Stupor and Coma Flashcards
What is consciousness? Requirements?
- total awarness of self and environment
- arousal (alertness)
- awareness (sum of cognitive mental functions)
consciousness depends on?
- arousal of cerebral cortex by brainstem ascending reticular activating system (RAS)
- input from sensory
- projects to hypothalamus, thalamus, cortex
impaired consciousness means?
- diffuse or b/l impairement of both hemispheres
- failure of brainstem ARAS
- both
confusion–what is it?
-orientation disturbed
delirium–what is it?
-hallucinations (visual)
obtundation–what is it?
-mental blunting, increased sleep, arouses to mild stimuli (voice)
stupor–what is it?
arouses only to noxious stimuli and not environmental
-only rudimentary awareness (purposeful motor responses)
coma–what is it?
-unarousable, unresponsive, unaware
persistent vegetative state
- arousal, awarness
- no reproducible response to stimuli
- eyes may be open, eye movements
- BP/pulse stable
akinetic mutism
-no spontaneous motor activity
locked in state
- normal sensation/ cognition
- complete paralysis except vertical eye movements
hypertension–consider
-pheochromocytoma, drugs, increased ICP
hyperthermia consider
-infection, heat stroke, serotonin syndrome, pontine hemorrhage
breath odor–musty
hepatic failure
neuro exam–2 purposes
- determine location and nature causing the impaired consciousness–anatomic level of brain involvement (supratentorial, subtentorial, diffuse)
- narrow differential possibilities
broad categories of lesions that produce coma
- supratentorial mass lesions–cause dysfunction in upper ARAS, cause downward herniation of brain to compress ARAS
- infratentorial mass lesions–involve brainstem
- diffuse/multifocal brain disease
supratentorial causes of coma
- unilateral–subdural hematoma, brain abcess, tumor
- bilateral–subarachnoid hemorrhage, multiple infarcts, cerebral edema, acute hydrocephalus
subtentorial causes of coma
- central pontine myelinolysis
- cerebellar hemorrhage/infarct, neoplasm, abcess
diffuse causes of coma
-hypoxia
-meningitis/encephalitis
-hypo/hyper-glycemia
-hyponatremia
-hepatic failure
-malignant hypertension
seizures (status epilepticus)
Neuro exam–essential elements
- pupillary responses
- corneal reflex
- extraocular movements
- cough/gag reflex
- motor responses
- resp pattern
Neuro exam–nearly essential elements
- neck stiffness
- carotid auscultation
- fundoscopic exam
pupillary response–sympathetic path
- hypothalamus
- lower cervical cord
- sympathetic chain
- superior cervical ganglion
- up carotid artery to CN V1, long cilicary nerve (dilator)
- Mueller’s muscle
pupillary response–parasympathetic path
- upper midbrain (edinger westphal nucleus)
- CN III
- ciliary ganglion
- short ciliary nerve (constrictor)
symp and parasymp pathways for pupillary response–anatomically adjacent to?
- ARAS
- absent or unequal responses imply brainstem lesion!!
dilated pupil on 1 side
-parasymp (CN III)
dilated pupil bilaterally
- b/l lesion to CN III
- post ictal
- barbiturate intoxication
constricted pupil
-symp dysfunction
pinpoint pupil
- pontine lesion
- opiates
- pilocarpine (3Ps)
midposition and unreactive pupil
symp and parasymp (midbrain)
frontal gaze, pontine gaze
- frontal–deviate eyes to opp side
- pontine–deviate eyes to same side
roving–conjugate, dysconjugate
- conjugate–brainstem intact
- dysconjugate–brainstem lesion
conjugate deviation at rest–hemispheric lesion
- destructive–toward lesion
- irritative-away from lesion
conjugate deviation at rest–brainstem lesion
-destructive–away from lesion
oculocephalic maneuver (dolls eyes)
Mid pons!
- CN 3,4,6
- horizontal/vertical head rotation–eyes move opposite
caloric (oculovestibular) reflex
Lower pons! -irrigate TM with cold water -eyes deviate to irrigated side -eye deviate downward if b/l irrigation (brainstem intact!)
decorticate?
arms flexed, legs extended
-hemispheric/ corte lesion
decerebrate
all extremities extended
-brainstem
flaccid?
pontomedullary or metabolic
Cheynes Stokes
- b/l hemispheres or diencephalon
- crescendo-decrescendo breathing pattern–hyperpnia alternating with apnea
stupor and coma–4 broad categories
- supratentorial
- subtentorial
- diffuse/metabolic
- psychiatric unresponsiveness
supratentorial mass lesions–characteristics
- focal!
