ACUTE VIRAL HEPATITIS By Dr Muhammad Ubaid Assistant Professor- Medicine
BILIRUBIN METABOLISM
BILIRUBIN METABOLISM
DEFINITIONS Hepatitis : inflammation of liver. Acute Hepatitis : symptoms last less than 6 months. Acute Hepatic Failure : is the appearance of severe complications rapidly after the first signs of liver disease (such as jaundice), & indicates that the liver has sustained severe damage (loss of function of 80-90% of liver cells ). Massive hepatic necrosis with impaired consciousness within 8 weeks of onset of illness . Fulminant Hepatitis : severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease. Chronic Hepatitis : Inflammation of liver for at least 6 months. Cirrhosis : Replacement of liver tissue with fibrosis(scar tissue).These changes lead to loss of liver function .
DEFINITIONS Hyperacute liver failure The onset of encephalopathy less than 7 days after the development of jaundice. Acute liver failure The onset of encephalopathy 8 to 28 days after the development of jaundice . Sub-acute liver failure The onset of encephalopathy more than 5 weeks but less than 12 weeks after the development of jaundice .
Clinical and Epidemiologic Features of Viral Hepatitis FEATURE HAV HBV HCV HDV HEV Incubation period in days 15–45 , mean 30 30–180, mean 60–90 15–160, mean 50 30–180 , mean 60–90 14–60 , mean 40 Onset Acute Insidious or acute Insidious or acute Insidious or acute Acute Age preference Children, young adults Young adults Any age, common in adults similar to HBV Epidemic young adults Sporadic older adults Transmission Mostly Fecal-oral Percutaneous Perinatal Sexual Percutaneous Perinatal Sexual Percutaneous Perinatal Sexual Percutaneous Perinatal Sexual Fecal-oral Clinical Severity Mild Occasionally severe Moderate Occasionally Severe Mild But Fulminant in Pregnancy Progression to chronicity No Yes Yes Yes No
PRODROMAL (PREICTERIC) PHASE Constitutional symptoms, Duration : 1-2 weeks Anorexia Nausea Vomiting Alterations in olfaction and taste Fatigue, malaise Arthralgias & myalgias Headache Photophobia Pharyngitis, cough, and coryza M ay precede the onset of jaundice by 1–2 weeks. Dark urine and clay- colored stools may be noticed by the patient from 1–5 days before the onset of clinical jaundice.
ICTERIC PHASE Clinical jaundice Dark urine Pruritus Resolution of fever Constitutional prodromal symptoms usually diminish, but in some patients, mild weight loss & symptoms continue A substantial proportion of patients with viral hepatitis never become icteric.
ICTERIC PHASE The liver becomes enlarged and tender Splenomegaly and cervical lymphadenopathy are present in 10–20% A few spider angiomas appear during the icteric phase and disappear during convalescence. Encephalopathy : Irritability, lethargy, confusion
CONVALESCENCE / RECOVERY PHASE Constitutional symptoms disappear Some liver enlargement and abnormalities in liver biochemical tests still evident. Duration: is variable 2 to 12 weeks More prolonged in acute hepatitis B and C. Complete clinical and biochemical recovery: 1–2 months hepatitis A and E 3–4 months in 75% of hepatitis B and C
JAUNDICE
JAUNDICE
Stool & Urine in Viral Hepatitis
SPIDER ANGIOMAS
CHOLESTATIC SCRATCH MARKS
INVESIGATIONS IN ACUTE VIRAL HEPATITIS Complete Blood Count / Complete Blood Picture Hb is usually normal Leukopenia, lymphocytosis Platelets are normal except usually in Sepsis/DIC Urine D/R Urobilinogen Urinary Bilirubin
INVESIGATIONS IN ACUTE VIRAL HEPATITIS Liver Function Tests Serum bilirubin typically rises to levels ranging from 5–20 mg/dl. The serum bilirubin may continue to rise despite falling serum aminotransferase levels. In most instances, the total bilirubin is equally divided between the conjugated and unconjugated fractions. Bilirubin levels >20 mg/dl extending and persisting late into the course of viral hepatitis are more likely to be associated with severe disease. In certain patients with underlying hemolytic anemia , unconjugated bilirubin can combine give levels upto even >30 mg/dl
INVESIGATIONS IN ACUTE VIRAL HEPATITIS Liver Function Tests The serum aminotransferases aspartate aminotransferase, AST and ALT (previously designated SGOT and SGPT) are the enzymes released during hepatocyte damage. The level of these enzymes, however, does not correlate well with the degree of liver cell damage . Peak levels vary from ~400 to ~4000 IU or more These levels are usually reached at the time the patient is clinically icteric and diminish progressively during the recovery phase of acute hepatitis Serum alkaline phosphatase may be normal or only mildly elevated
INVESIGATIONS IN ACUTE VIRAL HEPATITIS Liver Function Tests Prothrombin Time : prolonged value may reflect a severe hepatic synthetic defect, signify extensive hepatocellular necrosis, and indicate a worse prognosis RBS: Hypoglycemia Serum Protiens : May have hypoabuminemia
IDENTIFICATION OF VIRUS IN ACUTE VIRAL HEPATITIS (Antibodies) HEPATITIS A: Anti HAV- IgM : Acute Anti HAV- IgG : Chronic HEPATITIS B: HbsAg Anti HBc Antibody- IgM HbeAg
IDENTIFICATION OF VIRUS IN ACUTE VIRAL HEPATITIS (Antibodies) HEPATITIS C: Anti HCV: HEPATITIS D : Anti HDV HEPATITIS E: Anti HEV- IgM : Acute Anti HEV- IgG : Chronic
IDENTIFICATION OF VIRUS IN ACUTE VIRAL HEPATITIS (Identification of RNA/DNA) Isolation of Virus RNA or DNA by PCR technique Can be Qualitative or Quantitative Genotyping of Specific Sub type
MANAGEMENT OF ACUTE VIRAL HEPATITIS
MANAGEMENT OF ACUTE VIRAL HEPATITIS
MANAGEMENT OF ACUTE VIRAL HEPATITIS Most persons with acute hepatitis recover spontaneously. Specific treatment generally is not necessary. Hospitalization may be required for clinically severe illness, most patients do not require hospital care. Forced and prolonged bed rest is not essential for full recovery, but many patients will feel better with restricted physical activity. A high-calorie diet is desirable
MANAGEMENT OF ACUTE VIRAL HEPATITIS Intravenous feeding is necessary in the acute stage if the patient has persistent vomiting and cannot maintain oral intake Drugs capable of producing adverse reactions such as cholestasis and drugs metabolized by the liver should be avoided. If severe pruritus is present, the use of the bile salt-sequestering resin cholestyramine is helpful. Physical isolation of patients with hepatitis to a single room and bathroom is rarely necessary except in the case of fecal incontinence for hepatitis a and e or uncontrolled, voluminous bleeding for hepatitis B Universal precautions that have been adopted for all patients apply to patients with viral hepatitis.
COMPLICATIONS AND SEQUELAE OF ACUTE VIRAL HEPATITIS Relapsing Hepatitis Cholestatic Hepatitis Fulminant hepatitis (massive hepatic necrosis) Hepatitis B accounts for >50% Hepatitis E in up to 20% of cases in pregnant women. Chronic Hepatitis Rare complications: Pancreatitis Myocarditis Atypical pneumonia Aplastic anemia Transverse myelitis Peripheral neuropathy
PROPHYLAXIS Hand washing & hygiene Universal precaution No sharing of personal items (razor, toothbrush, nail clipper) Sexual barrier Vaccines: Hep A Hep B Hep E