COMA EXAMINATION OF COMATOSE

Prof. Ahmed Gaber Ass. Prof of Neurology Ain Shams University

Consciousness
Consciousness is an active state of arousal and awareness It is a function of the reticular activating system.

Classification
Consciousness is subdivided into: 1. Alertness (arousal) 2. Awareness

Alertness
It is the maintained arousal with intact sleep wake cycle. It is a function of the RAS at the level of brain stem (mesencephlon) and diencephalon (thalamus and hypothalamus). The arousal system act as the switch for the cortical awareness system.

Awareness
It is the higher level of integration of multiple sensory input that allow meaningful understanding of self and environment. It is a function of RAS at the level of interaction with the cortex. The arousal is conditional for awareness however one can be aroused but not aware. Awareness includes all cognitive functions of the brain (e.g. attention, orientation, abstraction, judgement).

Mechanisms Of Impaired Consciousness

Disorders of Awareness. Disorders of Alertness. Combined

Disorders Of Awareness
Bilateral diffuse Cerebral Cortex Failure

Due to disturbance of the RAS at the level of cortex. A state of arousal with impaired awareness Massive or diffuse cortical affection as in 1. Increase ICT (sinus thrombosis, SOL...) 2. Encephalitis 3. Postischemic anoxic (cardiac arrest)

Disorders of Awareness Clinical Presentation

Confusion: Inattentive +/- Disoriented Delirium: Confused + hallucinations +/- agitation Vegetative state (aroused but not aware) Abulia (Akinetic mute)

Disorders Of Arousal
Due to affection of the RAS at the diencephalic level, either from a disease primarily affecting this area (disorder of arousal from the start) or a as a progression of disorders of awareness ( start as disorder of awareness then continue as disorder of arousal)

Etiology
Primary brain stem pathology Secondary brain stem injury e.g. herniation

Disorders Of Arousal Clinical Presentations

Abnormal sleep wake cycle Lethargy apathy Sleepy Drowsy: awakened by verbal stimuli Stupor: awaken by painful stimuli Lightb coma: respond to painfuul stimuli (localizin

Combined Bilateral Cortical and Brain stem Failure

Encephalopathy (hepatic, uraemic ....) Intoxication

Clinical Approach

History
Rate of onset of coma As a disorder of arousal vs awareness Trauma, Drugs, illness, psychological troubles.

EXAMINATION OF THE COMATOSE GENERAL

Vital Data Breath odor Cardiac, chest and abdomen examination Skin for trauma and injection marks Head for signs of trauma.

NEUROLOGICAL
Mental Status Examination Type of Respiration Cranial N Examination Motor Function Sensory Function Cranium & spine Stretch signs

Mental State Examination

Level of consciousness Response to Auditory Stimuli Response to Visual Stimuli Response to Painful stimuli (applied centrally and to each limb separately)

Level Of Consciousness
Confused Delerious Vegetative Akinetic mute Lethargy Sleepy Drowsy Stuperous Light coma Deep coma

Psychogenic Unresponsiveness

Glascow Coma Scale

Motor Response
Normal Response Localizing Flexion (decortication) Abnormal Flexion Extension (Decerebration) No response

Verbal Response
Spontaneous speech Few words Uttering sounds In response to verbal stimuli In response to painful stimuli No response

Eye Response
Sponateous eye opening Eye opening to verbal stimuli Eye opening to painful stimuly No eye opening

Deep COMA
No Motor reponse No Verbal Response No Eye response

Respiratory Patterns
Respiration Cheyne-Stokes Description Localization Bilateral deep hemispheric and basal G dysfunction, upper B st may be affected Periods of hyperventilation gradually diminishing to apnea then build up again - variable duration Central Continuous rapid Neurogenic regular deep Hyperventilation hyperventilation (25/m)

No localizing Value Regularity poor sign DD metabolicacidosis, resp alkalosis

Respiratory Patterns
Respiration Apneustic Breathing (Inspiratory cramp) Description Localization Pontine Damage Prolonged inspiration followed by apnea , or clustered inspiration followed by apnea Ataxic Breathing Chotic breating. In (Gasping) gaspings : gasps followed by apnea of variable duration Depressed Shallow slow Breathing ineffective breathing

Medullary respiratory centers damage--- ominous sign Medullary depression by drugs

Cranial Nerve Examination

OPTIC: Reponse to visual threat Fundus OCCULOMOTORS: Gaze preference Pupils, light reflex Ptosis, Squint TRIGEMINAL: Jaw reflex, Corneal reflex FACIAL: Facial assymetry , facial tone and Glabellar reflex VESTIBULOCHOCLEAR: Dolls Sign = occulocephalic reflex (reflex conjugate eye movement) Caloric test BULBAR: Gag Reflex

Motor Function
Spontaneous (Voluntary/ Involuntary*) / Reflex withdrowal Asymmetric motor response (weakness) Tone (Flaccidity = poor prognosis) Reflexes (Areflexia = poor prognosis) Planter response *Involuntary contractions (mostly epiletic as myoclonic jerks, lid or facial twitches)

SENSORY FUNCTION
Response to noxious stimulus

Meningeal Signs
Neck stiffness ( DD rigidity) Sciatic or femoral stretch signs Upper limb stretch sign

Signs Of Poor Prognosis

Ataxic breathing Dilated fixed pupils Lost Dolls sign Lost Corneal reflex No response to pain Flaccidity Lost reflexes especially extensor planter

Differential Diagnosis
Locked In State Vegetative State Akinetic Mute state (Abulia) Non Convulsive status epilepticus Psychogenic Unresponsiveness

ETIOLOGY
Onset Disorder of Arousal Brain stem vascular, Traumatic, epileptic Inflammatory Disorder of Awareness Toxic

Dramatic, sudden

Rapid

Slow

SOL

ICT, encephalitis, encephalopathy SOL

Investigation
Vital Data Stabilization Glucose level Metabolic screening Urgent Ct brain or MRI CSF if needed Toxic screening EEG

Management
1. 2. 3. 4. 5. 6. 7. 8. Immediate Vital Data Stabilization Of the Etiology Care of the comatose: Ventilation Cardiac and fluid balance monitoring Skin care Bowel care Bladder care Eye care Nutrition Restlessness and agitation

Thank you