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Transient Ischemic Attack (TIA), Emergency Medicine


Basics


Description


  • 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%)

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, 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
  • Small vessel TIA syndromes:
    • 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 deficits
      • 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

History
  • Historical features suggestive of TIA:
    • 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
  • Historical features not suggestive of TIA:
    • 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

Physical Exam
  • 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


Lab
  • 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

Imaging
  • 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 hr
    • Diffusion-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 arteries
    • Carotid duplex ultrasound can be used to detect internal carotid stenosis
    • CT angiography:
      • Can be performed at the time of initial noncontrast head CT
      • Can be used to detect stenosis in intracranial and extracranial vessels
      • Requires contrast
    • MR angiography:
      • Can be used to detect stenosis in intracranial and extracranial vessels
      • Time of flight (TOF) sequences can provide angiographic images without contrast

Diagnostic Procedures/Surgery
  • 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 tissue
    • Prevent a subsequent stroke
  • BP management:
    • 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
  • Antiplatelet therapy:
    • 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
  • Anticoagulation:
    • 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
  • 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/dL
    • Key in patients upon discharge

Medication


  • Antiplatelet agents:
    • Aspirin 160 " “325 mg daily
    • Aspirin/dipyridamole 25 mg/200 mg daily
    • Clopidogrel 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/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)
  • Acute BP management:
    • 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


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

All children with TIA should be admitted for close neurologic observation, with strong consideration of ICU level care ‚  
Discharge Criteria
  • No clear discharge criteria exist:
    • Low risk for short-term stroke, with good follow-up

Issues for Referral
  • 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 disposition
    • Patients with carotid stenosis need rapid vascular surgery follow-up
  • Pitfalls:
    • 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
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