Hepatitis

By
Maged Albasmi, MSc, MD, PhD
Assist prof. of cardiovascular medicine
 Acute Hepatitis
Definition
It is a sudden widespread liver damage with hepatocyte necrosis.
Causes:
Non viral Hepatitis
1. Drugs
Salicylates (aspirin may cause Reye's syndrome),
Halothane (on repeated anesthesia), alpha methyl dopa
(aldomet)
2. Toxins:
Mushrooms, carbon tetrachloride
5. Bacterial
Leptospira, toxoplasma, Coxiella burnetti.
Viral Hepatitis:

Hepatitis viruses: The liver is the principal target

Hepatitis A & E viruses
Hepatitis B virus & related Delta virus
Hepatitis C virus
Others e.g. F & G

Non-hepatitis viruses: The liver is not the main target

Cytomegalo virus
Epstein-Barr virus
Herpes simplex virus
Yellow fever virus
Essentials of the Diagnosis
1. Anorexia (even aversion to smoking), nausea, vomiting.
2. Fever & flu-like symptoms.
3. Jaundice enlarged tender liver.
4. Low WBCs count + marked elevation of transaminases early
in the course.
5. Liver biopsy-if done- shows characteristic hepatocellular
necrosis + mononuclear cells infiltrate.
 Acute Viral Hepatitis
Clinical picture:
Viral hepatitis is almost always caused by one or another
of hepatitis viruses.

All these viruses give rise to similar clinical features:

• Prodromal phase (3-4 days):
It usually precedes the development of jaundice by
a few days to 2 weeks and include chills, headache,
malaise and distaste even for previously popular
foods
and cigarettes.
Gastrointestinal symptoms as anorexia, nausea,
vomiting, diarrhea and upper abdominal pain
may occur. Mild pyrexia occurs by the end of this
phase.
• Icteric phase (1-4 weeks):
1 Colour triad', dark urine + pale stools + yellow
sclera
2. Improvement of prodromal symptoms occurs
shortly after the appearance of jaundice.
3. Arthralgia and pruritus may occur especially with
HBV.
4. The liver (in 70%) becomes more easily palpable
and tender.
• Recovery phase (within 6 months):
Recovery from the acute illness occurs within 2-3
weeks in case of hepatitis A & 9 weeks in case of
hepatitis B & C. Lassitude & fatigue may persist for
some weeks.
Full clinical and biochemical recovery usually occur
within 6 months
• Investigations:
Biochemical tests:
1. Rise of serum transaminases activity (SGOT & SGPT) 10-50
folds the normal levels even before jaundice develops.
2. Elevation of the serum bilirubin.
3. The alkaline phosphatase activity (ALK) is rarely raised unles
markedly cholestasis develops.
4. Prolongation of the prothrombin time is an indication of
severe liver damage.
5. The white blood cell count is normal or low in
uncomplicated cases. Large lymphocytes resembling those
seen in infectious mononucleosis my be seen.
• Serological tests:
Serological tests can identify the incriminated virus.

