Neurocritical Care Flashcards
warfarin-related intracranial hemorrhage with high INR. treatment?
worst to best:
- IV vitamin K (takes 6-24 hours to make new coag factors)
- FFP - provides many coag factors quickly, but need to test compatibility and administer correctly, only transient correction. risk of fluid overload, infusion rxn
- PCC (prothrombin complex concentrates) - quickly correct INR if available. less complications.
protamine sulfate used for what?
reverse anticoagulation due to heparin
critical illness polyneuropathy - what kind of neuropathy is it? NCS/EMG findings?
axonal sensory and motor neuropathy that affects limbs and respiratory muscles - takes longer to recover than CIM
reduced CMAPs and SNAPs, with normal or mildly reduced conduction velocities
fibs and sharp waves on EMG
predictive factors after cardiac arrest
no pupillary response 24-72 hours after arrest - bad
no corneal reflexes or eye mvtments 72 hours out - bad
EEG showing burst suppression or generalized suppression - bad
evoked potentials with median nerve stimulation showing bilateral absent N20 responses at 24-72 hours - bad (best biomarker early on)
neuron specific enolase elevated - bad
duration of arrest, CT edema, physical exam before 72 hours not reliable
how to perform apnea test for brain death exam
preoxygenate x 10 minutes with FiO2 100%
baseline ABG - pCO2 should be 35-45
then disconnect from vent but give 6 L/min O2
observe for 10 min - look for chest rise/abd rise
after 10 min repeat ABG. if no resp movements and pCO2 > 60, supportive of brain death
BODY TEMP SHOULD BE 36.5 or higher and SBP >90
ancillary tests to support brain death (4)
EEG showing electrocerebral silence x 30 min
TCDs showing no flow signals
PET scan showing no isotope uptake in brain, no intracranial flow
Angiography showing no flow in circle of willis
decorticate rigidity - what does it look like and where is the lesion
arms flexed, legs extended
hemispheric dysfunction
lesion ABOVE RED NUCLEUS –> disinhibition of red nuclei, facilitation of rubrospinal tracts (which increase flexor tone in arms)
decerebrate - what does it look like and where is the lesion
extension + hyperpronation of arms, extended legs
pinpoint pupils
lesion in brainstem at/below superior colliculus and red nucleus, but ABOVE VESTIBULAR NUCLEI (enhance extensor tone)
lesions below vestibular nuclei –> flaccid limbs
Cerebral Perfusion Pressure equation
CPP = MAP - ICP
CPP ideally > 70
ICP normal 5-15
MAP >60
subfalcine herniation
cingulate gyrus (which hugs the corpus callosum) herniates under the falx cerebri (the sagittal membrane)
pericallosal and callosomarginal arteries compressed
uncal herniation
what sign occurs on exam?
medial temporal lobe herniates medially and down over tentorial edge
pushes onto midbrain –> fixed dilated pupil + contralateral hemiparesis (but if it pushes Kernohan’s notch on the other side, it can cause ipsilateral weakness)
PCA infarct can also occur
tonsillar herniation
cerebellar tonsils are pushed down through foramen magnum, compress medulla and block 4th vent –> hydrocephalus
transcalvarial herniation
brain tissue squeezes out through a skull defect (due to trauma or hemicrani)
central transtentorial herniation
expanding lesion in middle of brain causes downward displacement, pushing against midbrain
relationship between hematocrit and CBF
lower hematocrit = lower blood viscosity = increased CBF