COMAByThamrin 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 consciousnessContent of consciousness

LOC : an interaction between ARAS and cerebral cortexCOC : reflects cortical function

Decreasing LOC disturbs COC

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

Level of ConsciousnessStupor/sopor : patient can only react to strong stimuli (pain).Coma : A deep sleep; can not be aroused by strongest stimuli verbally or physically.

ComaEtiologi 1. Structural damage in brainSupratentorial ComaInfratentorail Coma2. Diffuse Metabolic-Toxic in both hemispheres(primary causes generally extracranial origin)

Causes of decreased LOC Intra-cranialExtra-cranialDiffuseMeningitis, EncephalitisFocal Stroke, Tumour, AbscessHeparRenalLungsDiabetesIntoxicationLumbal punctureCT-ScanLaboratory

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

Kocher-Cushing SyndromeTriad of : HypertensionBradicardiaDecreased LOC2. Process in lateral of medial cranial fossa compress ventral of NC. III pupil dilatation (anisocor)

3. Compression syndrome : Progress rostrocaudally in brain stem

Infratentorial ComaBased on patologic process, c/o :1. Primary lesion at brain stem :InfarctionBrain stem tumourTrauma at brain stem

2. Lesion outside brainstem that compresses and disturbs ARAS function :Cerebellar abscess or hemorrhage

Clinical presentationSupratentorial comaBeginning with focal neurologic deficit accroding to location/level of lesionThen followed by decreasing LOC. Compression starts rostrocaudaly :DiencephalonMidbrainPonsMedulla oblongata

Diencephalon StageSomnolence; stupor; restlessRegular respiration or Cheyne-Stokes Respiration (CSR)Positive occulocephalic reflexSmall reactive pupilPositive and bilaterla patologic reflexHypertonic ; rigidity; decorticate position

Midbrain - Pons StageStupor comaHyperthermiaHyperventilation Dilating pupilDisconjugate gazeNegative Dolls eye phenomenDecerebration position

Pons Medulla oblongata StageShallow, slow, and irregular respirationDilated pupil and negative corneal reflexNegative occulo-cephalic reflex (Dolls eye)Flaccid positionIrregular pulseAbrupt decreased blood pressure

Infratentorial ComaIrregular respiration, blood pressure, heart rateImpaired occular movementAlternating hemiparesis or tetraparesis

Toxic-Metabolic ComaMostly caused by :Hypoxia : Normal : 3.3 mL / 100 gm brain / minuteComa if < 2 mL / 100 gm brain / minuteHypoglycaemiaNormal : 2/3 of blood levelComa if below 10 mg/dLVarious toxinHepatic comaUremic coma

Metabolic ComaImpaired LOC or COC precedes neurologic deficitsSymmetric and bilateral neurologic deficitsRespiratory pattern CSR [ impairement of bilateral cortex and diencephalon]Isocor pupil with normal light reflexInvoluntary movementMyoclonusTremor , flaping

Assessment Objective :To find out the cause/etiologyprimer / structurallmetabolic / functionalTo decide the level or location of

Anamnesis Onset : abruptly, progressiveTraumaOther complaints :HeadacheVomitingConvulsionWeaknessPrevious historyMedication

Physical Examination : Vital SignsLevel of Consciousness : composmentis, somnolent, sopor, comaTemperature : Hypo/hyperthermia, related to systemic infectionPulse : slowness heart block> 140 bpm : ectopic cardiac rhythm decresased CBFBlood Pressure : Hypertension : Encephalopatic hypertension StrokeHypotension : myocardial infarction intoxication blood loss

Physical Examination : Vital SignsRespiration :

Hyper- / hypo-ventilationCSR periodic hyperpnea and apnea phase; result of loss of relation between repiratory center and cerebellumCNH (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 levelAtaxic iregular respiration, bioth in rhythm and deepness. Lesion at med oblngatq

GLASGOW COMA SCALEBest 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 HypoxiaIctericDry Skin ?Sweating ?Turgor ?

HEADBruises after punchBleeding Sign

CHEST Heart Lungs

ABDOMENLiver enlargementAscites EXTREMITIESEdema

MENINGEAL IRITATION4 NUCHAL RIGIDITY4 LASEAGUE / KERNIG SIGN4 BRUDZINSKI I, II, III

CRANIAL NERVES (CN) : CN I CN XII

PUPIL :4 MIDRYASIS : LESION IN MIDBRAIN4 PIN POINT : LESION IN PONS4 ANISOCOR: COMPRESSION OF CN III , BRAIN HERNIATION (UNCAL TYPE)

NEUROLOGIC EXAMINATION

EYE MOVEMENTCN III, IV, VI PALSIES4OCULAR BOBBING, EXTENT LESION IN PONS4ROVING EYE MOVEMENT : INTACT BRAIN STEM OCCULOMOTOR FUNCTION IN COMA STATE

REMEMBER : PUPILARY REFLEX IN METABOLIC COMA IS NORMAL.

PUPILARY REFLEX (MIDBRAIN)CORNERAL REFLEX (PONS)OCCULO-VESTIBULAR REFLEX =CALORIC REFLEX (PONS)OCCULOCEPHALIC REFLEX =DOLLS EYE PHENOMENA (PONS)GAG REFLEX (MEDULA OBLONGATA)

BRAIN STEM REFLEXES

MOTOR SYSTEM RESPONSE TO STIMULI : VERY HELPFUL IN DETERMINING LEVEL OF OF IMPAIREMENT IN NERVOUS SYSTEMDECORTICATION : HYPEREXTENSION : ARM FLEXION AND SUPRATENTORIAL LESIONDECEREBRATION : ARM AND LEG EXTENSION LESION IN MID BRAINDIFFUSE 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 TESTURINE : ROUTINE TEST, CULTURE

ECGEEGCT-SCANSKULL X-RAYANGIOGRAPHY

MANAGEMENT OF COMATOSE PATIENT GENERALCORRECT RESPIRATORY PROBLEMCORRECT CARDIOVASCULAR COMPROMISES NUTRITIONELECTROLYTE BALANCEANTIEDEMASPECIFIC ANTIDOTUMTREAT INFECTIONCATHETER

CAUSATIVE TREATMENTAFTER CONFIRMING DIAGNOSIS, E.G.

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

INFECTION : MENINGITIS APPROPRIATE ANTIBIOTICS

EPILEPSY ANTIEPILEPTICSUREMIC COMA DIALYSIS

BRAIN EDEMASIADHINFECTIONVEGETATIVE STATEDEHIDRATION

COMPLICATION

STRUCTURAL COMA : POORBRAIN STEM INSUFFICIENCY : POOR (BRAIN DEATH)SIGNS OF POOR PROGNOSIS4ABSENT PUPILARY REFLEX AND EYE MOVEMENT : DEATH IN 95%4ABSENT CORNEAL REFLEX4LIMB ATONIA4ABSENT OF VISUAL, AUDITORY, AND SOMATOSENSORY REFLEXESPROGNOSIS