eMedicine Specialties > Neurology > Neuro-vascular Diseases

Basilar Artery Thrombosis: Treatment & Medication

Author: Salvador Cruz-Flores, MD, MPH, Professor of Neurology, Director of Souers Stroke Institute, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Mid-America Stroke Network and Neuroscience Critical Care Unit, St Louis University Hospital
Coauthor(s): Sombat Muengtaweepongsa, MD, Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand
Contributor Information and Disclosures

Updated: Aug 18, 2009

Treatment

Medical Care

All patients should be admitted to a stroke unit. Patients with unstable or fluctuating neurological symptoms, decreased level of consciousness, active cardiac or respiratory comorbid conditions, hemodynamic instability, or a need for interventional therapies (eg, thrombolysis) must be admitted to a neurological intensive care unit.

  • General care
    • Care is required for all indwelling catheters, including monitoring for infection.
    • Control body temperature because evidence suggests that fever worsens the outcome in patients with stroke.
    • Glucose levels should be monitored to avoid hypoglycemia and hyperglycemia.
    • Aggressive pulmonary toilet is instituted to avoid pneumonia.
  • Hemodynamic management: The goal is to minimize ischemic injury.
    • Cerebral ischemia results in impaired autoregulation. Therefore, under ischemic conditions, cerebral blood flow becomes dependent on blood pressure. In patients with severe cerebral vascular occlusive disease, mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) become critical in maintaining cerebral blood flow (CPP = MAP - intracranial pressure).
    • No evidence from randomized trials indicates that treating hypertension is better than not treating it. Currently available guidelines for the management of acute stroke recommend the use of antihypertensives to lower blood pressure to less than a systolic value of 185 mm Hg or a diastolic value of less than 110 mm Hg only if thrombolysis is being considered. Additionally, some evidence suggests that induced hypertension in selected cases may be beneficial for limiting ischemic injury.
      • If the neurological condition is fluctuating and blood pressure requires close monitoring, an arterial catheter should be placed.
      • Hypertension should not be treated unless the patient has evidence of acute end organ damage such as hypertensive encephalopathy, unstable angina or acute myocardial infarction, heart failure, or acute renal failure. In the absence of any of these circumstances, treatment is indicated only when the diastolic blood pressure is greater than 120 mm Hg or systolic blood pressure is greater than 220 mm Hg.
      • Blood pressure treatment should be considered when thrombolytic therapy is to be administered, aiming to keep the diastolic blood pressure at less than 110 mm Hg and the systolic blood pressure at less than 185 mm Hg when thrombolysis will be used.
      • The preferred antihypertensive agents are nicardipine and labetalol.
      • When diastolic blood pressure is greater than 140 mm Hg and not responsive to nicardipine and labetalol, then nitroprusside should be used.
      • Overzealous treatment of hypertension should be avoided because it can exacerbate the ongoing ischemia.
    • Patients with hypotension should be treated to normalize the MAP and therefore to improve blood pressure–dependent cerebral blood flow.
      • Every effort should be made to maintain a normal intravascular volume by administering isotonic solutions.
      • If the MAP continues to be low despite fluid management, vasopressors such as dopamine, dobutamine, or phenylephrine should be used.
      • Dopamine can cause significant tachycardia; therefore, phenylephrine (Neo-Synephrine) and norepinephrine (Levophed) are the vasopressors of choice after dopamine. Dobutamine should be used with caution and with close monitoring of the cardiac index because it can often cause vasodilatation and hypotension.
      • Dobutamine is the pressor of choice in patients with congestive heart failure.
    • In patients whose intravascular volume status is unknown or who have comorbid conditions such as congestive heart failure or pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary wedge pressure. This allows better management and optimization of the intravascular volume to avoid volume overload.
  • Respiratory management: Early assessment and management of the airway is vital, given the frequent involvement of lower cranial nerves and impairment of consciousness in patients with brainstem ischemia. Other important aspects include assessment of the respiratory drive, the gag reflex, and the ability to handle secretions by a forceful cough.
    • Generally, endotracheal intubation should be considered in patients with a decreased level of consciousness and Glasgow Coma Scale score of less than 8.
    • Endotracheal intubation is recommended in most patients to keep their airway clear while maintaining normal ventilation. Of the mechanical ventilation modes, pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation are used most often.
