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RABIA

Egidia Miftode

Caz VD- F
Mucat de cine (necunoscut) pe 16-17 dec
2011 la nivelul pleopei- GO dr
Fr PEP
Efectuat VTA

Manifestri clinice
20.02 2012 febr, vrsturi
21.02 contracturi musculare ale extremitilor

hidrofobie

iritabilitate
23.03 intensificarea contracturilor musculare

agitaie psiho-motorie

sialoree

Ex. fizic la internare


Nistagmus vertical
Tremor intenional
Perioade de contacturi musculare ale
membrelor
Sensibilitate exagerat

Ex. biologice

CT uoar lrgire a anurilor intergirale


L=14150/mmc
PN=68%
VSH=40/1h, TGP=N, uree=68mg/dl, gl=1.2g/l
LCR: 84 elem/mmc, Lf=85%
Alb=0.42g/l
Gl=0.83
Cl=7.9
Recoltare serologie pt v. rabic

Evoluie
26.02 halucinaii auditive i vizuale,
tahicardic, cu agitaie psiho-motorie
27.02 desaturare important IOT
hTA
Stop cardiac ireversibil

Perioada de incubaie a rabiei = foarte


variabil - ntre zile i ani (de obicei 30-90
de zile).
Perioada prodromal i simptomele clinice
precoce au o durat de 2-10 zile:
parestezii / durere la locul mucturii,
stare general alterat, febr, mialgii, cefalee,
grea, vrsturi, dureri abdominale, diaree.

Boala neurologic acut (2-7 zile) poate fi


clasificat n dou forme:
1. ,,rabia furioas ( 80%):
agitaie, halucinaii, anxietate, tuburri de
comportament,
hidrofobie,
convulsii,
disfuncii autonome: tahicardie, aritmii,
hipotensiune.

2. rabia paralitic (20%) :


paralizii ale unuia sau ale tuturor membrelor,
ileus, retenie urinar,
sindrom Guillain-Barre (cu afectare
combinat motorie i senzitiv).

Coma poate aprea imediat dup debutul


bolii sau poate surveni pn la 14 zile
dup debut.

Profilaxia post- expunere


Expunerea este reprezentat de:
muctura de animal sau om,
contaminarea unei plgi deschise sau a mucoaselor
cu saliv sau esut infectat de la animale sau om,
sau contact similar cu virusul rabiei, viu.
Riscul rabiei dup muctura de animal rabigen
(5-80%) este de aproape 50 de ori mai mare dect
riscul dup zgrietur (0,1-1%).

Splarea imediat i corespunztoare a


plgilor mucate i zgrieturilor cu ap i
spun reduce conisderabil riscul de rabie

Circumstane
1.Persoan nevaccinat anterior

Animalul nu a fost capturat


Animalul a decedat

Animalul triete i poate fi supravegheat

2.Persoan vaccinat anterior

Conduit
Igiena plgii cu ap i spun;
Imunoglobulin antirabic: 20 mg/kgc;
Vaccinare: 1 ml. vaccin i.m.(m. deltoid) n
zilele 0, 3, 7, 14, 28.
Ig.antirabic+vaccin
Iniierea profilaxiei i stopare n funcie de
examenul de laborator (Testul de
imunofluorescen direct a creierului
animalului);
Iniierea profilaxiei* i stopare dac animalul
nu prezint nici un semn de boal (vaccinare
zilele 0, 3, 7, 14).
Igiena local a plgii
Ig. nu trebuie administrate
Vaccin n ziua 0 i 3 i apoi n funcie de
starea animalului.

Tipul de expunere
*
Persoan care a fost lins pe pielea intact: nu este
necesar profilaxie
Plag superficial,
Muctur sau contaminare cu saliv a unei plgi
deschise ale tegumentului/ mucoasei: Imunoglobuline
umane i vaccin.

