Transient Ischemic Attack (TIA), Emergency Medicine

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Transient Ischemic Attack (TIA), Emergency Medicine

Basics

Description

All children with TIA should be admitted for close neurologic observation, with strong consideration of ICU level care

• TIA " “ an episode of reversible neurologic deficit caused by a temporary decrease in blood flow to an area of the central nervous system (CNS)
• Classically described as symptoms lasting <24 hr, but most TIA symptoms resolve in <1 hr
• A warning for stroke, as 12 " “30% of strokes will be preceded by TIA

Etiology

• Transient decrease in perfusion to an area of the CNS, which can be caused by:Thrombosis in medium to large arteries with atherosclerosis (25%)Intracranial small vessel disease (25%)Embolic cause from the heart (20%)Miscellaneous, including arterial dissection, vasculitis, and hypercoagulable states (5%)No clear predisposing vascular cause found (25%)

• Thrombosis in medium to large arteries with atherosclerosis (25%)
• Intracranial small vessel disease (25%)
• Embolic cause from the heart (20%)
• Miscellaneous, including arterial dissection, vasculitis, and hypercoagulable states (5%)
• No clear predisposing vascular cause found (25%)

Diagnosis

Signs and Symptoms

• Symptoms are determined by the vascular territories which are affected
• Large vessel TIA syndromes:Anterior cerebral artery (ACA) " “ unilateral motor/sensory loss to leg > arm, disinhibitionMiddle cerebral artery (MCA) " “ unilateral motor/sensory loss to face/arm > leg, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsiaPosterior cerebral artery (PCA) " “ homonymous hemianopsia, may have alexia, prosopagnosia (cant recognize faces)Anterior inferior cerebellar artery (AICA) " “ unilateral deafness, vertigo, tinnitus, vomiting, ipsilateral facial weakness and limb ataxia, contralateral decrease in pain and temperature sensationPosterior inferior cerebellar artery (PICA) " “ unilateral palatal weakness, unilateral limb ataxia, unilateral Horner's syndrome, decreased pain/temperature sensation on contralateral body:Wallenberg syndromeVertebrobasilar artery " “ ataxia, oculomotor palsies, facial paresis, loss of consciousness, quadriplegiaCarotid artery " “ unilateral motor/sensory loss to face/leg/arm, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsia
• Small vessel TIA syndromes:Amaurosis fugax " “ transient monocular blindness from occlusion of ophthalmic branch of internal carotidLacunar infarcts " “ occlusion of a deep penetrating artery of the brain. Usually produce pure motor or pure sensory deficitsInternal capsule " “ hemiparesis or dysarthria with clumsy handCorona radiata " “ hemiparesisPons " “ dysarthria with clumsy handThalamus " “ sensory loss to 1 side of the body

• Anterior cerebral artery (ACA) " “ unilateral motor/sensory loss to leg > arm, disinhibition
• Middle cerebral artery (MCA) " “ unilateral motor/sensory loss to face/arm > leg, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsia
• Posterior cerebral artery (PCA) " “ homonymous hemianopsia, may have alexia, prosopagnosia (cant recognize faces)
• Anterior inferior cerebellar artery (AICA) " “ unilateral deafness, vertigo, tinnitus, vomiting, ipsilateral facial weakness and limb ataxia, contralateral decrease in pain and temperature sensation
• Posterior inferior cerebellar artery (PICA) " “ unilateral palatal weakness, unilateral limb ataxia, unilateral Horner's syndrome, decreased pain/temperature sensation on contralateral body:Wallenberg syndrome
• Vertebrobasilar artery " “ ataxia, oculomotor palsies, facial paresis, loss of consciousness, quadriplegia
• Carotid artery " “ unilateral motor/sensory loss to face/leg/arm, aphasia if dominant hemisphere, neglect if nondominant hemisphere, homonymous hemianopsia

• Wallenberg syndrome

• Amaurosis fugax " “ transient monocular blindness from occlusion of ophthalmic branch of internal carotid
• Lacunar infarcts " “ occlusion of a deep penetrating artery of the brain. Usually produce pure motor or pure sensory deficitsInternal capsule " “ hemiparesis or dysarthria with clumsy handCorona radiata " “ hemiparesisPons " “ dysarthria with clumsy handThalamus " “ sensory loss to 1 side of the body

• Internal capsule " “ hemiparesis or dysarthria with clumsy hand
• Corona radiata " “ hemiparesis
• Pons " “ dysarthria with clumsy hand
• Thalamus " “ sensory loss to 1 side of the body