    • For patients with good respiratory drive, the most comfortable mode is PSV. In this mode, the ventilator does not deliver a set of breaths but provides enough pressure support to maintain the desired tidal volume. The usual goal is to maintain a tidal volume of 5 mL/kg. Most patients with no comorbid pulmonary condition reach this goal with a PSV of 5-10.
    • For patients with poor respiratory drive, synchronized intermittent mandatory ventilation may be a better mode. This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with the patient's inspiratory effort while allowing the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort during the extra breaths.
    • Sedation and paralysis should be avoided because they interfere with the neurologic assessment. Certain circumstances, such as neurogenic hyperventilation, may require the use of sedation and paralysis to avoid hypocarbia, which can worsen the ischemic process. However, sedation alone can and should be used to maintain comfort.
  • Thrombolysis: Tissue plasminogen activator (tPA) is the only pharmaceutical agent approved by the US Food and Drug Administration (FDA) for the treatment of acute ischemic stroke within the first 3 hours of onset. Its approval was based on data from the trial by the National Institute for Neurological Disorders and Stroke. However, the trial did not include patients in stupor or coma and, thus, probably excluded patients who experienced a basilar artery occlusion. Moreover, the trial did not systematically study vascular anatomy in all patients.
  • Intra-arterial thrombolysis: This has emerged as a therapeutic strategy despite the absence of data from randomized clinical trials.
    • Several case series have been published. The average time to treatment has ranged from 8-48 hours. Overall mortality rates have decreased from 46-75% to 26-60%. The rate of hemorrhagic transformation is approximately 8%, which a little higher than that of intravenous thrombolysis in anterior circulation, confirmed by another study in animal models. The patient's condition at presentation is, apparently, the major prognostic factor; patients with quadriplegia and/or coma have worse outcomes than other patients. Despite these efforts, intra-arterial thrombolysis for vertebrobasilar occlusion has not been studied systematically in randomized controlled trials.
    • Thrombolytic agents include urokinase, pro-urokinase, streptokinase, and tPA.
      • Urokinase is not on the market in the United States because of concerns with its production.
      • Streptokinase has not been used for stroke since multicenter European, Italian, and Australian trials were stopped because of greater mortality rates in treated patients than in untreated patients.
      • Pro-urokinase was tested in a prospective randomized fashion. The trial involved only patients with occlusion of the middle cerebral artery stem. Results showed a better outcome in treated patients. However, pro-urokinase was not approved for use in acute stroke; therefore, the only option in the United States is tPA. This drug has been studied prospectively in trials involving combined intravenous and intra-arterial thrombolysis; the dosage used is 0.3 mg/kg, up to a maximum of 10-20 mg intra-arterially.
      • An ongoing phase 3 trial is combining intravenous and intra-arterial thrombolysis with the addition of intravascular ultrasound or with the Merci Retriever, although the intervention is not focused only on basilar artery occlusion.
      • Because the rate of reocclusion is approximately 30%, some investigators have reported limited experience with the use of glycoprotein IIb/IIIa inhibitors such as abciximab to block platelet function and rethrombosis.
    • A recent systematic analysis demonstrated that the morbidity and mortality of patients treated with intra-arterial thrombolysis is not all that different from the effect of intravenous thrombolysis, although recanalization was achieved more frequently with intra-arterial thrombolysis.9
    • Ideally, patients with basilar artery occlusion should be treated within the context of a randomized trial. In the absence of this option, many stroke experts would advocate the use of intra-arterial thrombolysis. This decision, however, should be made with knowledge of the background information just described and with recognition of the absence of evidence from randomized trials.
    • Some general guidelines should be followed when treating a patient with intravenous or intra-arterial thrombolysis, as follows:
      • Patients with a stuttering course of longer than 3 hours and up to 12 hours should be considered for intra-arterial thrombolysis, provided that ischemic changes are not present on the CT scan. However, the care team should recognize that under these circumstances, the therapy is offered in a compassionate fashion, given the poor prognosis of basilar artery occlusion.
      • Despite reports of the successful use of anticoagulation immediately following thrombolysis, avoiding systemic anticoagulation is recommended for the first 24 hours after thrombolysis, given the risk of hemorrhagic complications.
