Transient Ischemic Attack

Description

Transient ischemic attacks (TIAs) are a sudden, temporary, stroke-like condition of presumed vascular origin. The traditional or historical definition describes it as, "cerebral dysfunction of ischemic nature lasting no longer than 24 hours with a tendency to recur."
A modified, tissue-based definition implements neuroimaging findings and describes TIAs as, "a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms lasting less than an hour and without neuroimaging evidence of acute infarction."
Patients with a history of TIAs may present for urgent or emergent carotid endarterectomy, craniotomy, or minimally invasive interventional procedures. Additionally, patients may present for surgery unrelated to the disease or have postoperative manifestations of TIAs.

Epidemiology

Incidence

In the US: 200,000–500,000/year

Morbidity

Ninety-day risk of stroke following a TIA: 10–20%
Five-year risk of stroke following a TIA: 30%

Mortality

Combined 10-year risk of stroke, MI, or vascular death of 42.8% (~4% per year).
Stroke is the second most common cause of death worldwide (1).

Etiology/Risk Factors

Risk factors for experiencing a TIA include

Hypertension; most prevalent and significant (2)
Cigarette smoking
Obesity
Hyperlipidemia
Heart disease
Carotid artery disease
Diabetes
Alcoholism
Atherosclerosis
Polycythemia
Sickle cell anemia

Physiology/Pathophysiology

TIA may be considered an ischemic penumbra of varied duration; it can proceed to cerebral infarction or resolve, but must be considered a harbinger of stroke.
It is the result of temporary hypoperfusion secondary to various causes. The most common cause is an embolus that frequently arises from distant sites like the aorta, cardiac clots (atrial fibrillation), or bifurcation of the internal carotid, middle, or anterior cerebral arteries. They are typically comprised of platelet-fibrin or atherosclerotic material.

Anesthetic GOALS/GUIDING Principles

Patients on anticoagulation who are presenting for surgery unrelated to their TIAs should be discussed with the surgeon, neurologist, cardiologist, or primary care physician regarding ideal management. Consider bridging therapy prior to the surgery with low molecular weight heparin and reinstituting therapy as soon as possible.
Patients who present postoperatively with TIAs should be evaluated expeditiously with appropriate neurological evaluation, so that intervention such as anticoagulation or invasive radiological therapy has the chance to interrupt or limit progression to stroke.

Diagnosis ⬆ ⬇

Symptoms

Syncope, loss of balance, vision changes, weakness or heaviness in extremities, numbness especially in the face, arms or legs, change in speech pattern or recognition.

History

Brief episode(s) of stroke-type symptoms with rapid resolution and complete recovery.
Risk factors, including atrial fibrillation, cardiac shunts and lesions such as artificial valves, may be completely or partially evaluated.
Patients may have coincident decreases in level of cognition, orientation, and neurological function, which should be noted to facilitate postoperative evaluation.

Signs/Physical Exam

Because TIA is defined as the resolution of stroke type symptoms, the physical exam is often benign. However, neurological deficits should be determined and documented appropriately.
Carotid bruits, irregularly irregular rhythm, or cardiac murmurs.

Treatment History

Corrective procedures: Carotid endarterectomy, intracranial–extracranial bypass, or invasive radiological procedures (stenting).
Electrophysiologic ablation procedures

Medications

"Blood thinners:" Aspirin, clopidogrel, heparin
Statins (for their pleiotropic, membrane stabilizing properties)
Antidysrhythmics

Diagnostic Tests & Interpretation

Labs/Studies

CBC
Electrolytes, BUN, Cr, glucose
Evaluation of hypercoagulability
EKG; cardiac rhythm disturbances, such as atrial fibrillation, should be completely evaluated and treated.
Echocardiogram to evaluate chamber size, clots, and shunts (PFO).
Carotid Doppler studies
C-reactive protein is of interest and may be helpful to predict future stroke and TIA, but may not be useful as an immediate preoperative test (3).
MRI/CT

CONCOMITANT ORGAN DYSFUNCTION

Vascular disease (coronary artery and renal disease)
Diabetes can complicate large vessel occlusive disease with small vessel disease; worsening perfusion problems.
Hypertension makes the risk of end-organ ischemia under anesthesia, secondary to relative hypotension, a concern.
Arrhythmias

Circumstances to delay/Conditions

Partially or improperly evaluated TIAs need proper investigation prior to elective surgery.
Recent or accelerating episodes of TIA.
Uncontrolled hypertension. SBP >200 mm Hg and DBP <100 mm Hg are reasons to consider delay.
Potassium and electrolytes should be optimized to reduce the incidence of rhythm disturbance in patients with a history of, or strong risk factors for TIAs or stroke.

