When a patient presents with acute focal neurologic deficits consistent with ischemic stroke, the immediate goal is to determine whether the patient is eligible for reperfusion therapies with intravenous thrombolysis (tissue plasminogen activator, tPA) and/or endovascular therapy with mechanical thrombectomy (MT). Assessment is based on clinical symptoms which are typically assessed with the National Institutes of Health Stroke Scale (NIHSS), timing, and neuroimaging. A detailed description of the NIHSS can be found in Appendix 2. Evaluation and treatment decisions must be made as quickly as possible, keeping in mind the mantra that “time is brain”—there is clear evidence that faster treatment results in a greater likelihood of neurologic recovery.
A focused history should establish the time of symptom onset. When the exact time of symptom onset is unclear, the time at which the patient was last known normal should be used. The NIHSS serves as a rapid neurologic exam to quantify the neurologic deficit. A fingerstick glucose should be checked to ensure hypo- or hyperglycemia is not causing a stroke mimic.
In patients with mild, non-disabling deficits, the risk of thrombolytic therapy likely outweighs the benefit, so withholding tPA is reasonable. No specific threshold value of the NIHSS can discriminate between disabling and non-disabling deficits, therefore clinical judgment in the individual patient is required.
Patients within 4.5 hours of the time last known normal may be eligible for intravenous (IV) thrombolysis. Noncontrast head computed tomography (CT) can exclude hemorrhage. IV tPA exclusion criteria should be quickly assessed (see Table 41.1), and tPA should be administered as rapidly as possible if the deficit is perceived to be disabling (see Table 41.1 in Appendix 1). If blood pressure elevation precludes tPA, administer IV antihypertensive medication such as labetalol or nicardipine to achieve an acceptable blood pressure. It is not necessary to wait for the results of laboratory testing other than fingerstick glucose unless the patient is on anticoagulation (if on warfarin, international normalized ratio [INR] > 1.7 precludes tPA) or has a clinical history raising suspicion of thrombocytopenia (e.g., sepsis, malignancy).
A patient with a severe deficit and a contraindication to tPA may benefit from MT, so CT angiogram (CTA) should be obtained to evaluate for large vessel occlusion. Depending on workflow, CTA may also be obtained with the initial CT in order to speed evaluation.
When > 4.5 hours from onset, tPA should not be given, but if significant neurologic deficit is present, then rapid CTA (MRA is also acceptable, though generally more time-consuming) should be used to assess for the presence of a large vessel occlusion, in which case MT should be considered. When < 6 hours from onset, perfusion imaging is generally not necessary.
In the 6–24-hour time window, if large vessel occlusion is present, perfusion imaging should be performed to identify patients that are likely to benefit from MT (small infarct core and large territory at risk).
If occlusion of the internal carotid artery (ICA) or proximal middle cerebral artery (MCA) is identified, MT should be pursued in patients with significant deficits < 6 hours from onset unless there is extensive ischemic injury on CT. In the 6-24-hour window, results of perfusion imaging should be considered in making an assessment of potential benefit of treatment. Thrombectomy for basilar artery occlusion has not been well studied, but given the severity of the disease, it is reasonable to treat based on similar principles. If no large vessel occlusion is present, the patient is not eligible for MT.
Beyond 24 hours, the benefit of MT is uncertain; urgent CTA is appropriate if there is symptom fluctuation or progression.
Patients that receive reperfusion therapy warrant intensive monitoring per a standard protocol, particularly during the first 24 hours, due the risk of intracranial bleeding. A blood pressure goal of < 180/105 mmHg is appropriate. Antithrombotic therapy and deep vein thrombosis prophylaxis should be withheld for 24 hours following IV tPA, until head imaging confirms there is no hemorrhage. After MT, antithrombotic therapy can be started immediately if the risk of procedural bleeding complications is felt to be low; this is often assessed with a repeat head CT postprocedure to exclude intracranial bleeding.
In patients not treated with tPA or MT, early administration of aspirin is indicated to reduce the risk of recurrent stroke. Within the first 24 hours of symptom onset, patients with minor stroke should be treated with combination aspirin and clopidogrel, assuming no contraindication, for 21 days, then switched to antiplatelet monotherapy.
Aggressive intravenous hydration should be administered to all stroke patients unless there is concern for heart failure. Positioning the head of bed flat may improve cerebral blood flow in some patients. Formal dysphagia screening should be performed prior to allowing oral intake.