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Coma-S1
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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