a

e
r
,
a
a
t
s
S
a
o
t
a
m
e
o
l
i
c
r
a
r
u
b
l
tu
de tienta
s
n
co

,
C
U
I
L
RI
V
A
.G
MF
S
M
.
U
f
ie
Pro
g
o
l
u
o
n
r
a
u
t
i
Ne
e
t em
s
d
e
a
T
e
dr
cate Nicola

Lear
ning
Ob

jectiv

es

To b

e
and able to
d
r
state istingui ecogniz
sh f r
e co
s t ha
ma
o
md
t are
i
st
clini
To k
cally inct
si m i
n
lar.
work ow the a
p
pres up for a propria
e
t
p
inclu nting w atient e initial
it
d
exam ing a ta h coma,
rget
.
ed n
euro
logic
To b
e fam
trea
tme iliar wit
nt o
h th
appr
f
c
opria
oma e early
te f o
r mo that is
st et
iolog
i es.

:
atos
com
Boln
avu
l

nu v
orbe
ste
nu n
nu c telege

omu
nic
antu
cu
raju
l
form
sub

nici
o
nu-s
i des
ch i d
prez
e oc
int
hii
in c o
sfnc
ntin
teria
ent
n

 Con

Aci
unil
e

trolu
l i a
func
sigu
iilor
rare
I n di
vital
a
e
care
a co
glice
ntro
miei
lu lu i
exam
i a
Ana ene de laaltor
m ne
bo r a
s
Apre
to r
ticul
actu
ciere
alei
de in
a in s
str
c
t
o
a
i
n
l

tien
Exa
r ii s t

r ii
men
u l in
gene
tern
r
a
l
istic
Exa
men
ul n e
Exa
urolo
men
gic
u l co
m ple
men
tar

EX A

M EN
UL P
A C IE
FR
NTU
CO
LUI
N T
IE N

Pier

dere
a ac
con
ut
tien
stare
ei es a
t
majo de urge e o
n
r n
paci
entu care so
arta
lui n
ms
ur
m
are
d
rapi
e
p
inde
ditat
de
ea m
tera
peut
sur
ic e
ilor
diag
i de
nost
ic n
de c
trep
tre
rinse
pers
med
onal
ical.
ul

la
mei
a co
c a uz
zuri noate.
e ca
u
mult nu se c
arte
e
n fo admiter

te
a
t
i
t
en
o
ce
e
t
a
f
s
e
r
da
nu
,
A
e
m
s
M
e
r
l
O
e
b
C
p r-o pro
c
i
C,
g
V
o
t
A
l
n
,
nozo arte di hipoxie ent
p
l ( nsufci
a
c
i
).
med atism, i tic etc.
a
m
trau sau hep
al

What is CONSCIOUSNESS?
Descartes:
1) The physical brain
worked by the flow of
animal spirits through
its cavities.
2) The immaterial soul
was connected to the
body and brain through
the pineal gland which
lies in the midline.

Gilbert Ryle:
the dogma of the
Ghost in the
Machine.

CON
SCI

Wha
OUS
t is
NES
S?

DEF
IN

ITIO
N

Co n

s c io
usne
spon
s s is
ta n e
the
state
ousl
y oc
o
f
a
c
self
and warenes urring
envi
ronm s of
ent.
Con
s ci o
us ne
dim e
ss h
n s io
a s tw
wa k
n
s

efuln
o
a wa
ess
a nd
rene
s s [M
Soci
ety T
ultia
the
Pers sk Forc
isten
e on
Vege
t
tativ
e St
ate,
1994
].

BAZA ANATOMICA A CONSTIINTEI

NORMAL STATE OF CONSCIOUSNESS

Level of consciousness (state/clarity of consciousness, quantitative

level of consciousness, vigilance, alertness, arousability);

Content of consciousness (quality of consciousness, awareness);

and Wakefulness.

D i s tu
r
Con bances
sc i o
usne of
ss

Acut
e

Normal Consciousness

This is the condition of the

normal person when
awake.

Cara
c

teri
s
tica
de i
str
nco
ii
nti
en

Este

nevo
cuno
i
ate e a
a le s
p
trii atru st
adii
(vigi
de v
lene
eghe
va n
i). In
c
i
paci erca a v ial se
entu
orbi
l
paci
cu
entu . Dac
l rs
ntre
pund
bri
nde
e la
i
pline
care
te m
au u
dete
n sc icri
op
rmin
este
at, a
tunc
trea
vigil
i el
z
(
s
en
tare
de
depl
in).

Impaired Consciousness
Inattention and Confusion .

In these conditions
the patient does not
take into account all
elements of his
immediate
environment.

teri
s
tica
de i
str
nco
ii
nti
en

Cara
c

n c

azul
de
som
nole
paci
entu n,
l la e
uoa
xcita
r se
este
ie
t
r
e
z
capa
e
te
men
b
il s
i
in
stare
vigil
en
a de
disc

uiei n decur
sul
cu m
edic
ul .

Impaired Consciousness

Drowsiness denotes an
inability to sustain a wakeful
state without external stimuli.
Stupor describes a patient
who can be roused only by
vigorous and repeated
stimuli.

teri
s
tica
de i
str
nco
ii
nti
en

Cara
c

Se n

ume
te s
dere
glare
tupo
con
a st
a
re
tien
r
paci
a t ii d e
unci
entu
l poa
cnd
men
inu
te f
t
prin
t
aplic reaz do
exci
ar
taii are de
pute
repe
rnice
tate
.

Cara
c

teri
s
tica
de i
str
nco
ii
nti
en

Star

ea d
e co
defn
m
ete
con
l
tien ipsa de
aplic
ch
i ar
area
i
stim
u
la
n
ei
ulr
i ma
Exci
sive
taii
.
le d u
se a
rero
p lic
ase
cres

n
o
cnd
rdin
e
extr
(a
emit
ting
erea
ilo
scut
r,
urat
ul de
cioc
nire
ume
dege
a ste
ri,
rnul
tul).
ui cu

STIMULUS

Calling patients name

Simple commands
Light touch with soft scrap by surface of eyelash,

ear, nose, lips

Patting on the face
Shaking the shoulders
Pricking the arms or thighs
Pressing distal phalanx
Knuckle the sternum
Gag reflex
Supraorbital or temporo-manibular joint projection
pressure

e
ul d
men
ta
Exa
rgen
u

rea
a
z
i
r
le
ola
a
c
n
s
o
,
ers
za
nt
p
e
a
n
n
e
sm,
i
i
t
t
m
a
m
a
a
o
D

oan
ad
aum
r
r
r
e
e
t
t
f
e
s
e
i
Em amaneza, h ral: urmelodare etc. tura
An men genexterne, pa e, tempera utie,
Exeamoragii e eshidratar ectie, perc
h
nsp
ed
i
d
:
e
e
rac
a si
o
e
emn
t
r
S
a
,

palp
ratia
i
,
p
s
l
s
Reuscultatie lar: TA, pui cordului ercutie,
a
,p
e
ascu aselor s
r
v
a
o
p
i
d
al
v
Caurscultatia spectie, p
loje zical
,
i
i
n
i
a
g
ora
en:
l ve
u
m
m
b
e
o
o
h
Abudscultatie mictiune,tentie la gl
a
,a
tal:
u
i
r
n
t
e
s
ro-g hipoga
U
nale,
re
gice
o
l
o
crin
o
(!)
d
n
ee
n
m
Se

pa r a

Con
met
t ro l
r i l or
ul
vita
li

La p

acie
nii f
con
r
tien
se c

treb
ontr
ui e s
olez
rnd

p
n
prim
(resp arame
ul
trii v
irai
itali
cont
a, fr
ecve
rac
ii lo r
na
tens
card
iune
iace
a ar
aa
,
teria
mo d
l) n
func
pent
iile
ru ca
vital
(resp
e
irato
card
iocir rie i
cula
se a
torie
fe n
) s
sigu
r an
.

