transient ischemic attacks- advances in diagnosis & mx

Transient Ischemic Attacks:Advances in Diagnosis and Management

in the Emergency Department

Dr Sazwan RSEmergency Physician, HoSHAS

Temerloh

• Definitation: “episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a 24 hours; they leave no persistent neurologic deficit” Advisory Council for the National Institute of Neurological and Communicative Disorders and Stroke. A classification and outline of cerebrovascular diseases,II. Stroke 1975;6:564–616

• It is estimated that 30% of the events that were previously diagnosed as TIA actually have infarcted brain.

Sacco RL, Kasner SE, Broderick JP, et al, American Heart Association Stroke Council, Council on Cardiovascular Surgery and Anesthesia. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:2064–89.• New definition of TIA has evolved into a tissue-based

definition: “transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.”

Stat CT Brain?

• CT is not nearly as sensitive as MRI and may require 12 hours after the event to demonstrate injury.

• MRI more sensitive and more specific for acute injury and turns positive much sooner.

• Although most TIAs last less than 1 hour, up to 50% of patients with TIA lasting 1 to 24 hours have negative MRI, confirming the absence of stroke.

TIA- tissue base defination

Nondisabling stroke• transitory presence of

neurologic symptoms with mild (National Institutes of Health Stroke Scale 3) to absence of persistent clinical deficits in the presence of imaging evidence of necrosis.

Silent stroke• is the radiologic finding of

cerebral necrosis without neurologic findings.

Risk of developing stroke

• Early outcome studies on the risk of stroke after TIA estimated an incidence of 3% to 10% at 2 days and 9% to 17% at 90 days.

Mozaffarian D, Benjamin EJ, Go AS, et al, American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics– 2015 update: a report from the American Heart Association. Circulation 2015;131(4):e29–322

Etiology• Cardioembolic

etiologies approximately 34% of TIAs.

• artery occlusion/disease (10%–18%)

• large artery atherothrombosis (9%–13%)

• other causes (3%–6%).

Look hard for etiology!!

• Cardioembolism has been associated with severely debilitating strokes, and is an independent predictor of mortality.

• Atrial fibrillation is the most common cause, has a highly variable average annual risk of first-time stroke in patients who are not anticoagulated.

High priority to rule out

• hypoglycemia,• Stroke• central nervous system (CNS) mass lesions• CNS vasculitis• CNS infections • hypokalemia (Although rare, has been

reported in case reports to present with focal deficits)

History

Negative symptomsA loss of a function:• such as motor (weakness),• speech (decreased or

altered speech)• visual (diminished vision)• sensation (anesthesia)

(suggest ischemia or infarction)

Positive symptomsPresence of something that is not normal:• such as motor (involuntary

motions)• speech (increased volume of

incomprehensible speech)• visual (flashes of light or

scintillating scotoma)• sensation (dysesthesias), and

sometimes pain

(suggest migraine or seizure-related diagnoses)

History

“if the symptoms have not resolved, TIA cannot be diagnosed and the patient should be assumed to have a stroke, or a stroke mimic”• “dizziness,” which, at least in the case of

vertigo, is a positive symptom and can be due to posterior circulation ischemia; in particular, even without any other neurologic sign, it has been associated with TIA or stroke in 0.7% of dizzy patients”

• Most TIAs are brief, most lasting less than 1 hour; in up to 50% of patients with symptoms lasting more than 1 hour, radiologic evidence of infarction can be found.

• Physical examination: Normal in full CNS examination

• Lab investigation : FBC -> thrombocytosis

Cardiac assessment

• An electrocardiogram (ECG) is recommended to assess for a cardioembolic mechanism, including atrial fibrillation, ventricular hypertrophy, or signs of cardiac ischemia (Class of evidence IB).

• Transthoracic echocardiography (TTE) is used to assess for evidence of cardiac hypertrophy, ventricular hypokinesis or thrombus, mitral stenosis, and valve disease (Class of evidence IIaA).

Brain Imaging

• The 2013 ASA guidelines state that patients with transient ischemic neurologic symptoms should undergo neuroimaging evaluation within 24 hours of symptom onset or as soon as possible in patients with delayed presentations.

• The sensitivity of CT scan in identifying stroke within 12 hours of symptom onset is only 0.39.

• MRI>>>CT Brain

A 78-year-old man with episode of dysarthria lasting 20 minutes. Head CT scan (onthe left) done after 3 hours from episode showing no acute alteration. DWI MRI (on the right) done right after the CT revealing punctate area of restricted diffusion in

the right insula (arrow) compatible with infarction

Risk Stratification

Limitation of ABCD2 Score • up to 41% of the patients with a high score (>4) have been

found to have TIA mimics, • up to 21% of patients with low score have a high-risk

etiology, such as atrial fibrillation or carotid stenosis.• measurements favor identifying anterior circulation strokes

and miss posterior circulation findings, such as dizziness or sensory loss.

“ABCD2 score does provide a framework for approaching clinical decision making in these patients.”

NEW: ABCD2-I score has been proposed in which neuroimaging is added to the formula

Which Score To Use?

“The perfect scoring system has yet to be developed, and clinical acumen based on a careful history and physical must be incorporated into the clinical decision making”

Kiyohara T, Kamouchi M, Kumai Y, et al. ABCD3 and ABCD3-I scores are superior to ABCD2 score in the prediction of short- and long-term risks of stroke after transient ischemic attack. Stroke 2014;45(2):418–25

Treatment• The goal in TIA treatment is

to prevent subsequent stroke.

• There are 3 main therapeutic actions that reduce stroke occurrence:

antiplatelet therapy anticoagulant therapy surgical or endovascular

treatment of significant arterial stenosis

• Underlying disease eg HPT, DM, hypercholesrolemia.

Immediate Rx

• One trial it has been shown that the supine position ensures an increased cerebral flow compared with the seating or standing position.

• Oxygen administration is recommended only in case of hypoxia (ie oxygen saturation <94% on room air) and should be avoided in nonhypoxic patients(Class of evidence IIIB).

Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013;44:870–947

Anticoagulant

• In cases of nonvalvular atrial fibrillation, the 2013 ASA stroke guidelines recommend starting an anticoagulant within 14 days of the event.

Antiplatelet• Antiplatelet therapy is recommended in all cases of noncardioembolic

TIA (Level of evidence IA).• There are 5 conditions when double antiplatelet therapy with aspirin

and clopidogrel should be considered: high-risk TIA (large artery atherosclerosis and cardioembolic disease)

within the first 24 hours, TIA associated with severe (70%–99%) intracranial arterial stenosis

within the first 3 days TIA with intracranial or carotid symptomatic stenosis with microembolic

signs within 7 days extracranial vertebral stenting with bare metal stents, TIA with aortic arch atherosclerotic plaque or mobile thrombosis or

patches.

Disposition

• 2009 AHA guidelines used the ABCD2 score recommending that hospitalization:

ABCD2 score greater than 2evidence of focal ischemiaor for any patient in whom rapid follow-up as

an outpatient cannot realistically be obtained within 2 days

Reference