COMA and Related

Disorders of
Consciousness
Dr.Budhi Suwarma SpS
FK UNJANI
COMA and Related
Disorders of
Consciousness
3% of all admissions to the Emergency W.

82% of the comatose patients:

alcoholism, Cerebral Trauma and CVD
(Boston City H)

Other major causes : Epilepsy, Drug

intoxi cation, Severe infection
Consciousness
Psychologist : a state of continuous
awareness of ones self and ones
environment
Physicians : the state of the
patients momentary awareness of
self and environment and his/her
responsive ness to external
stimulation and inner need
Consciousness
Level of consciousness : the state of
arousal or the degree of variation from
normal alertness
Content of consciousness : the quality
and coherence of thought and behavior
Normal consciousness : fully responsive
to stimuli and indicates by his/her
behavior and speech
Confusion
Inability to think with customary speed
and clarity, usually marked by some
degree of inattentiveness and
disorientation
Most often results from a process that
influences the brain globally
(toxin,meta- bolic disturbances or
dementia) but can also accompany
focal cerebral diseases
 Confusion (cont.)
Thinking : variably to problem solving or
to coherence of ideas about a subject

Severely confused, moderately confused

and mild degree of confusion

Delirium : a confusional state in which

hyperactivity may be prominent
 Consciousness (level )
Drowsiness : inability to sustain a wakefull
state without ext.stimuli (speak/tactile)
Stupor : can be aroused only by vigorous&
repeated stimulieyes open look at the
examiner,no/slow/inadequate response,
restless stereotyped motor activity
Coma : appears to be asleep, can not be
aroused by ext.stimuli / inner needs
Sleep
May still respond to unaccustomed
stimuli
At times are capable of some mental
activity (dream)
Cerebral 02 uptake does not
decrease
EEG, Cerebral Evoked Response,
Spontaneous motor activity differ
Persistent Vegetative State
Blink to gesture threatening, roving eye,
seemingly follow object/fixating
momenta ry to the physician/family
member, inatten tive, no speech, no
signs of awareness of the
environment/inner need

Responsiveness is limited to premature

postural/reflex movement of the limbs
Apallic
syndrome/Neocortical
death
Presence of autonomic and
respiratory function without
cognition
Locked-in
syndrome/Deafferented
state
Due most often to a lesion of the
basis pontis
Spare both somatosensory pathway
and ascending neuronal system
Wakefull
Depriving of speech and capacity to
respond in anyway except vertical
gaze and blinking
Coma vigile
Appear to be awake but
unresponsive
Able to answer in whispered
monosyllable
Akinetic mutism
Silent and inert
Result of bilateral frontal lobe lesion
Normal integrity of motor and
sensory pathway
Lacking to an extreme degree
psychic drive or impulse to action
(abulia)
Brain Death
Absence of cerebral functions

Absence of brainstem functions +

no spontaneous respiration

Irreversibility of the state

Brain Death cont.
Absence of cerebral function

Deep coma
Total lack of spontaneous movement
Total lack of motor and vocal rasponse
to all visual,auditory and cutaneous
stimulation
Spinal reflex may persist in some cases
Brain Death cont.
Absence of brainstem function
Absence of spontaneous eye movement
Mid position of the eyes
Lack of response to OC and OV testing
Fixed dilated / midposition fixed pupil
No facial movement and no gag, cough,
corneal, sucking reflex
Absence of decerebrate respons
No respiratory movement (PaC02 50-60)
Brain Death cont.
Most institutions demand proof of EEG (ECS,
flat, isoelectric, no wave > 2V during 30 min
recording)
Wait about 24 h before pronouncing the
patient death (6h massive cerebral
hemorrhage/trauma)
Exclude :
Profound hypothermia
Intoxication with hypnotic-sedative drugs
Immediately following cardiac arrest
Physiology and Morbid
anatomy of Coma
The state of consciousness depends on a
continuously active central generator (ARAS)
Sensory stimulation has a double effect
Convey information to the brain from somatic
structure and the environment
Activates ARAS
Cortex not only receives impuls from ARAS
but also modulates it via corticofu -gal
projection to centrencephalic
 Disease mechanism that
disturb consciousness
Interfere metabolic activities of neuron
cortex (hypoxia,hypoglycemia,hyper/hypo-
osmoler,acidosis,alkalosis,hyperammonemi
a etc.)
Acute drop in CBF to 25 ml/min/100 gr
syncope ; 12-15 ml ECS coma.N(55)
CMR (metabolic encephalopathy)
O2 to 2 mg/min/100 gr (N=4)
Disease mechanism that
disturb consciousness
(cont.)
Body temperature > 41C or < 30C
DM : acetone bodies (acetoacetic acid,
-hydroxybutiric acid)
Uremia : phenolic derivates of the
aromatic amino acid
Hepatic coma : NH3 5-6 X N
Lactic acidosis : blood pH < 7
Pulmonary insufficiency : hypercapnia
Disease mechanism that
disturb consciousness
(cont.)
Hyponatremia < 120 mEq/L : water IC

