WORKUP	Section 5 of 10
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Lab Studies:

• Serum chemistry profile

• Coagulation studies

• Erythrocyte sedimentation rate (ESR)

• Syphilis serology

• Complete blood count

• Platelet count

• Antiphospholipid antibodies

• Glucose level

• Drug screens

• Cardiac index markers (may be considered)

• Optional studies

• Screening for hypercoagulable states (particularly in patients younger than 50 years)

• Levels of protein C and protein S

• Antithrombin III level

• Thrombin time

• Hemoglobin electrophoresis

• Serum protein electrophoresis

• Cerebrospinal fluid examination

• Testing for silent myocardial ischemia

• Anemia and elevated ESR (>100 mm/h) - Hallmarks of temporal artery arteritis

Imaging Studies:

• Location of the disease is very important for treatment and prognosis. Evaluation of the patient with a TIA includes diagnostic tests for the following:

• Carotid or vertebral artery plaques that produce arteriogenic emboli

• Flow-limiting stenosis

• Penetrating cerebral artery disease

• Noncontrast cranial CT scan of the head: An area of infarction appropriate for the TIA symptoms has been identified in 29-34% of patients with TIA. Support for obtaining a cranial CT scan includes the following:

• Locating the new area of ischemia or infarction

• Locating a silent infarction from a previous undocumented stroke (may predict prognosis for further TIA/stroke)

• Excluding other lesions that simulate TIA (eg, subdural hematoma, brain tumor, arteriovenous malformation, cerebral aneurysm)

• MRI of the brain

• Acute infarcts are located more accurately using MRI than CT scan.

• Abnormal vascular flow can be detected within minutes of onset of symptoms.

• Limited availability and cost of MRI scanners restrict the immediate requirement for a stat MRI. MRI can be obtained on a less urgent or outpatient basis if less-costly tests do not identify the cause of TIA symptoms.

• Magnetic resonance angiography: MRA provides noninvasive images of carotid and vertebral arteries.

• Cerebral arteriography: Selective catheterization of the cerebral vessels is necessary to evaluate the carotid arteries prior to carotid endarterectomy, identify the vertebral and basilar arteries, and define intracranial stenosis or occlusion.

• Cerebral arterial imaging: Carotid and vertebral artery ultrasound is required to identify the surgical candidate with high-grade carotid stenosis.

Other Tests:

• 12-lead electrocardiogram

• 12-lead ECG is indicated to assess the rhythm and guide case management.

• Rhythms such as atrial fibrillation are associated with cardioembolic events.

• Lumbar puncture (LP) is indicated if the diagnosis is in doubt and subarachnoid hemorrhage, infectious etiology, or demyelinating disease is to be excluded.

	TREATMENT	Section 6 of 10
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Prehospital Care:

• Rapid transport is essential to evaluate the patient who may have fleeting symptoms.

• The following can facilitate immediate intervention and reduce delay in evaluation once the patient has arrived in the ED:

• Cardiac monitoring

• Rapid glucose assessment

• Pulse oximetry

• Establishing intravenous (IV) access

• Administer supplemental oxygen.

• EMS personnel should collect prescription bottles and instruct family members or witnesses to go to the ED.

Emergency Department Care: Global CNS depression and airway or cardiac compromise are not features of a TIA. Therefore, ED intervention is relatively minimal.

• Supporting the airway and restoring perfusion or a stable rhythm are tenets of emergency care. By definition, patients with TIA are hemodynamically stable and able to support their own airways. Rapid assessment excludes those conditions that mimic a TIA such as hypoglycemia or an intracranial hemorrhage.

• Vital signs must be obtained promptly and addressed as indicated. Place the patient on a cardiac monitor and a pulse oximeter and establish an IV line (if one has not already been established by EMS).

• Obtain a fingerstick glucose level and treat accordingly.

• Obtain an ECG and initiate treatment for symptomatic rhythms or evidence of ischemia.

• A significant area of controversy is whether to treat hypotension or hypertension during a stroke. For patients with TIA who are diabetic, recent evidence indicates that blood pressure (BP) treatment targets should be lower than previously recommended to less than 130/85 mm Hg.

