Coma

Pathological unresponsiveness No response, other than reflex, to external stimuli or inner needs A symptom, not a disease Multiple causes

Coma
Continuum of consciousness alert lethargic obtunded stuporous comatose

Coma - the rule of 4

1. Think glucose/thiamine/naloxone 2. Two mechanisms for coma: either bilateral hemisphere or brainstem retic. form. dysfunction 3. Three general disease processes structural metabolic seizures 4. Four key aspects to the exam

Mechanisms of coma
1. Hemisphere destruction/dysfunction - bilateral Examples - diffuse anoxia/ischemia after cardiac arrest with neuronal loss throughout entire cerebral cortex -> irreversible coma; barbiturate OD -> reversible depression of cortex 2. Upper midbrain - pontine reticular formation destruction/dysfunction - structural or functional May be caused by primary lesion in the brainstem or compression from cerebral displacement - herniation

Reticular formation
Central core of the brainstem Involved in. Control of movement - pontomedullary Modulation of pain - midbrain & pontine Autonomic reflexes Arousal and consciousness -midbrain/upper pons

Reticular activating system

RAS -- found in the reticular formation in the core of the upper brainstem Inputs from every sensory system Projections to thalamus - esp. diffuse intralaminar nuclei, basal forebrain, hypothalamus, and to cortex Physiologically involved in sleep/wake regulation and arousal/consciousness

Mechanisms of coma
Structural - hematoma, infarct, abscess, tumor, etc. = usually associated with an abnormal imaging study - a lesion that occupies space, above or below the tentorium Seizure-associated ictal - status epilepticus postictal Metabolic - imaging usually normal

Metabolic coma
Substrate deprivation - 02, glucose Derangements in water, electrolyte, osmolar balance, hyperglycemia Hypo- / hyperthermia Vitamin deficiencies - e.g. thiamine Diffuse infections - encephalitis / meningitis Microvascular occlusions - widespread
malaria, DIC, thrombotic thrombocytopenic purpura, multiple emboli

Organ failure [endogenous poisoning] hepatic, renal Exogenous toxins Subarachnoid hemorrhage

Coma - emergency management

Assume
airway, ventilation, BP adequate C - spine cleared by X- ray

Send gluc., elecs., renal, liver function tests, coags., CBC, toxicology Consider naloxone, thiamine, D50 Arterial blood gases Treat seizures - if necessary History Examination

Coma - the rule of 4

1. Think glucose/thiamine/naloxone 2. Two mechanisms for coma either bilateral hemisphere dysfunction or brainstem RF dysfunction 3. Three general disease processes structural metabolic seizures 4. Four key aspects to the exam

Coma - history
Sudden onset - vascular origin, esp. postr. fossa or SAH, or hypoglycemia Progression from hemispheric signs to coma in minutes - hrs. suggests hemispheric ICH Slower progression from hemispheric signs to coma suggests other space-taking lesion Coma preceded by confusion or delirium w/o lateralizing signs suggests metabolic derangement

Coma - approach to diagnosis

Signs of trauma basilar skull fx. hemotympanum CSF oto- rhinorrhea - dural tear

Vital signs
hypothermia w/ EtOH, myxedema, Wernickes, sedative OD, hypoglycemia hyperthermia w/ infection, anticholinergic drug intoxication

???? Meningeal irritation Optic fundi - papilledema / hemorrhages

Coma - approach to diagnosis

Four aspects of neurologic exam important...

Pupils Eye movements Motor response Ventilation pattern - acid base status
Important questions. Whats the cause of the coma ? Is the brainstem intact ? Is the patient improving, stable, or deteriorating ?

Coma respiration/acid base

Resp. acidosis
sedative - hypnotic drug OD

Resp. alkalosis
hepatic encephalopathy salicylate intox. sepsis

Metabolic acidosis
diabetic ketoacidosis uremia lactic acidosis paraldehyde, MeOH, ethylene glycol, INH, salicylate OD

Pupils in coma
Pupillary reaction to light -- the brainstem reflex that is most resistant to metabolic depression Divergent sym/parasym pathways help in diagnosis

Pupils
Dual sym / parasym innervation parasympathetic = CN III sympathetic = from hypothalamus via spinal cord and sympathetic chain Ablate sympath => miosis Ablate parasym => mydriasis

Pinpoint pupils
Pontine hemorrhage Organophosphate poisoning [acetylcholine esterase inhibitors] Narcotics Syphilis Constrictor drops

The fixed, dilated pupil in coma

May be seen ipsilateral to an expanding hemispheric mass Implies worsening of clinical state and impending catastrophe due to brain tissue displacement and herniation

Metabolic fixed pupils

Anoxia - severe Major barbiturate O.D. Anticholinergic drug poisoning [atropine] Hypothermia - severe

Coma - motor patterns

Limited repertoire in response to pain Purposeful - away from midline Absent Seizure fragments Reflex - towards midline

Reflex movements in coma

decerebrate - extensor decorticate - flexor not = classic animal models seen in metabolic coma - symmetric if asymmetric, implies structural disease contralateral

Eye movements in coma

Oculocephalic -- dolls eyes

Oculovestibular - ice water calorics Normal eye movements in coma mean the brainstem pathways subserving these reflexes are intact from upper medulla to midbrain

Herniation
Displacement of brain tissue into tentorial notch [or foramen magnum] Compression of midline, deep structures mediating arousal: thalami and midbrain Especially important are the pupils and CN III

Ipsilateral [occas. contralat] fixed, dilated pupil Kernohans notch