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36 Cards in this Set
- Front
- Back
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Risk factors for SAH |
hypertension, smoking, family history, cocaine use |
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aneurysms that have higher risk of rupture |
larger (>7mm), located in posterior circulation, on the Pcomm |
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is there a familial clustering of SAH? |
yes, first degree relatives of SAH patients = 3x more likely to suffer from SAH compared to general population |
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connective tissue disorders associated with intracranial aneurysms |
Ehlers-Danlos syndrome NF1 Marfan's ADPKD (most convincing) |
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what are perimesencephalic hemorrhages |
10% of SAH 2/3s of angio NEG SAH blood predominantly located in perimesencephalic and prepontine cisterns |
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typical clinical picture of perimesencephalic hemorrhages |
>50y/o, less severe neuro symptoms, rare seizures or focal deficits |
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why is it important to distinguish perimesencephalic hemorrhages from other aneurysmal SAH? |
rebleeding and DCI related to vasospasm is extremely unusual |
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most common cause of non-aneurysmal SAH |
head traum |
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how can one differentiate traumatic and nontraumatic SAH based on the CT? |
Usually traumatic SAH has a thin layer of blood in the subarachnoid space around cerebral convexities or within Sylvian fissure; less common to see blood in basal cisterns or surrounding circle of Willis due to trauma (suspect aSAH) |
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aside from aneursymal and traumatic causes of SAH, are there other causes of SAH? |
dural AV fistulas, septic / mycotic aneurysms, pituitary apoplexy, Moya moya disease, cocaine or stimulant abuse, cerebral vasculitis |
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CN III palsy in an otherwise healthy individual |
Pcomm aneurysm |
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CN sign of elevated ICP |
CN VI palsy |
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sensitivity of CT relative to onset of symptoms |
Sn 100% within first 6 hours of onset of hemorrhage 85% at 5 days 50% at 1 week |
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What to do with NEG angio SAH? |
10-20% will have negative angio if not perimesencaphalic or if high suspicion, repeat angio as to when? still controversial - 1 week to 3 months? |
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when should LP be done after SAH? |
ideally delay for 6-12 hours after onset of symptoms |
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these findings on CT are strongly associated with development of DCI |
thick cisternal clot IVH |
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what is the most important prevention strategy for prevention of rebleeding in SAH |
to treat and secure the aneuryms as early as possible |
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when should surgical clipping of aneurysms be done? |
early clipping within first 3d preferred to reduce rate of rebleeding and to avoid surgery within peak of DCI |
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trial that compared clipping to coiling |
ISAT (international subarachnoid aneurysm trial) - found favorable outcome in certain subgroups of patients treated with endovascular coiling |
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define vasospasm |
radiographic narrowing of cerebral arteries following aSAH |
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incidence of vasospasm |
70% |
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define DCI |
delayed cerebral ischemia - neuro deterioration related to cerebral ischemia |
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incidence of DCI |
20-30% of aSAH patients |
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mechanism of DCI |
oxyhemoglobin in subarachnoid space - production of superoxide free radicals - inactivates / decreases production of NO - increases intracellular calcium - prolonged sm muscle contraction - narrowing of vessel lumen |
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TCD mean blood flow velocity threshold |
<120 = absence of vasospasm; >200 presence of vasospasm |
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Methods to screen for cerebral vasospasm |
frequent serial neuro assessment; TCD; CT angio; CT perf, Xenon CT, MRI with perfusion and DWI, PbtO2, direct CBF monitoring, cerebral microdialysis, continuous EEG |
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triple H therapy |
HTN, hypervolemia, hemodilution |
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complications of triple H therapy |
pulmonary edema, MI, hyponatremia, cerebral hyperemia and hemorrhage |
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components of the Triple H therapy which remain a mainstay of treatment in symptomatic vasospasm |
induced HTN and volume expansion |
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nimodipine dose |
60mg q4h x 21d |
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why is nimodipine given in SAH? |
reduces risk of poor outcome and secondary ischemia |
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gold standard for evaluation of vasospasm |
cath angio - allows for endovascular treatment with angioplasty or localized IA infusion of vasodilators |
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types of HCP in SAH |
acute due to obstruction of flow in ventricular system and late due to impairment of arachnoid granulations resulting in poor CSF reabsorption |
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treatment of HCP in SAH |
acute may need EVD; late may need VPS |
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what causes the pupillary changes and downward deviation of eyes in SAH with acute HCP? |
dilatation of cerebral aqueduct |
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risk factors for seizures after SAH |
older age, surgical aneurysm treatment, IPH, ant circulation aneurysms |