Ana
mn

eza

C t

de m
paci
u lt s
entu
e af
l fr

con

tien
paci

entu ? Cum
a fos
l gs
paci
entu
t
it? C
l a fo
nd
ultim
st v
a da
loc c
t? A
zut
eva
deos avut
mom
ebit
entu
con
n
l p ie
tien
rder
trau
ii de

?
S
mat
-a
oare
paci
entu
l?

Ana
mn

eza

S u fe

r
care oare p
v
a
Adm a boli cu cientul
de
inist
nosc
r
care
va m eaz pa ute?
cien
mod
edic
tu l
ame
regu
n te
m ed
n
icam lat? Ce
adm
en t e
in
rece istrat p eventua
n
a
l
paci t? Cons cientul a
u
e
Dac ntul dro m oare
guri
d
a
/alco
,
fost
c

t
ol?
de in
co n s
de u
u
t
ltime mul n d ens a
zile/
ecur
spt le
s
m
ni/lu
ni?

Insp
eci
a

O in

spec

furn
izea ie atent
z e

i n fo r
v
e
m
cauz aii ref ntuale
erito
ele u
are
con
nei p
la
tien
i
e
r
d
cum
. Im
eri d
s
e
tegu e prezin portant
este
men
t co
:
au e
t
le as elor pac loraia
ie
livid
p
n ca ect pali ntului,
d, ro
cian
d
r
u
l une
oze?
z sa
u
i
sem
S
u
n
t
n
de e e de lez prezent
e
x
a
sau emplu v re exter
hem
n

atoa nti, r ,
n i
me?

Insp
eci
a

Nu

i-a m
paci
entu ucat
l l im
o ma
ba?
nifes
(la f
unui
tare
el
acce
p
r
opri
Cum
s ep
e
i
e
l
e
s
ptic)
te st
gene
.
area
ral
paci
entu a
lu i ?
un m
S
e sim
i
r
o
s
Efec
oare
tuea
care te
z p
mic
?
acie
r i s
ntul
pont
Care
a
e
s
t
e tip ne?
resp
ul de
irai
e?

D
LIZE
ERA
GEN
S
es
URE
izur
c Se Mal)
SEIZ
loni
ic-C (Grand
Ton

n
o
i
t
c
tra
n
o
C the jaw
of
es
l
c
s
e
mu
s
u
a
c
y
a
m
f
o
g
n
.
e
biti
u
g
on
t
e
th

Insp
eci
a

Se o

b
pete serv h
emo
iale
ragii
rezu
d
i
f
u
ltatu
ze n
coag
l
ulare tulburr
man
i
ifest ? Exist i de

lez
rilor ri propr careva
ii
orga
inter
n
n
ud? e? Este elor
M
p
poat iciunea acientu
e
l
acce f o ma involun
tar
nifes
s ep
ilept
cnd
tare
i
c
de
(n c
dezb pacient
ul es azul
rca
t
cu a
t
ten se vor e deja
ie ha
exam
inele
ina
lui).

EVALUATION OF THE COMATOSE PATIENT

Temperature

Pulse

Respiratory rate

Blood pressure

Posturing

Skin

Meningeal signs

Neuro Exam

Labs

EEG

CT, MRI

Evaluation temperature
FEVER

HYPOTHERMIA

Systemic infection (pneumonia,

bacterial meningitidis)

Alcoholic intoxication
Barbiturate intoxication

Heat stroke
Drowning
Anticholinergic drug toxicity
Exposure to cold
Disturbing the temperature
regulating centers (very rare)

Peripheral circulatory failure

Myxedema

Eval
uatio
n

- pul

se

Rate

(if ex
sugg
cepti
e st h
onall
eart
with
block y slow,
p e r io
shou
, or d ic b
hype
ld
r
i
rtens
eath
f c om
i
i
n
intra
bined
cran on - an in g and
ial pr
cr e a
e
s e in
s
Rhyt
sure
)

hm
Volu
me
Forc
e
Equ
ality
Con

ditio
n of
wall
arter
ial

Evaluation
respiratory rate
SLOW
Opiate intoxication

RAPID
Pneumonia

Barbiturate intoxication

Diabetic or uremic
acidosis

Hypothyroidism
Pulmonary edema
Central neurogenic
hyperventilation

BREATHING PATTERNS AND LOCALIZATION:

Evaluation
blood pressure
Marked HYPERtension
Cerebral hemorrhage

HYPOtension
Diabetes intoxication
Alcohol intoxication

Hypertensive
encephalopathy

Barbiturate intoxication
Internal hemorrhage

Greatly increased
intracranial pressure

Myocardial infarction
Dissecting aortic aneurysm
Septicemia
Addison disease
Massive brain trauma

Evaluation posturing
Eval

ation

u
uring
post

Evaluation posturing
Eval

ation

u
uring
post

The predominant
postures of the limbs
and body, the
presence or absence
of spontaneous
movements, the
position of the head
and eyes


ation

u
uring
post

movements
Yawning
Shifting of body
positions

Eval

Vocalization
Grimacing
Deft avoidance

of th

uatio

c ti o n

Eval

e
insp

Cyanosis of the lips

and nail beds inadequate
oxygenation.

in

e sk

of th

uatio

c ti o n

Eval

e
insp

in

e sk

Cherry-red
coloration carbon monoxide
poisoning.

of th

uatio

c ti o n

Eval

e
insp

in

e sk

Multiple bruises cranial fracture

and
intracranial
trauma.

of th

uatio

c ti o n

Eval

e
insp

in

e sk

Telangiectasia's
and hyperemia of
the face and
conjunctivae
alcoholism.

of th

in

e sk

uatio

c ti o n

Eval
e
insp

Marked pallor internal

hemorrhage.

