brain tumors
what causes the neuro deficits with tumors
mass effects- leading to increased ICP, papilledema, headache, AMS, mobility impairment, vomiting, seizure, autonomic dysfunction
occluded anterior cerebral artery
contralateral weakness
blood is supplied to the brain from
internal carotid arteries and veterbral arteries
2 reliable predictors of outcome in hemorrhagic stroke
estimated blood volume and change in LOC
symptoms of cerebral aneursysm
headache, photophobia, confusion, hemiparesis, coma
out of the astrocytomas which are the most benign, which are the most devastating
gliomas - primary tumors least aggressive
pilocytic astrocytomas - mostly benign
anaplastic astrocytomas - poor differentiated usually evolve into glioblastoma mutliforme
glioblastoma multiforme - carry a high mortality, requiring surgical debulking and chemo; life expectancy is within weeks even with treatment
occluded middle cerebral artery
contralateral hemiparesis and hemisensory deficit
aphasia
contralateral visual field deficit
where does the circle of willis form
inferior surface of the brain to for collateral circulation to multiple areas of the brain
IPH, SDH, EDH, IVH, SAH
IPH - in the brain
EDH - epidural
SDH - subdural
SAH- subarchoid space
IVH - ventricular system
risk factors for cerebral aneursym
HTN, smoking, female, oral contraceptives, cocaine use
pituitary adenomas
noncancerous, varying subtypes
transsphenioidal or open crani for removal is curative
occluded posterior cerebral artery
contralateral visual field deficit
contralateral hemiparesis
ischemic CVA treatment
PO aspirin
IV or intra-arterial TPA
thrombectomy to stent/remove clots
revascularization
treatment of hemorrhagic CVA
reduce ICP
BP control
seizure precautions
vigilant monitoring
hematoma evacuation (Burr Holes, EVD)
preanesthesia considerations for cerebral aneursym
CT/MRI, EKG, ECHO, CBC, BMP, T&C with blood available
*BP control, mannitol
seizure prophylaxis
treatment: stenting, coiling, trapping/bypass
acoustic neuromas
usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal
occluded penetrating artery
contralateral hemiparesis
contralateral hemisensory deficits
revascularization preanesthesia considerations
baseline neuro assessment
ability to lay flat safely, CV function
sedation or secure an airway
CV risk factors: HTN, DM, CAD, afib, valvular disease can impact vasoactive drug choices and hemodynamic goals
anticoags for prophylaxis =
high risk pts for CVA on long acting anticoags =
new anticoag for thrombus = no elective cases within 3 months
anticoags for prophylaxis = consult presciber for protocol
high risk pts for CVA on long acting anticoags = need short acting anticoags to bridge the gap
vasospasm watch period and causes
day 3-15 post bleed
free Hgb triggers inflammatory mediators which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
radiatio damage may lead to lethargy and AMS
chemo may lead to neuro deficits
patients often on steroids to minimize cerebral edema
anticonvulsants are common (supratentorial lesions closer to motor cortex)
autonomic dysfunction may manifest on EKG, labile HR & BP
CBC, BMP, EKG
CT/MRI
preopsteroid and antiseziure per surgeon
mannitol
basilar artery occluded
oculomotor deficits and or ataxia with crossed sensory motor deficits
veterbral artery occlusion
lower cranial nerve deficits and or ataxia with cross sensory deficits
CVA prerop
review Hx, deficits, imaging, treatments, co-existing disease
assess orientation, pupils, grip strength, LE strength
headaches, tinnitus, vision/memory loss, bathroom issues
look at route of case of CVA
preop EKG,
CBC, BMP, T&C
cererbral oximetry
2 IV and/or CVC, ALINE
treatment for vasopasms
hemodilution, hypervolemia, HTN
interventional - balloon dilation, direct injection of vasodilators relieve the spasm