Quick viewing(Text Mode)

Coma ƒ Obtundation ƒ Stupor Lewis B

Coma ƒ Obtundation ƒ Stupor Lewis B

Definitions and Descriptions of Altered Mental Status

ƒ Lethargy ƒ ƒ Lewis B. Eberly, MD ƒ Coma Alfaneurology ƒ VCU School of Medicine Inova Campus ƒ Dementia ƒ

1 2

Levels of altered mental Levels of altered mental status / coma status / coma

ƒ Delirium - confusional state, may be ƒ Obtundation marked by agitation or lethargy or – lethargic, blunted cognition waxing and waning mental status – awake but somnolent or slowed – arousable –DT’s ƒ Stupor – complex partial – asleep/semi comatose – drug induced delirium – only arouses when stimulated – – reverts back to when stimulus withdrawn

3 4

Unconsciousness occurs Definition of Coma when either:

ƒ Unresponsive to the environment ƒ Both cerebral hemispheres are ƒ Unable to communicate depressed ƒ Unarousable ƒ The reticular activating system is dysfunctional

5 6 Etiologies of Coma Etiologies of Coma

ƒ Supratentorial mass lesions ƒ Infratentorial lesions – intracerebral hematoma – infarction – – pontine hemorrhage – large ischemic infarction – brainstem demyelination – – cerebellar tumor – – cerebellar abscess – – cerebellar hemorrhage

7 8

Etiologies of Coma Etiologies of coma

ƒ Metabolic and other diffuse disorders – drug toxicity ƒ : Mortality 5-10% – anoxic-ischemic encephalopathy ƒ Metabolic: Mortality 50% – ƒ Head Trauma: Mortality 50% – endocrine disorders – acid-base disorders ƒ Anoxia: Mortality 90% – encephalitis and encephalomyelitis ƒ : Mortality 80% – – hyper- – uremic encephalopathy 9 10

The RAS and Essential Neurotransmitters ƒ Epinephrine Locus Coeruleus is ƒ Serotonin: Median Raphe Dependent on an Intact ƒ Acetylcholine: Basal Reticular Activating System!

11 12 Initial Neurological Exam: Exam points Primary Question ƒ Nuchal rigidity – sub arachnoid ƒ Is the coma due to: hemorrhage – toxic, infectious, metabolic coma? –meningitis ƒ Rash OR – meningococcus, – acute neurosurgical cause? – spiders • bleed – drug reaction • ƒ Ecchymosis over orbit or • mastoid • increased intracranial pressure ƒ Papilledema

13 ƒ Subhyaloid hemmorrhage 14

Abnormal postures in a comatose Initial Exam

ƒ Pupils - Unilateral Dilated Pupil - R/o herniation ƒ Fundi - r/o Papilledema ƒ Oculocephalic and oculovestibular ƒ Motor response –withdrawal – decortication – decerebration ƒ Progression suggests – expanding or worsening mass 15 16

Initial Exam Initial Exam

ƒ Bilateral dilated pupils – transtentorial herniation of both temporal ƒ 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 ƒ Bilateral pinpoint pupils slowly, suggests rapidly expanding – mophine poisoning ipsilateral mass compressing midbrain or – pontine hemorrhage – organophosphates or eye drops (miotic)

17 18 Initial Exam

ƒ 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 ( drugs)

19 20

Etiologies-toxic metabolic Metabolic Coma

ƒ Drug overdose – narcotics, tricyclics, stimulants ƒ of toxic - ƒ Metabolic metabolic coma – – pupils small - narcotics – hepatic encephalopathy – pupils large - tricyclics – uremic encephalopathy – - dilantin, pcp – – hypothyroid () – respiratory depression - narcotics – ETOH withdrawal/intoxication – tremor / asterixis - , etoh, hepatic – anoxic encephalopathy

21 22

Signs of increased Locked-in State ICP / Herniation ƒ Pupils ƒ Quadriplegia – unilateral dilated pupil is a sign of? ƒ Paralysis of lower – bilateral small poorly reactive pupils are a sign of? ƒ Eye movements ƒ Lesion of basis pontis (RAS not affected) – third nerve palsy? ƒ Preservation of consciousness – sixth nerve palsy? – can be assesses by cold caloric ƒ Fundoscopy – signs of papilledema? ƒ Respiratory pattern?

23 24 Signs of herniation (cont’d)

ƒ Can be detected by a deterioration in mental status, pupils, or motor exam – withdrawal to transitioning to flexor withdrawal – flexor withdrawal to extensor posturing • decortication - flexor withdrawal - lesion above • decerebration -extensor posturing - lesion below red nucleus

25 26

Initial Management Initial Management

ƒ Protect airway- ƒ Stat ƒ If Narcotic OD ƒ If ETOH withdrawal (72-96 Support vitals – fingerstick for dextrose suspected, give hrs post ETOH) – CBC, electrolytes, BUN/Cr, ƒ If evidence of trauma, – naloxone 1 - 2 amps – (confusion, hallucinations, immobilize spine, get Calcium, ABG, LFT’s, tremor, tachycardia, HTN) , UA, serum and – repeat in 15 minutes stat c-spine – thiamine 100 mg/IM urine tox screen, blood ƒ If ƒ IV, Pulse ox, frequent cultures if febrile – librium 25-100 mg q6hrs overdose suspected, vitals and ƒ Dextrose (1 amp = 25 ƒ For ETOH seizures – flumazenil .2 mg neurochecks grams dextrose) – (12-24 hours post withdrawal) – repeat q 1 minute up to ƒ 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, • 2 mg IV q 6-8 increased risk of hours Korsakoffs 27 28

If bacterial menigitis or SAH Increased ICP suspected ƒ For SAH, STAT CT of brain ƒ : 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 ƒ If bacterial meningitis suspected, do not delay for CT- Start empiric therapy ƒ 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 ƒ Mannitol and lasix are synergistic. immunocompromised ƒ 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 29 30 Increased Intracranial Pressure: Hyperventilation

ƒ 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 ƒ Reduction of CO2 beyond a p CO2 of 30 has little benefit 12 1

31 32

Predictors of Persistent Vegetative State Awakening / Good Outcome ƒ Preserved vegetative functions (sleep-wake ƒ EEG: ƒ EP’s: Median Nerve cycle, autonomic and respiratory control) – strong predictor only – strong predictor only of ƒ No for poor outcome in poor outcome ƒ No appropriate response to the environment coma - 0/138 good – absent cortical potential recovery if: to median nerve ƒ Spontaneous movements, but no • stimulation (N20) purposeful or voluntary responses to • low voltage – poor prognosis >95% stimulation •PLEDS ƒ Preservation of hypothalamic and brainstem function

33 34

Persistent Vegetative State

ƒ Recovery of consciousness is rare after 3 months ƒ May survive for years ƒ Mortality rate is 80% in 3 years, 95% in 5 years

35