Evaluation
inspection of the skin

A maculohemorrhagic rash meningococcal infection,

staphylococcal endocarditis,
typhus, or Rocky
Mountain spotted fever.

of th

uatio

c ti o n

Eval

e
insp

in

e sk

Excessive
sweating hypoglycemia or
shock.

of th

uatio

c ti o n

Eval

e
insp

in

e sk

Excessively
dry skin diabetic
acidosis,
uremia, or
drug overdose
with
anticholinergic
effect.

Evaluation - the
odor of the breath
The ODOR

Etiology of coma

Alcohol

Alcoholic intoxication
(vodka is odorless)

The spoiled-fruit odor

Diabetic coma

Uriniferous odor

Uremia

Musty fetor

Hepatic coma

Burnt almond

Cyanide poisoning

E
xam
r ni s
tic g enul
en e
ra l
i nt e

Exa

men
ul pa
in c o
cien
ntie
tulu
ntot
nt cu
i
deau
prin
exam
de
na o
gene inare co
rpor
ral
al
deta
foar
te
liat
.

sc
za
a
a
e
f
c
n
itali entilare
p
s
pre bare si v ul nu
nt
tu
o indac pacieu prezint

t
t an
men
a

t
a
r
t
stric
lui
ga
r
u
t
ilibru

h
l
c

e
p
s
ez
ea d
ctar rolitic
e
r
o
c
ct
oele
hidr

e
u ri d
Ms
nt
e
urg

za

n fa liceasc
a
faza c,
spit
n

si
as
e
sa
a
c

C
i
r
l
i
ut
c
a
o
t

i
resp turi
f
p
e

pre nu s-a
ub a r e i
t
vrs
n
i
n
e
c
en
a
t e d a c o lo a t
n
d
i
m
a
a
e
n
s

r
x
i
a
x
o imobiliz dac e iciune
ic , e
r
o
t
p
e
s
s
l
su
ica
o I eneral si rapid
c er v a i m i c a ei
m
g
re
g ic
o
l
c e a c i de n t a
o
r
d a c
u
c
e
e
a
t
n
i
e
d

tinit cauza
go w
n oa s
i
s
e
r
a
v
l
u
G
ie
Ms noaste
o lin la de com unctiilor
o
cu
e
af
sc a
s
une
e
r
p
a
z
o
nt
i
m
i
r
e
g
e
ito
r
s
n
u
o
si
CT
B 1)
t
o mvitale
a
n
n
i
e
m
x am
( v i ta
E

n
i
o
e de
n
ia m g i/ v
T
e
o 100 m
xa m o r
/v
i
E
g
o b o r at
50
enul
oz
:
m
c
l
a
u
l
a
u
l
ex
o G e st e c a z I C
i
r
o
c
nt
lH
Une
o da tratamentut anticonvulsiva
o

LC R
men
tic
ipire
trata

Sca
la G
l a sg
(Gla
ow
sgo
Sca w Com
le , G
a
SC)

Ras
p
D

un
es
Descche spo s oc
Desc hide la ntan ular
(
Fr hide la coma 4
Nu p rspun durer nd
e
oate
s
2 3
f ap 1
recia
Ras
t
p

Orie
uns
n
t
C o n a t 5 ve r
bal
Cuvifuz, de
(V
Sunente inczorien
Fr te nei oeren tat
Nu p rspu nteligi te 3 4
oate ns 1 bile
f ap
2
Ras
recia
t (in
Exec puns
t ub a
u
Loca t la mo
t)
Flex lizeazcomantor (
Flex ie norm durer d 6 M )
Exte ie anor al 4 ea 5
Fr nsie 2 mal 3
r s p
u ns 1

S co

r GS
C=
O+
V+
M

O)

Rsp

uns

o cu l

ar

Desc
h
verb ide spo
Desc ali = 4 punntan dar s
i la s
h
cte
timu
verb ide la c
li
oma
ali =
n
senz
3
punc d sa
orial
u s ti
te ( b
reac
nu
muli
o
tion
l

n
n
a
t
e
v
Desc eaz la lege c ul cu a
oma
h
stim
nda fazie
stim ide la d
u
l
i
verb
dar
u
u
ali)
nive lul dure rere =
2
ro
lu
si n l fetei d rs nu s puncte,
Fr chiderea foeoarece ree aplic la
r tat
r
actia
boln spuns
a
poat
oc h i
avul
=1
ef
l
o
pu n c
stim
r
nu-s
uli n
i
t
Reac
ocic deschid , cnd
tia e
eptiv
e os
t ra u
mat ste greu
i
chii
i
s me
o rb i
d
nici
e
a
tare
le cr
p
r
la
e
c
anio
cu l
pal
iat

pe
ez
sa
-fa
cons bral, da iuni loca ciale cu u chiar
im
r ac e
e mn
l
at.
st im e, edem implicar posibil
e
n
pedi
s
men au hem a regiun
a
t tre
ii
buie tom

Rsp

uns

o cu l

ar

Desc
h
verb ide spo
Desc ali = 4 punntan dar s
i la s
h
cte
timu
verb ide la c
li
oma
ali =
n
senz
3
punc d sa
orial
u s ti
te ( b
reac
nu
muli
o
tion
l

n
n
a
t
e
v
Desc eaz la lege c ul cu a
oma
h
stim
nda fazie
stim ide la d
u
l
i
verb
dar
u
u
ali)
nive lul dure rere =
2
ro
lu
si n l fetei d rs nu s puncte,
Fr chiderea foeoarece ree aplic la
r tat
r
actia
boln spuns
a
poat
oc h i
avul
=1
ef
l
o
pu n c
stim
r
nu-s
uli n
i
t
Reac
ocic deschid , cnd
tia e
eptiv
e os
t ra u
mat ste greu
i
chii
i
s me
o rb i
d
nici
e
a
tare
le cr
p
r
la
e
c
anio
cu l
pal
iat

pe
ez
sa
-fa
cons bral, da iuni loca ciale cu u chiar
im
r ac e
e mn
l
at.
st im e, edem implicar posibil
e
n
pedi
s
men au hem a regiun
a
t tre
ii
buie tom

lu
su
pun i acest
s

R
s
bat
intu

nde mele,
u
p
l rs stie nu patiu
u
v
olna erent, mp si s
b
,
ncte este co at n ti
l s au
i
u
g
p
i
5
ri,
ent
te v d ar
=

i
s
r
b
t
e
o
e
a
,
r
nt
te
ie
te
nt
Orie vat la ale, es 4 punc discut ste
e
n
a
c
ade e perso entat = ticip l i mare
l
zori sor, par sau ma
date
e
d
l nu r
u
z,

u
c
u
t
i
i
f
v
z
n
a
oln te doa
b
Cooate f trseur maiumz
,
e
nct
stes
f
p

u
o
n
r
p
m
o
,
c
o
= 3 rsatie
e
ntr- rientat,
t
n
ve
ul
re
n
v
o
e
o
a
z
o
c
n
e
c
d
bol
,
e in enat n
uli
t
e
t
n
m
i
i
c
t
r
v
n
Cuoate fanet potrivite le = 2 pui doar la s
vul
i
r
p
n
a
b
o
i
n
e
e
l
g
t
i
n
l
in
d b o t iv i
inte eme, u
n
cuv
e

n
ete este, g
zul c ocicep
n
a
c
u
S olboros
t, n timuli n avul este
c
n
b
si
1 pu et la s ac boln
o
r
=
e
dur
uns un sun precia d
p
s
a
i
r
r ate nic se poate notat.
F
u sco bal nu rebuie
t
r
n
l ve
cru