Acute HAV Anti-HAV IgM positive

Acute HBV HBs Ag positive
Anti-HBc IgM positive
Acute HDV Anti-HDV IgM positive
Acute HEV Anti-HEV IgM positive
Acute HCV Anti-HCV IgM positive (after
2-6 m) by:
o ELISA (second generation
Anti-HCV) or
o Immunoblot assay
(RIBA2).
Complications & non classic presentations:
1- Fulminant hepatic failure.
2- Relapsing hepatitis: occurs in up to 15% of cases. It is
indicated by re-rise of serum transaminases or bilirubin.
Recovery of relapses is usually complete..
3- Cholestatic hepatitis: jaundice deepens rapidly and within 3
weeks the patient starts to itch. After few weeks the patient
improves but the jaundice persists. Laboratory tests of liver
function indicate cholestasis (hyperbilirubinaemia +
bilirubinuria + elevated alkaline phosphatase & cholesterol).
Resolution occurs later on and is usually complete.
4- Post hepatitis syndrome: the patient feels unwell for a
variable period of time. The patient is usually an anxious
one. He feels right upper abdominal discomfort and the liver
edge may be palpable and tender. Serum transaminases may
be raised & biopsy shows mild residual portal cellularity.
5- Chronic hepatitis.
6- Extrahepatic complications: e.g. aplastic anaemia,
neurological complications etc.
Management:
"There are no specific treatment for acute viral
hepatitis“
Bed rest: Should be advised and continued until
symptoms and signs have disappeared and
liver function tests have returned towards
normal. Bed rest is especially needed for those
over 50 years, the pregnant women and when
symptoms are marked.
Diet:
A nutritious but bland diet with good protein
intake. The content of the diet is better
determined by the patient's wishes. Intravenous
fluids and glucose may be required if vomiting is
severe.
Drugs:
should be avoided (specially in severe hepatitis and
especially sedatives & hypnotics) because many
drugs are metabolized in the liver.
Hepatitis A Virus:
Incubation period:
The incubation period is usually 2-4 weeks. The
patient is infectious before clinical illness and
remains infectious for approximately a week
thereafter. It is safest to regard stools
infectious for 2 weeks from the onset of
illness. Blood, urine and other intestinal juices
can also transmit the infection.
Transmission:
• transmission of hepatitis A virus occurs mainly by the
FAECAL ORAL route; rarely it occurs through blood-borne or
sexual transmission
• transmission in sporadic cases occurs through:
1. Food contaminated during preparation.
2. Promiscuous homosexual habits.
• Transmission in epidemics occurs through:
1. Water borne epidemics: through contaminated water
2. Food borne epidemics: through contaminated foods e.g.
from food handlers (e.g. cold meat) or soil fertilized with
human sewage.
3. Recently it has become recognized that hepatitis A spreads
among neonatal Intensive care units or children in day care
centers.
Prevention.
The blood & stools are infectious during the incubation period & early
in the disease till the peaking of transaminases levels. There is no
carrier state for HAV. Prevention of transmission can be achieved
through:
1. Maintaining good sanitation and personal hygiene.
2 Immune serum globulin:
It should be given before exposure (i.e. earlier than 2weeks before
The start of the clinical illness)
3. Hepatitis A vaccine is recently developed.

Prognosis:
Usually it resolves without treatment. Chronicity does not occur.
Hepatitis B Virus
Transmission:
1.Blood borne:
Blood products are the best recognized infectious
materials.
HBs Ag is quite stable in these media and can
survive for long periods in dried blood. Not only
transfusion of large volumes of blood can
transmit the infection, but minor amounts are
sufficient for parenteral transmission e.g.
• Contaminated syringes among drug abusers, needles
used in tattooing instruments used in medical and
dental procedures especially, bites of mosquitoes and
bed bugs…. etc.
• Transmission can also occurs if infected blood comes in
contact with minor abrasions: non-parenteral
transmission e.g. razors at barber shops, tooth brushes,
, bah brushes during surgical operations on patients
with HB Ag positive and skin disease of the hands.

Generally, those at close contact with patients are

found to be at higher risk of getting the infection.
2. Other body fluids and secretions:
All body fluids are potentially infectious; saliva,
semen, CSF, pleura & peritoneal fluids.
However, the urine hardly ever seems to
transmit infection
Sexual contact is a well known route of
transmission and promiscuous sexual habits
e.g. homosexuality increases risk of infection.
3. Vertical transmission:
Transmission from mothers to their new born
infants occurs when an infected mother is HB
Ag positive at delivery.
Prevention:
1) Immune globulin:
Hepatitis B can not be prevented reliably by
standard immune globulin. Hepatitis B immune
globulin, containing a high titre of anti HBs, can
prevent or attenuate the disease following
exposure to the hepatitis B virus. A dose of 0.04
0.06 ml/kg is probably sufficient. This dose
Should be given as early as possible within 48
hours of parenteral exposure.
2) Vaccines:
The most recent vaccine is the yeast vaccine. Yeast cells
are forced to synthesize hepatitis B surface antigen
through a recombinant DNA technique.
It is given in 3 doses of 1 ml (20 μg) each by I.M.I, in the
deltoid muscle.
The second dose is given after 1 month and the third
dose by the 6th month. The good response is ushered
by the production of anti HBs and is followed by a high
degree of protection against hepatitis B virus infection
for about 5 years.
 Meningitis

Definition:
Classification:
-Acute:
-Subacute
Mode of spread:
-Direct:
-Septic focus.
-Trauma.
-Blood stream .
 Meningococcal Meningitis

