Gastroenterology

Fernanda Freire Tovar, MD

Hepatitis A

Epidemical jaundice has afflicted civilization for centuries. Precise identification of cause occurred 20 yeas ago, when the hepatitis A virus (HAV) was discovered in feces of infected human volunteers.

THE VIRUS:

TRANSMISSION:

INTRODUCTION:

The use of immune globulin (IG) to prevent infection in contacts of hepatitis A works in individuals cases and the protection afforded by IG is only temporary (1-3 months).In addition, because hepatitis A can be asymptomatic, epidemics continue. A safer and more effective prophylactic method should be developed
.

The clinical picture of viral hepatitis is extremely variable ranging from asymptotic infection without jaundice to a fulminating disease and death in a few days

In 1997 in USA, about 100 deaths occur from hepatitisA annually and the disease accounts for up to 30% of fulminate hepatitis cases. Twenty to 50% of this patients due to hepatitis A will die. The case fatality among all cases of hepatitis A is thought to be 0,3%. However, there case fatality rate increases to 2,5% among older persons. Over 70% of reported deaths are among persons >49 ys old, even though this age group accounts for only 8% of infections. Because the antibody rate HAV is decreasing among older Americans, this group will increasingly become susceptible to severe disease if they are infected. Deaths due to this disease must now be considered vaccine preventable

TYPICAL COURSE:

*SYMPTOMS:
A)Prodromal phase:
#general malaise
# myalgia
# arthalgia
# easy fatigability
# upper respiratory symptoms (nasal discharge pharyngitis)
#anorexia
fever (38-39ºC)
#nausea
#vomiting
#diarrhea
#constipation
#adominal pain is usually mild and constant in the right upper quadrant or epigastrium and is often aggravated by jarring or exertion rarely it is severe enough to simulate cholecystitis or cholelithiasis).

B)ICTERIC PHASE:
#may appear at the same time of the initial symptomatology or after 5-10 days
#with onset of jaundice, there is often an intensification of prodromal symptoms followed by progressive clinical improvement.
#most patients never develop clinical icterus.

C)CONVALESCENT PHASE:
#increasing sense of well-being
#return to appetite
#desappearance of abdominal pain and tenderness, jaundice and fatigability.
#the acute illness usually subsides over 2-3 weeks
#clinical and laboratory recovery by 9 weeks
#in some cases, clinical, biochemical and serologic recovery may be followed by one or two relapses, but ultimate recovery is the rule.
#hepatitis A is usually self-limited and does not result in chronic infection.

D)COMPLICATIONS:
# more protracted course
#cholestatic hepatitis (rare)
#fulminate hepatitis (in 0.1% of the cases).
#hepatitis A may persist for up to 1 year and clinical and biochemical recovery may occur before full recovery.
#the mortality rate is less than 0.3% and the severity of the disease decrease with the age of the patient and the presence of other diseases.

SIGNS:

LABORATORY FINDINGS:

IMMUNOGENETICY:

Both IgM and IgG anti HAV are detectable in serum soon after the onset of the illness. Peak titers of IgM is a excellent test to diagnosing acute disease and occur during the first week of clinical disease and disappear within 3-6 months. Titers of IgG anti HAV peak after one month of the disease and may persist for years. The presence of IgG alone indicates previous exposure to HAV, noninfectivity, and immunity to recurring HAV infection.
...............graphic 1........................

DIAGNOSTIC METHOD:

DIFFERENTIAL DIAGNOSIS:

TREATMENT DURING ACUTE PHASE:

PREVENTION:

FULMINATE HEPATIC FAILURE:

There is an extensive necrosis of large area of the liver, acute liver atrophy and the symptoms, sings and laboratory testes show severe hepatocelular damage

A)Symptoms and signs:

#toxemia
#gastrointestinal symptoms
#hemorragic phenomena
#absolut or minimal jaundice
#ascites
#edema (it may be found)

B)Laboratory findings:
#elevated serum aminotransferase
#elevated serum bilirubin
#prolonged protrombin time
#low serum albumin

C)Signs of encephalopathy:
#sleep reversal
#delirium
#tremor
#drowsiness
#coma

D)Treatment:
The treatment is directed toward those metabolic abnormalities associated with severe liver cell dysfunction (coagulation defects, disordered fluid electrolyte and acidbase balance, renal failure, hypoglycemia and encephalpathy):
#prophylatic antibiotictherapy - decrease the risk of infection
#manitol - 100-200 mL of a 20% solution by rapid intravenous infusion - decrease the cerebral edema
#early transfer to a liver transplantation center - emergency liver transplantation has been associated with 80% survival rate at 1 year.

E)Mortality rate:
#as high as 80% for patients with severe encephalopathy.

Bibliography

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