eMedicine Specialties > Emergency Medicine > Neurology
Transient Ischemic Attack: Treatment & Medication
Updated: Oct 23, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
- Rapid transport is essential to evaluate the patient who may have fleeting or stuttering symptoms.
- Fingerstick glucose can quickly rule out hypoglycemia.
- Intravenous (IV) access can be established, although transport should not be delayed for this.
- Collect all the patient’s prescription bottles.
- The family or witnesses should be instructed to go to the ED, or contact information for these individuals should be obtained.
- Some communities may have EMS preferentially transfer patients with high-risk stroke symptoms to centers with specific stroke expertise.11
Emergency Department Care
- Global CNS depression and airway or cardiac compromise are not typically features of a TIA. In fact, the level of consciousness and neurologic examination are expected to be at the patient's baseline.
- Initial assessment is aimed at excluding emergent conditions that can mimic a TIA such as hypoglycemia, seizure, or intracranial hemorrhage.
- Vital signs must be obtained promptly and addressed as indicated.
- Cardiac monitoring can capture a relevant dysrhythmia.
- Pulse oximetry can evaluate for hypoxia.
- Intravenous access (if not already established by EMS) should be obtained.
- Obtain a fingerstick glucose level and treat accordingly.
- Laboratory studies, including CBC, coagulation studies, and electrolytes levels, can be obtained.
- Obtain an ECG and evaluate for symptomatic rhythms or evidence of ischemia.
- Patients may be significantly hypertensive. Unless there is specific concern for end-organ damage from a hypertensive emergency, blood pressure should be managed conservatively while ischemic stroke is being ruled out.
- For acute ischemic stroke, the American Heart Association recommends initiating antihypertensive therapy only if blood pressure is more than 220/120 mm Hg, or mean arterial pressure greater than 130 mm Hg. Unless there is a concerning comorbid cardiac or other condition requiring blood pressure lowering, allowing the patient's blood pressure to autoregulate at a higher level (during the acute phase) may help maximize cerebral perfusion pressure.12
- Brain imaging is typically indicated to rule out an emergent cause of neurologic dysfunction. A noncontrast head CT, as a widely accessible study, is a reasonable first choice.13
Consultations
- Neurologist: There is clear consensus on the need for rapid evaluation, and patients who undergo neurology evaluation and risk stratification within 24 hours versus within a few days appear to have a significantly decreased short-term risk of stroke. Therefore, decisions regarding ED evaluation, and inpatient versus rapid outpatient followup, are ideally made in concert with a neurologist.
- Primary care physician: This is the most important consultation that can occur, as the primary care physician will monitor the patient long term and ensure risk factor and lifestyle modification. In addition, rapid neurology consultation is not available in many communities, and the primary care doctor may well be primarily responsible for managing urgent risk stratification.
- Cardiologist: This consultation can be considered for those with clear findings that influence stroke risk, such as atrial fibrillation, patent foramen ovale, intracardiac thrombus, or valvular abnormalities.
- Vascular surgeon: This consultation should be considered for those with significant vessel stenosis or occlusion.
Medication
Medical management is aimed at reducing both short- and long-term risk of stroke. Antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out, given the high short-term risk of stroke following TIA. One set of guidelines from the American Stroke Association (and supported by the American Academy of Neurology) are summarized here:14
Noncardioembolic TIA (or for those in whom no source is determined)
- Antiplatelet agents are recommended rather than oral anticoagulation as initial therapy. Aspirin (50-325 mg/d), combination aspirin/extended-release dipyridamole, and clopidogrel are all reasonable first-line options (class I recommendation).
- Combination aspirin/extended-release dipyridamole (Aggrenox) may be superior to aspirin alone (class IIa recommendation).15
- Clopidogrel may be considered instead of aspirin alone (class IIb recommendation).
- Aspirin in combination with clopidogrel increases the risk of hemorrhage and is not routinely recommended for patients with TIA (class III recommendation).
For those with a known cardioembolic source
- Atrial fibrillation: Long-term anticoagulation (goal INR 2-3) is typically recommended. Aspirin 325 mg/d is recommended for those unable to take oral anticoagulants.
- Acute MI with left ventricular thrombus
- Oral anticoagulation (goal INR 2-3) is reasonable
- Aspirin up to 162 mg/d should be used concurrently for ischemic coronary artery disease.
- Dilated cardiomyopathy: Either oral anticoagulation (goal INR 2-3) or antiplatelet therapy may be considered.
- Rheumatic mitral valve disease: Oral anticoagulation (goal INR 2-3) is reasonable. Antiplatelet agents would not normally be added to warfarin unless patients experience recurrent embolism despite a therapeutic INR.
- Mitral valve prolapse: Long-term antiplatelet therapy is reasonable.
- Mitral annular calcification: Antiplatelet therapy can be considered. Those with mitral regurgitation can be considered for warfarin or antiplatelet therapy.
- Aortic valve disease: Antiplatelet therapy may be considered.