R
n
u
p
s
ve r
l
a
b

Rsp

uns

mot
or

Se p
unct
eaz
bun
rsp
uns, cel mai
exem
de
p
l
u
mem
n f e
x ie c
bru
exte
s
nsie uperior u un
ia n
s i n
cu c
e
cons
llal
sau
i
t
d
e
r
n ca
atie , se
fexi
zul b
hem
a,
ipleg
olna
rsp
v il o r
ic i s
e ap
unsu
recia
din p
l cel
z
mai
arte
neaf
b
ecta hemicor un
t
pulu
i

Rsp

uns

mot
or

Rsp
u
punc nde la
c
t
spon e, (de e omenzi
Loca tane nu sxeemplu: Rpirin execu
t
dica
li
iau
ti m area mis
nerv zeaz d
n
c

o
u
c
n
nsid
s
dup i contin rerea =
erat a!). Mis rii = 6
i
c
u
e
5
rile
.
cerc care bo u nervu puncte
lnav
l
nd
(
s
se c
upr
u
5 pu
s
ncte ndep l si fect aorbita omprim
r de

l en
puti
eaz
n p n cazul rteze s
p
l
m
a
n
e
timu
n la
ul os i si
mbr
n ca
Flex
l
u
u
o
re b
man
ie no
olna l durero l superio s,
dibu
=4
rma
v
r
r
l.
s
ul s
l
p
i duc ). Se ac
com uncte (o , de ap
r
e
o
p
d
r
mn
si f rim cu unghie are, bol
a ce
ecte
d
n
un o
l
e la
avul
a
com
b
pres z mem iect du mna b si retra
ol
r
ia
b
mn
g
a nu nervul rul supe (stilou), navului e mna
u
se
la
rio
Flex
aj
i
ie an unge p supraor r din co care bo
b
lnav
t,
n la
stim
o
itar
ul
se p sau la
ulul rmal (
n
i
v
d
e
r
n
fexi
o
e
l
o
u
d
c
c
l ma
u
ort
ice
a len
ndib ce fexi
sau
t a ptiv sup icare) =
a da
u
lei).
n
m
r
infer cheietu embru raorbita 3 punct
lui s
r sau
e (d
ra m
ioare
up
up

Exte
, rea
s
ctia inii, exte erior la ternal u
nsie
es
n iv
rm
ns
dure
=
ros s 2 punc te bilate ia mem elul co eaz
tulu
ume
brelo
t
ral)
i
rilor eproduc e /dece
.
r
, ext
rebr
e
Lips
e
x
a
ensi
a re
a me tensia c re/ (dup
actie
o
sti
m
i=1
brelo tului,
m
r
pun
o
r
tatia ulul
infer
ct .
ioare
inter
n a
.

Rsp

uns

mot
or

Rsp
u
punc nde la
c
t
spon e, (de e omenzi
Loca tane nu sxeemplu: Rpirin execu
t
dica
li
iau
ti m area mis
nerv zeaz d
n
c

o
u
c
n
nsid
s
dup i contin rerea =
erat a!). Mis rii = 6
i
c
u
e
5
rile
.
cerc care bo u nervu puncte
lnav
l
nd
(
s
se c
upr
u
5 pu
s
ncte ndep l si fect aorbita omprim
r de

l en
puti
eaz
n p n cazul rteze s
p
l
m
a
n
e
timu
n la
ul os i si
mbr
n ca
Flex
l
u
u
o
re b
man
ie no
olna l durero l superio s,
dibu
=4
rma
v
r
r
l.
s
ul s
l
p
i duc ). Se ac
com uncte (o , de ap
r
e
o
p
d
r
mn
si f rim cu unghie are, bol
a ce
ecte
d
n
un o
l
e la
avul
a
com
b
pres z mem iect du mna b si retra
ol
r
ia
b
mn
g
a nu nervul rul supe (stilou), navului e mna
u
se
la
rio
Flex
aj
i
ie an unge p supraor r din co care bo
b
lnav
t,
n la
stim
o
itar
ul
se p sau la
ulul rmal (
n
i
v
d
e
r
n
fexi
o
e
l
o
u
d
c
c
l ma
u
ort
ice
a len
ndib ce fexi
sau
t a ptiv sup icare) =
a da
u
lei).
n
m
r
infer cheietu embru raorbita 3 punct
lui s
r sau
e (d
ra m
ioare
up
up

Exte
, rea
s
ctia inii, exte erior la ternal u
nsie
es
n iv
rm
ns
dure
=
ros s 2 punc te bilate ia mem elul co eaz
tulu
ume
brelo
t
ral)
i
rilor eproduc e /dece
.
r
, ext
rebr
e
Lips
e
x
a
ensi
a re
a me tensia c re/ (dup
actie
o
sti
m
i=1
brelo tului,
m
r
pun
o
r
tatia ulul
infer
ct .
ioare
inter
n a
.

(G
w
)
o
C
g
S
s
G
a
l
,
e
G
l
a
a
l
c
a
S
Sc
a
om
C
w
o
g
las

Pentru a
permite
reevalur
i corecte
ulterioare
se
noteaz
scorul
GSC = 11
puncte O
(3) + V
(3) + M
(5)

s
(Gla

ow
lasg
ale,
la G
a Sc
Sca
Com
gow
)
GSC

t o si
GS C
a
,
i
r
m
co
i n
a
m
l
a
r
x
doa
te e t
l

a
c
z
i
i
l
a
s
p
n
e
i
a
e
c
t
i
se
ren
e f a i n s u fc
e
u
s
f
i
n
i
s
d
o m a t o ie d a r
nu
e
t
ele
c
r
c
n
o
e
t
r
a
u
l
t
a
c,
p
i
n
n o bl i g

t
3
p

e
pile ie,
e
m d profund
fi
i

n
i
z
a
cr i
lm
erm
t
u

m
o
r
o
p
p
o
i
c
u
sc cesul si apare d ever, h
de
t i,
f a ls s i u n e s
a
t
c
i
i
g
ia l
ia
i
c
or m ipoten
v
a
c
f
a
s
so c, h t e
o ln
b
t is m
a
a
l
n
m
t
n

a me
e ci a cu t r u a o ci a t
r
c
i
p
d
a
me
cei ar as
de
a
u
l
e
,
r
du l
te g intubati
e
s
m
e
a z i ci ,
i une
z
e
l
f
a
sa u )
r
e
v
se
egie
l
p
a
(tetr
C:
S
G
PRE
S
E
TD
A
N
O
NTI
E
M
DE

