clinical manifestation of rabies include different between encephalitic rabies and paralytic rabies and how to compute dose for rabies

1. -DR.VEKARIYA KUSHAL
CLINICAL MANIFESTATION
PRODROMAL FEATURES
ENCEPHALITIC RABIES
PARALYTIC RABIES

2. CLINICAL MANIFESTATION
• EMPHASIS MUST BE ON POST EXPOSURE PROPHYLAXIS INITIATED BEFORE ANY
SYMPTOMS OR SIGNS DEVELOP
• USUALLY BE SUSPECTED ON THE BASIS OF THE CLINICAL PRESENTATION.
• THE DISEASE USUALLY PRESENTS AS AN ATYPICAL ENCEPHALITIS WITH RELATIVE
PRESERVATION OF CONSCIOUSNESS.
• IT DIFFICULT TO RECOGNIZE IN THE LATE STAGE .(EX :- COMA )
• A MINORITY OF PATIENTS PRESENT WITH ACUTE FLACCID PARALYSIS.
• THERE ARE PRODROMAL, ACUTE NEUROLOGIC, AND COMATOSE PHASES THAT
USUALLY PROGRESS TO DEATH DESPITE AGGRESSIVE THERAPY

4. PRODROMAL FEATURES
• THE WOUND HAS USUALLY HEALED BY THIS POINT, AND SYMPTOMS
PROBABLY REFLECT INFECTION WITH ASSOCIATED INFLAMMATORY
CHANGES IN LOCAL DORSAL ROOT OR CRANIAL SENSORY GANGLIA.
Earliest specific
neurologic symptoms of
rabies
paresthesia, pain, or pruritus near the site
of the exposure, which occurs in 50–80%
of patients and strongly suggests rabies.
The earliest clinical
features of rabies begin
with nonspecific
prodromal
manifestations
fever, malaise, headache,
nausea, and vomiting. Anxiety
or agitation

5. ENCEPHALITIC RABIES
• IN ENCEPHALITIC RABIES, EPISODES OF
HYPER EXCITABILITY ARE TYPICALLY
FOLLOWED BY PERIODS OF COMPLETE
LUCIDITY THAT BECOME SHORTER AS
THE DISEASE PROGRESSES.
Encephalitic rabies
Two acute neurologic
forms of rabies are
seen in humans:
1Encephali
tic (furious)
in 80%
2paralytic
in 20%.
Manifestations of
encephalitic rabies may be
seen in other viral
encephalitides
include
fever,
confusion,
hallucinatio
ns,
combativene
ss, and
seizures.
Autonomic
dysfunction is
common
hypersalivati
ongoosefles
h, cardiac
arrhythmia,
and
priapism.

6. • THESE SYMPTOMS ARE PROBABLY DUE TO DYSFUNCTION OF INFECTED BRAINSTEM
NEURONS THAT NORMALLY INHIBIT INSPIRATORY NEURONS NEAR THE NUCLEUS
AMBIGUOUS (GROUP OF LARGE MOTOR NEURON) RESULTING IN EXAGGERATED
DEFENSE REFLEXES THAT PROTECT THE RESPIRATORY TRACT.
In rabies early
brainstem involvement
hydrophobia
aerophobia
involuntary, painful contraction of
the diaphragm and accessory
respiratory, laryngeal, and
pharyngeal muscles in response to
swallowing liquids.
The combination of
hyper salivation and
pharyngeal dysfunction
responsi
ble
“foaming at the mouth”.

7. BRAINSTEM DYSFUNCTION PROGRESSES RAPIDLY, AND COMA FOLLOWED WITHIN
DAYS BY DEATH IS THE RULE UNLESS THE COURSE IS PROLONGED BY SUPPORTIVE
MEASURES.
cardiac and/or respiratory failure, disturbances of
water balance (syndrome of inappropriate
antidiuretic hormone secretion or diabetes
insipidus), noncardiogenic pulmonary edema, and
gastrointestinal hemorrhage.
late complications
Cardiac arrhythmias may be due to dysfunction affecting vital centers in the
brainstem or to myocarditis. Multiple-organ failure is common in patients
treated aggressively in critical care units.

8. PARALYTIC RABIES
• PATIENTS WITH PARALYTIC RABIES GENERALLY SURVIVE A FEW DAYS LONGER
THAN THOSE WITH ENCEPHALITIC RABIES, BUT MULTIPLE-ORGAN FAILURE
NEVERTHELESS ENSUES.
20%.
which muscle
weakness
predominates
cardinal features of encephalitic rabies
(hyperexcitability, hydrophobia, and
aerophobia) are lacking.
There is early and prominent flaccid
muscle weakness, often beginning in the
bitten extremity and spreading to
produce quadriparesis and facial
weakness.
Sphincter involvement is
common
sensory involvement is usually mild, and these cases are
commonly misdiagnosed as Guillain-Barré syndrome.

9. THANK YOU