After The Diagnosis Of TIA – Determining The Urgency Of The Workup

Two days ago I watched and studied the TIA Rapid Review videos from Emergency Medicine Cases and linked to them. Resource (1)

Today, I review and post excerpts from Emergency Medicine Cases podcast and shownotes Episode 6: Transient Ischemic Attack [Resource (2)] which is the basis of Rapid Review Videos referenced in the previous post.  For me, the most important points in the resource are the following from Episode 6:

Acute TIA management

  • Maximize cerebral blood flow by rehydrating dehydrated patients, and by resisting the urge to rapidly lowering the blood pressure
  • Antiplatelet medications (decreases the risk of stroke – and MI – by 1/4)
  • ASA should almost always be the first option, and given as soon as there is no bleed as confirmed by CT head, with loading dose of 160‐325mg NON‐enteric coated chewed, then 81mg dailyIn severe ASA allergy, Clopidogrel is the only choice
  • If ASA failure (ensure compliance first), Plavix™ and Aggrenox™ are equally effective and at least as good as ASA, but Plavix™ has a better side‐effects profile
  • Plavix™ (Clopidogrel) should be given either as a loading dose of 300mg (onset of action 6‐7hrs) then 75mg daily, or overlapped with ASA for 3‐4d if no loading dose is given (onset of action 3‐4d); do not combine ASA + Clopidogrel for extended periods as the risks of major bleeding and ICH outweight the benefits (MATCH trial)
  • Aggrenox™ (dipyridamole 200mg + ASA 25mg) should be given BID, but patients should be warned of the frequent severe headaches accompanying the medication, and therefore should be directed to take acetaminophen with the first few doses
  • Heparin should probably never be started by the EP (even in the setting of a.fib), except possibly in crescendo TIAs with suspected critical carotid artery stenosis or tight basilar artery occlusion in consultation with a neurologist

Vascular Imaging (NASCET trial)

Essential to organize early imaging (1‐3d max) given that carotid endarterectomy (CEA) performed within 2wks of TIA gives an absolute risk reduction (ARR) of 30%, or a number needed to treat (NNT) of 3 – unparalleled in terms of benefit compared to other treatments we can offer; early treatment is crucial given that the ARR drops to 16% if CEA is performed 2‐4wks after TIA, and close to 0% if after 4 weeks; interestingly, the benefit of early CEA seems to drop in women after3wks, emphasizing the need for prompt treatment
Consider CTA if there is no renal dysfunction nor allergies to contrast, especially in a convincing TIA story or concern for dissection (the vascular imaging will be done immediately and admission will be considered, as opposed to a few‐days outpatient management); carotid Doppler, although still good, cannot assess intracranial circulation and is an imprecise measure in certain cases
Echocardiography: lower priority test as the yield is low, especially if there is no known cardiac disease; consider it in patients for which there is no explanation of the TIA/stroke  [and especially if the patient has silent infarcts in different vascular territories on diffusion weighted MRI. TW]

Transient Ischemic Attack is a clinical diagnosis based on the patient’s history as the patient will almost certainly be normal by the time he or she presents to the clinician. Pts with a TIA are at increased risk of a stroke especially immediately after the TIA. So once you determine that the episode is a TIA and not a TIA mimic, attention shifts to trying to prevent a stroke. First you need to determine the etiology of the stroke. And then you need to begin preventive treatment depending on the etiology of the TIA:

So to determine the etiology of the TIA, you will want to order:

  • A CT scan of the head to rule out intracranial hemorrhage.
  • An electrocardiogram to look for evidence of an arrythmia or of heart damage.
  • A CT angiogram to look for evidence of carotid and/or intracerebral vascular disease.
    • Carotid duplex scan is okay but it won’t give any information about the intracranial vessels and it won’t necessarily demonstrate internal carotid artery dissection (an etiology in younger patients) that often occurs at a level above what the carotid duplex can see.
  • A diffusion weighted MRI of the brain to look for previous clinically silent cerebrovascular accidents.
    • Previous silent CVAs in several different vascular territories might be a clue that the heart is the etiology of the TIA and silent stroke.
      • In this case you might want to get a stat transthoracic echocardiogram or even an esophageal echocardiogram.
  • Laboratory tests including CBC, ESR, Chem 21, and perhaps others depending on clinical circumstances.

The key question is how urgently do the above tests, if indicated, need to be obtained.


[11-23-2018: The ABCD2 Score should no longer be used for the determination of the urgency of evaluation. Please see Ep 117 TIA Update – Risk Stratification, Workup and Dual Antiplatelet Therapy November 2018 from Emergency Medicine Cases.

Patients who have had a TIA are at increased risk of a stroke especially immediately after the TIA. It is critical to determine the urgency of evaluation because we can’t begin the appropriate preventive stroke treatment until we know the etiology.



The higher the risk, the more urgently the evaluation must be performed.]


The following are more excerpts from Episode 6: Transient Ischemic Attack: Resource (2)

TIA classification and tests (rule of 4s – 4 types and 4 investigations)

 Types of TIA Appropriate investigations
Cardioembolic (1/4 of TIAs) ECG: Look for a.fib (12‐16% of stroke) and other cardiac problems that might cause embolic phenomena from the heart: CHF, recent MI, left ventricular aneurysm, rheumatoid heart disease, valvular disease); if the ECG looks like acute MI and a severe headache ispresent, think of ICH and SAH
Lacunar (small arteries) TIAs (1/4 of TIAs)

  • Classically: pure motor and pure sensory, or mixed‐motor‐sensory but without cortical findings (below)
Unenhanced CT head: To rule out TIA mimics (tumor, SDH, ICH, SAH – especially given that ASA will be given), and see old strokes
Large arteries in neck, brain (1/4 of TIAs)

  • Cortical findings: aphasia (sometimes mistaken for confusion) means left hemispheric involvement; neglect means right‐hemispheric involvement; visual disturbances (field cuts)
Vascular imaging: Organize for carotid Doppler in the neck 1‐3d maximum, or consider adding CT‐angiogram to CT head (which can assess for intracranial arteries) – see discussion below
Other TIAs (1/4 of TIAs)

  • Intracranial hemorrhages (15%), cryptogenic, clotting diosrders, PFOs
Blood: Accucheck and blood work (CBC, lytes and blood sugar, BUN, Cr, INR)

Other important causes of TIA:

  • Carotid dissection: young patient with no risk factors, especially if associated with trauma or sudden, rapid movement of the neck, neck pain (anterior pain in carotid dissection, posterior pain in vertebral dissection), vertigo or headache
  • Endocarditis: unwell for weeks, flu‐like symptoms, recurring fever, weight loss, and headache


(1)  “TIA Parts 1 and 2” From EMC’s Awesome Rapid Reviews Videos
Posted on August 19, 2017 by Tom Wade MD

(2) Episode 6: Transient Ischemic Attack from Emergency Medicine Cases

(2) Diagnosis of Transient Ischemic Attack (TIA) Using the ABCD2 Score from the Ischemic Stroke Module of the Emergency Neurological Life Support Course
Posted on September 11, 2015 by Tom Wade MD

(1) 2014 Preventing Stroke In Pts With Stroke and Transient Ischemic Attack (TIA) And References That Cite The Article Posted on March 5, 2016 by Tom Wade MD



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