Exa
m en
n eu
u
l
r ol o
g ic

Men
Ref ingismul

e
cere xele tr
unc
bral
hiul
pupi
(
R
e
ui
lar.
acia
ocul
ocef Refexul
alic.
vest
Refe
ibulo
corn
- o cu
xul
e
la
Refe al. Refe r. Refe
x
x
x
la ex ul de tu ul farin ul
gian
cita
se. G
.
Refe
ie du
rima
x
exci ul de c reroas. s
lipire
taie
de c
a cu s
l
lipire
tic. a
vizu
al.) la excit Refexu
aie
l

Evaluation meningeal signs

Eval

m en

gns
al si

uatio

inge

Evaluation meningeal signs

Eval

m en

gns
al si

uatio

inge

Exam
trun enul ref
chiu
e
xelo
la p a
lu i c
ereb r
ci e n
ral
t ul c
oma
to s

 Tulb

Exa
m en
n eu
u
l
r ol o
g ic

u
ocu rri de
lar
ocul
(Poz motrici
ari.
tate
i io n
D
a
Mic
area eviaia p rea glob
o cu l
ilor
ari. spontan rivirii.
o cu
Rea
ag
l
a
lobil
r bo
c ia
or
bbin
dure
la e
g
Ref roas. xcitaie
e
(RO xele os
T)
teoextr
e m i t . C n d d
ten d
ile
e ex
refe
inoa
e
x
r
prov ul mass efexele mplu de
se
e te r
o ac
se p
pe t
ia
n
ro
o
d

ivelu
ate
n es
v oa
elo
tran l trecer c, atunc te aboli c uor
sv e r
,
t
i
i
s d i cranio leziune sau nu iar
-c
e niv
a
s
Ton
el su ervicale se af e
usu
l
l mu perior). (leziune a

s cu l
ar.

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light reflex (II, III)

il
Pup

ion
luat
Eva
flex
ns
t Re
esio
Ligh
al L
c tu r
lar y
St r u

er
n
r

H
e
om
n
r
o
d
i
n
s
y
e
l
s
ed
d
i
s
one brainstem
e
of th
us
or
m
a
l
a
h
t
o
p
hy
a
o
t
r
o
ng
i
t
c
e
e
h
t
s
s
f
i
o
d
m
s
y
r
y
u
l
l
e
tid
a
n
o
r
r
a
e
a
t
d
lc
a
n
Unila and fixe
r
te
n
i
d
e
dilat ncal
ry
e
t
r
a
U

n
o
i
t
a
i
hern

ly
l
a
r
e
Bilat icted
tr
s
s
n
n
o
o
i
c
s
le
e
n
i
t
Pon

Claud Bernard-Horner syndrome

Evaluation
Pupillary Light Reflex
Toxic
Ingestions
MIOSIS (small
pupils)
Alcohol

MYDRIASIS (large
pupils)
Anticholinergics

Opiates

Antihistamines

Barbiturates

TCAs

Organophosphates

Cocaine /
Amphetamines

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light reflex (II, III)
Oculocephalic / Dolls eye reflex (III, IV, VI, VIII)

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light reflex (II, III)
Oculocephalic / Dolls eye reflex (III, IV, VI, VIII)
Oculovestibular reflex (III, IV, VI, VIII)

Evaluation
Oculovestibular Reflex

Patients head is raised 30 degrees from the

horizontal. (Orients the semi-circular canals)

Cold water is infused into the auditory canal.

In an intact reflex, both eyes deviate towards the
ipsilateral side

Evaluation Oculocephalic Reflex

and Oculovestibular Reflex

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light reflex (II, III)
Oculocephalic / Dolls eye reflex (III, IV, VI, VIII)
Oculovestibular reflex (III, IV, VI, VIII)
Corneal reflex (V, VII, III)

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light reflex (II, III)
Oculocephalic / Dolls eye reflex (III, IV, VI, VIII)
Oculovestibular reflex (III, IV, VI, VIII)
Corneal reflex (V, VII, III)
Gag reflex (IX, X)

Exa
m en
n eu
u
l
r ol o
g ic

Ton
Act usul musc

i v i ta
ular
te a
.
sp o
nt a n
mus
R ef
cula
.
r
prim exel
e pr
i
sunt tive ace
imit
le
p
mat rezente refexe
i
uriz
care ve. Se
l
a
n
rii d
en
ou
n
n

cef
-n
ume
m
is
sc
apar alului re par. n le scut, ia od fziol
ogi c
r pe
iia.
fexe
ziun
p
e
le re
Se m
spec difuze arcusul
al
tive
ne l e
i fa e
c din
palm piram
no u
i da
o-

me n
le. R
Refe
t
efex
o
xu l l
nier.
ul
ab ia
preh
l. Re
e n si
fexu
(apu
une
l de
care
). Re
fexu
l de
suge
re.

Evaluation NEURO EXAM

Mental status
Cranial nerves
Blink to threat (II)
Pupillary light refex (II, III)
Oculocephalic / Dolls eye refex (III, IV, VI, VIII)
Oculovestibular refex (III, IV, VI, VIII)
Corneal refex (V, VII, III)
Gag refex (IX, X)

Muscle tonus
Deep tendon refexes
Babinski refex

Sist
e mu
nerv l
ve g
o
etat s
iv.

Se v

a
tenis observ
a mo
iunii
frecv
d
a
ene rteriale ifcarea
card
iace i contrac i a
Brad
la

icard excita iilor

re ex
spec
i
ial la a, care
tern
i

n jo
n
s es poziion tervine .
te o
a c iu
area
n
m
ne c
c
a
creie
omp nifesta apului
r
r
r
regiu ului. La esiv as e de
u
o
tulb nii hipot aciune pra
u
a
term rare a fu lamice a asupra
o
n
r
exem reglare ciei de e loc o
, ca r
p
l
u
e de
prin
se p
o
h
cent iperterm ate man
ral.
if e s t
ie de
a
origi
ne

Sist
e mu
nerv l
ve g
o
etat s
iv.

Ref

exul
cilio
Aplic
spin
area
a l.
dure
u
n
ei ex
roas
cita
e n
trap
ii
ezoi
regiu
d s
este
nea
a
uaf
nso
pupi
it
eii
d e l
lelor
. Ace
rgire
pato
logic
st re
de s
fex
e
s
t
e re
istem
a liz a
ul si
t
mpa
tic.

1)Extreme

COM
A

unresponsivene
ss.

2) No voluntary
movement or
behavior.

FIZIOPATOLOGIA COMEI
PRINCIPALELE CAUZE CARE PRODUC COMA:

1. O leziune a
trunchiului cerebral sau
tulburri metabolice ce
lezeaz sau deprim
Sistemul Reticular
Activator (SRA).
2. O leziune emisferic
bilateral sau o inhibitie
a activittii emisferelor.

