COMA

By
Thamrin Syamsudin, dr., Sp.S(K)
INTRODUCTION

DISTURBANCE OF CENTRAL
NERVOUS SYSTEM, ESPECIALLY
BRAIN, CAN LEAD TO BOTH
DECREASED LEVEL OF
CONSCIOUSNESS AND
BEHAVIOUR DISTURBANCE
WHATEVER THE CAUSES.

IT IS OUR TASK TO FIND THE CAUSE

AND TO DO THE APPROPRIATE
TREATMENT.
Consciousness

A state that reflect an optimal integration

between afferent stimuli and efferent
response.

Normally it needs an interaction between

cerebral hemispheres and reticular formation
in brain stem

Two aspects of consciousness

•Level of consciousness (LOC)
•Content of consciousness (COC)
LOC : an interaction between ARAS
and cerebral cortex
COC : reflects cortical function

Decreasing LOC à disturbs COC

Level of Consciousness

Composmentis : state of awareness,

alertness; knowing and recognising of
ownself to environment, place, time and
person
Lethargic/somnolence : state of drowsy,
but react to stimuli, can be
accompanied by COC disturbance
Level of Consciousness

Stupor/sopor : patient can only

react to strong stimuli (pain).
Coma : A deep sleep; can not be
aroused by strongest stimuli
verbally or physically.
 Coma

Etiologi
1. Structural damage in brain
Supratentorial Coma
Infratentorail Coma
2. Diffuse Metabolic-Toxic in both
hemispheres
(primary causes generally
extracranial origin)
 Causes of decreased LOC

Intra-cranial Extra-cranial

Diffuse Focal Hepar

Meningitis, Stroke, Renal
Encephalitis Tumour, Lungs
Abscess
Diabetes
Intoxication
Lumbal CT-Scan
puncture
Laboratory
Supratentorial Coma

Occur in Space Occupying Lesion/process

àStep of progresivity according to level
involved : Diencephalon-> Midbrain-> Pons->
Medulla oblongata
Space Occupying Process occurred in :
1. Abrupt increased of ICP in supratentorial
area [ICH, EDH, SDH]
à compression of infratentorial structure
à Kocher-Cushing Syndrome
à Kocher-Cushing Syndrome

Triad of :
•Hypertension
•Bradicardia
•Decreased LOC

2. Process in lateral of medial cranial fossa

à compress ventral of NC. III
à pupil dilatation (anisocor)
3. Compression syndrome :
Progress rostrocaudally in brain stem
Infratentorial Coma

Based on patologic process, c/o :

1. Primary lesion at brain stem :
•Infarction
•Brain stem tumour
•Trauma at brain stem

2. Lesion outside brainstem that

compresses and disturbs ARAS
function :
Cerebellar abscess or hemorrhage
Clinical presentation

Supratentorial coma
Beginning with focal neurologic deficit
accroding to location/level of lesion
Then followed by decreasing LOC.
Compression starts rostrocaudaly :
…Diencephalon
…Midbrain
…Pons
…Medulla oblongata
Diencephalon Stage

8Somnolence; stupor; restless

8Regular respiration or Cheyne-Stokes
Respiration (CSR)
8Positive occulocephalic reflex
8Small reactive pupil
8Positive and bilaterla patologic reflex
8Hypertonic ; rigidity; decorticate position
Midbrain - Pons Stage

]Stupor à coma
]Hyperthermia
]Hyperventilation
]Dilating pupil
]Disconjugate gaze
]Negative Doll’s eye phenomen
]Decerebration position
Pons – Medulla oblongata Stage

{Shallow, slow, and irregular respiration

{Dilated pupil and negative corneal reflex
{Negative occulo-cephalic reflex (Doll’s eye)
{Flaccid position
{Irregular pulse
{Abrupt decreased blood pressure
Infratentorial Coma

°Irregular respiration, blood pressure, heart rate

°Impaired occular movement
°Alternating hemiparesis or tetraparesis
Toxic-Metabolic Coma

Mostly caused by :
²Hypoxia :
²Normal : 3.3 mL / 100 gm brain / minute
²Coma if < 2 mL / 100 gm brain / minute
²Hypoglycaemia
²Normal : 2/3 of blood level
²Coma if below 10 mg/dL
²Various toxin
²Hepatic coma
²Uremic coma
 Metabolic Coma

YImpaired LOC or COC precedes neurologic

deficits
YSymmetric and bilateral neurologic deficits
YRespiratory pattern – CSR [ impairement of
bilateral cortex and diencephalon]
YIsocor pupil with normal light reflex
YInvoluntary movement
žMyoclonus
žTremor , flaping
Assessment

Objective :
qTo find out the cause/etiology
üprimer / structurall
ümetabolic / functional
qTo decide the level or location of
Anamnesis