Classifications

ABCD2 classification for TIA helps to define risk (higher scores are associated with increased risk of stroke) and guide treatment.
- A: Age over 60 years is 1 point
- B: BP >140/90 mm Hg is 1 point
- C: Clinical features, including unilateral weakness, are 2 points and speech disturbance without weakness is 1 point.
- D2: Diabetes is 1 point and duration of symptoms 1 point for <60 minutes and 2 points for >60 minutes (4).
CHADS2 scoring aids with assessing the risk of stroke in patients with atrial fibrillation.
- CHF, hypertension, age over 75, diabetes, and stroke get one point for each of the risk factors.
- Prior stroke or TIA receives 2 points.
- A score of five or six, history of a stroke or TIA within 3 months, or rheumatic valvular heart disease are at high risk (5).

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Continue scheduled antiarrhythmics and antihypertensives on schedule.
Perioperative beta-blockers have been associated with an increase in stroke, possibly due to hypotension. If utilized, they should be done cautiously while maintaining adequate cerebral perfusion pressures.

INTRAOPERATIVE CARE

Choice of Anesthesia

Depends on the surgical procedure, comorbidities, and patient preference.
Neuraxial techniques may be contraindicated by anticoagulants.

Monitors

Standard ASA monitors
Arterial line may be appropriate in patients with severe cerebrovascular disease to ensure adequate cerebral perfusion pressures or with cardiac arrhythmias (in concordance with the surgical procedure).
BIS monitoring may be helpful in detecting CNS ischemia/TIA (6).

Induction/Airway Management

Induction agent choice should maintain stable hemodynamics (avoid hypotension, hypertension, sympathetic stimulation that can exacerbate arrhythmias).

Maintenance

No specific anesthetic technique (volatile versus IV) has been shown to decrease the incidence of intraoperative cerebral ischemia, TIAs, or postoperative stroke.

Extubation/Emergence

Hypertension may require antihypertensives like labetalol, esmolol, or nitroglycerin.
Wakefulness post emergence aids the immediate neurological evaluation.

Follow-Up ⬆ ⬇

Bed Acuity

Depends on the surgical procedure, patient comorbidities, and intraoperative events

Medications/Lab Studies/Consults

Delayed emergence can occasionally simulate postoperative TIA so a brief period (15 minutes) of observation may be warranted prior to further workup. Neurology consultation and diagnostic studies such as CT scan or MRI scan as appropriate.
Reinstitution of "blood thinners" should be done as soon as safely possible.
Reinstitution of antihypertensives and stains should be performed as soon as possible.

Complications

Stroke
Confusion

References ⬆ ⬇

Gage BF , et al. Validation of clinical classification schemes for predicting stroke. JAMA. 2001;285(22):2864–2870.
Easton OJ , et al. Definition and evaluation of transient ischemic attack. Stroke. 2009;doi:1 0.1161/STROKEAHA.1 08.192218 (A).
Di Napoli M , et al. Evaluation of C-reactive protein measurement for assessing the risk and prognosis in ischemic stroke. Stroke. 2005;36(6):1316–1329 (B).
Mora S , Ridker PM. Justification for use of statins in primary prevention. Am J Cardiol. 2006;97(2A):33A–41A. (B)
Johnston SC , et al. Validation and refinement of scores to predict very early stroke risk after TIA. Lancet. 2007;369:283–292. (B)
Bleeker CP , et al. Bispectral index changes during acute brainstem TIA/ischemia. Case Reports in Medicine. 2010; Article 697185. doi:10.1155/2010/697185 (C).
Sacco RL , Adams R , Albers G , et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: A statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: Cosponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Circulation. 2006;113:e409–449. (B)
Rost N , et al. Plasma concentration of c-reactive protein and risk of ischemic stroke and transient ischemic attack. Stroke. 2001;32:2575. (A)
Veenith TV , et al. Perioperative care of a patient with stroke. Int Archf Med. 2010;3:33 DOI:10.1186/1755-3-33. (B)
Wolf PA , Clagett GP , Easton JD , et al. Preventing ischemic stroke in patients with prior stroke and transient ischemic attack: A statement for healthcare professionals from the Stroke Council of the American Heart Association. Stroke. 1999;30:1991–1994. (A)

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Basics ⬇