1+2

ul
rium
De l i

Este
o
si cu tulbura
n
r
prin oastere e de co
nstie
, car
dezo
a
aten
n
r
tiei, ientare, cterizat ta

tu l b
(halu
dimi
u
n
r
gnd cinatii), ri de p uarea
tulb
erce
ire, t
u
ptie
com
port ulburri rri de
ame
nelin
de m
n
i
t
tulb ste psih inadec emorie,
u
v
o
acut rri de s motorie at,
,
o
(
de d de mult mn, cu
d
u
e
cte rat lim ori noa ebut
v
p
it
spt a zile p at (de tea) si
m
l
ni). n la 3-4 a

Deli
ul
riu m

ai
m

ativ ac
c
f
i
)d
mn
e
%
p.
s
5
m
2
i
e
t
t
la
es

di n
a
n
t
e

a
t
t
p
a
(
a
oi
r
lit
c
t
i
c
a
i
i
d
t
n
s
r
me
at
Mo a vrst
c
i

t
t
s
u
za
l
o
c
u
n
a
a
s
g
c
e
e
l
a
te
dia
un
i
a
la
t
e
o
c
t
t
p
s
e
n
f
e
e

a
cv
er
nu
v
e
ce
i
r
re
e
r
f
a
s
l
o
i
i
a
u
c
a
ti
m
sc
Prac gical m i apare ziuni va e, n
r
u
r
i
otus aj, n le fectioas
h
t
c
,
m
u
vr
in
i
e
,
r
i
s
l
e
c
e

i
d
p
ze
at
i
u
r
d
m
c
cu
i
u

c
e
a
i
l
p
l
r
i
t
a
du
et
er
le,
n
u
a
e
a
r
,
s
g
b
cere n cursul fectiuni lmonar

a
u
HIC, tice, n cient p l,
a
p
f
epile , n insu tic, ren dup
a

ii,
febr c, hep eoplaz rvetii
n
ia
te
,
d
n
e
i
r
i
,
a
c
em
al
c
r
i
l
e
g
n
hipo ezie ge c.
t
t
anes gicale e
r
chiru

Clasifcarea fziopatologic
a comelor
Dou categorii majore de come
1. Come neurogene (primare cerebrale)
prin leziuni supratentoriale
prin leziuni subtentoriale
2. Come toxico / metabolice (secundare)

Clasifcarea comelor
Coma neurogen (com
primar)
-leziune neurologic
- semne neurologice de
focar
Com metabolic /
toxic (com
secundar)
- atingere metabolic
sau toxic
- semne neurologice
simetrice.

DIAGNOSTICUL DIFERENTIAL AL COMEI

I. Maladii ce nu provoac semne neurologice de
focar sau de lateralizare, cu pstrarea funciilor
trunchiului cerebral. Examenul CT i RM cerebral,
numrul de celule n LCR este normal.
A. Intoxicaii: alcool, barbiturate i alte droguri
sedative, opiate, etc.
B. Afeciuni metabolice: anoxia, acidoza
diabetic, uremia, coma hepatic,
hipoglicemia, boala Addison, deficiena
nutriional profund.
C. Infecii de sistem severe : pneumonia, febra
tifoid, malaria, septicemia, sindromul
Waterhouse-Friderichsen.
D. Colapsul (ocul) circulator de orice cauz.

DIAGNOSTICUL DIFERENTIAL AL COMEI

I. Maladii ce nu provoac semne neurologice de
focar sau de lateralizare, cu pstrarea funciilor
trunchiului cerebral. Examenul CT i RM cerebral,
numrul de celule n LCR este normal.
E. Starea postcritic (dup acces epileptic).
F. Encefalopatia hipertensiv i eclampsia.
G. Hipertermia sau hipotermia.
H. Comoia cerebral.
I. Stupoarea i coma idiopatic.
J. Hidrocefalia acut.

DIAGNOSTICUL DIFERENTIAL AL COMEI

II. Maladii care cauzeaz iritaie meningeal cu
sau fr febr, cu un exces de eritrocite sau
leucocite n LCR, de obicei fr semne de focar,
de lateralizare sau de implicare a trunchiului
cerebral. CT sau RMN care preced puncia
lombar este normal sau anormal.
A. Hemoragie subarahnoidian din erupie de
anevrism, malformaie arterio-venoas,
ocazional post-traumatic.
B. Meningit acut bacterian.
C. Unle forme de encefalite virale.

DIAGNOSTICUL DIFERENTIAL AL COMEI

III. Maladii care provoac semne de lezare de
focar a trunchiului cerebral sau semne de
lateralizare cerebral, cu sau fr modificri ale
LCR. CT i RMN de obicei sunt anormale.
A. Hemoragie sau infarct cerebral emisferial.
B. Infarct de trunchi cerebral prin tromboz
sau embolism.
C. Abces cerebral, empiem subdural.
D. Hemoragie cerebral epidural i subdural,
contuzie cerebral.
E. Tumori cerebrale.
F. Cauze mixte: tromboz de vene corticale, unele
forme de encefalite virale, encefalomalacie de focar
embolic pe motiv de endocardit bacterian,
leucoencefalit hemoragic acut, encefalomielit
acut (post-infecioas), i altele.

apte cauze frecvente ale

comei
1.Otrvire, alcool
2.Leziuni ale capului (contuzie, hematom subdural, extradural)
3.Ictus ( hemoragie subarahnoidian, ictus ntins ischemic sau
hemoragic)

4.Status epileptic (convulsiv sau non-convulsiv)

5.Tulburri metabolice (diabetice, uremice, hepatice)
6.Infecii (meningite, encefalite)
7.Anoxii

(pneumonie, encefalopatie hipoxico-hipotensiv)

Come reversibile

Hipoglicemia

Hematomul extra- i
subdural (mai frecvent
intr-un context
traumatic)

Meningita i
meningoencefalita

Evaluation Labs

Blood Glucose!
Chemical-toxicologic analysis of blood and urine
Arterial blood-gas analysis
Measurements of electrolytes, calcium, osmolarity
Renal function (blood urea nitrogen)
Hepatic function
Drug levels of any prescription meds in the home
CSF examination
If etiology remains obscure, consider: NH 4+, TSH,
cortisol, lactate, serum osmoles, co-oximetry

Laboratory Procedures in Comatos Patient

In patients with
evidence or even a
suspicion of increased
intracranial pressure, a
CT scan or MRI should
be obtained as a
primary procedure.

