Transient Ischaemic Attack in the Acute Setting – Diagnosis, Management and Treatment

Transient Ischaemic Attack in the Acute Setting – Diagnosis, Management and Treatment

Bhatt Archit, Glynn Ted, Reeves Mathew J
European Neurology - Volume 3 Issue 2
US Neurology - Volume 4 Issue 2
Published: March 2009
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More than 700,000 acute strokes1 and 300,000 transient ischaemic attacks (TIAs)2,3 occur annually in the US. It is estimated that between 15 and 26% of acute stroke cases have a prior history of TIA.4 TIAs are important because they are associated with high short-term risk of both stroke and cardiac events. In a widely quoted emergency department (ED) study of over 1,700 TIA cases from California, the three-month stroke risk was found to be 10.5%.5 A recent meta-analysis of 11 TIA cohort studies found that the summary estimate for the 90-day stroke risk was 9.2% – very similar to the Californian study.6 This meta-analysis also confirmed that most of this stroke risk occurs in the first few days after the TIA event; the risk of stroke was 3.5% at two days and 8.0% at 30 days.6 Similar findings were found in another recent meta-analysis of 18 cohort studies, which estimated that the seven-day risk of stroke was 5.2%.7 Patients with TIA are also at high risk of other cardiovascular events. In a meta-analysis of 39 cohort studies, the annual risk of myocardial infarction and non-stroke vascular death following TIA was 2.2 and 2.1%, respectively.8 These studies, which serve to illustrate the high risk of cardiovascular events following a TIA, suggest that patients suspected of having a TIA event require an expedited clinical work-up. Historically, TIA has been defined on the basis of focal neurological deficits due to transient and reversible cerebral or retinal hypoperfusion lasting for less than 24 hours.9 However, because the duration of symptoms for most TIAs is much less than 24 hours – typically less than TIA10 – there has been a proposed change in the definition of TIA to include only cases with a symptom duration of less than one hour.11,12 The advent of diffusion-weighted imaging (DWI) technology adds further challenges to the traditional definition of TIA – up to 50% of TIA patients ave DWI abnormalities indicating ischaemic changes.13–15 The presenceof positive DWI changes in TIA cases has been shown to be associated with longer symptom duration (>60 mins), the presence of speech disturbance, atrial fibrillation and ipsilateral carotid stenosis.13

Accuracy of Transient Ischaemic Attack Diagnosis in the Urgent Setting
The diagnosis of TIA has always been a clinical challenge even for neurologists. Two carefully conducted diagnostic studies undertaken in outpatient or non-acute settings demonstrated that the inter-rater agreement among neurologists for the diagnosis of TIA was actually good (kappa = 0.65–0.77).16,17 In one study of 56 patients, the overall agreement for TIA diagnosis between pairs of neurologists who each interviewed the patients was very high (85%; n=48).16 In the other study evaluating the validity of TIA diagnosis in 72 patients, the overall agreement between neurologists was also very high (88%; n=64).17 However, many cases of TIA present to the ED, where an ED physician rather than a neurologist evaluates them. Achieving optimal diagnostic accuracy for TIA is even more challenging in the ED setting. The reported accuracy of TIA diagnosis among non-neurologists is quite variable, with overall agreement rates varying between 39 and 67%.18–21 In a recent study of 100 hospitalised patients who had a presumptive ED-based diagnosis of TIA, a retrospective chart review by two stroke neurologists found that 60% were misdiagnosed.22 However, such results should not be interpreted as necessarily reflecting the clinical skills of neurologists and ED physicians; rather, these data are a reflection of the fact that more complete and definitive diagnostic information (e.g. brain imaging, carotid imaging) is typically not obtained until after the patient is admitted to the hospital.22 Difficulties in making an accurate diagnosis of TIA in the ED setting arise from several factors. First, time constraints resulting from prehospital delays23,24 and rapid triage and assessment requirements make the process especially difficult in a busy ED. Second, differentiating common stroke mimics from TIA can be difficult, particularly for nonstroke physicians.25 Even differentiating TIA from ischaemic stroke can be challenging when reliable information on the exact onset time of symptoms is lacking. Third, terms such as ‘TIA’, ‘TND’ (transient neurological deficits), ‘mini stroke’ and ‘minor stroke’, which may signify different underlying pathology and aetiology, are often liberally applied in the ED setting, and may or may not identify a patient who meets the formal definition of TIA (i.e. transient focal neurological symptoms of <24 hours’ duration). Fourth, the frequent use of terms such as ‘rule-out TIA’, ‘suspect TIA’, ‘possible TIA’ or ‘TIA/stroke’ in the ED setting may reflect either a reluctance on behalf of the ED physician to make a definitive diagnosis based on limited clinical information, and/or the inherent difficulty in ruling out alternative diagnoses in the limited time available. Finally, and perhaps most importantly, the recent emphasis on the rapid identification and evaluation of TIA cases in the ED setting means that the target population of interest shifts from confirmed TIA cases to ‘suspect TIA’ cases,26 who may or may not have a final diagnosis of TIA. This shift in focus makes the appropriate identification of suspect TIAs, as well as the confirmation of their true TIA status, even more challenging.

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Keywords:
Atrial Fibrillation, Carotrid Artery Stenosis, Carotid Endarterectomy, Transient Ischemic Attack, Transient Ischaemic Attacks, Ischemic Attack Symptoms, Acute Ischemic Attack, Temporary Ischemic Attack

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