• While BP and perfusion should be supported, cerebral perfusion pressure may respond inconsistently to antihypertensive therapy.

• Even a modest reduction in BP can extend a fragile ischemic penumbra.

• If an antihypertensive agent is administered, closely monitor the patient's response by repeating the physical examination.

• Consensus suggests not treating hypertension during an acute stroke unless the mean arterial peripheral pressure exceeds 130 mm Hg. Mean pressure is calculated as (systolic BP + [2 x diastolic BP]) /3.

• When a TIA is caused by large or small vessel arteritis, distinguishing between pure arteritis and arteritis that produces penetrating arterial disease is important. The former is treated with dexamethasone, often on an outpatient basis, but the latter is better treated with IV steroids and observation.

Consultations:

• Contact the patient's primary care physician. Any further specialist consultation needed (eg, neurologist, vascular surgeon, cardiologist) should occur after consulting the patient's primary care provider. The decision to admit after a TIA appears to vary regionally; all patients require additional workup on an inpatient or outpatient basis.

• Neurologist (particularly if questioning whether the presentation is consistent with TIA)

• Vascular surgeon (not typically performed in the ED)

• Cardiologist: Although not typically performed in the ED, cardiology consultation is useful, in particular when a cardiac etiology is suspected (eg, atrial fibrillation, valvular disease).

	MEDICATION	Section 7 of 10
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Rapid pharmacologic intervention in patients with TIAs caused by atherosclerosis is limited to antiplatelet or anticoagulation therapy. Treatment for TIA caused by dysrhythmias, extracranial embolisms, or metabolic disorders can require a specific treatment dictated by the cause.

Emergency physicians may be in the unique position to limit the progression of the TIA. Emergency physicians must know when to initiate single-agent antiplatelet therapy, adjust existing antiplatelet therapy, initiate anticoagulant therapy, or advance other pharmacologic treatment. Recent therapeutic intervention and outcome studies have advanced the understanding of TIA. Patient outcomes are no longer clumped with "all stroke patients." We appreciate unique TIA therapy is available. Emergency physicians must closely examine the therapeutic options for patients who experience a TIA.

If the patient is already taking aspirin, he or she may be a candidate to take aspirin plus extended-release dipyridamole. Recent reports suggest that this combination is more effective than aspirin alone at preventing stroke, particularly in patients at high risk for stroke. Although dual therapy carries the increased risk of GI bleeding.

A possible benefit may exist by administering antiplatelet therapy with aspirin and clopidogrel to patients who are showering the cerebral circulation with microemboli.

Several new oral anticoagulant medications, including ximelagatran, are in the final stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke. Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Emergency physicians interested in keeping abreast of the challenging field of post-TIA therapy must closely follow the results of the PRoFESS (the Prevention Regimen for Effectively Avoiding Second Strokes) study. This is a randomized, double blind interventional study designed to compare 25 mg aspirin/200 mg extended-release dipyridamole with clopidogrel monotherapy and to compare telmisartan with placebo in the prevention of recurrent stroke.

	MISCELLANEOUS	Section 9 of 10
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Medical/Legal Pitfalls:

• The emergency physician must be aware that a TIA can be a harbinger of an impending stroke. It has been reported that a quarter of the patients with a TIA will have a stroke within 24 hours. In one study, 17% of patients with an acute ischemic stroke had a TIA on the day of the stroke. The take home message is: TIA is a warning for an impending stroke.

Special Concerns:

• The following are possible discharge criteria for the patient with a TIA:

• Institutionalized individual with severe preexisting irreversible disability such as untreatable dementia, terminal illness, or profound irreversible neurologic deficits

• Noninstitutionalized individual with preexisting disability or terminal illness who has adequate home support

• Mild neurologic deficits not due to unruptured aneurysm, infection, trauma, or cerebrovascular shunt malfunction, which are identified more than 48 hours after symptom onset and can receive expeditious outpatient evaluation

• Mild neurologic deficit due to lacunar stroke syndrome and normal cranial CT scan (excluding previous documented CT scan findings), no risk for embolic event, uncontrolled diabetes, or cardiac event (eg, uncontrolled hypertension)

• Transient neurologic symptoms limited to monocular blindness or amnesia