2. A 20 year old , 24 weeks ANC was admitted on
14 /06/13 with chief c/o
1. Weakness of both lower limbs since 7 days
2. Fever since 2 days
3. Retension of urine since 2 day
4. Abnormal behavior since 1 day
No h/o headache /vomiting/convulsion
3. No h/o lm / vomiting
No back pain
No h/o trauma
No h/o vaccination
H/o dog bite lt leg 6 month before
Not received ARV/ARG
4. On examination
Not cooperative
Disoriented
Agitated
Febrile
Pulse =104/min
Resp =18/min thoracoabdominal
Bp =140/90 mmhg
No edema feet
No neck stiffness
Spine was normal
Hydrophobia +
Aerophobia +
Photophobia +
5. On examination
Patient catheterised (ub)
Power – gr ‘o” in both lower limb
moving upper limbs
DTR absent lower limbs ,normal upper limbs
Planters –absent
Sensory/ cerebellar can not be tested
P/A –uterus gravid , 24 weeks , FHS +
RS- wnl
CVS -wnl
14. Introduction
Rabies is an acute highly fatal viral disease caused by lyssavirus type
-1,belongs to family Rhabdoviridae .
Occurs in more than 100 countries and territories.
Australia,Taiwan, Cyprus, Iceland, Ireland, Japan, Malta, UK & Islands
of western pacific Norway ,Swedan are free from disease.
The annual number of human rabies deaths globally is estimated in
2010 to be from 26 400 to 61 000
15. In India
India is reported highest incidence globally.
A multicentre study in 2003 showed that 20 565 human deaths
annually
Disease occurs in all parts of country except Lakshadweep,Andaman
& Nicobar group of Islands.
Transmitted mainly by animal bite, particularly rabid Dog bites, licks
on abraded skin and mucosa.
Aerosols and man to man transmission although rare is possible
16. Clinical features
The clinical stages of rabies are:
Incubation,
Prodrome,
Acute neurological signs,
Coma, and
Death.
17. Clinical features
furious rabies: cardinal features are
o fluctuating consciousness,
o hydrophobia or aerophobia,
o inspiratory spasms,
o signs of autonomic dysfunction
They might not be evident at the same time, and disappear during
coma.
Comatose patients with furious rabies develop flaccid limb
weakness, which has been frequently misinterpreted as paralytic
rabies.
18. Clinical features
paralytic rabies
LMN type ascending weakness with only motor disturbance is
the initial manifestation
Consciousness is preserved until the preterminal phase
Atypical signs and symptoms of rabies associated with infection
with either bat or dog increasingly recognised.
Presentation of transverse myelitis as neuromyelitis optica or
tetanus-like symptoms , focal brainstem signs, myoclonus,
hemichorea, and Horner’s syndrome have been reported.
Excitation is less evident in paralytic rabies, and phobic spasms may
appear in only 50% of such patients.
Paralytic rabies, which resembles GBS, although progression to
coma, myoedema, and bladder clearly differentiate these two
disorders
19. Percussion myoedema
During the early stages of paralytic rabies,
notable signs may include myoedema at
percussion sites.
Percussion myoedema is most readily elicited on
the chest, deltoid, and thigh regions; it consists of
mounding of the muscle at the percussion site,
which then disappears over a few seconds.74
The reason why percussion myoedema is
associated with paralytic rabies is unknown, but
this sign is not observed in GBS or encephalitic
rabies, or in neuroparalytic accidents after
neural-tissue vaccination.
Has to be interpreted with caution, because it
can be found in extreme cachexia,
hyponatraemia, and the syndrome of
inappropriate secretion of antidiuretic hormone,
hypothyroidism, and renal failure usually in the
region of the chest, deltoid muscle and thigh,
piloerection and fasciculation.
20. Average survival with furious rabies and paralytic rabies after
infection 5.1 and 11 days respectively
Survival can be extended to 1 month or longer with intensive care
support.
21. Clinical case definition
a subject presenting with an acute neurological syndrome (i.e.
encephalitis) dominated by forms of hyperactivity (i.e. furious rabies) or
paralytic syndromes (i.e. dumb rabies) progressing towards coma and
death, usually by cardiac or respiratory failure, typically within 7–10 days
after the first sign, if no intensive care is instituted.
