Transient Ischemic Attack
annals review article (Annals of Emergency Medicine Volume 43, Issue 5 , May 2004, Pages 592-604)
resolves within 24 hrs, if resolves in > then RIND
We probably should change this definition to one hour (Albers GW, TIA Working Group. Transient ischemic attack–proposal for a new definition. N Engl J Med 2002;347:1713-6).
First, the symptoms are acute in onset; symptoms reach maximum intensity within seconds, and all symptoms begin at the same time. Patients with migraine with aura and partial seizures, on the other hand, often present with symptoms that march from one area to another, over a period of seconds to minutes.
in differential are:
migraines with aura-symptoms typically march over 5 to 30 min
seizures-usually sx precede seizure activity though Todds can confuse
In order to be TIA, symptoms must all occur simultaneously within seconds
Kaiser TIA Study (JAMA2000; 284:2901-2906
1700 patients for 90 days after being diagnosed with TIA by the emergency physician.
Neurologist reviewed the ED chart of all patients and felt that TIA was unlikely in only 5.6% of the patients
Stroke occurred in 10.5% of patients at 90 days,
Half of the strokes occurred within the first 48 hours.
Stroke was fatal in 21% and only 7% of patients had non-disabling stroke and were not hospitalized.5 independent risk-factors for stroke:
- age greater than 60 years,
- diabetes mellitus,
- duration of episode longer than 10 minutes,
- weakness with the episode,
- speech impairment with the episode.
Risk of stroke increased with the number of risk factors, from 0% with no risk factors, to 34% with 5 risk factors. Finally, 25% of patients experienced either stroke, cardiovascular hospitalization, death, or recurrent TIA within 90 days after their TIA, and more than half of these events occurred within the first 4 days.
In a prospective cohort study, the risk of recurrent stroke after TIA was 8% at 7 days, 11.5% at one month, and 17.3% at three months. After mild stroke, the rates were 11.5%, 15%, and 18.5% respectively. (BMJ 26 Jan 2004)
In another with similar numbers (Stroke 34:e138, Aug 2003)
most recent multi-center eval showed it not to be accurate enough (Ann emerg med 2010;55(2):201)
Hemiparesis, unilateral sensory loss, visual field defect (monocular), gaze preference, aphasia, left sided neglect
carotid dopplers, or possible MRA/CTA
hemiparesis, quadriparesis, hemisensory loss or loss in all 4 extremities, crossed deficits, diplopia, disconjugate gaze, gaze palsy, nystagmus, dysarthria, vertigo, decreased LOC, limb or gait ataxia, intractable vomiting
transcranial dopplers or MRA of vertebrobasilar system.
cardiac source (acute or previous MI, AF, valvular disease, new murmur
On the other hand, if the dysphagia was prominent, or especially if the facial weakness was on the right, I’d be concerned about basilar artery ischemia
Diener HC, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet 2004;364:331-7
Young TIA Patients
headache and neck pain possible with trauma could be carotid or vertebral artery dissection
Classically in carotid dissection,
head face or neck pain
will be present
in Vertebral, occipital headache and brainstem ischemia may be the presentation.
