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
