Definitions and Descriptions of Altered Mental Status Lethargy Coma Obtundation Stupor Lewis B. Eberly, MD Coma Alfaneurology Delirium VCU School of Medicine Inova Campus Dementia Brain Death 1 2 Levels of altered mental Levels of altered mental status / coma status / coma Delirium - confusional state, may be Obtundation marked by agitation or lethargy or – lethargic, blunted cognition waxing and waning mental status – awake but somnolent or slowed – arousable –DT’s Stupor – complex partial seizures – asleep/semi comatose – drug induced delirium – only arouses when stimulated –hypoxia – reverts back to sleep when stimulus withdrawn 3 4 Unconsciousness occurs Definition of Coma when either: Unresponsive to the environment Both cerebral hemispheres are Unable to communicate depressed Unarousable The reticular activating system is dysfunctional 5 6 Etiologies of Coma Etiologies of Coma Supratentorial mass lesions Infratentorial lesions – intracerebral hematoma – brainstem infarction – subdural hematoma – pontine hemorrhage – large ischemic infarction – brainstem demyelination – brain tumor – cerebellar tumor – brain abscess – cerebellar abscess – epidural hematoma – cerebellar hemorrhage 7 8 Etiologies of Coma Etiologies of coma Metabolic and other diffuse disorders – drug toxicity Drug Overdose: Mortality 5-10% – anoxic-ischemic encephalopathy Metabolic: Mortality 50% – hepatic encephalopathy Head Trauma: Mortality 50% – endocrine disorders – acid-base disorders Anoxia: Mortality 90% – encephalitis and encephalomyelitis Stroke: Mortality 80% – subarachnoid hemorrhage – hyper- hypothermia – uremic encephalopathy 9 10 The RAS and Essential Neurotransmitters Epinephrine Locus Coeruleus Consciousness is Serotonin: Median Raphe Dependent on an Intact Acetylcholine: Basal Nucleus Reticular Activating System! 11 12 Initial Neurological Exam: Exam points Primary Question Nuchal rigidity – sub arachnoid Is the coma due to: hemorrhage – toxic, infectious, metabolic coma? –meningitis Rash OR – meningococcus, – acute neurosurgical cause? – spiders • bleed – drug reaction • neoplasm Ecchymosis over orbit or • infection mastoid • increased intracranial pressure Papilledema 13 Subhyaloid hemmorrhage 14 Abnormal postures in a comatose patient Initial Exam Pupils - Unilateral Dilated Pupil - R/o herniation Fundi - r/o Papilledema Oculocephalic and oculovestibular Motor response –withdrawal – decortication – decerebration Progression suggests – expanding or worsening mass 15 16 Initial Exam Initial Exam Bilateral dilated pupils – transtentorial herniation of both temporal Asymmetric pupils (anisocoria) lobes – difference of 1mm or less and normal – anticholinergic of sympathomimetic drug constriction may be normal intoxication – if the dilated pupil does not react or reacts Bilateral pinpoint pupils slowly, suggests rapidly expanding – mophine poisoning ipsilateral mass compressing midbrain or – pontine hemorrhage oculomotor nerve – organophosphates or eye drops (miotic) 17 18 Initial Exam Extraocular Movements – oculocephalic (dolls eyes), and oculovestibular (cold calorics) reflexes • normal – full doll’s eye movements and tonic conjugate eye movement to side of ice water irrigation • abnormal – lesions of oculomotor nerve or midbrain –no response – structural lesion or metabolic (sedative drugs) 19 20 Etiologies-toxic metabolic Metabolic Coma Drug overdose – narcotics, tricyclics, stimulants Signs and symptoms of toxic - Metabolic metabolic coma – sepsis – pupils small - narcotics – hepatic encephalopathy – pupils large - tricyclics – uremic encephalopathy – nystagmus - dilantin, pcp – hypoglycemia – hypothyroid (myxedema coma) – respiratory depression - narcotics – ETOH withdrawal/intoxication – tremor / asterixis - uremia, etoh, hepatic – anoxic encephalopathy 21 22 Signs of increased Locked-in State ICP / Herniation Pupils Quadriplegia – unilateral dilated pupil is a sign of? Paralysis of lower cranial nerves – bilateral small poorly reactive pupils are a sign of? Eye movements Lesion of basis pontis (RAS not affected) – third nerve palsy? Preservation of consciousness – sixth nerve palsy? – can be assesses by cold caloric Fundoscopy – signs of papilledema? Respiratory pattern? 