1) Etiology: 4) Investigations:
Meningococcal represent 25% - CT scan.
2) Clinical picture: - CSF exam.
- Symptoms. - Blood exam.
- Signs: - Detection of source of infection.
• General=vital signs 5) Treatment:
• Meningeal irritation - prophylactic
• Neurological deficit - curative
3) Complications: 6) DD:
- CNS - Acute general infection
- CVS - Meningism
- Eyes - Encephalitis
- Genito urinary - Sub Arachnoid Hemorrhage
- Other types of Meningitis
Meningitis
Definition:
It is the inflammation of the membranes covering
the CNS, including the dura, arachnoid & pia
maters
Inflammation of the dura mater is rare & is known
as pachymeningitis
Inflammation of the pia-arachnoid is more
common and is known as leptomeningitis.
 CLASSIFICATION:
Leptomeningitis can be classified into two groups:
1. Acute pyogenic (purulent) meningitis:
The C.S.F. contains mainly polymorphs, due to
infection of the meninges by pyogenic organisms as:
• Meningococci (most common)
• Streptococci
• Pneumococci
• Haemophilus influenza
2. Subacute lymphocytic meningitis:
The C.S.F. contains mainly lymphocytes due to
infection of the meninges by organisms that do not
form pus as:
a) Viruses: Acute anterior poliomyelitis, acute
anterior lymphocytic choriomeningitis, mumps
and viral encephalitis.
b) Bacteria: Tuberculous bacilli, spirochaetes (as
syphilis) and trypanosomes.
c) Fungi: Cryptococcosis and mucomycosis
MODE OF INFECTION:
1. Blood stream as in the course of septicaemia or as a
metastases from Infection of the heart, lungs or other
viscera
2. Direct spread from:
a) Septic focus in the skull (sinusitis, otitis media),spine
(osteitis, Pott's disease) or parenchyma of the C.N.S.
(brain abscess, encephalitis, myelitis).
b) Trauma: organisms may be introduced from outside
the C.N.S. (lumbar puncture, penetrating wound) or
from the inside (closed head injuries involving the
nasal sinuses or the petrous part of the temporal bone)
 MENINGOCOCCAL MENINGITIS
( Acute Cerebro-Spinal Fever )
I. AETIOLOGY
1. The causative organism is the meninogococcus which is responsible
for 25% of all cases of purulent meningitis.
2. The disease occurs sporadically or in epidemics.
3. The disease spreads by droplet infection and is predisposed to by
overcrowding (e.g., schools, soldier's barracks).
4. The disease affects mainly children & young adults.
5. The organisms are implanted on the nasopharynx and gain access
to the meninges mainly by the blood stream and to a lesser extent
directly through the cribriform plate of the ethmoid bone.
II . CLINICAL PICTURE
A . Symptoms:
Acute onset with sudden chills, fever, headache, vomiting, backache,
blurring of vision, stiffness of the neck and prostration.
B . Signs:
1) General:
1. Temperature: 38°-39°C, maybe more.
2. Pulse rate is usually rapid except if there is increased intracranial
tension where the pulse rate will be slow
3. Respiratory rate is increased & may be irregular.
4. Blood pressure is usually normal except in severe cases where there
is hypotension.
5. Haemorrhagic skin rash may appear on the trunk and extremities,
6. Restlessness and irritability.
2) Signs of Meningeal Irritation:
1. Neck rigidity: passive flexion of the neck is difficult and painful
2. Neck retraction and may be opisthotonus
3. Positive Kerning, Brudzinski and Lassegue signs.

3) Signs of Neurological Deficits:

1. Clouding of consciousness, stupor or coma.
2. Convulsions.
3. Blurring of the margins of the optic discs.
4. Transient cranial nerve palsies due to exudation around the nerves.
5. Diminution of the deep reflexes may occur but other focal
neurological signs are rare.
N.B: Waterhouse-Freidreichson's syndrome is an acute
fulminating meningococcal septicaemia associated with:
a. Purpura fulminans causing petechial haemorrhages
which may coalesce leading to gangrene.
b. Adrenal haemorrhage (Addissons crisis) with prostration,
low B.P.& coma.