General anesthetic,alcohol,opiates,pheny
toin,antidepressant,diazepines direct
effect on neuronal membrane,neurotrans-
mitter and their receptor

Methyl alcohol,ethylene glycol,paraldehy

de metabolic acidosis
Disease mechanism that
disturb consciousness
(cont.)
General epileptic seizure : sudden
and excessive neuronal discharge
Concussion :
- enormous increase in ICP 200-700 lb/m2
lasting a few thousandth of a second
- Sudden swirling motion of the brain
rotation of the hemisphere around the
axis of the upper brainstem
Patho-anatomy
Displacements of the Brain
Tissue (Herniation)
Central syndrome:downward displacement
and bilateral compression of the upper
brainstem (rostro-caudal deterioration)
Confusion,apathy,drowsiness,CSR
Miosis, RC , OC & OV elicitable (fast compo
nent ), bilateral Babinskidecerebrate post.
Coma, CNH, midposisi fixed pupil, decrebrate
OV-, slow-irregular breathing death
Uncal syndrome:drowsiness is
accompanied or preceded by unilateral
pupillary dilatation.
Patho-anatomy
Displacements of the Brain
Tissue

(cont.)
Subfalcial herniation : Paraparesis or tri
paresis, bilateral babinski signs

Upward herniation of fossa posterior via

cerebellar tentorium

Downward herniation of fossa posterior

via foramen magnum (tonsillar cerebelli
dis- placement)
Clinical Approach to the
Comatose Patient
The physician must have a broad
know- ledge of disease and a
methodical approach that leaves
none of the common and treatable
causes of coma unexplored
Make certain the airway is clear, not
in hemodynamic shock,in case of
trauma no bleeding from a wound
or rupture organ (spleen or liver)
Clinical Approach to the
Comatose Patient (cont.)
If shock or bleeding central venous
line, blood,glucosa (after blood glucose
ex.), colloid.
If breath normally, an oropharyngeal air-
way is usually adequate
If respiration
cease/hypoventilation/emesis with a
threat of aspiration tracheal intu-
bation and mechanical ventilation.
Clinical Approach to the
Comatose Patient (cont.)
Head injury may also have suffered a
fracture of C.vertebrae be cautious about
moving the head and neck
Immediate inquiry the previous health: DM,
head injury, convulsion,alcohol/drug
use,prior episode of coma / attempted
suicide, circumstances in which the patient
was found
The big 3 common causes of coma: severe
head injury, alcoholic/drug intoxication,
hypertensive brain hemorrhage
 Clinical Approach to the
Comatose Patient (cont.)
Fever systemic infection (pneumonia /
bacterial meningitis.Temperature 42-43C
+ dry skinHeat stroke/Anticholinergic int.
Brain lesion disturb the temperature regula
ting center (central fever) a very rare
occurrence !
Hypothermia alcoholic/barbiturate intox.,
drowning,exposure to cold,peripheral circu
latory failure, myxedema.
Clinical Approach to the
Comatose Patient (cont.)
Slow breathing : opiate / barbiturate
intox., hypothyroidism
Deep rapid breathing : pneumonia
(expira tory grunt,cyanosis,fever), DM /
uremic acidosis, pulmonary edema, CNH
Slow,irregular,periodic CSR brain
damage + raise ICP
Pulse rate slow heart block
Clinical Approach to the
Comatose Patient (cont.)
Slow pulse rate + periodic breathing +
hypertension raise ICP
Marked hypertension ICH, HE, ICP
Hypotension : DM, alcohol / barbiturate in
tox.,internal hemorrhage, MCI, dissecting
aortic aneurysm, septichemia, Addison
dis
Cyanosis lips and nail beds inadequate
oxygenation
Clinical Approach to the
Comatose Patient (cont.)
Cherry red coloration CO poisoning
Multiple bruises scalp, bleeding/CSF
leak- age from ear/nose,brill
hematome intra cranial trauma
Teleangiectasia and hyperemia of the
face and conjunctiva alcoholism
Puffiness of the face myxedema
Marked pallor internal hemorrhage
 Clinical Approach to the
Comatose Patient (cont.)
Maculohemorrhagic rash meningococcal
infection, staphylococcal endocarditis,
typhus, Rocky mountain spotted fever
Skin lesion exposed to the sun pellagra
Excessive sweatinghypoglycemia,shock
Excessive dry skin DM acidosis, uremia,
anticholinergic overdose, antidepressant
Turgor dehydration
Clinical Approach to the
Comatose Patient (cont.)
Large blood blisters over pressure points
acute barbiturate, alcohol, opiate
intox
Breath odor
Alcohol ethanol drink (vodka odorless!)
Spoiled fruit odor DM coma
Urine ferous odor uremia
Musty fetor hepatic coma
Burnt almond odor cyanide poisoning
Neurologic Examination of
the Stuporous / Comatous
patients
Watching
Posture of the limbs and body
Spontaneous movements
The position of the head and eyes
Rate/depth/rhytm of respiration
Respons to
Calling his name
Simple command
Noxious stimuli
Neurologic Examination of
the Stuporous/Comatous
patients(cont)
Vocalization may persist in stupor
Grimacing and avoidance movements are
preserved in light
coma(hemihypesthesi?)
GCS is usefull
Determine meningeal irritation, focal cere
bral/brainstem diseases (CN,hemiparesis,
deviation conjugae,lips puff out,Babinski)
 GLASGOW COMA SCALE