- neuro signs–1 anatomic location
- progression of signs rostral to caudal
- motor signs–asymmetric
herniation syndromes caused by?
expanding supratentorial mass lesions
-displace brain tissue–rostral to caudal progression
uncal transtentorial
uncus under tentorium
-compress CN III, contralateral brainstem (ipsilateral hemiparesis), resp abnormalities
central transtentorial
herniate into foramen magnum
-resp arrest, death
cingulate gyrus
-herniates under falx
subtentorial mass lesions characteristics
- localizing brainstem signs preceed coma–always include oculovestibular abnormality (eye movement)
- CN palsies usually present
- bizarre respiratory patterns
diffuse/metabolic characteristics and causes
- confusion, stupor precede motor signs
- motor signs symmetrical
- pupillary reactions preserved!!
- asterixis (liver flap-flaps wrist down and up), myoclonus
- acid-base imbalance
hepatic/renal failure -hyper/hypoglycemia -hypoxia electrolyte imbalance--hyper/hyponatremia, calcium -sepsis
global cerebral ischemia
- blood flow inadequate to meet metabolic requirements of brain (cardiac, pul arrest)
- ranges from reversible to brain death
global cerebral ischemia reversible when?
-
prolonged ischemic episodes
- comatose at least 12 hours
- lasting focal or multifocal motor, sensory, cognitive deficits
persistent vegetative state
- awake but functionally decorticate, unaware of surroundings
- eye opening, eye movements, sleep-wake cycles
brain death definition
- irreversibility
- complete cessation of brain function (including respirations but not heartbeat)
- persistance
irreversibility–what must be ruled out?
-cause of coma known–irreversible
sedative intoxication, hypothermia (
cessation of brain function
- unresponsiveness to all sensory input
- absent brainstem reflexes–respiratory responses absent 8-10 minutes after patients pCO2 rises to 60 mmHg
absent brainstem reflexes
- pupillary light reflex-2,3
- dolls eyes, cold water irrigation–3,6,8
- pain reflex, pinch supraorbital n–5,7
- corneal reflex–5,7
- gag reflex–9,10
brain death–persistence
- 6 hours with confirmatory isoelectric (flat) EEG
- 12 hours without confirmatory EEG
- 24 hours for anoxic brain injury without confirmatory EEG
manage comatose patients–1st steps
- A-patent airways
- B-breathing, oxygenation
- C-circulation, bleeding
manage comatose patients–next steps
- history, exam, EKG
- glucose, thiamine
- antidote
- adjust body T
- control agitation
- stop seizures if present
manage comatose patients–Lab evaluation
- venous blood–glucose, electrolytes, BUN/creatinine, osmolality, drug screen, liver function, ammonia, coagulation studies, blood cultures
- arterial blood–pH, pO2, pCO2, HCO3, HbCO
- urine–UA, culture, drug screen
- if febrile–blood cultures
- if stiff neck–LP after CT
manage comatose patient–diagnostic testing
- non-contrast CT (blood, space occupying lesion)
- LP (xanthochromia–hemorrhage, infection)
- MRI (posterior fossa, infarct)–not done right away!
- EEG–if expect seizures
manage comatose patient–specific interventions–reduce elevated intracranial P
- elvate head of bed
- intubate/hyperventilate to PCO2 of 20 mm (constricts BVs)
- mannitol for ischemic lesions (hyperosmolar conc–will suck water/edema out of brain)
- decadron for tumor, abcess, cerebral hemorrhage
- Lasix–for dehydration
manage comatose patient–specific interventions–treat seizures
- lorazepam
- phenytoin
glascow coma sclae
(3-15)
- eye opening–1-4
- best verbal response-1-5
- best motor response-1-6
KEY to accuracy in diagnosis and management lies in 2 steps
- physical signs–determine anatomic level of brain involvement
- determine supratentorial, subtentorial, or metabolic
