CVA 2 Flashcards
intercerebral hemorrhage
bleeding in brain parenchyma
typically 2/2 HTN (poorly controlled, microaneurysm)
how do ICHs injure brain
direct pressure of expanding clot and irritation of tissue
increased ICP and herniation
where do ICH typically occur (5)
basal ganglia pons thalamus cerebellum cerebrum
s/s ICH
occur without warning and with routine activity
worsen over minutes to hrs
HA, vomiting, LOC, focal deficit, behavior change
ICH diagnosis
Non contrast CT
new blood = white, old blood = gray
NO LP bc elevated ICP/herniation risk
ICH tx
no effective tx - ICU, neuro checks
manage BP (nicardipine), cent support (HOB 30), eve resale of anticoagulation, seizure prophylaxis, DVT prophylaxis
HTN control in ICH
nicardipine is DOC
optimal range = 160/90, MAP 110
AVOID NITROPRUSSIDE
reversal agents
vitamin K IV, Praxbind, prothrombin complex
clinical course ICH
deteriorating LOC in 24-48hrs
high risk of herniation 2/2 vasogenic edema
high risk fo seizures
specific measure to reduce ICP
mannitol/hypertonic saline
hypothermia
hyperventillation
decompressive craniotomy
ICH prevention
HTN goal management (<130/80)
smoking cessation, limited alcohol, exercise, healthy weight
SAH
blood bt Pia and arachnoid mater
secondary to trauma or spontaneous
SAH clinical picture
sudden, severe headache
“worst HA I’ve ver had”
symptoms being following strenuous activity
+/- n/v, LOC, meningeal signs
SAH diagnostics
non-contrast CT – may miss
follow up LP to observe for blood in CSF
LP findings in SAH
done if high clinical suspicion but negative imaging
Xanthrochromia in all 4 viles
CTA SAH would show
extrvasion of contrast
dye will be out of the vessel and into CSF
SAH management
hospitalize
periodic re-eval with CT
bed/bowel regime to decrease ICP
HA pain magnet, BP management, prevention of vasospasm, statins
vasospasm prevention
Nimodipine(Nimotop) non-DHP CCB
IV then PO
SAH diagnostics AVM
bilateral carotid and vetetnral angiography to evaluate for aneurysm
clipping nad cooling done to prevent re bleeding
SAH complications
hydrocephalus, hyponatremia, rebreeding
family history and SAH
first degree relatives have increased risk of lifetime SAH
AV malformation
congenital malformed communication between arteries and veins
70% will bleed, and cerebral ones do before age 40
AV malformation rules
small (<2/5) more likely to bleed than >5
AVMs are likely to rebelled
cerebral AVMS are often associated with aneurysm
AVM symptom
HA, seizures, focal neuro deficits in unruptured AV
types of aneurysms
fusiform
mycotic
saccular
occur at vessel bifurcation
fusiform aneurysm
LARGE arteries, caused by arteriosclerosis
typically in older, vertebrobasilar system
not easily accessible to surgeon
fusiform aneurysm symptoms due to
compression of brain or cranial nerves by thrombosis or take off vessel
mycotic aneurysm
septic emboli lodge within peripheral cerebral vessel
2/2 infective endocarditis and abscess rupture
typically have >1 aneurysm`\
saccular aneurysm
small round berry out poaching (typically in circle of willis)
heomdynamicaly induced by degenerative vascular injury
MC In women, MC type of aneurysm
diseases associated with saccular aneurysm
PCKD
marfans/CT disorders
coarctation of aorta
familial tendency
HTN, hyperlipidemia, smoking
highest risk of rupture saccular aneurysm
found in posterior circulation
increased size
s/s of saccular aneurysm
asymptomatic until rupture
small working leaks produce HA, nausea, meningeal signs hrs/weeks before rupture
aneurysm study of choice
cerebral angiography gold stnd
excludes multiplicity
tx aneurysm goal
prevention of further hemorrhage
surgical clipping, coil
