COMA bisa

di otak dan
di luar otak
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 >tingkat
Content of consciousness >isi
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, Stroke, Renal
Encephalitis Tumour, Lungs
Abscess
Diabetes
Intoxication
Lumbal CT-Scan
puncture
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 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 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

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
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