One or more of the following laboratory criteria should be used to
confirm a clinical case:
■■ presence of viral antigens;
■■ isolation of virus in cell culture or in laboratory animals;
■■ presence of viral-specific antibodies in the cerebrospinal fluid or
the serum of an unvaccinated person; or
presence of viral nucleic acids detected by molecular methods in
samples (e.g. brain biopsy, skin, saliva, concentrated urine) collected
post mortem or intra vitam
22. Clinical case definition
Cases of rabies are basically classified as follows:
■■ suspected: a case that is compatible with a clinical case
definition
■■ probable: a suspected case plus a reliable history of contact
with a
suspected rabid animal
■■ confirmed: a suspected or probable case that is laboratory-
confirmed.
In some situations, a clinical suspicion of encephalitis or a history of
animal exposure may be lacking; however, a case would still be
considered confirmed by appropriate laboratory diagnostic testing.
23. Sampling
For intra-vitam diagnosis in humans
Secretions, biological fluids (e.g. saliva, spinal fluid, tears) and tissues (skin biopsy
samples and hair follicles at the nape of the neck) can be used to diagnose
rabies during life
Three saliva samples taken at intervals of 3–6 h, skin and hair follicules are the
most sensitive samples.
Ideally, samples should be stored at –20 °C or less. Serum should be collected
from blood samples before freezing and stored at –20 °C or less.
For post-mortem diagnosis in humans
Brain tissue is the preferred specimen for post-mortem diagnosis in both
humans and other animals
If a brain biopsy cannot be performed, such as in field studies, tissue samples can be
collected via the trans-orbital or trans-foramen magnum route (1). Preservation
in glycerine (at +4 °C or –20 °C) or drying smears of brain tissue on filter paper
containing proper inactivating chemicals (at +30 °C) allows safe, stable
transport of infected material, but safe, effective viral inactivation must be
ensured before shipment
Other specimens, such as skin and hair follicles taken at the nape of the neck, are
also highly sensitive for post-mortem diagnosis
24. Techniques for intra-vitam diagnosis
1.Viral antigen detection
Direct fluorescent antibody test
Immunochromatographic methods
2.Viral antibody detection
Rapid fluorescent focus inhibition test
Fluorescent antibody virus neutralization test
3 .Viral RNA detection by RT-PCR
Post-mortem diagnosis of rabies BY
Direct fluorescent antibody technique
Enzyme linked immunosorbent assays (ELISAs) and
Direct rapid immunohistochemistry tests,
Virus isolation,Viral RNA detection
25. Neuroimaging
MRI abnormalities provide clues for differential diagnosis with
other encephalitides, in terms of preferential sites and extent of
involvement
Typically, MRI abnormalities are hypersignalT2 changes without
contrast enhancement involving the spinal cord, brainstem, thalamus,
limbic structures, and white matter during the non-comatose phase
Both clinical forms of rabies in man have similar MRI features Lesions
in the brachial plexus, spinal cord, and nerve roots are already seen at
the prodromal stage as signal intensity abnormalities or enhancement.
During the comatose phase, widespreadT2 hyperintense lesions in
the brainstem and forebrain can be seen; these are probably due to
virus-induced neuronal injury and superimposed hypoxic insult.
26.
27. Management
No proven standard treatment exists
Recovery after rabies, reported in four patients with bat RABV
variant rabies
Importantly, all four rabies survivors , had a vigorous and early
immune response, with autosterilisation (ie, no detected virus or
RNA in tissue or biological fluids) and rabies antibodies detected in
serum and CSF.
28. Management
The Milwaukee protocol
Initially aimed to induce coma with an electroencephalographic
stage of burst suppression.
Various sedatives (midazolam barbiturates,ketamine), amantadine,
which is supposed to reduce brain excitotoxicity, and ribavirin were
given to a patient who then recovered with minimal sequelae.
However, following the protocol did not save more than two dozen
fully alert, previously healthy, young, or middle-aged patients with
symptomatic rabies.
Current Milwaukee protocol consists of ketamineand midazolam,
similar to what is used by physicians in dog RABV variant endemic
countries to relieve suff ering and dysautonomia. Nimodipine has
also been added to the protocol to relieve vasospasm
Coma induction is no longer recommended in the protocol..
