An Update on Transient Ischemic Attacks

Janice Hinkle

Disclosures

J Neurosci Nurs. 2005;37(5):243-248. 

In This Article

Abstract and Introduction

Abstract

Each year in the United States 200,000–500,00bstract: 500,000 people have a transient ischemic attack (TIA). These episodes of brief neurologic deficits were thought to be fairly benign, but this view is changing. In 2002, a new definition for TIA was proposed, and a more intensive diagnostic workup recommended to look for a probable cause of the transient neurologic deficit. Implementation of prevention strategies is essential because the risk of a stroke following a TIA is approximately 30% within 5 years. These changes have important implications for nursing care and patient advocacy. In addition, patient and family education must be addressed by the entire healthcare team.

Introduction

Current estimates are that between 200,000 and 500,000 people have transient ischemic attacks (TIA) each year in the United States (Johnston, 2002). Approximately 5 million adults in the United States have had a transient ischemic attack (TIA), and many are undiagnosed (Johnston et al., 2003). These episodes of a sudden, brief neurologic deficit used to be thought of as fairly benign events. In 2002, a new pathophysiologically based definition was proposed for TIAs. The current evaluation, including laboratory and diagnostic tests, is aggressive and intensive. These changes have important implications for nursing care, patient advocacy, and pertinent patient and family teaching.

Many changes have occurred in the last two decades regarding TIAs. This article provides a historical perspective on the evolution of the definition of TIA and reviews the associated pathophysiology and symptoms. The laboratory and diagnostic tests a neuroscience nurse can expect in the evaluation of a patient following a TIA are identified. Nursing interventions a neuroscience nurse needs to use in the emergency department (ED) and during inpatient stay for TIA also are addressed. Patient and family teaching regarding modifiable risk factors associated with a TIA are an important component of care.

Historical Perspective

The definition of TIA as a time-based event was discussed in the 1950s and 1960s when the proposed temporal criteria varied widely (Albers et al., 2002). A National Institutes of Health committee on the classification of cerebrovascular disease suggested in 1958 that a TIA could last several hours, but typically ranged from a few seconds to 10 minutes; the upper duration was 1 hour (Winn, 2004).

In 1964, Acheson and Hutchinson reported their observations of 82 patients with what was then referred to as episodes of transient cerebral ischemia. In this study, which took place before computed tomography (CT), there was a predominance of males over females and a mean age of 56 years (Acheson & Hutchinson, 1964). Forty of the episodes were classified as TIA, using the time frame of less than 1 hour (Acheson & Hutchinson). The authors noted that little was known about the natural history of TIA at that time.

The 1975 classification of cerebrovascular diseases defined TIA as lasting up to 24 hours (National Institute of Neurologic Diseases and Stroke ad hoc Committee on Cerebrovascular Diseases, 1975). Dyken and colleagues (1977) reported on a large cooperative study of hospital frequency and characteristics of TIAs. TIAs were then acknowledged as a warning sign of an impending stroke. This study, funded by a National Institute of Neurological Diseases and Stroke contract in 1972, gathered data on 1,323 patients with TIA-like symptoms at six major medical institutions (Dyken et al., 1977). Sixty-six percent of patients who had carotid artery symptoms and 63% of those who had vertebral artery symptoms were male; the median age was 63 years and 7% were African American (Dyken et al.). The median duration of the TIA was 14 minutes for those with carotid artery symptoms and 8 minutes for those who had vertebral artery symptoms. The majority of TIAs (90%) in the study were reported to have cleared within 10 minutes.

Levy (1988) reported on 1,343 hospitalized patients included in a database of patients with TIA (defined as acute neurologic changes resolving within 24 hours of onset), reversible ischemic neurological deficit (defined as resolving between 24 hours and 4 weeks of onset), and ischemic stroke. Fifty six percent of the patients were male with a mean age of 66 years (Levy, 1988). In 382 patients, TIA was diagnosed and of these 191 (50%) had episodes that lasted less than 30 minutes, and 9% had symptoms that lasted 30–60 minutes. These authors suggested less than 24 hours as the longest permissible duration for TIA. Understanding the natural history of TIAs was becoming more important as the pilot studies using intravenous (IV) tissue plasminogen activators (t-PA), such as Activase, for ischemic stroke were taking place. Differentiating between patients for whom early treatment would bring favorable clinical outcomes or those for whom it could cause harm became more important with a potential therapy on the horizon.

Werdelin and Juhler (1988) reported on 78 patients admitted to hospital with their first episode of presumed ischemic origin to decide whether the differential diagnosis of stroke versus TIA could be made earlier than 24 hours. Within the first hour, 50% of TIA patients had recovered; 90% recovered within 4 hours. CT scans obtained on half of the patients with TIA showed infarction in two, multiple infarctions in one, and no infarction in the remainder of the cases (Werdelin & Juhler).

The 1990s brought a flurry of algorithms and clinical guidelines to assist healthcare practitioners in managing TIAs. Brown and colleagues (1994) published a costeffective, scientifically based algorithm for the evaluation and treatment of TIA and minor ischemic stroke. That same year the stroke council of the American Heart Association (AHA) published guidelines for the management of TIAs (Feinberg et al., 1994). In 1999 these guidelines were updated to include prevention strategies (Wolf et al., 1999). That same year a supplement to the AHA guidelines, which addressed risk-factor modification and provided an update of TIA medical and surgical management, was published (Albers, Hart, Lutsep, Newell, & Sacco, 1999).

TIA is still defined as a “neurological deficit lasting less than 24 hours that is attributed to focal cerebral or retinal ischemia’ (Johnston, 2002, p. 1687). The 24-hour time limit is arbitrary, was adopted before the widespread availability of neurodiagnostic studies, and remains debatable (Albers et al., 2002; Dyken et al., 1977; Fisher, 2002; Levy, 1988). Disadvantages of time-based TIA definitions include the following:

  • the suggestion that TIA symptoms are benign

  • the promotion of diagnosis based on a temporal course rather than pathophysiology

  • delays in interventions for acute cerebral ischemia because the definition inaccurately predicts the presence or absence of ischemic brain injury

  • overlooking the distinction between angina and myocardial infarction (MI); angina is a symptom of MI (Albers et al., 2002).

Because of these limitations a new diagnostic description was proposed: A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of acute infarctions (Albers et al., 2002). The advantagesof this new definition are that it is based on the presence or absence of a biologic end point, indicates that transient ischemic symptoms can cause permanent brain injury, encourages use of neurodiagnostic tests to identify brain injury and its cause, more accurately reflects the presence or absence of ischemic brain injury, and is more consistent with the distinction of angina as a symptom of MI (Albers et al.). The current consensus is that TIA is not a benign event and should not be ignored (Daffertshofer, Mielke, Pullwitt, Felsenstein, & Hennerici, 2004).

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