Through 2008, of the 7 reported rabies survivors


to hospital discharge [1, 4, 7], only the index MP
case did not receive PEP.
More recently, abortive rabies was described in an
adolescent female who developed neurologic
symptoms after bat exposure and had high rabies
antibody titer, without isolation of rabies virus

2008
We reviewed indigenously acquired cases of bat-variant
rabies in humans in Canada and the United
States from 1950 through 2007.
Results. Of 61 cases identified 5 occurred after organ
transplantation and were excluded from further analysis.
A bite was reported by 22 (39%) of the case patients, 9
(16%) had a direct contact (i.e., were touched by a bat)
but no history of a bite, 6 (11%) found bats in their home
(2 [4%] in the room where they slept) but reported
no direct contact, and 19 (34%) reported no history of bat
exposure whatsoever

Caz 1 supravietuitor
The patient continued to excel in school and play sports until one
month after exposure, when she experienced generalized fatigue and
paresthesia of the left hand.
Two days later diplopia developed and she felt unsteady.
The next day, she had nausea and vomiting without fever. A
neurologist noted
partial bilateral sixth-nerve palsy and ataxia. The results of magnetic
resonance imaging and angiography of her brain were unremarkable.
By the fourth day after the onset of symptoms, blurred vision,
weakness of the left leg, and a gait abnormality were present.
On the fifth day, fever (38.8C), slurred speech, nystagmus, and
tremors of the left arm developed.

Milwaukee Protocol (MP) [1].


This protocol includes therapeutic coma (to prevent early
life-threatening dysautonomia) (Coma was induced with
ketamine and midazolam infusions, as recommended in the
MP (version 1.1), for presumed rabies.), antiviral therapy,
cerebral
Vasospasm management, and
avoidance of immunization (The rabies antibody response
typically appears by 2 weeks. The MP postulates that a
vigorous immune response may exacerbatethe disease
process [5], and it avoids active immunization)

On HD1, upon diagnosis of rabies, and after discussion


with the California Department of Public Health, CDC,
and authors of the MP:
intravenous ribavirin and enteral amantidine,
tetrahydrobiopterin
(BH4), coenzyme Q10, and ascorbic acid were
initiated.
All subsequent titrations and modifications of the MP
were made in direct consultation with the MP primary
investigator
ribavirin may delay the antibody response and is no longer
recommended [8].

On hospital day 1 (HD1), direct fluorescent antibody (DFA)


detected rabies virus antigen in corneal impressions; serum and
cerebrospinal fluid (CSF) serologies were negative. From a saliva
sample on HD3, molecular testing performed at the Centers for
Disease Control and Prevention (CDC) detected rabies virus
RNA, corresponding genetically to Philippine dog rabies. Antirabies
immunoglobulin G (IgG) was first detected via indirect
immunofluorescence in serum and CSF on HD11 and HD13,
respectively. Initial nuchal biopsy was positive by DFA on HD3
and again on HD19.

Given concerns for development of cerebral


electrical silence,
vasospasm, and edema, intense neurologic
monitoring was initiated.
This included continuous electroencephalogram
(EEG),
continuous cerebral regional oxygen saturation
measurement by near-infrared spectroscopy
(NIRS), and daily transcranial Doppler (TCD).

Cerebral vasospasm was suggested by TCD on HD6 and


HD10HD12, as reported elsewhere [3]; vasospasmtargeted
therapies included escalating doses of BH4, followed by
milrinone
and L-arginine. Serial EEG revealed slowing, progressing
to
burst suppression by HD13; anticonvulsant prophylaxis
included fosphenytoin, midazolam, and phenobarbital.
On HD21 topiramate was administered for multifocal
spikes;

The hospital course included multiple secondary


complications previously described in rabies:
transient hyponatremia,
hemidiaphragmatic paralysis, pancreatitis,
hypothyroidism, and
heart block requiring transvenous pacing.
Additional complications included ventilatorassociated pneumonia and peripheral
thrombophlebitis.
Hospitalization charges exceeded $700 000.

Ex ana - pat
edematous brain, with diffuse lymphocytic
encephalitis and widespread loss of neurons in the
cortex, with
many residual neurons undergoing necrosis. The
cerebellum
demonstrated extensive loss of Purkinje cells and
internal granule
cell neurons. Negri bodies microinfarcts and small
perivascular hemorrhages

As reported to date in the MP Rabies Registry, variations of


the MP have been applied to 25 additional patients, with 3
minimally documented survivors [5]. A girl from Colombia
[6] and a man from Peru died (HD76 and HD70, respectively)
after presumed viral clearance and discharge from the ICU, from
nonrabies attributable medical complications (R. E. Willoughby,
personal communication, 2011). The third survivor, a Brazilian
boy with bat rabies [7] who received partial PEP before onset of
symptoms, is living at home.

Genetic variabilities in the host and virus


likely contribute to survival. Indeed, there
are reports of animals surviving rabies
without therapy [11].
Thus, application of the MP may be more
successful in specific subgroups of patients.

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