-DR.VEKARIYA KUSHAL

CLINICAL MANIFESTATION PRODROMAL FEATURESENCEPHALITIC RABIESPARALYTIC RABIES

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

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

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:

1Encephalitic (furious)

in 80%

2paralytic in 20%.

Manifestations of encephalitic rabies may be

seen in other viral encephalitides

include fever,

confusion, hallucinatio

ns, combativen

ess, and seizures.

Autonomic dysfunction is

common

hypersalivationgooseflesh, cardiac arrhythmia,

and priapism.

• 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 dysfunctionresponsi

ble “foaming at the mouth”.

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.

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

predominatescardinal 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.

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