23 24 Signs of herniation (cont’d) Can be detected by a deterioration in mental status, pupils, or motor exam – withdrawal to pain transitioning to flexor withdrawal – flexor withdrawal to extensor posturing • decortication - flexor withdrawal - lesion above red nucleus • decerebration -extensor posturing - lesion below red nucleus 25 26 Initial Management Initial Management Protect airway- Stat If Narcotic OD If ETOH withdrawal (72-96 Support vitals – fingerstick for dextrose suspected, give hrs post ETOH) – CBC, electrolytes, BUN/Cr, If evidence of trauma, – naloxone 1 - 2 amps – (confusion, hallucinations, immobilize spine, get Calcium, ABG, LFT’s, tremor, tachycardia, HTN) ammonia, UA, serum and – repeat in 15 minutes stat c-spine – thiamine 100 mg/IM urine tox screen, blood If benzodiazepine IV, Pulse ox, frequent cultures if febrile – librium 25-100 mg q6hrs overdose suspected, vitals and Dextrose (1 amp = 25 For ETOH seizures – flumazenil .2 mg neurochecks grams dextrose) – (12-24 hours post withdrawal) – repeat q 1 minute up to Intubate if GCS < 10 or – always follow with Thiamine • give thiamine 100mg if any question of 100 mg IM 1.0 mg, may produce seizures. • stat fingerstick for dextrose ability to protect • improves recovery of airway Wernickes, if delayed, • lorazepam 2 mg IV q 6-8 increased risk of hours Korsakoffs 27 28 If bacterial menigitis or SAH Increased ICP suspected For SAH, STAT CT of brain Hyperventilation: Reduces ICP – 90% yield for SAH immediately, peak effect 1-2 hours – notify neurosurgery stat if suspected – NO BENEFIT TO drop PCo2 < 25, Ideal = 30 If bacterial meningitis suspected, do not delay for CT- Start empiric therapy Mannitol: Onset in 30 minutes lasts 4-6 – ceftriaxone 2 grams q12 hours IV hours – vancomycin 750-1000 mg q 12 hours IV – ampicillin 2 grams q 4 hours IV age > 65 or if Mannitol and lasix are synergistic. immunocompromised LP: L3-L4 interspace – 1 - 2 grams/kg bolus – obtain opening pressure – 0.5 - 1 gram/kg q 6 hours – cell count tubes 1 and 4 – tubes 2 and3, gram stain, Cocci, AFB, india ink, – monitor sodium, osmolality, BUN, carefully – protein and glucose 29 30 Increased Intracranial Pressure: Hyperventilation Hyperventilation 36 The prognosis of coma is reduces ICP p acutely, but ICP CO2 primarily dictated by returns to baseline ic p etiology within 1-2 hours icp Reduction of CO2 beyond a p CO2 of 30 has little benefit 12 1 31 32 Predictors of Persistent Vegetative State Awakening / Good Outcome Preserved vegetative functions (sleep-wake EEG: EP’s: Median Nerve cycle, autonomic and respiratory control) – strong predictor only – strong predictor only of No awareness for poor outcome in poor outcome No appropriate response to the environment coma - 0/138 good – absent cortical potential recovery if: to median nerve Spontaneous movements, but no • burst suppression stimulation (N20) purposeful or voluntary responses to • low voltage – poor prognosis >95% stimulation •PLEDS Preservation of hypothalamic and brainstem function 33 34 Persistent Vegetative State Recovery of consciousness is rare after 3 months May survive for years Mortality rate is 80% in 3 years, 95% in 5 years 35.