• Historical features suggestive of TIA:Sudden onsetShort duration (as >60% of events last <1 hr)Negative symptoms " “ CNS is underperfused and therefore, not functioning, so TIA syndromes generally produce loss of neurologic function " “ i.e., weakness or aphasiaSymptoms are focal, related to specific vascular territory
• Historical features not suggestive of TIA:Gradual onsetPositive symptoms " “ increased neurologic function in a particular area, such as convulsion, tingling, or twitching, suggests increased CNS activity as with migraine or seizure

• Sudden onset
• Short duration (as >60% of events last <1 hr)
• Negative symptoms " “ CNS is underperfused and therefore, not functioning, so TIA syndromes generally produce loss of neurologic function " “ i.e., weakness or aphasia
• Symptoms are focal, related to specific vascular territory

• Gradual onset
• Positive symptoms " “ increased neurologic function in a particular area, such as convulsion, tingling, or twitching, suggests increased CNS activity as with migraine or seizure

• Detailed neurologic exam: Strength, sensation, coordination, gait, naming/speech, and visual fields
• Persistent neurologic deficits suggest acute stroke rather than TIA
• The National Institute of Health Stroke Scale (NIHSS) is a reliable and easily repeatable neurologic exam (http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf)

Essential Workup

• Rapid history and physical exam including detailed neurologic exam
• Fingerstick glucose " “ hypoglycemia can produce focal neurologic deficits
• Noncontrast CT head " “ rule out hemorrhage
• If patients present with persistent deficits, obtain STAT neurologic consultation with concern for acute stroke rather than TIA

Diagnosis Tests & Interpretation

• Glucose
• Chemistry panel " “ check Na, renal function
• CBC " “ exclude anemia, polycytosis
• Troponin " “ rule out concomitant ACS or demand ischemia
• Hemoglobin A1C and fasting lipid panel for patients being admitted/observed

• CT:Upon arrival to ED, STAT noncontrast head CT to rule out CNS hemorrhage
• MRI:Up to 50% of patients that clinically have a TIA will have evidence of infarction on MRI:Goal is to have MRI in <24 hrDiffusion-weighted imaging (DWI) is the most sensitive protocol for detection of tissue infarction
• Vascular imaging:Either with initial imaging or inpatient workup, perform vascular imaging of the head and neck:Almost 50% of patients with TIA have stenosis or occlusion of large arteriesCarotid duplex ultrasound can be used to detect internal carotid stenosisCT angiography:Can be performed at the time of initial noncontrast head CTCan be used to detect stenosis in intracranial and extracranial vesselsRequires contrastMR angiography:Can be used to detect stenosis in intracranial and extracranial vesselsTime of flight (TOF) sequences can provide angiographic images without contrast

• Upon arrival to ED, STAT noncontrast head CT to rule out CNS hemorrhage

• Up to 50% of patients that clinically have a TIA will have evidence of infarction on MRI:Goal is to have MRI in <24 hr
• Diffusion-weighted imaging (DWI) is the most sensitive protocol for detection of tissue infarction

• Goal is to have MRI in <24 hr

• Either with initial imaging or inpatient workup, perform vascular imaging of the head and neck:Almost 50% of patients with TIA have stenosis or occlusion of large arteries
• Carotid duplex ultrasound can be used to detect internal carotid stenosis
• CT angiography:Can be performed at the time of initial noncontrast head CTCan be used to detect stenosis in intracranial and extracranial vesselsRequires contrast
• MR angiography:Can be used to detect stenosis in intracranial and extracranial vesselsTime of flight (TOF) sequences can provide angiographic images without contrast

• Almost 50% of patients with TIA have stenosis or occlusion of large arteries

• Can be performed at the time of initial noncontrast head CT
• Can be used to detect stenosis in intracranial and extracranial vessels
• Requires contrast

• Can be used to detect stenosis in intracranial and extracranial vessels
• Time of flight (TOF) sequences can provide angiographic images without contrast

• ECG " “ evaluate for thrombogenic rhythms such as atrial fibrillation
• Echocardiography in patients with no other cause for TIA " “ exclude existing thrombus and abnormal wall motion or aneurysms that cause thrombus

Differential Diagnosis

• Hypoglycemia
• Seizure
• Paralysis after seizure (Todds paralysis)
• Atypical migraine
• Psychiatric disease
• Stroke
• CNS tumors or metastases
• Subdural hemorrhage
• Subarachnoid hemorrhage
• Multiple sclerosis
• Intracerebral hemorrhage
• Air embolism
• Vasculitis
• Arterial dissection

