Both antiplatelet and anticoagulant therapy are often considered in the acute therapy of ischemic stroke, and one or both may be appropriate, but randomized trials have shown that anticoagulants should not be routinely employed acutely. Trials have shown that antiplatelets have only a modest benefit, and no studies have yet shown the benefit of urgent antiplatelet treatment.
Acute antiplatelet therapy
Aspirin for acute stroke has been shown to be effective, though only marginally, when studied in thousands of patients.5,6*
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Acute therapy and optimization of neurological status 17
Table 3.1.Approach to arterial hypertension in acute ischemic stroke.
Indication that patient is eligible for treatment with intravenous rtPA or other acute reperfusion intervention
Blood pressure level
Systolic > 185 mm Hg or diastolic > 110 mm Hg
Labetalol 10 to 20 mg IV over 1 to 2 minutes, may repeat × 1 or
Nitropaste 1 to 2 inches or
Nicardipine infusion, 5 mg/h, titrate up by 2.5 mg/h at 5- to 15- minute intervals, maximum dose 15 mg/h; when desired blood pressure attained, reduce to 3 mg/h
If blood pressure does not decline and remains > 185/110 mm Hg, do not administer rtPA
Management of blood pressure during and after treatment with rtPA or other acute reperfusion intervention
Monitor blood pressure every 15 minutes during treatment and then for another 2 hours, then every 30 minutes for 6 hours, and then every hour for 16 hours
Blood pressure level
Systolic 180 to 230 mm Hg or diastolic 105 to 120 mm Hg Labetalol 10 mg IV over 1 to 2 minutes, may repeat every 10 to 20 minutes, maximum dose of 300 mg
or
Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min Systolic > 230 mm Hg or diastolic 121 to 140 mm Hg
Labetalol 10 mg IV over 1 to 2 minutes, may repeat every 10 to 20 minutes, maximum dose of 300 mg
or
Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min or
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18 Ischemic stroke
Antiplatelet treatment beyond aspirin is driven by evidence from acute cardiovascular trials until there are more stroke data available, remembering of course the greater propensity of the brain to develop hemorrhagic complications.
We give aspirin 81–325 mg to most patients. In patients who have had strokes or TIAs while already on antiplatelet therapy, who have afluctuating neurological course, or who have a heavy burden of atherosclerotic risk factors or atherosclerotic lesions, we will often orally load the patient in the emergency department with clopidogrel (Plavix) 375 mg, and then aspirin 81 mg and clopidogrel 75 mg once daily for thefirst few days. The idea of an oral load stems from studies in patients undergoing coronary procedures who have less peri-procedural ischemic complications if they receive a load pre-procedure. We then switch to aspirin alone,* or aspirin/dipyridamole combination (Aggrenox, Asasantin),* or clopidogrel alone* if the patient is going home on antiplatelets.
Acute anticoagulant therapy
Anticoagulation for acute ischemic stroke has never been shown to be effective.5Even among those with atrialfibrillation, the stroke
Table 3.1.(cont.)
Management of blood pressure during and after treatment with rtPA or other acute reperfusion intervention
Nicardipine infusion, 5 mg/h, titrate up to desired effect by increasing 2.5 mg/h every 5 minutes to maximum of 15 mg/h
If blood pressure not controlled, consider sodium nitroprusside Source:Adams HP Jr, del Zoppo G, Alberts MJ,et al., Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association.Stroke2007;38: 1655–
711.1Reproduced with permission from Lippincott Williams & Wilkins.
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Acute therapy and optimization of neurological status 19
recurrence rate is only ~5–8% in thefirst 14 days, which is not reduced by early acute anticoagulation.7,8* Anticoagulation is mostly used for long-term secondary prevention in patients with atrialfibrillation and cardioembolic stroke at this point.
Without convincing supporting data, some clinicians advocate acute anticoagulation with heparin in certain cases. These include patients with a cardioembolic condition at high risk for recurrence (thrombus on valves, or mural thrombus), documented large- artery (ICA, MCA, or basilar artery ) occlusive clot at risk for distal embolism, arterial dissection, or venous thrombosis. Such patients may be started on heparin acutely and transitioned to warfarin (Coumadin). If ordering heparin, use weight-adjusted algorithm withnobolus*. Enoxaparin (Lovenox) at 1 mg/kg subcutaneously every 12 hours may be used in place of heparin.
Most patients who need long-term anticoagulation with warfarin and related coumarin derivatives might not need adjusted heparin or enoxaprin to“bridge”until INR reaches the goal level.
Observational study has indicated higher risk of hemorrhagic conversion with heparin“bridging.”9
How long should you wait before starting anticoagulation? There are no clear data on this topic. There is concern that the risk of hemorrhagic conversion is increased with anticoagulation, particularly in patients with large strokes. Hemorrhagic transformation is frequent in the evolution of large infarcts, especially those that have been reperfused either by spontaneous recanalization or with thrombolytics. One should be particularly careful about early anticoagulation in these patients. One generally waits 2–14 days before starting anticoagulation, the specific duration depending on the urgency of the indication versus the risks. You must carefully weigh the risks and benefits on a case by case basis, andnever start anticoagulants without obtaining brain imaging first, to exclude ongoing hemorrhagic evolution or brain swelling.
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20 Ischemic stroke