- Prosthetic heart valves
- For mechanical prosthetic valves, oral anticoagulants (goal INR 2.5-3.5) are recommended. For those with TIAs despite therapeutic INR, aspirin 75-100 mg/d can be added to the regimen.
- For bioprosthetic valves, patients with TIA and no other source of thromboembolism can be considered for oral anticoagulation (INR 2-3).
Antiplatelet Agent
These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. See above for recommendations for specific agents from the American Stroke Association.
Aspirin (Anacin, Ascriptin, Ecotrin, Bufferin, Bayer Aspirin)
Blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis and prevents formation of platelet-aggregating thromboxane A2.
Adult
50-325 mg/d PO
Pediatric
10-15 mg/kg/dose PO q4-6h; not to exceed 60-80 mg/kg/d
Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding times; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma
Because of association with Reye syndrome, do not use in children (<16 y) with flu
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Aspirin 25 mg/dipyridamole 200 mg
Drug combination with antithrombotic action. This combination may be superior to aspirin alone in preventing cardiovascular events following TIAs.
Aspirin irreversibly inhibits formation of cyclooxygenase, thus preventing formation of thromboxane A2, a platelet aggregator and vasoconstrictor. Platelet-inhibition lasts for life of cell (approximately 10 d).
Dipyridamole is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3',5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.
Each capsule contains 25 mg aspirin and 200 mg dipyridamole for total of 50 mg aspirin and 400 mg dipyridamole to be given per day.
Adult
1 cap PO bid
Pediatric
Not established
Theophylline may decrease hypotensive effects of dipyridamole; antiplatelet activity of dipyridamole may increase heparin toxicity
Aspirin effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; children <16 y (due to association of aspirin with Reye syndrome)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Aspirin may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Caution in hypotension; dipyridamole has peripheral vasodilating effects
Clopidogrel (Plavix)
Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.
Adult
75 mg PO qd
Pediatric
Not established
Naproxen associated with increased occult GI blood loss; prolongs bleeding time; safety of coadministration with warfarin not established
Documented hypersensitivity; active pathological bleeding, such as peptic ulcer or intracranial hemorrhage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)
Dipyridamole (Persantine)
Administer to complement usual warfarin therapy. Inhibits platelet adhesion, which may inhibit adenosine uptake by RBCs. May increase cyclic-3',5'-AMP within platelets and formation of potent platelet activator thromboxane A2. May reduce the risk of stroke when used as monotherapy instead of aspirin.
Adult
200 mg PO bid
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Theophylline may decrease hypotensive effects; because of antiplatelet effects, may increase heparin toxicity
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution with hypotension; has peripheral vasodilating effects
Ticlopidine (Ticlid)
Second-line antiplatelet therapy for patients who cannot tolerate or do not respond to aspirin therapy. In some circumstances, it can be an alternative to clopidogrel.
Adult
250 mg PO bid
Pediatric
Not established
Corticosteroids and antacids may decrease effects; theophylline, cimetidine, aspirin, and NSAIDs increase toxicity
Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage; active bleeding disorders
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue if absolute neutrophil count falls to <1200/mm3 or if platelet count falls to <80,000/mm3
Anticoagulant
These agents are used to prevent venous thrombosis, pulmonary embolism, and thromboembolic disorders.
Warfarin (Coumadin)
Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.
Adult
5-15 mg/d PO for 2-5 d
Pediatric
0.05-0.34 mg/kg/d PO (infants may require doses at, or near, high end of this range)
Many medications may impact warfarin activity
Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac
Documented hypersensitivity; severe liver or kidney disease; open wounds; GI ulcers
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not switch brand after achieving therapeutic response; caution with active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis
More on Transient Ischemic Attack |
| Overview: Transient Ischemic Attack |
| Differential Diagnoses & Workup: Transient Ischemic Attack |
 Treatment & Medication: Transient Ischemic Attack |
| Follow-up: Transient Ischemic Attack |
| References |
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References
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Further Reading
Keywords
transient ischemic attack, TIA, temporary and focal loss of cerebral function, cerebral blood flow reduction, stroke, ischemic stroke, carotid artery atherosclerotic disease, vertebral artery atherosclerotic disease, hypertension, hypotension, impending stroke, atherosclerotic disease, coronary artery disease, carotid artery dissection, vertebral artery dissection, necrotizing vasculitis
vertebral artery stenosis, carotid artery stenosis, cerebral embolism, valvular heart disease, ventricular thrombus, atrial fibrillation, arterial dissection, arteritis, cocaine abuse, subdural hematomas, congenital heart disease, cerebral thromboembolism, clotting disorders, CNS infection, vasculitis, idiopathic progressive arteriopathy of childhood, moyamoya, fibromuscular dysplasia, Marfan disease, tuberous sclerosis, tumor, neurofibromatosis, carotid endarterectomy scars, pacemaker, atrioseptal defects, ventricular aneurysm, cranial nerve dysfunction, nodular cranial arteries