Hypercoagulable states can also cause TIAs and strokes in this age group
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2009 AHA Recs
Class I Recommendations1. Patients with TIA should preferably undergo neuroimaging evaluation within 24 hours of symptom onset. MRI, including DWI, is the preferred brain diagnostic imaging modality. If MRI is not available, head CT should be performed (Class I, Level of Evidence B). 2. Noninvasive imaging of the cervicocephalic vessels should be performed routinely as part of the evaluation of patients with suspected TIAs (Class I, Level of Evidence A).3. Noninvasive testing of the intracranial vasculature reliably excludes the presence of intracranial stenosis (Class I, Level of Evidence A) and is reasonable to obtain when knowledge of intracranial steno-occlusive disease will alter management. Reliable diagnosis of the presence and degree of intracranial stenosis requires the performance of catheter angiography to confirm abnormalities detected with noninvasive testing. 4. Patients with suspected TIA should be evaluated as soon as possible after an event (Class I, Level of Evidence B).Class II Recommendations1. Initial assessment of the extracranial vasculature may involve any of the following: CUS/TCD, MRA, or CTA, depending on local availability and expertise, and characteristics of the patient (Class IIa, Level of Evidence B).2. If only noninvasive testing is performed before endarterectomy, it is reasonable to pursue 2 concordant noninvasive findings; otherwise, catheter angiography should be considered (Class IIa, Level of Evidence B).3. The role of plaque characteristics and detection of MESs is not yet defined (Class IIb, Level of Evidence B).4. ECG should occur as soon as possible after TIA (Class I, Level of Evidence B). Prolonged cardiac monitoring (inpatient telemetry or Holter monitor) is useful in patients with an unclear origin after initial brain imaging and electrocardiography (Class IIa, Level of Evidence B).5. Echocardiography (at least TTE) is reasonable in the evaluation of patients with suspected TIAs, especially in patients in whom no cause has been identified by other elements of the workup (Class IIa, Level of Evidence B). TEE is useful in identifying PFO, aortic arch atherosclerosis, and valvular disease and is reasonable when identification of these conditions will alter management (Class IIa, Level of Evidence B).6. Routine blood tests (complete blood count, chemistry panel, prothrombin time and partial thromboplastin time, and fasting lipid panel) are reasonable in the evaluation of patients with suspected TIAs (Class IIa, Level of Evidence B).7. It is reasonable to hospitalize patients with TIA if they present within 72 hours of the event and any of the following criteria are present:a. ABCD2 score of =3 (Class IIa, Level of Evidence C).b. ABCD2 score of 0 to 2 and uncertainty that diagnostic workup can be completed within 2 days as an outpatient (Class IIa, Level of Evidence C).c. ABCD2 score of 0 to 2 and other evidence that indicates the patients event was caused by focal ischemia (Class IIa, Level of Evidence C).
The New EMedHome Clinical Pearl is: Acute Treatment of a TIABack to top
Acute Treatment of a TIA
Emergency Physicians are accustomed to diagnosing a TIA and initiating the diagnostic work-up, usually via hospital admission. There has not been much emphasis placed on the acute treatment of a TIA.
Initial treatment of a TIA begins with optimizing potentially compromised cerebral blood flow (1). In a study of 69 patients with an acute TIA, 1/3 had evidence of a perfusion abnormality on MRI perfusion imaging (2). Changing head position is a simple, often overlooked measure to increase cerebral perfusion. Studies using transcranial Doppler monitoring have shown that flow velocity in the MCA can increase 20% when head position is lowered from 30° to 0° (3). Some patients will have demonstrable recovery of neurologic deficits when positioned flat, particularly in cases of large vessel occlusion or high-grade stenosis.
In the setting of acute cerebrovascular ischemia, cerebral autoregulation may be impaired, and cerebral perfusion, particularly in regions dependent on collateral blood flow, may be directly dependent on systemic blood pressure. Isotonic IV fluids should be given to ensure euvolemia and maintain intravascular volume. A 500-mL bolus of NS followed by 100 – 150 mL/hour is reasonable for patients without heart failure (1).
Antithrombotic therapy should be started once neuroimaging, typically CT, has excluded cerebral hemorrhage. There is very little data from randomized trials specifically involving treatment of TIA; a larger amount of data exists for ischemic stroke, and it is logical to extrapolate the benefits of aspirin to TIA. However, there are 2 reasons why aspirin may be of even greater benefit with a TIA: (1) It is likely that patients with TIA have a lower risk of bleeding complications compared with patients with stroke and (2) the risk of early recurrent stroke is higher in patients with TIA than completed ischemic stroke, such that interventions might have a greater treatment effect.
References:(1) Cucchiara B, Ross M. Transient ischemic attack: risk stratification and treatment Ann Emerg Med 2008;52(2):S27-39.(2) Krol AL, et al. VSG Perfusion MRI abnormalities in speech or motor transient ischemic attack patients Stroke 2005;36:24872489.(3) Wojner-Alexander AW, et al. Heads down: flat positioning improves blood flow velocity in acute ischemic stroke Neurology 2005;64:13541357.
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