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
Content of consciousness

LOC : an interaction between ARAS

and cerebral cortex
COC : reflects cortical function
Decreasing LOC 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,
Encephalitis

Stroke,
Tumour,
Abscess

Renal

Lumbal
puncture

CT-Scan

Lungs
Diabetes
Intoxication

Laboratory

Supratentorial Coma
Occur in Space Occupying Lesion/process
Step 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]
compression of infratentorial structure
Kocher-Cushing Syndrome

 Kocher-Cushing Syndrome
Triad of :
Hypertension
Bradicardia
Decreased LOC
2. Process in lateral of medial cranial fossa
compress ventral of NC. III
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
Somnolence; stupor; restless
Regular respiration or Cheyne-Stokes
Respiration (CSR)
Positive occulocephalic reflex
Small reactive pupil
Positive and bilaterla patologic reflex
Hypertonic ; rigidity; decorticate position

Midbrain - Pons Stage

Stupor coma
Hyperthermia
Hyperventilation
Dilating pupil
Disconjugate gaze
Negative Dolls eye phenomen
Decerebration position

Pons Medulla oblongata Stage

Shallow, slow, and irregular respiration
Dilated pupil and negative corneal reflex
Negative occulo-cephalic reflex (Dolls 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 :
Hypoxia :
Normal : 3.3 mL / 100 gm brain / minute
Coma if < 2 mL / 100 gm brain / minute
Hypoglycaemia
Normal : 2/3 of blood level
Coma if below 10 mg/dL
Various toxin
Hepatic coma
Uremic coma

Metabolic Coma
Impaired LOC or COC precedes neurologic
deficits
Symmetric and bilateral neurologic deficits
Respiratory pattern CSR [ impairement of
bilateral cortex and diencephalon]
Isocor pupil with normal light reflex
Involuntary movement
Myoclonus
Tremor , flaping

Assessment
Objective :
To find out the cause/etiology
primer / structurall
metabolic / functional
To decide the level or location of

Anamnesis
Onset : abruptly, progressive
Trauma
Other complaints :
Headache
Vomiting
Convulsion
Weakness
Previous history
Medication

Physical Examination : Vital Signs

Level of Consciousness : composmentis,
somnolent, sopor, coma
Temperature : Hypo/hyperthermia,
related to systemic infection
Pulse :
slowness heart block
> 140 bpm : ectopic cardiac rhythm
decresased CBF
Blood Pressure :
Hypertension : Encephalopatic hypertension
Stroke
Hypotension : 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
Response

Best Verbal
Response

Eye
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 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
NUCHAL RIGIDITY
LASEAGUE / KERNIG SIGN
BRUDZINSKI I, II, III
CRANIAL NERVES (CN) : CN I CN XII
PUPIL :
MIDRYASIS : LESION IN MIDBRAIN
PIN POINT : LESION IN PONS
ANISOCOR: COMPRESSION OF CN III ,
BRAIN HERNIATION (UNCAL TYPE)

EYE MOVEMENT
CN III, IV, VI PALSIES
OCULAR BOBBING, EXTENT LESION IN PONS
ROVING EYE MOVEMENT : INTACT BRAIN
STEM OCCULOMOTOR FUNCTION IN COMA STATE
REMEMBER :
PUPILARY REFLEX IN METABOLIC COMA
IS NORMAL.

BRAIN STEM REFLEXES

PUPILARY REFLEX (MIDBRAIN)
CORNERAL REFLEX (PONS)
OCCULO-VESTIBULAR

REFLEX

=CALORIC REFLEX (PONS)

OCCULOCEPHALIC REFLEX
=DOLLS EYE PHENOMENA (PONS)
GAG REFLEX (MEDULA OBLONGATA)

MOTOR SYSTEM
RESPONSE TO STIMULI : VERY HELPFUL IN
DETERMINING LEVEL OF OF IMPAIREMENT
IN NERVOUS SYSTEM
DECORTICATION : HYPEREXTENSION :
ARM FLEXION AND SUPRATENTORIAL
LESION
DECEREBRATION : ARM AND LEG
EXTENSION 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
APPROPRIATE ANTIBIOTICS
EPILEPSY ANTIEPILEPTICS
UREMIC COMA DIALYSIS

COMPLICATION
BRAIN EDEMA
SIADH
INFECTION
VEGETATIVE STATE
DEHIDRATION

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