Evaluation Imaging

CT of head without contrast is test of choice. If

initial work-up unrevealing, and patient is stable,

can consider MRI

MRI is better for CT in detecting coma due to:

Brainstem and cerebellar infarcts
Early cerebral infarcts
Herpes encephalitis
Anoxic encephalopathy

ACCES CT 24/24
CLRA
I

Laboratory Procedures in Comatos Patient

If poisoning is
suspected, aspiration
and analysis of the
gastric contents is
sometimes helpful, but
greater reliance should
be placed on
chromatographic
analysis of the blood
and urine. Accurate
means are available for
measuring the blood
concentrations of
phenytoin, barbiturates,
alcohol, and a wide
range of other toxic

Laboratory Procedures in Comatos Patient

Lumbar puncture,
although carrying a
certain risk of
promoting further
herniation, is
nevertheless necessary
in some instances to
rule out bacterial
meningitis,
encephalitis, or a
primary subarachnoid
hemorrhage that is not
visible by CT, although
such a patient would
not likely be comatose.


ion
lu at
Eva panum
otym

Hem

Evaluation Papilledema

n
uatio
Eval
ma
llede
Papi

Optic disk modification in increased intracranial

pressure

Normal retina

Stagnant Optic

Papilledema

Atrophy after
stagnation

Ev a lu atio n

ct
e
t
e
nd
a
c
G
iv e
s
E
l
E
u
nconv
no
s
statu ticus
p
l
epile , as wel
)
E
S
N
s
(
u
o
i
r
a
as v malities
r
abno may
h
whic st
e
g
g
u
s
fc
i
c
e
sp
al
n
o
i
t
addi oses.
n
diag

EEG

S TA
TE S
ING
COM
A

Brain death

Persistent vegetative state

Minimally conscious state

ICK

Locked-in syndrome

Psychogenic
unresponsiveness

MIM

ts
n
e
i
t
pa
f
o
e
s
e
e
t
ta
Th
s
a
n
are i coma.
g in
p
e
e
b
e
d
ey
h
t
Then en their
in
to op at frst
,
eyes nse to
o
li
p
u
s
m
e
i
r
st
l
u
f
pain ter
y
la
and aneousl
t
n
o
p
s
for
d
n
g ly
a
n
i
s
a
incre ged
n
o
l
o
r
p
s.
d
o
i
r
pe

Minimally
s
e
t
a
t
S
s
u
o
i
c
s
Co n

Locked-in syndrome
ed-in
Lock
rome
synd

Is a de-efferented
state in which the
patient is fully
conscious but can
make no
spontaneous
movements except
lid and vertical eye
movements.

Sind
rom
ul lo
in s
cked
au s
de d
in d r
omu
ez e
fere
l
ntar
e

Tetra
p
doar legie cu
vert a misc pstrar
ea
rilor
icale
ocul
misc
n su
are
rile
s
s
i une
Apar
pleo
ori
e n
apel
leziu
pont
or.
ine c
nile
cilo
u afe
r co r
ctar
cort
t
icon icospin ea
ucel
al e s
obic
are,
i
ei de
de
isch
c
a
uz
emic
sa
hem
u
o r ag
ic .

Locked-in Syndrome, and Akinetic Mutism

A patient is fully conscious
and able to see but unable
to feel, or move because of
brainstem damage. Lockedin patients can often move
their eyes to stimuli

and move their

eyes voluntarily
if only upwards.

Persistent vegetative state

(apallic syndrome)
Is caused by
extensive injury to
the cerebral cortex,
subcortical white
matter, or thalamus.
The patients are
awake but
unconscious (loss of
cortical function).

,
z
u
f
i
d

l
r
a

c
f
i
t
r
r
co
l da
i
e
i
g
t
i
c
v
fun parent
s
i
d
au
s
o
a

e
d
t
t
Es
fin
ien
t
l
li,
s
u
a
n
nd
v
b
i
o
a
r
f
c
e
n
l
v
e
e
bo
ct i
tar
uli
a
n
m
e
u
i
r
l
t
s
vo
n
nt
i
u
nici o onal la
u
s
a
e
s
e
tiv
ti
x
a
o
e
t
n,
f
e
m
e
m
g
e
r
o
e
s
e
v
ele
h
i
ril
i
g
c
t
s
e.
c
e
i
r
v
n
a
m
l
u
c
f
i
u
le,
tm
ort
op
i
i
t
c
r
b
s
i
e
i
(
s
s
d
l
po
a
ca
rin
r
p
e
b
t
,
e
a
a
v
r
r
e
a
e
t
t
r
c
s
a
ia
p
eg
i
idit
x
g
o
m
i
n
r
e
ia
a
c
e
t
i
l
r
f
u
l
g
a
e
o
o
p
a
ip
at
Ev
h
o
.
,
p
)
r

a
o
re
s
Cauz -respirat al extin s sau sta e
d
r
io
e
card ie cereb tre dec doar cea
c
uz
i
t
si
e
n

c
o
t
i
c
al
n
b
u
e
o
t
t
s
n
e
i
e
d
s
este ativ per ate f ev
o
t
p
e
g

t
e
v
ra
u
d

t
scur ibil.
rs
reve

e
r
a
t
S
a
et
g
e
v

v
i
t
a
s
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s
r
pe

t
n
te
sau
r
d
n
i
s
l
u
m
o
lic
a
p
a

The Persistent Vegetative State

Patients who survived for indefnite periods without
regaining any meaningful mental function. For the frst
week or two after the cerebral injury, these patients are
in a state of deep coma. Then they begin to open their
eyes, at frst in response to painful stimuli and later
spontaneously and for increasingly prolonged periods.
The patient may blink in response to threat or to light
and intermittently the eyes move from side to side,
seemingly following objects or fxating momentarily on
the physician or a family member and giving the
erroneous impression of recognition.
In brief, there is arousal or wakefulness, and alternating
arousal-nonarousal cycles are established, but the
patient regains neither awareness nor purposeful
behavior of any kind.

Akinetic mutism
etic
Akin
sm
muti

The patient is awake

but the drive to
voluntary movement
is severely impaired
and the patient does
not speak (mutism).

i
ic
n
e
c
fa
u
n
l
u
v
a
ln
Bo
o miscare, nu se
l
u
t
c
a
t
n
o
c
a
lu
e
t
a
o
p
cu el, uneori ns
a
e
ir
iv
r
p
u
c
e
t
s
e
r
urm
iar ritmul veghesomn poate f
pstrat. Apare n
leziuni ale liniei
l,
mediane (diencefa
talamus, partea
superioar a
mezencefalului,
leziuni frontale
bilaterale mediobazale).
u
a
s
c
i
t
e
in
h
c
a
e
l
d
u
l
m
u
s
i
m
t
o
e
r
Mu sindr
a
t
n
e
r
e
f
a
z
de

r
o
l
i
h
c
o
a
e
re
v
i
e
t
d
i
c
a
h
c
e
r
s
,
e
e
d
c
i
a
r
l
t
e
t
m
n
i
e
s
t
e
,
s
c
i
i
e
l
z
g
a
e
o
R ile norm r neurol pozitiile
p
lo
u
e

P
z
n
a
m

e
ct
se
e
a
r
s
o
p
c
i
i
L
s

e
u
d
v
a
e
n
n
ol
B
comode sunt sem
u
in
n
i
e
ic
b
o
Decotinent
a
m
in
oco

d
u

e
n
s
e
P
g
o
h
psi

Psyc
distu hogen
ic
r ba n
cons
ces
of
ciou
snes
s

Are
relat
ively
di a g
n
r
can ose. Th are and
e lac
be e
i
k of difcult
p sy c
t h er
arou
to
hiatr
an e
s
or a
cute ic disea xpressio ability
se ( c
n of
stres
d ep r
o
a
ess i o
s renver
delib
s
n
a
erat , catato ction, s ion
e
so m
etim fabrica nic stup evere
or) o
es f o
tion.
h i st o
r
u
r
C
amin y or on nd in th lues ar a
e
n eu r
e ca
ation
s
o
aver
sive (e. g., p logical e e
clos
ing, refexes resence x, a cpres
and
of
e
t
vest
i
r
v
e ey
i- bu ved op
n y st
tokin e
lo - o c
a gm
etic
us
stere
u
otyp , catale lar
ed p
p
ostu sy,
re).

