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By Gilang Nispu Saputra

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COMA

By
Gilang Nispu Saputra
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, 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 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 :
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
    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
=DOLL’S 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

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