Once a clinical diagnosis of TIA is made, an ABCD2 score (age, blood pressure, clinical features, duration of TIA, presence of diabetes) can be used to predict the short-term risk of subsequent stroke (see Table 2).6,7 A general rule of thumb is to admit patients who present within 72 hours of the event and have an ABCD2 score of three or higher for observation, work-up, and initiation of secondary prevention.1
Although only a small percentage of patients with TIA will have a stroke during the period of observation in the hospital, this approach may be cost effective based on the assumption that hospitalized patients are more likely to receive intravenous tissue plasminogen activator.8 The decision should also be guided by clinical judgment. It is reasonable to admit a patient whose diagnostic workup cannot be rapidly completed.1
The workup for TIA includes routine labs, EKG with cardiac monitoring, and brain imaging. Labs are useful to evaluate for other mimics of TIA such as hyponatremia and glucose abnormalities. In addition, risk factors such as hyperlipidemia and diabetes should be evaluated with fasting lipid panel and blood glucose. The purpose of EKG and telemetry is to identify MI and capture paroxysmal AF. The goal of imaging is to ascertain the presence of vascular disease and to exclude a non-ischemic etiology. While less likely to cause transient neurologic symptoms, a hemorrhagic event must be ruled out, as it would trigger a different management pathway.
Imaging for TIA
There are two primary modes of brain imaging: computed tomography (CT) and MRI. Most patients who are suspected to have had a TIA undergo CT scan, and an infarct is seen about 20% of the time.1 The presence of an infarct usually correlates with the duration of symptoms and has prognostic value. In one study, a new infarct was associated with four times higher risk of stroke in the subsequent 90 days.9 Diffusion-weighted imaging, an MR-based technique, is the preferred modality when it is available because of its higher sensitivity and specificity for identifying acute lesions.1 In an international and multicenter study, incorporating imaging data increased the discriminatory power of stroke prediction.10
Extracranial imaging is mandatory to rule out carotid stenosis as a potential etiology of TIA. The least invasive modality is ultrasound, which can detect carotid stenosis with a sensitivity and specificity approaching 80%.1 While both the intra- and extracranial vasculature can be concurrently assessed using MR- or CT-angiography (CTA), this is not usually necessary in the acute setting, because only detecting carotid stenosis will result in a management change.1
Carotid endarterectomy is standard for symptomatic patients with greater than 70% stenosis and is a consideration for symptomatic patients with greater than 50% stenosis if it is the most probable explanation for the ischemic event.11 Despite a comprehensive workup, about 50% of TIA cases remain cryptogenic.12 In some of these patients, AF can be detected using extended ambulatory cardiac monitoring.12
The goal of admitting high-risk patients is to expedite workup and initiate therapy. Two studies have shown that immediate initiation of preventative treatment significantly reduces the risk of stroke by as much as 80%.13,14 Unless there is a specific indication for anticoagulation, all TIA patients should be started on an antiplatelet agent such as aspirin or clopidogrel. A large randomized trial conducted in China and published in 2013 demonstrated that dual antiplatelet therapy with aspirin and clopidogrel for 21 days, followed by clopidogrel monotherapy, reduced the risk of stroke compared to aspirin monotherapy. An international multicenter trial designed to test the efficacy of short-term dual antiplatelet therapy is ongoing, and if the benefit of this approach is confirmed, this will likely become the standard of care. Evidence-based indications for anticoagulation after TIA are restricted to AF and mural thrombus in the setting of recent MI. Patients with implanted mechanical devices, including left ventricular assist devices and metal heart valves, should also receive anticoagulation.15