• Congenital heart disease
• Vasculitis
• Arterial dissection
• Sickle cell disease
• Neurocutaneous syndromes
• Vascular malformations
• Meningitis

Treatment

Pre-Hospital

• Rapid assessment of neurologic deficits
• Consider transport to a stroke center, when available, if deficits persist

Initial Stabilization/Therapy

• IV access
• Cardiac monitoring
• Supplemental oxygen if hypoxic

Ed Treatment/Procedures

• Main goals in the management of TIA:Improve perfusion to ischemic tissuePrevent a subsequent stroke
• BP management:BP should not be lowered acutely unless over 220/120 mm HgHypertensive patients with TIA should have their BP lowered if stable at 24 hr after TIAKey in patients upon discharge1st line " “ HCTZ or ACE inhibitor
• Antiplatelet therapy:All patients, in the absence of contraindications, need antiplatelet therapy for stroke prevention1st line " “ aspirin (ASA):Safe, cheap, effectiveASA allergy " “ clopidogrel, ticlopidineASA/dipyridamole may be more effective than ASA alone
• Anticoagulation:Indicated for new onset atrial fibrillation or existing atrial fibrillation not on anticoagulantsOptions include heparin/low-molecular-weight heparin with a transition to warfarin or dabigatranThe decision to anticoagulate is not emergent; discuss with admitting physician
• Carotid endarterectomy (CEA):CEA within 2 wk after TIA in patients with >70% carotid stenosis reduces stroke risk by 10 " “15%
• Lipid therapy:AHA guidelines recommend statin therapy for patients with TIA with a goal LDL of under 70 mg/dLKey in patients upon discharge

• Improve perfusion to ischemic tissue
• Prevent a subsequent stroke

• BP should not be lowered acutely unless over 220/120 mm Hg
• Hypertensive patients with TIA should have their BP lowered if stable at 24 hr after TIA
• Key in patients upon discharge
• 1st line " “ HCTZ or ACE inhibitor

• All patients, in the absence of contraindications, need antiplatelet therapy for stroke prevention
• 1st line " “ aspirin (ASA):Safe, cheap, effective
• ASA allergy " “ clopidogrel, ticlopidine
• ASA/dipyridamole may be more effective than ASA alone

• Safe, cheap, effective

• Indicated for new onset atrial fibrillation or existing atrial fibrillation not on anticoagulants
• Options include heparin/low-molecular-weight heparin with a transition to warfarin or dabigatran
• The decision to anticoagulate is not emergent; discuss with admitting physician

• CEA within 2 wk after TIA in patients with >70% carotid stenosis reduces stroke risk by 10 " “15%

• AHA guidelines recommend statin therapy for patients with TIA with a goal LDL of under 70 mg/dL
• Key in patients upon discharge

Medication

• Antiplatelet agents:Aspirin 160 " “325 mg dailyAspirin/dipyridamole 25 mg/200 mg dailyClopidogrel 300 mg initially then 75 mg daily
• Anticoagulation:Heparin 5,000 " “7,500 U IV bolus, followed by 1,000 U/h infusion OR 80 U/kg IV bolus then 18 U/kg/hWarfarin dose is dependent on age and weight, but goal INR for atrial fibrillation is 2 " “3Dabigatran 150 mg daily (normal renal function)
• Acute BP management:Labetalol 20 mg IV bolus, followed by 20 " “80 mg IV every 10 min; max. cumulative dose of 300 mgNicardipine 5 mg/h infection, increase by 2.5 mg/h every 5 " “15 min; max. dose of 15 mg/h

• Aspirin 160 " “325 mg daily
• Aspirin/dipyridamole 25 mg/200 mg daily
• Clopidogrel 300 mg initially then 75 mg daily

• Heparin 5,000 " “7,500 U IV bolus, followed by 1,000 U/h infusion OR 80 U/kg IV bolus then 18 U/kg/h
• Warfarin dose is dependent on age and weight, but goal INR for atrial fibrillation is 2 " “3
• Dabigatran 150 mg daily (normal renal function)

• Labetalol 20 mg IV bolus, followed by 20 " “80 mg IV every 10 min; max. cumulative dose of 300 mg
• Nicardipine 5 mg/h infection, increase by 2.5 mg/h every 5 " “15 min; max. dose of 15 mg/h