Best Motor Best Verbal Eye

Response Response Opening
6 - Obeys commands 5 - Oriented 4 - Spontaneous
5 - Localizes pain 4 - Confused 3 - To speech
4 - Withdraws to pain 3 - Inappropriate words 2 - To pain
3 - Abnormal flexion 2 - Incomprehensible 1 - None
2 - Abnormal extension 1 - None
1 - None

TOTAL (3-15): _____

Neurologic Examination of
the Stuporous/Comatous
patients(cont)
Check brainstem functions :

Pupillary size and reactivity

Ocular movement,eyelid,cornea

Spontaneous limb movements

 Check Brainstem
Functions (pupillary size
and activity)
Unilaterally mydriasis > 5 mm e.c. stretch-
ing/compression of 3rd CN
Bilateral fixed dilated:massive midbrain les
Extrem miotic<1 mm:pontin tegmen lesion
Cilio-spinal reflex lost :brainstem lesions
Horners syndrome :i.l.brainstem/hypothal.
Opiate pinpoint; barbiturat miosis; atropin/
tricyclic fixed dilated # physostigmin
Check Brainstem Functions
(Ocular
movement,eyelid,cornea)
Roving eye movement : light coma
Unilateral lateral slight downward:3rd CN palsy
Unilateral medial deviation : 6th CN palsy
Looking toward the lesion : hemisphere lesion
Looking away the lesion : pontin lesion
During seizure : eye turn and jerk opposite to
the irritative focus
Eyes looking at the nose : thalamic / upper
midbrain lesion (parinaud)
 Check Brainstem Functions
(Ocular
movement,eyelid,cornea)
Retraction and convergence nystagmus :
midbrain tegmen lesion
Ocular bobbing : pontin lesion
Ocular dipping : anoxia,intoxication
OC hor.:intactness 3rd,4th ,6th CN-midbrain-
pontin tegmen structure + loss cortical
inh. OC ver. : intactness upper brainstem
OV : fast corrective phase is lost in coma
Check Brainstem Functions
(Ocular
movement,eyelid,cornea)
Sedative or anticonvulsant
intoxication may obliterate OC / OV

Spontaneous blinking reduction

loss then loss to eyelash touching
and finally loss to corneal touch
 Check Brainstem Functions
(Spontaneous limb
movements)
Bilateral : corticospinal tracts are more or
less intact and usually not profound coma

Focal motor seizure : corticospinal path-

way is intact

Choreic,athetotic,hemiballistic : disorder of
the basal ganglionic and subthalamic ncl
 Postural changes in the
comatose patients
Decebrate rigidity : opisthotonus,clenching
of the jaws,stiff extension of the limbs,inter
nal rotation of the arm,plantar flexion of the
feet (transect intercollicular)

Decorticate rigidity : arms in flexion-adduc

tion and leg extended (cerebral white
matter/internal capsule/thalamus lesion)
 Postural changes in the
comatose patients
Diagonal posture : one arm flex, the oppo
site arm & leg extension (supratentorial
lesion)

Lesion level 8th CN nucleus : forceful exten

sor of the arms and weak flexor of the legs

Lesion below this level : flaccidity and

abolition of all postures and movements
Pattern of breathing in
coma
CSR + drowsy/stupor : massive
supratent orial lesion,bilateral deep-
seated cerebral lesions,metabolic
disturbance isolation of the brainstem
respiratory center from the cerebrum
more sensitive to CO2

CSR + coma : intoxication, severe

metabo lic derangement
Pattern of breathing in
coma
CNH : low midbrain - upper pontin
tegmen lesion.
Apneustic : low pontin lesion

Ataxic / chaotic rhythm : dorso medial

part of the medulla

Prolonged inspiratory gasp apnoe