CVA/Stroke ========= þ 2010 AHA ACLS Guidelines for CVA HTN: - if OK for tPA but BP >185/110 - Labetalol 10-20 mg IV/1-2 mins, may repeat x1 - Nicardipine 5 mg/hr IV, tritrate by 2.5 mg/hr every 5-15 min, max 15 mg/hr; when desired BP reached, decreased to 3 mg/hr - consier hydralazine, enalprilat - during and after tPA, check BP Q15' x 24 hrs + if systeolic 180-230 or disastolic 105-120, then + Labetalol 10 mg IV then 2-8 mg/min + Nicardipine 5 mg/hr, then titrate up 2.5 mg Q 5-15 min, max 15 mg/hr + if not controlled, especially if DBP >140 consider nipride þ IMS III Trial at UPMC Mercy - Start standard (0.9 mg/kg) tPA prior to randomization and enrollment - Goals + >= 50% of subjects treated within 1 hour + <= 40 minutes from IV completion to IA initiation - Stop IV tPA at 2/3 of total dose, then do intraarterial - only for hyperacute strokes - no change in our current protocols - won't enroll if NIHSS > 20 won't likely enroll - Tech or RN will bring in telemedicine unit for stroke neurologist to do NIHSS þ Sopt Sign - CTA in ICH shows "spot" indicating ongoing bleed - May be an indication for Factor VII or an investigational drug þ Headache: - classically associated with posterior cerebral artery ischemic CVAs þ Early CT changes: - Those with poor collateral circulation may have findings on CT even acutely after an ischemic CVA. - CT 95% sensitive for SAH. - Look for hyperdense (white) vessels: but can see lots of them (false positives common) not all that useful. - New (Acute) CVA: 1-10 ASPECT score correlates with prognosis (rating for findings on CT) - Medium (Subacute) CVA - Old CVA þ MRI: - Stroke Protocol: diffusion-weighted imaging + stays positive for up to 7 days + Can show ischemic CVA in 10 minutes - FLAIR Imaging: + Positive 3-6 hours after CVA + Shows every little tiny CVA anyone's ever had - MPGR/GRE: shows bleeds, vessel occlusions. May show tiny hemorrhage around ischemic infarct that is missed by CT; however, in real life this is very rare, and such tiny bleeds not a contraindication for tPA. - MRA: computer model of flow. Affected by stenosis, makes it look much worse distally than it really is - Clearing for MRI: þ TIA: - The classic definition of a transient ischemic attack is a neurologic deficit caused by focal brain ischemia that completely resolves within 24 hours. In 2002, a group of stroke specialists publicly debated the accuracy and utility of this definition and proposed a new one in its place. The new proposed definition by the Transient Ischemic Attack Working Group is "a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction." - 5% risk of stroke within 2 days or 8.6% risk within 1 week after a transient ischemic attack. - Civil suits for failure to evaluate for carotid stenosis and failure to initiate antiplatelet agents after a transient ischemic attack are common claims filed in the US courts with respect to transient ischemic attacks. - Many hospitals and physicians have instituted the practice of admitting all patients with transient ischemic attacks (or at least consulting a neurologist). - TIA Syndromes: + Anterior Circulation - Hemiparesis - Unilateral sensory loss - Visual field deficit (monocular blindness) - Gaze preference - Aphasia - Left-sided spatial neglect or hemiattention + Posterior Circulation - Several of the following usually present: - Hemiparesis - Quadriparesis ("locked-in" syndrome allows movement of the upper lids only) - Hemisensory loss or sensory loss in all 4 extremities - "Crossed" deficits* - Diplopia - Disconjugate gaze - Gaze palsy - Nystagmus - Dysarthria with dysphagia - Vertigo - Decreased level of consciousness - Limb or gait ataxia - Intractable vomiting *Cranial nerve findings one side of body, with contralateral motor or sensory signs. - A "march" of symptoms with different body parts affected in succession is unlikely because of transient ischemic attack and more likely suggests a migraine headache or seizure. - Nonfocal signs and symptoms, such as loss of consciousness, vague "dizziness," generalized weakness, mental confusion, loss of vision with reduced level of consciousness, and incontinence of feces or urine, are rarely caused by a transient ischemic attack; similarly, the following symptoms, if in isolation, are unlikely to be caused by a transient ischemic attack: vertigo, diplopia, dysphagia, loss of balance, tinnitus, sensory symptoms confined to part of one limb or the face, scintillating scotomas, amnesia, drop attacks, and (usually) dysarthria. All of these dicta are, for the most part, true, but exceptions may exist to each of these. It is generally accepted that isolated vertigo is rarely a manifestation of transient ischemic attack; however, this premise may not be reliable among the elderly, given one small study of 24 elderly patients with isolated vertigo: 6 patients (25%) were discovered to have caudal cerebellar infarcts. - Posterior TIAs: ertigo, ataxia, nausea, and vomiting are the most common symptoms. Dysarthria, dysphagia, and diplopia caused by disconjugate gaze, hemiparesis, and hemisensory loss may also occur in posterior circulation ischemia. Because so many long tracts and cranial nerve nuclei are so closely positioned in the brain stem, it is distinctly unusual for any of these symptoms to occur in isolation. - Also deep TIAs with clumsy hand syndrome, widespread but mild sx. - Minimial TIA workup: + neurologic examination + ECG (2% of patients with TIA have new a. fib.) (4% will have a new infarct) + brain imaging (CT or MRI) If anterior TIA: + Carotid Dopplers either stat or with excellent followup as outpatient. (89% specificity and 93% sensitivity for high-grade stenosis, using cerebral angiography as the criterion standard.) If posterior TIA: + Transcranial Dopplers. MRA is acceptable alternative to either. + If Dopplers negative, needs echo to rule out clot. - Immediate admission for further evaluation and treatment: (1) "aspirin failure" transient ischemic attack, (2) possible cardioembolic stroke (eg, atrial fibrillation), (3) "crescendo" transient ischemic attack (>3/72hrs, ramping up in severity), and (4) Johnston's "high-risk" group based on certain risk factors [Johnston SC, Gress DR, Browner WS, et al. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000;284:2901-2906.]:  Age >60 y  Diabetes mellitus  Duration of episode >10 min  Weakness during the episode  Speech impairment during the episode # of Risk Factors # of Strokes Within 90 Days, 0 0 1 3 2 7 3 11 4 15 5 34 - If a. fib and no bleed on CT: admit, anticoagulate. - If SBE, do NOT anticoagulate. - If focal neurologic deficit does not resolve within 1 hour or rapidly improve within 3 hours, the vast majority of these patients (>98%) will have a cerebral infarct. - Rx: + ASA: 50 to 325 mg daily. + United Kingdom Transient Ischemic Attack Aspirin Trial (300 versus 1,200) and Dutch Transient Ischemic Attack Trial (283 versus 30) compared low and high doses of aspirin and found no statistical difference + Aggrenox (dipyridamole + ASA): slightly better than ASA but not firstline. + Ticlopidine (e.g., Ticlid): slightly better than ASA but only for ASA failure given the side effect of neutropenia, need CBC Q2wk for 3 months after starting. [DON'T USE: KC] (Adenosine diphophate inhibitor.) + Clipidogrel (e.g., Plavix): like Ticlid but no neutropenia. + Coumadin: no better than ASA unless has a. fib. European Atrial Fibrillation Trial: 8% vs 15% CVA in Coumadin vs ASA groups (19% in placebo). [EAFT (European Atrial Fibrillation Trial) Study Group. Secondary prevention in nonrheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet. 1993;342:1255-1262.] + Heparin: bridge during hypercoagulable state when starting Coumadin. + Who to heparinize: "In one survey of 280 neurologists in the United States, 47% stated they would heparinize a patient who presented with multiple or crescendo transient ischemic attacks.72 Because there are no clear guidelines and no large, well-designed studies demonstrating a benefit to this practice, one should consider discussion with local experts before initiating anticoagulation. [Al-Sadat A, Sunbulli M, Chaturvedi S. Use of intravenous heparin by North American neurologists: do the data matter? Stroke. 2002;33:1574-1577.] "The only accepted indication for heparinization for transient ischemic attack patient is atrial fibrillation. In all other circumstances, the emergency physician should consult a neurologist." - Carotid Endarterectomy (CEA): + "existing literature falls short when establishing the appropriate time frame for CEA." + Amaurosis Fugax: low risk, can discharge for outpatient studies and readmit for CEA if appropriate as low risk of CVA in next 30 days. - Who to send home: + 5% of those with TIA had CVA within next 2 days. [Johnston SC, Gress DR, Browner WS, et al. