoxic damage of hepatocytes. Non-
inflammatory centrilobular cell necrosis is
found in nearly 70% of cases
• Both the acute and chronic forms result in
severe centrilobular congestion and
hepatocellular necrosis and atrophy
Treatment