Death may, occur within 24 hours due to disseminated

intravascular coagulopathy (D.I.C.).
III. COMPLICATONS
1. Neurological
-Hydrocephalus
- Deafness
- Other focal neurological lesions are rare.
2. Cardiac:
-Pericarditis.
-Endocarditis
3. Eye:
-Conjunctivitis
- Keratitis
- iridocyclitis
 4. Genitourinary:
- Nephritis
- Pyelitis.
- Epididymitis
- Orchitis
5. Joint: Purulent arthritis specially in the knee and
shoulder.
IV. INVESTIGATIONS
1. CT Scan to exclude subarachnoid hemorrhage, or an intracranial
mass
2. C.S.F Examination
a. The pressure is raised
b. The C.S.F. is purulent.
c. Cells, mainly polymorphs are markedly increased up to 2000-
20.000/mm.
d. Proteins are markedly increased. (N: 20-40 mg/dl)
e. Sugar is markedly decreased to below 20 mg/dl. (N: 50-80mg/dl)
f. Chlorides are moderately decreased (N:720-750 mg/dl)
g. Organisms can be detected by Gram-stain or culture of C.S.F.
3. Blood examination for:
-Leucocytosis up to 30.000/cubic mm.
-Culture shows the organism in most cases
4. Detection of the source of infection:
-Chest X-ray (for pneumonia).
-Skull X-ray (for fracture).
-Sinus X-ray (for sinusitis)
V. TREATMENT:
A. Prophylactic:
1. Isolate the patient & avoid overcrowding during epidemics.
2. Chemoprophylaxis: rifampicin 600 mg twice daily orally for 2 days for
contacts.
3. Immunoprophylaxis: meningococcal live attenuated vaccine 1/2 ml s.c. for
children.
B. Curative:
1. General care: proper nursing adequate fluids, analgesics & sedatives.
2. Specific: once meningitis is suspected start Treatment Immediately, even
before culture:
a. Antibacterial:
-Cefotaxime (Claforan) 2-4 gm I.V/day or
-Penicillin G 20 million units I.V /day or ampicillin 100 mg/kg I.V /day or
-Chloramphenicol 100 mg/kg/day in penicillin-sensitive patients
b. Corticosteroids:
-For severe cases as Waterhouse- Freidereichson syndrome along with
blood transfusion, dopamine & heparin in suspected D.I.C.
VI. DIFFERENTIAL DIAGNOSIS:

1. Acute general infections: associated with delirium and headache

as typhoid. pneumonia and typhus, they are differentiated by the
characteristic clinical picture of the disease and by the absence of
signs of meningeal irritation.

2. Meningism:
This is a condition in which there are Signs of meningeal irritation in
the absence of meningitis. It occurs in acute Infections of children
and young adults in typhoid, pneumonia and acute exanthemata. In
these cases there is water retention and blood dilution. As the
blood is hypotonic to the C.S.F., an attempt is made by the body to
reestablish an equilibrium by transferring water from the blood to
the C.S.F through the choroid plexus. As a result the C.S.F. becomes
diluted (protein and chloride contents become reduced) while its
pressure is raised. This use of C.S.F. pressure) will lead to the
symptoms and sign? of meningeal Irritation which are relieved by
lumbar puncture or diuresis.
3. Encephalitis of various types, and brain abscesses:
They may be associated with signs of meningeal irritation
but is differentiated by the presence of early and marked
signs of cerebral and brain stem lesion and by the normal
sugar and chloride contents of the C.S.F.
4. Subarachnoid haemorrhage:
There are signs of meningeal irritation and sometimes
fever but the onset is more sudden and the C.S.F. is bloody.
5. Other types of meningitis:
a. Other causes of pyogenic meningitis: differentiated by
C.S.F. culture.
b. Causes of lymphocytic meningitis especially:
- T.B. meningitis.
- Acute lymphocytic choriomeningitis.
T.B.MENINGITIS:
-The onset is insidious and usually preceded by prodromal symptoms of
malaise, night fever and sweat and loss of weight (symptoms of toxaemia).
-Signs of meningeal irritation are mild but vomiting and headache are
pronounced.
-The presence of a primary tuberculous focus in the body and the typical
C.S.F. findings are diagnostic.
- C.S.F. findings:
1. The pressure is raised.
2. Appearance is cloudy or ground glass.
3. Cells, mainly lymphocytes are increased up to 500 cells/cubic mm.
4. Proteins are Increased.
5. Sugar is decreased to 20-40 mg/dl.
6. Chlorides are markedly decreased and may reach below 600 mg/dL
7. No organisms can be demonstrated by the usual staining methods, but
may be revealed by the Ziehl-Nielsen stain.
Treatment of T.B meningitis: Antituberculous drugs:
-Streptomycin 1gm/i.m./daily.
-Isonicotinic acid hydrazide INH 300-800 mg/orally/
daily.
-Rifampicin 600 mg/orally/daily.
Anti tuberculous drugs should be given for 1-2 years
except Streptomycin which is given for 3 months only
for fear of nerve deafness.
 ACUTE LYMPHOCYTIC CHORIOMENINGITIS
This is an acute benign viral infection of the meninges,
choroid plexus and rarely the brain substance. It is
differentiated from meningococcal meningitis by the
presence of excess lymphocytes in the C.S.F and from
T.B meningitis by the acute onset and by the normal
sugar and chloride contents: The virus can be isolated
from the C.S.F. by special methods.
Thank you