Approach
• Utility of thrombolysis is time limited. Must distinguish TIA, ischemic or hemorrhagic CVA.
• Quick assessment of ABCs & fingerstick glucose
• History: Time of onset (or “last seen nl”) is key to determining eligibility for lytics
• RFs: HTN/HLD, DM, AF, CAD, PVD, CHF, PFO, tobacco, valve dz, hyper- or hypocoagulable, OCP, cocaine, amphetamines
• Complaints may be vague (AMS, numb, weak, vision Δ, dysarthria)
• Consider concurrent aortic dissection, hypertensive encephalopathy
• Consider recrudescence (“unmasking”) of old stroke (eg, due to UTI), & other causes of focal neuro deficits (Todd’s paralysis, ↓ glucose, mass, complex migraine)
• Physical: Quick but detailed neuro exam. NIH Stroke Scale (see below) is useful for this. Also check for arrhythmia, murmur, bruits, & rectal for occult blood if considering lytics.
• Evaluation: All pts need glucose, CBC, coags
• ECG may show cerebral T waves (deep symmetric precordial) suggesting bleed, or AF
• CTH to r/o hemorrhage, & LP if story concerning for SAH
Transient Ischemic Attack
Definition
• Neuro deficit lasting <24 h (frequently <1 h) w/ complete resolution
• Due to atherosclerosis, emboli, small vessel dz (lacunar), or hypotension w/ stenosis
• ↑ CVA risk: 20% will have CVA in 1 mo, 50% in 1 yr. ABCD2 score (below) predicts stroke risk.
Presentation
• Posterior circulation: Nonlateralizing sxs (eg, diplopia, dysarthria, dysphagia, ataxia)
• Anterior circulation: Unilateral motor/sensory deficit (eg, numbness, weakness, facial droop, monocular blindness [amaurosis fugax], aphasia)
Evaluation
• Initial assessment same as for CVA, consult neurology
• Need to find etiology of TIA (echo, carotid imaging, Holter, MRI/MRA), usually as inpt
Treatment
• ASA or clopidogrel
• BP control: If no prior h/o HTN, goal is <160/90. If prior HTN, keep BP at baseline.
Disposition
• Admit if 1st TIA, multiple TIAs in short time, cardiogenic, or posterior circulation
• In some stroke centers, select cases can be managed outpt (eg, recent full w/u)
• ABCD2 is a useful data point but not well validated as a disposition tool
Pearl
• Recurrent TIAs w/ different sxs are likely cardiac emboli; if same sxs, likely cerebral
Ischemic Stroke
Approach
• See above
• Hx & findings will depend on stroke location (see table below)
• All pts need head CT (bleed vs. infarct), usually followed by CTA or MRI/MRA to eval patency of vessels, look for e/o recent infarct, r/o venous thrombosis
Management
• Neurology consult, ASA. May use clopidogrel, ticlopidine, or warfarin per neurology.
• BP control: Rapid & titratable: Labetalol, esmolol, nicardipine are 1st line
• If thrombolytic candidate: Goal is 185/110, lysis is contraindicated if refractory to 2 doses
• If not candidate: Avoid rapid decrease, avoid decrease more than 10–20%. Treat only if persistently >220/120, or signs of other end-organ damage (eg, AMI).
• Decide whether thrombolysis is appropriate
• See table below for inclusion criteria, absolute & relative CIs
• Some stroke centers will do intra-arterial thrombolysis if longer time since onset of sx
• Close monitoring, repeat exams to look for signs of ↑ ICP (edema, bleed)
• If arterial dissection or suspected cardioembolic stroke, may consider heparin
• If septic emboli suspected, start appropriate abx
Disposition
• Small strokes usually to telemetry
• Large strokes to ICU (risk of edema or hemorrhagic conversion)
• Rarely, pts w/ small strokes who have had full w/u & are on maximal medical therapy can be managed as outpts w/ close neurology f/u
Pearls
• 70% localized to anterior circulation, MCA territory most common
• Inpt w/u includes carotid imaging, echo, Holter monitor, advanced serology (hypercoagulability, lipids, bleeding diathesis, ESR, ANA)
• NIHSS correlates w/ neurologic outcome at 3 mo; performs poorly for posterior CVAs
Hemorrhagic Stroke
Presentation
• Hx & findings will depend on stroke location (see table below)
• Generally sudden onset, often w/ AMS or LOC, N/V, new onset sz, severe HA
• RFs: Long-standing HTN, coagulopathy, cocaine/other sympathomimetic use
• H/o cancer (GBM, melanoma, renal cell carcinoma, lung)
• Personal hx or FH of cerebral aneurysms or PCKD, cerebral AVM, aortic coarctation, or connective tissue dz (Ehlers–Danlos syndrome, Marfan syndrome)
• SAH presentation discussed in detail above in “Headache” section
• May have focal neuro deficits or nuchal rigidity
• Cushing reflex (HTN + bradycardia) is late finding that suggests herniation
Evaluation
• See general approach to stroke above
• All pts need head CT (90% sens for bleed in 1st 24 h)
• If working up for SAH, need LP to eval for RBCs, xanthochromia
• If LP+, CTA to look for aneurysm, AVM, mets, amyloid
Management
• Consult neurology & neurosurgery
• BP control: Rapid & titratable: Labetalol, esmolol, nicardipine enalaprilat are 1st line
• Avoid rapid decrease & avoid decrease more than 10–20%
• Treat only if persistently >220/120, or signs of other end-organ damage (eg, AMI)
• Goal <160/105, place A-line for close monitoring
• If coagulopathy present, correct w/ Vit K or FFP
• In consultation w/ neurosurgery, consider:
• Antiepileptics: Dilantin load (15–20 mg/kg IV) vs. levetiracetam (1 g IV)
• Nimodipine (60 mg PO) for arterial vasospasm in SAH (1/3 cases)
• If signs of ↑ ICP/edema: Hypertonic saline, mannitol, or dexamethasone
Disposition
• Admit to ICU
