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Paralytic RABIES
This document describes a case of paralytic rabies in a 20-year-old pregnant woman. She was admitted with weakness in her lower limbs, fever, difficulty urinating, and abnormal behavior. She had a history of being bitten by a dog 6 months prior but did not receive post-exposure prophylaxis. On examination, she displayed signs of hydrophobia, aerophobia, and photophobia. Tests revealed weakness and loss of reflexes in her lower limbs. She was diagnosed with paralytic rabies and expired two days later due to cardiorespiratory arrest. The document then provides background information on rabies epidemiology, clinical presentation, diagnosis, and management.
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Paralytic RABIES
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- 2. A 20year 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/olm / 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 Notcooperative 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 Patientcatheterised (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
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- 11. Probable diagnosis ANCwith Paralytic Rabies
- 12. Outcome Patient expiredon 16/6/13 d/t CRA
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- 14. Introduction Rabies isan 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 Indiais 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 clinicalstages of rabies are: Incubation, Prodrome, Acute neurological signs, Coma, and Death.
- 17. Clinical features furiousrabies: 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 Duringthe 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 survivalwith 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-vitamdiagnosis 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-vitamdiagnosis 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 abnormalitiesprovide 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.
- 27. Management No provenstandard 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 Milwaukeeprotocol 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..
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