Coma and Brain Death Flashcards
Define coma
sleep-like, unarousable, unresponsive state
-obtunded/stuporous are pts with impaired consciousness but some limited degree of responding
What is clinically testable in coma?
only BRAIN STEM REFLEXES since cortical function is absent
persistent vegetative state-whats going on?
- eyes periodically open or move
- sleep and wake cycle occur
- pain responsiveness may return, but meaningful interaction remains absent since severe cortical impairment persists
what can cause coma
severe metabolic or systemic conditions that diffusely depress cortical function
what can directly impair neuronal function
- hypoxia
- inadequate cerebral blood flow
- hypoglycemia
- drug intoxication or overdose
what can indirectly affect cerebral cortex
- systemic infection
- metabolic disturbances
- hepatic or renal failure
what in particular can cause permanent cortical deficits
the hypo’s:
- severe hypotension
- hypoxia
- hypoglycemia
relationship between solitary cerebral lesions and coma
a solitary unilateral cerebral lesions doesn’t produce coma UNLESS it adversely affects the opposite hemisphere via brain edema or herniation
what is the ship between coma and reticular formation
coma may be produced by a brainstem lesion if it disrupts the reticular formation
(the tegmental brain stem reticular formation, projecting to thalamic and subcortical nuclei, is important for wakefulness and arousal)
what is the use of serial repeated observations?
may show progressive loss of neurological function and BS reflexes, often indicative of a rostral to caudal deterioration d.t edema or inflammation
limited examination in an unresponsive pt
- evaluation of motor responses
- breathing patterns
- pupil size and reactivity
- reflexive ocular movements
symmetrical vs asymmetrical abnormalities
- asymmetrical neurological signs strongly suggest a structural lesions (such as ischemic infarction, hemorrhage, or tumor)
- symmetrical abnormalities usually are due to a more diffuse or toxi-metabolic process (ie anoxia)
do motor responses occur in coma?
no. motor responses to command or withdrawal to painful stimuli do not occur in coma.
- an appropriate localizing response to a noxious stimulus requires some cortical function
Posturing (two types)
- decorticate=flexion of upper limbs with extension of lower limbs; associated with a lesions at the level of the cerebral cortex or hemisphere
- decerebrate=extension of the upper and lower limbs; associated with a lesions at the level of the midbrain (red nucleus)
abnormal breathing patterns in a coma
-Cheyne-Stokes respiration-alternating tachypnea and apnea (crescendo-decrescendo respiration)
….can also be seen in CHF and health elderly
How is Cheyne-Stokes respiration produced in a ca comatose pt?
- b/l cortical involvement d/t:
- -metabolic encephalopathy (ie renal failure)
- -unilat lesions with severe brain edema
- -b/l structural lesions in cerebral cortex
central neurogenic hyperventilation
-rarely ma result from a lesion or edema in the low midbrain to upper pons
ataxic respiration pattern
- consists of variable breaths at an irregular rate from a lesion or edema in the medulla, involving cardiorespiratory control centers there
- ominous for intubation
pupillary light reflex in unconscious pt
- important!!
- in coma f/m metabolic causes pupillary light reflex is preserved
sympathetic vs. parasympathetic fibers
- sympathetic (pupilloDILATOR) fibers travel down entire brainstem
- PS (pupilloCONSTRICTOR, CN3) fibers are a circuit at the midbrain level
tectal (dorsal) midbrain lesion
-selectively involves the PS fibers=LARGE FIXED pupils (unopposed sympathetic)
uncal herniation (neurologic emergency!)
-larger, BLOWN, fixed pupil unresponsive consensually or directly to light d/t compression of ipso CN3 f/m swollen temporal lobe
pontine lesion
- selectively involves the sympathetic fibers=SMALL PINPOINT pupils (unopposed PS fibers)
- sans pontine lesion…same pupils d/t high doses of narcotics or cholinergic eyedrops used to treat glaucoma
Reflexive eye movements
- important to check in every unresponsive pt
- may be suppressed by vestibulotoxic drugs (such as BZ) in absence of BS lesion
oculocephalic reflex aka “doll’s eye reflex”
-normally: eye should move in the direction OPPOSITE to the lateral turn of the head by the examiner
oculovestibular (cold caloric) reflex
- first: exclude ear canal blockage or ruptured TM
- nml: eyes move slowly toward cold (irrigated ear)
emergency tx of comatose pt
-ABCs
-rule out hypoglycemia or empirically give 50% dextrose iv
(hypoxia and hypoglycemia cause neuronal death is not promptly corrected)
structural causes of coma
=hemorrhage, ischemic infarction, mass lesion
–more likely in presence of asymmetrical neurologic signs
unless it is ruled out what does a comatose trauma pt have?
intracranial bleed! brain CT or MRI needed, in addition to ABCs
mechanism of hyperventilation to ICP
-intracranial blood volume is reduced since hypocarbia causes arterial vasoconstriction
mechanism of osmotic diuretics (mannitol) on ICP
-reduced cerebral water volume, by osmotics effects on intact BBB in nml brain tissue
iv corticosteroids (dexamethasone) vs edema
-dex can counter edema produced by a cerebral tumor, abscess, or encephalitis (not from ischemic infarction or hemorrhage)
define brain death
-irreversible loss of function for both cerebrum and brain stem
causes of brain death
- hemorrhage from trauma
- uncontrolled HTN
- ruptured berry aneurysm
- large/multiple ischemic infarctions
- meningoencephalitis
- anoxia f/m cardiac arrest…fragile gross brain
where is there evidence of herniation caused by edema
temporal lobes and foramen magnum
where is necrosis most severe
cerebral cortex and cerebellar folia
red neurons vs Purkinje cells
- ischemic red neurons: found in cerebral cortex and appear eosinophilic and shrunken
- cerebellum Purkinje cells: ischemic or absent
What is necessary for brain death declaration
- apparent cause should be known and must be of sufficient severity to account for the irreversible coma
- no neurological improvement despite adequate tc of any reversible causes of coma (such as drug intoxication, circulatory shock, or hypothermia–core temp <32C)
what is the generally accepted observation period when the etiology of coma is known and no reversible causes require tx?
SIX HOURS
- 7d-2mo: 48 hr
- 2mo-1yr: 24 hr
- > 1yr: 12-24 hr
bedside neurological exam in a brain dead pt
-shouldnt show any hint or suggestion of cerebral function in a comatose pt unresponsive to painful stimuli
=NO: decorticate/decerebrate, sz, swallowing, yawning, vocalization, pupillary rxn to light, light and corneal reflex, dolls eyes, cold caloric, gag reflex
-all CN or BS reflexes must be absent sans spontaneous respirations
what specific testing can be used to verify apnea?
- give ventilated pt 100% oxygen for 10mins to create an oxygen reserve in lungs and test baseline ABG
- d/c vent while 100% is still supplied though tubing
- if ensuing hypercarbia induces respiratory movements apnea is RULED OUT
- If no respiratory movements happen after 10 mins test another ABG
- apnea is CONFIRMED if no breathing observed despite reaching pCO2 of 60mmHg (or pCO2 20mmHg above baseline)
When are confirmatory tests of brain death used?
when bedside examination of CN and BS reflexes are hard to do–severe facial and ocular trauma or edema.
-also should always be done in comatose kids <1yo
What are two classical confirmatory tests of brain death
- a flat line or isoelectric EEG after 30 mins of recording
2. cerebral angiography which showed failure of any intracranial blood flow over a 10 min period d/t a fatal brain edema
What is often the currently preferred confirmatory test?
a radioisotope brain scan