MOARTEA CEREBRAL
MANIFESTRI
CLINICE:

Moartea cerebral poate f

suspectat la orice pacient n stare de
com profund cu apnee, rezultat
dintr-o leziune cerebral profund sau
difuz.
Criteriile cardinale de diagnostic
ale morii cerebrale sunt:
(1) coma profund cu areactivitate
complet,
(2) stare de apnee, indiferent de
hipercapnie,
(3) absena tuturor refelexelor trunchilui
cerebral i a celor susinute de nervii
cranieni,
(4) prezena leziunilor cerebrale
structurale, sufciente pentru
producerea manifestrilor clinice,

Care of the Comatose Patient

1. The management of shock, if it is present, takes precedence
over all other diagnostic and therapeutic measures.
2. Shallow and irregular respirations, stertorous breathing
(indicating obstruction to inspiration), and cyanosis require the
establishment of a clear airway and delivery of oxygen. The
patient should initially be placed in a lateral position so that
secretions and vomitus do not enter the tracheobronchial tree.
Secretions should be removed by suctioning as soon as they
accumulate; otherwise they will lead to atelectasis and
bronchopneumonia. Arterial blood gases should be measured
and further observed by monitoring of oxygen saturation. A
patient's inability to protect against aspiration and the presence
of either hypoxia or hypoventilation dictates the use of
endotracheal intubation and a positive-pressure respirator.

Care of the Comatose Patient

3. Concomitantly, an intravenous line is established and blood
samples are drawn for determination of glucose, drugs, and
electrolytes and for tests of liver and kidney function. Naloxone, 0.5
mg, should be given intravenously if a narcotic overdose is a
possibility. Hypoglycemia that has produced stupor or coma demands
the infusion of 25 to 50 mL of 50% glucose, followed by a 5%
infusion; this must be supplemented with thiamine.
4. With the development of elevated intracranial pressure, mannitol,
25 to 50 g in a 20% solution, should be given intravenously over 10 to
20 min and hyperventilation instituted if deterioration from a mass
lesion occurs, as judged by pupillary enlargement or deepening
coma. Repeated CT scanning allows the physician to follow the size
of the lesion and degree of localized edema and to detect herniations
of cerebral tissue. With massive cerebral lesions, it may be
appropriate to place a pressure-measuring device in the cranium.

Care of the Comatose Patient

5. A lumbar puncture should be performed if meningitis or
subarachnoid hemorrhage is suspected, keeping in mind the
risks of this procedure and the means of dealing with them. A
CT scan may have disclosed a subarachnoid hemorrhage, in
which case no lumbar puncture is necessary.
6. Convulsions should be controlled by special measure.
7. As indicated above, gastric aspiration and lavage with
normal saline may be useful in some instances of coma due
to drug ingestion. Salicylates, opiates, and anticholinergic
drugs (tricyclic antidepressants, phenothiazines,
scopolamine), all of which induce gastric atony, may be
recovered many hours after ingestion. Caustic materials
should not be lavaged because of the danger of perforation.

Care of the Comatose Patient

8. The temperature-regulating mechanisms may be
disturbed, and extreme hypothermia, hyperthermia, or
poikilothermia may occur. In severe hyperthermia,
evaporative-cooling measures are indicated in addition
to antipyretics.
9. The bladder should not be permitted to become
distended; if the patient does not void, decompression
should be carried out with an indwelling catheter.
Needless to say, the patient should not be permitted to
lie in a wet or soiled bed.

Care of the Comatose Patient

10. Diseases of the CNS may disrupt the control of
water, glucose, and sodium. The unconscious patient
can no longer adjust the intake of food and fluids by
hunger and thirst. Both salt-losing and salt-retaining
syndromes have been described with brain disease.
Water intoxication and severe hyponatremia may of
themselves prove damaging. If coma is prolonged, the
insertion of a gastric tube will ease the problems of
feeding the patient and maintaining fluid and electrolyte
balance. Otherwise, approximately 35 mL/kg of isotonic
fluid should be administered per 24 h (5% dextrose in
0.45% saline with potassium supplementation unless
there is brain edema, in which case isotonic normal
saline is preferable).

Care of the Comatose Patient

11. Aspiration pneumonia is avoided by prevention of
vomiting (gastric tube and endotracheal intubation),
proper positioning of the patient, and restriction of oral
fluids. Should aspiration pneumonia occur, it requires
treatment with appropriate antibiotics, and aggressive
pulmonary physical therapy.
12. Leg vein thrombosis - a common occurrence in
comatose and hemiplegic patients - often does not
manifest itself by obvious clinical signs. An attempt may
be made to prevent it by the subcutaneous
administration of heparin, 5000 units q 12 h, and by the
use of intermittent pneumatic compression boots.

Care of the Comatose Patient

13. If the patient is capable of moving, suitable
restraints should be used to prevent falling out of bed
and self-injury from convulsions.
14. Regular conjunctival lubrication and oral cleansing
should be instituted.

Prognosis of Coma
As a general rule, recovery from metabolic and toxic causes of coma
is far better than from anoxic coma, with head injury occupying an
intermediate prognostic position. If there are no pupillary, corneal, or
oculovestibular responses within several hours of the onset of coma,
the chances of regaining independent function are practically nil (see
Levy et al). Other unfavorable prognostic signs are absence of
corneal reflexes and eye-opening responses and atonia of the limbs
at 1 and 3 days after the onset of coma and absence of the cortical
component of the somatosensory evoked responses on both sides.

REFERENCES
PLUM F, POSNER JB: Diagnosis of Stupor and Coma,
3rd ed. Philadelphia, Davis, 1980.
ADAMS R, VICTOR M: Principles of Neurology, New
York McGraw-Hill, 1985.
CARONNA JJ, SIMON RP: The comatose patient: A
diagnostic approach and treatment. Int Anesthesiol Clin
17(2/3):3, 1979.
WEINER HL, LEVITT LP: Neurology. Fifth edition.
Williams & Wilkins, 1998.
MAIESE K: Metabolic Coma. Neurobase. Third 1999
Edition.

THE END
QUESTIONS ???