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000;284:2901-2906.] [Lovett JK, Dennis MS, Sandercock PA, et al. Very early risk of stroke after a first transient ischemic attack. Stroke. 2003;34:e138-140.] "Johnston has subsequently recommended hospitalization if the appropriate evaluation cannot be conducted in 24 hours on an outpatient basis, which is unlikely to occur in most medical systems." [Johnston SC. Clinical practice: transient ischemic attack. N Engl J Med. 2002;347:1687-1692.] TIA Presentation Reasonable/Acceptable Patient Disposition Atrial fibrillation or flutter Admit and anticoagulate Presumed cardioembolic source Admit; urgent echocardiography Presumed carotid source Admit; urgent carotid studies and consultation Crescendo or recurrent transient Admit; consider fluid resuscitation if ischemic attack hypovolemic Johnston's "high risk" group Admit; urgent evaluation (>=3 risk factors) Amarosis fugax (transient Arrange urgent carotid imaging by monocular blindness) primary care physician and discharge on antiplatelet therapy No carotid stenosis and low Discharge on antiplatelet therapy and suspicion of embolic source arrange further urgent outpatient workup (eg, echocardiography) by primary care physician Contraindications to anti- Discharge on antiplatelet therapy and coagulation and surgery arrange close follow-up with primary care physician Transient ischemic attack Discharge on antiplatelet therapy and >1 week before ED visit arrange outpatient workup by primary care physician Complete negative evaluation Consult with primary care physician or within weeks neurologist Transient ischemic attack despite Consult with primary care physician or being on antiplatelet therapy neurologist Patient follow-up unsure for Admit for urgent evaluation social or logistic reasons Significant ambiguity as to Admit for observation, urgent evaluation, diagnosis and consultation Duration of transient ischemic Admit for observation, urgent evaluation, attack >1 h and consultation *These dispositions are the opinions of the authors and are based on analysis of the medical literature. There are no definitive data to validate either the need for admission or the safety of discharge, and the decisions must be individualized. The underlying purpose is to find and treat treatable causes of stroke before the stroke occurs. Therefore, in general, the emergency physician should have a low threshold to admit for urgent evaluation. - [Shah KH, Edlow JA.Transient ischemic attack: Review for the emergency physician. Ann Emerg Med. 2004;43:592-604.] þ Older TIA information: - acute loss of focal cerebral function with sx lass than 24 hrs, thought to be due to local ischemia. - 10-fold increased risk of CVA over 10 years - if carotid disease, 50% risk of CVA þ Johnston TIA study [Johnston et al, JAMA 2000] - 10% risk of CVA after TIA in ED, half (5%) in 48 hours after ED visit: ^ risk if + > 60 yrs, + DM, + > 10' episode, + weakness, or + speech impairment - 2.6% risk of death, 25% risk of adverse event (CVA, death, recurrent TIA, cardiovascular incident, in 90 days þ Kernan Score: [Kernan et al. The Stroke Prognosis Instrument II: Stroke 2000] þ Choice of antiplatelet agents - ASA: cheap, 13-17% risk reduction, does not important 30 mg vs. 283 mg (Farrell et all 1991) 300 vs 1200 (Dutch TIA 1991): only difference is in GI upset - ASA failures: no evidence - TICLID: more effective for secondary prevention, in some studies, but more side effects (neutropenia, thrombocytopenia, jaundice) - Plavix: more expensive, more bleeding, but no difference compared to ASA in some studies, - Persantine and ASA: up and coming - anticoagulation: + Ann Neurology 1997: ASA vs. coumadin, INR 3-4.5, stopped trial early due to bleeding + Mohr et al Stroke 2000: Coumadin helped compared to ASA + Algra et al: oral anticoagulants after TIA or minor stroke, no benefit (meta-analysis) þ Standard of Care for TIAs: - first TIA: admit, consider anticoagulation until carotid stenosis ruled out (CEM Grand Rounds 5/30/02) þ RIND: - as above, resolves in 1-2 wks. þ Mercy tPA protocol for CVA þ ASA vs. Coumadin for CVA þ Studies on CVA/Thrombolytics: - MAST-I + SK + stopped early due to safety concerns due to bleeding + but showed some longterm benefit - MAST-E + SK + higher intracranial hemorrhage (21%) in SK group + stopped early due to safety concerns + [N Engl J Med 1996;335:145-50.] - ASK study + SK + stopped early due to high mortality in those treated more than 3 hours after start of CVA + better disability outcomes in those treated early + [JAMA 1996;276:961-6.] - ECASS + European Cooperative Acute Stroke Study + rt-PA 1.1 mg/kg + heparin + patients excluded if any edema or hemorrhage on CT + many enrolled inappropriately due to misread of CT + used Barthel's/Rankin indices + shortened hospital stay + no differnece in mortality + of those inappropriately treated due to misread CT, twice as many died of a bleed + [JAMA 1995; 274:1017-25.] - NINDS study + any CVA (except if seizure) within 3 hours + tPA vs. placebo + no anticoagulants or antiplatelet agents for 24 hours. + improvment of those particularly within 90 minutes; beg difference at 3 months. + CT read by neuroradiologist. + [N Engl J Med 1995;33:1581-7.] þ A few pithy comments on the current fad for thrombolysis for strokes: þ "Brain Attack": rapid transport to ED to check for: - carotid stenosis (? stat endarterectomy) - emboli from new atrial fibrillation (anticoagulate to prevent more) - check for other problems (meningitis, SAH, hypoglycemia) - consider surgery for hemorrhagic CVA (better outcome) - trial of neuroprotective agents (e.g., fosphenytoin at Mercy) þ Initial Stroke Management - ABCs/neuro exam - EKG, CXR, CBC, platelet count, PT/PTT, lytes, glucose (ABG, ethanol, and drug screen when indicated) - IV LR or NS (NO dextrose), slow rate, and oxygen - non-contrast head CT - if suspect carotids, do emergency carotid dopplers - "stroke cocktail?" + ?heparin (see below) + low molecular weight heparin (Chinese study showed decreased mortality and dependency at six months) + ASA: NOT in acute CVA, but appropriate if it's a TIA; after CVA, may start a few days later. þ Ischemic CVA: - ABCs - treat ^BP only if: + SBP > 220 or DPB > 120 continues for 30-60 minutes + MI + aortic dissection see also HTN and CVA - load with Dilantin (and other drugs if needed) for seizures - urgent neurosurg evaluation if cerebellar infarct þ Heparin if: - Stroke in evolution - recurrent TIAs - Evidence of embolic CVA with negative head CT þ Intracerebral Hemorrhage: - ABCs - urgent neurosurg consult if cerebellar hemorrhage or acute hydrocephalus - treat ^BP if >220 systolic or >120 diastolic - if ^ICP: mannitol; consider Lasix, hyperventilation þ Subarachnoid Hemorrhage: - ABCs - neurosurgical consult - treat ^BP when higher than pre-SAH BP - start nimodipine 60 mg PO Q6H for grades 1,2,3. - treat seizures with meds, include full loading dose of Dilantin - analgesics and sedatives as needed - consider angiography, invasive hemodynamic monitoring, and early surgery. SAH grading: þ Stroke Definitions - TIA: resolves totally in 24 hours - RIND: resolves over about 3 weeks þ Stroke Background - 85% ischemic (65% thrombotic, 35% cardiogenic) - 10% hemorrhagic (1/3 SAH, 2/3 HTN) - 5% other þ NSA Consensus Statement (Stroke Clinical Updates, May 1993): þ Hyperglycemia and CVA - hyperglycemia is associated with a poor prognosis in humans. - animal studies show that induced hyperglycemia causes worse infarcts. [Browning RG, Olson DW, Stueven HA, Mateer JR. 50% destrose: Antidote or toxin? Ann Emerg Med June 1990;19:683-687.] [Yip PK, He YY, Hsu CY, Garg N, Marangos P, Hogan EL. Effect of plasma glucose on infarct size in focal cerebral ischemia-reperfusion. Neurology 1991;41:899-905.] - still not clear what's going on in humans; one study suggests human hyperglycemia is reactive to stroke. [Tracey F, Crawfor VLS, Lawson JT, Buchanan KD, Stout RW. Hyperglycaemia and motrality from acute stroke. Q J Med 1993;86:439- 446.] þ Fluids: - hypotonic fluids clearly not good. - isotonic fluids to replace fluid losses appropriate. þ SPECT vs. Xenon CT - SPECT gives only _relative_ blood flow; hard to tell if an area has low blood flow or if other areas have high flow. - Xenon CT shows absolute blood flow, thus better for CVA evaluation. þ LMW heparin - NEJM 1995 article suggests it helps þ Thrombolysis - European ECASS trial with 6 hour: no benefit - tPA with 3-hour window: some benefit