Symptoms of Hepatitis A Infection
Hepatitis A may cause no symptoms at all when it is contracted, especially in children. Such individuals will only know they were infected (and have become immune – you can only get hepatitis A once) by getting a blood test later in life. In fact, symptomatic hepatitis A infection is directly related to age. Seventy percent of hepatitis A infections in children younger than six years of age are asymptomatic; in older children and adults, infection tends to be symptomatic with seventy percent of patients developing jaundice (CDC, 2007).
Symptoms typically begin about 28 days after contracting the hepatitis A virus, but can begin as early as 15 days or as late as 50 days after exposure (Koff, 1998), and include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise. After a few days of the aforementioned symptoms, jaundice (also termed “icterus”) sets in. Jaundice is a yellowing of the skin, eyes and mucous membranes that occurs because bile flows poorly through the liver and backs up into the blood. The urine will also turn dark with bile and the stool light or clay-colored from lack of bile. When jaundice sets in, the initial systemic manifestations begin to subside.
The severity of illness associated with hepatitis A increases with age. In general, the period of acute illness lasts from ten days to three weeks, at which time patients tend to recapture some sense of wellness as serum chemistries begin to normalize. It is not unusual, however, for serum chemistries to remain abnormal for six months (or more), prolonging the patient’s recovery for up to a year.
The jaundice so commonly associated with hepatitis A can linger for a prolonged period in some infected persons – sometimes as long as eight months. Additionally, pruritus, or severe “itchiness” of the skin, can also persist for several months after the onset of symptoms. These conditions are frequently accompanied by diarrhea, anorexia, and fatigue.
In addition, relapse is possible with hepatitis A. This usually occurs within three months of the initial onset of symptoms. Although relapse is more common in children, it does occur with some regularity in adults.
On average, the time to full recovery takes about 2 months, but 10-15 percent of persons have a prolonged or relapsing course lasting up to six months (Gilkson, et al., 1992; Willner, et al., 1998). The vast majority of persons who contract hepatitis A fully recover, and it does not lead to chronic hepatitis. Persons do not carry hepatitis A long-term (as with hepatitis B and C).
Fulminant Hepatitis A
Fulminant hepatitis A is a rare but devastating complication of a hepatitis A infection that results in approximately 100 deaths per year in the U.S. Among reported cases for all ages, the fatality rate is approximately 0.3%. This figure, however, increases with age. For sufferers of fulminant hepatitis over 40 years old, the fatality rate is approximately 2% (CDC, 2007).
Fulminant hepatitis affects the liver. Weighing around three pounds, the liver is the body’s largest organ. The hepatitis A virus (HAV) infects the liver’s parenchymal cells (internal liver cells). Once a cell has been penetrated by the viral particles, the hepatitis A virus releases its own toxins which cause, in essence, a hostile takeover of the host cell’s system. The cell then produces new viral components that are released into the bile caniculi that run between the liver’s parenchymal cells. Thereafter, the affected liver cells are no longer able to perform their function. This process - i.e. the pathologic death of liver cells - is called hepatic necrosis.
The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells - upwards of three-quarters of the liver’s total cell count - that the liver can no longer perform its multifaceted job.
Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema. Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function. Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure. Intracranial hypertension leading to stem death and sepsis with multiple organ failure are the leading causes of death in patients suffering from fulminant hepatic failure (Detry, 2006).
Treatment of those suffering from fulminant hepatic failure turns largely on the victim’s status. Those who have not become encephalopathic generally undergo an intense course of supportive treatment. But for those whose liver failure is so complete that it has lead to encephalopathy or cerebral edema, timely liver transplantation is often the only option. For these unlucky few, the process of necrosis has left their liver scarred and useless. Unfortunately, many patients with irreversible liver failure do not receive a transplant because of contraindications or the unavailability of donor livers (Feldman, 2002).
Persons most at risk of suffering fulminant hepatitis A include those with:
- Pre-existing chronic liver disease (Gilkson, et al., 1992)
- Chronic hepatitis B
- Chronic hepatitis C (there are 3.9 million such persons in the U.S. [MMWR, Oct. 9, 1999])
- Alcohol-induced chronic hepatitis or cirrhosis
- Older individuals, over the age of 50