00:00
So what then are the clinical features of viral hepatitis? It should be stated at the outset
that asymptomatic infections are 10 to 30x more common than symptomatic in all of them.
00:17
When they do present clinical manifestations, they are all pretty similar and just on the basis
of the way they feel and on physical exam, none clearly distinguish one from the other. The
onset of virtually all viral hepatitis is flu-like in about 25% where the patients may have
malaise, fatigue, myalgia, arthralgia and headache. Anorexia, nausea and vomiting are also
common and strangely alterations in olfaction and taste. Back in the days when so many
patients used to smoke cigarettes, I was often struck by how often a patient told me that they
have to stop smoking because their cigarettes did not taste right. Low-grade fever is also
fairly common but I want to emphasize that it is low grade. In other words, if you have a
severely jaundice patient you think has hepatitis but their temperature is say 39, think again.
01:27
That's not very common in viral hepatitis. The low-grade fever, if it occurs, is more common in
hepatitis A and E than it is in B or C. Many of them will have dark urine and clay-colored stools
for 1 to 5 days before the jaundice and that's because there is some back-up of bile production
in the liver and many patients never become jaundiced even though they had some of the
other symptoms. Many will have right upper quadrant tenderness which is in keeping with
swelling of the liver and stretching of Glisson's capsule. Splenomegaly and cervical
lymphadenopathy are found in about 10 to 20%. So let's now talk about fulminant hepatitis.
02:22
I mean, where it's life threatening. It would be defined as severe liver failure within 8 weeks
of the onset of symptoms. This is seen primarily with these 2 viruses, hepatitis B or the
combination of B and D. In fact, that's the leading cause in Japan and France of fulminant
hepatitis. It's also common to occur in patients who already have chronic hepatitis due to
hepatitis C. So if they get hepatitis B plus or minus hepatitis D and they already have hepatitis C,
they're in trouble. Hepatitis A is generally a pretty benign disease. Most of us, as we mention,
never even knew they had the disease but if it does cause fulminant hepatitis, it is in older
patients unless a person already has hepatitis C and is sort of incubating a severe liver
infection already. Hepatitis E actually is the leading cause of fulminant hepatitis in India,
although it's much more common in women than in men and remember that 20% of pregnant
women who get hepatitis E develop fulminant hepatitis. So how does that act? Well, someone
with fulminant hepatitis is going to have hepatic encephalopathy. In other words, they're not
going to be able to process ammonia and other important chemicals that need to be disposed
off by the liver. Instead of liver getting large, the liver shrinks because of the widespread
destruction of liver cells. Many of the patients will develop ascites related to low albumin
production and therefore peripheral edema. Their bilirubin will be sky high and if someone is in
deep coma when they present with fulminant hepatitis, their mortality is more than 80%.
04:47
On the good side, if a patient survives fulminant hepatitis, they generally have a complete
recovery with the possible exception of patients who also have chronic hepatitis B and C.
05:01
Important pearl, hepatitis A does not cause chronic hepatitis. Now, it may cause prolonged
hepatocellular necrosis and inflammation but not for 6 months. That is hepatitis B, C and
hepatitis B associated hepatitis D and hepatitis E. So hepatitis A does not cause chronic
hepatitis. Hepatitis E only causes chronic hepatitis in someone who is immunosuppressed and
remember it's the immune system that attacks the infected liver cells and removes them and if
you're immunosuppressed that may not happen. Let's talk now about chronic hepatitis B. This
is a highly replicative infection. We're talking about greater than 10⁵ to 10⁶ IU/mL and they
have a greater risk to transmit the infection by needlestick and they have a greater risk to
develop hepatocellular carcinoma. More than 90% of newborns of mothers with chronic
hepatitis B get chronic hepatitis. Fewer than 1% of immunocompetent adults with clinically
apparent hepatitis B get chronic hepatitis B. The symptoms of chronic hepatitis B are from no
symptoms at all to severe debilitating and life-threatening liver problems and furthermore it
may be complicated by extrahepatic manifestations such as vasculitis, arthritis and even
glomerulonephritis. The histology can vary from no necrosis at all to cirrhosis. Chronic hepatitis
C occurs more often in men than women, in blacks than whites and it's more often anicteric,
no jaundice more than it is jaundice. Certain individuals, based on their HLA type, are more
predisposed to get hepatitis C and not unexpectedly immunocompromised persons are more
likely to get chronic hepatitis C. In chronic hepatitis C, the histologic features are the best
predictors of the disease progression. So that would mean that mild inflammation and mild
fibrosis is making the patient less likely to develop frank cirrhosis and the level of virus in the
bloodstream and the hepatitis C genotype do not correlate with whether it's going to progress
to cirrhosis. Symptoms early are none. Later, probably nothing more than fatigue. On physical
exam, most of them will have evidence of hypersplenism meaning that the spleen plucks out
platelets and white cells leading to low counts and there are extrahepatic manifestations of
hepatitis C such as cryoglobulinemia. Now chronic hepatitis E occurs most commonly in
immunocompromised patients especially organ transplant recipients or HIV-infected patients
and most commonly it's genotype 3 and the symptoms, signs and histopathology are similar to
the other forms of chronic hepatitis. Interestingly, most patients are not jaundiced and the
liver tests are only modestly abnormal. So what are the manifestations outside the liver in
these chronic forms of hepatitis? Well, first there's glomerulonephritis and cryoglobulinemia,
Guillain-Barré syndrome, Bell's palsy or peripheral neuropathy, even worse transverse myolitis
or acute meningoencephalitis.