COnset : abruptly, progressive

CTrauma
COther complaints :
CHeadache
CVomiting
CConvulsion
CWeakness
CPrevious history
CMedication
Physical Examination : Vital Signs
ØLevel of Consciousness : composmentis,
somnolent, sopor, coma
ØTemperature : Hypo/hyperthermia,
related to systemic infection
ØPulse : slowness à heart block
> 140 bpm : ectopic cardiac rhythm
àdecresased CBF
ØBlood Pressure :
üHypertension : Encephalopatic hypertension
Stroke
üHypotension : myocardial infarction
intoxication
blood loss
Physical Examination : Vital Signs
Respiration :

|Hyper- / hypo-ventilation
|CSR – periodic hyperpnea and apnea phase;
result of loss of relation between repiratory
center and cerebellum
|CNH (Central Neurogenic Hyperventilation) –
rapid and deep respiration as a result of
disturbance of tegmenrtum
|Cluster – group fof repiration followed by
apnea phase; lesion at pons and medulla
oblongata level
|Ataxic – iregular respiration, bioth in
rhythm and deepness. Lesion at med
oblngatq
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): _____

SKIN
Cyanotic, Nail-Bed à Hypoxia
Icteric
Dry Skin ?
Sweating ?
Turgor ?

HEAD
Bruises after punch
Bleeding Sign
CHEST
Heart
Lungs

ABDOMEN
Liver enlargement
Ascites

EXTREMITIES
Edema
NEUROLOGIC EXAMINATION

MENINGEAL IRITATION
4 NUCHAL RIGIDITY
4 LASEAGUE / KERNIG SIGN
4 BRUDZINSKI I, II, III

CRANIAL NERVES (CN) : CN I – CN XII

PUPIL :
4 MIDRYASIS : LESION IN MIDBRAIN
4 PIN POINT : LESION IN PONS
4 ANISOCOR: COMPRESSION OF CN III ,
BRAIN HERNIATION (UNCAL TYPE)
EYE MOVEMENT
CN III, IV, VI PALSIES
4OCULAR BOBBING, EXTENT LESION IN PONS
4ROVING EYE MOVEMENT : INTACT BRAIN
STEM OCCULOMOTOR FUNCTION IN COMA
STATE

REMEMBER :
PUPILARY REFLEX IN METABOLIC COMA
IS NORMAL.
BRAIN STEM REFLEXES

qPUPILARY REFLEX (MIDBRAIN)

qCORNERAL REFLEX (PONS)
qOCCULO-VESTIBULAR REFLEX
=CALORIC REFLEX (PONS)
qOCCULOCEPHALIC REFLEX
=DOLL’S EYE PHENOMENA (PONS)
qGAG REFLEX (MEDULA OBLONGATA)
MOTOR SYSTEM

•RESPONSE TO STIMULI : VERY HELPFUL IN

DETERMINING LEVEL OF OF IMPAIREMENT
IN NERVOUS SYSTEM
•DECORTICATION : HYPEREXTENSION :
ARM FLEXION AND à SUPRATENTORIAL
LESION
•DECEREBRATION : ARM AND LEG
EXTENSION à LESION IN MID BRAIN
•DIFFUSE BRAIN FLACCIDITY : OCCURRED
IN BRAIN STEM LESION OR DISTAL TO
PONTO MEDULLAIR
SUPPORTING MEASURES

LABORATORY

•BLOOD : HB, LEUCO, PCV,

GLUCOSE, UREA-N, CREATININE,
GAS ANALYSIS, ELECTROLYTES
(NA, K, CA, MG), LIVER FUNCTION
TEST
•URINE : ROUTINE TEST, CULTURE
•ECG
•EEG
•CT-SCAN
•SKULL X-RAY
•ANGIOGRAPHY
MANAGEMENT OF COMATOSE PATIENT

GENERAL
•CORRECT RESPIRATORY PROBLEM
•CORRECT CARDIOVASCULAR COMPROMISES
•NUTRITION
•ELECTROLYTE BALANCE
•ANTIEDEMASPECIFIC ANTIDOTUM
•TREAT INFECTION
•CATHETER
CAUSATIVE TREATMENT

AFTER CONFIRMING DIAGNOSIS, E.G.

STROKE CAUSED BY INTRACEREBRAL

HEMORRHAGE : SUPPORTIVE, AND
SURGERY IF NEEDED

INFECTION : MENINGITIS ß
APPROPRIATE ANTIBIOTICS

EPILEPSY ß ANTIEPILEPTICS
UREMIC COMA ß DIALYSIS
COMPLICATION

BRAIN EDEMA
SIADH
INFECTION
VEGETATIVE STATE
DEHIDRATION
PROGNOSIS

STRUCTURAL COMA : POOR

BRAIN STEM INSUFFICIENCY : POOR
(BRAIN DEATH)
SIGNS OF POOR PROGNOSIS
4 ABSENT PUPILARY REFLEX AND EYE
MOVEMENT : DEATH IN 95%
4 ABSENT CORNEAL REFLEX
4 LIMB ATONIA
4 ABSENT OF VISUAL, AUDITORY, AND
SOMATOSENSORY REFLEXES