Follow-Up

Disposition

• There are no clear indications for admission or discharge
• Patients with TIA have variable short-term risk of stroke
• Goal of admission is to prevent subsequent stroke in high-risk patients
• Scoring systems have been developed to predict short-term risk of stroke and therefore can guide disposition
• Most common = ABCD2 score:Age >60 = 1 pointBP >140/90 = 1 pointClinical features:Unilateral weakness = 2 pointsSpeech difficulty alone = 1 pointDuration:>60 min = 2 points10 " “59 min = 1 point<10 min = 0 pointsDiabetes = 1 point
• ABCD2 score 0 " “3 = low risk of stroke ( ¢ ˆ ¼1% at 7 days)
• ABCD2 score 4 " “5 = moderate risk for stroke ( ¢ ˆ ¼6% at 7 days)
• ABCD2 score 6 " “7 = high risk for stroke ( ¢ ˆ ¼12% at 7 days)
• Patients with moderate to high risk for short-term stroke = admission
• Patients with low risk for short-term stroke, but poor follow-up = observation unit

• Age >60 = 1 point
• BP >140/90 = 1 point
• Clinical features:Unilateral weakness = 2 pointsSpeech difficulty alone = 1 point
• Duration:>60 min = 2 points10 " “59 min = 1 point<10 min = 0 points
• Diabetes = 1 point

• Unilateral weakness = 2 points
• Speech difficulty alone = 1 point

• >60 min = 2 points
• 10 " “59 min = 1 point
• <10 min = 0 points

• No clear discharge criteria exist:Low risk for short-term stroke, with good follow-up

• Low risk for short-term stroke, with good follow-up

• The risk of stroke after TIA is highest within 2 days of symptoms
• Discharged patients need to see neurology/primary care within 24 " “48 hr

Follow-Up Recommendations

• Primary Care/Neurology " “ management of risk factors for cerebrovascular disease (hypertension, diabetes, etc.)
• Vascular surgery " “ for carotid stenosis. Follow-up within 1 wk, plan for possible CEA within 2 wk
• Cardiology " “ for those patients with cardiac cause of stroke, such as atrial fibrillation or cardiomyopathy

Pearls and Pitfalls

• Pearls:Risk stratification scores (such as ABCD2) can help guide dispositionPatients with carotid stenosis need rapid vascular surgery follow-up
• Pitfalls:Failure to recognize the subtle lacunar TIA syndromes, such as sensory lossFailure to rapidly check a glucose in a patient with a focal neurologic deficitDischarging patients with TIA without close outpatient follow-up

• Risk stratification scores (such as ABCD2) can help guide disposition
• Patients with carotid stenosis need rapid vascular surgery follow-up

• Failure to recognize the subtle lacunar TIA syndromes, such as sensory loss
• Failure to rapidly check a glucose in a patient with a focal neurologic deficit
• Discharging patients with TIA without close outpatient follow-up

Additional Reading

• Davis ‚ SM, Donnan ‚ GA. Clinical practice. Secondary prevention after ischemic stroke or transient ischemic attack. New Engl J Med. 2012;366:1914 " “1922.
• Panagos ‚ PD. Transient ischemic attack (TIA): The initial diagnostic and therapeutic dilemma. Am J Emerg Med. 2012;30:794 " “799.
• Pare ‚ JR, Kahn ‚ JH. Basic neuroanatomy and stroke syndromes. Emerg Med Clin North Am. 2012;30:601 " “615.
• Siket ‚ MS, Edlow ‚ JA. Transient ischemic attack: Reviewing the evolution of the definition, diagnosis, risk stratification, and management for the emergency physician. Emerg Med Clin North Am. 2012;30:745 " “770.
• Sorensen ‚ AG, Ay ‚ H. Transient ischemic attack: Definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011;21:303 " “313.

Codes

ICD9

• 435.3 Vertebrobasilar artery syndrome
• 435.8 Other specified transient cerebral ischemias
• 435.9 Unspecified transient cerebral ischemia

ICD10

• G45.8 Oth transient cerebral ischemic attacks and related synd
• G45.9 Transient cerebral ischemic attack, unspecified
• G46.1 Anterior cerebral artery syndrome
• G46.0 Middle cerebral artery syndrome
• G46.2 Posterior cerebral artery syndrome

SNOMED

• 266257000 Transient ischemic attack (disorder)
• 195210002 Anterior cerebral artery syndrome (disorder)
• 195209007 Middle cerebral artery syndrome (disorder)
• 195211003 Posterior cerebral artery syndrome (disorder)
• 230716006 Carotid territory transient ischemic attack