COMA

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 : like 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
Meningitis,
Encephalitis
Focal
Stroke,
Tumour,
Abscess
Hepar
Renal
Lungs
Diabetes
Intoxication
Lumbal
puncture
CT-Scan
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
according 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
Bilateral 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
4Impaired LOC or COC precedes neurologic
deficits
4Symmetric and bilateral neurologic deficits
4Respiratory pattern CSR [ impairement of
bilateral cortex and diencephalon]
4Isocor pupil with normal light reflex
4Involuntary movement
Myoclonus
Tremor , flaping
Assessment
Objective :
OTo find out the cause/etiology
-primer / structurall
-metabolic / functional
OTo 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 tegmentum

=Cluster group of 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

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)

NEUROLOGIC EXAMINATION
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.

OPUPILARY REFLEX (MIDBRAIN)
OCORNERAL REFLEX (PONS)
OOCCULO-VESTIBULAR REFLEX
=CALORIC REFLEX (PONS)
OOCCULOCEPHALIC REFLEX
=DOLLS EYE PHENOMENA (PONS)
OGAG REFLEX (MEDULA OBLONGATA)

BRAIN STEM REFLEXES
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
ANTI EDEMAS .SPECIFIC ANTIDOTUM
TREAT INFECTION
CATHETER
CAUSATIVE TREATMENT
AFTER CONFIRMING DIAGNOSIS ;

STROKE CAUSED BY INTRACEREBRAL
HEMORRHAGE : SUPPORTIVE, AND
SURGERY IF NEEDED

INFECTION : MENINGITIS
APPROPRIATE ANTIBIOTICS

EPILEPSY ANTIEPILEPTICS
UREMIC COMA DIALYSIS
BRAIN EDEMA
SIADH
INFECTION
VEGETATIVE STATE
DEHIDRATION

COMPLICATION
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
PROGNOSIS