      • Although treatment as late as 24-48 hours after symptom onset has been reported, the authors recommend caution because of the high risk of hemorrhagic complications. Systemic anticoagulation may be an alternative for patients with contraindications for thrombolysis, although no evidence clearly indicates any beneficial effect.
      • With rare exceptions, patients should not be treated with thrombolysis if more than 12 hours have elapsed since the onset of more major symptoms or if they have marked ischemic changes on the CT scan, regardless of the time course.
      • The benefits of intra-arterial thrombolysis in selected groups of patients with basilar artery thrombosis, such as patients with minor deficit or old patients with extensive brain stem infarcts, is even less clear.
  • Other therapies
    • Anticoagulation with heparin or low molecular weight heparinoids has been used, but no evidence shows that this has an impact on outcome.
    • The role of other antiplatelets, such as clopidogrel and the combination of aspirin and dipyridamole, in the treatment of acute basilar artery occlusion is not known.
    • Angioplasty with or without stent placement has been performed to treat patients with atherosclerotic stenosis or to mechanically dislodge thrombi. The advantage of angioplasty is the excellent and quick anatomical recanalization, but the success rate is still low. Angioplasty has been performed in patients with acute vertebrobasilar occlusion and in patients selected electively. The morbidity rates cited in the published case series range from 0-50%. The mortality rate is as high as 33%. The role of angioplasty in the therapy for this disorder is not known.
    • Only one case report has described successful endovascular embolectomy in basilar artery thrombosis.10 In the MERCI and Multi MERCI trials, mechanical embolectomy in 27 patients resulted in a 78% recanalization rate, a mortality rate of 44%, and a good clinical outcome in 41% of patients. Patients who underwent recanalization had better outcomes than those without recanalization.11
    • Thrombus retrieval has been more recently added to the armamentarium by way of the Merci Retriever device. The FDA approved its use for blood vessel recanalization, although its impact in improving neurological outcome is not known.
    • For patients with atherosclerotic stenosis who survive basilar artery occlusion, the estimated annual risk of recurrent stroke is 20%. Antiplatelet agents such as aspirin, clopidogrel, and the combination aspirin/dipyridamole (Aggrenox) could be used for stroke prophylaxis. No trials have been reported that directly compare clopidogrel with aspirin/dipyridamole. The most recent secondary prevention trials showed that these agents are marginally better than aspirin alone, and, therefore, they may be the drugs of choice. Long-term anticoagulation with warfarin was advocated as the treatment of choice, but the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study Group demonstrated that warfarin is no better than aspirin in preventing strokes in patients with intracranial artery stenosis and is associated with bleeding complications.
  • Combination therapy
    • The combination of intravenous thrombolysis with consecutive on-demand endovascular mechanical thrombectomy may allow for early treatment initiation with high recanalization. In one small study, recanalization was achieved in 15 of 16 patients who received the combination therapy.12
  • Conclusion
    • Recanalization of the basilar artery is key to the successful treatment of basilar artery thrombosis and for improving its prognosis. Some unresolved issues need further clarification, such as the best method of recanalization (intra-arterial thrombolysis, mechanical thrombolysis, or combination), the time window for the treatment, and patient selection.
    • In the absence of clear evidence, treating these patients in the context of a clinical trial seems most reasonable. If such an alternative is not available and given the limited time window, then intravenous thrombolysis within 3 hours seems to be a reasonable alternative. In institutions with the service available, intra-arterial pharmacological or mechanical thrombolysis can be considered.

Consultations

  • Physical therapy and occupational therapy should be started soon after admission depending on the condition of the patient. Once the symptoms have stabilized, the patient should be mobilized out of bed and allowed full physical and occupational therapy activities.
  • Speech therapy should address the concerns of aspiration in patients with profound dysarthria and depressed cough reflex.

Diet

  • The patient should be restricted to taking nothing by mouth until the swallowing mechanism has been assessed and cleared and the airway has been protected. If the patient has a high risk of aspiration, a nasogastric or nasoduodenal tube should be placed.
  • If the swallowing abnormalities are so severe that recovery is expected to take weeks or months, a gastrostomy tube should be placed either surgically or percutaneously.

Activity

Some patients have fluctuating symptoms and signs, and these are often position related. Because of this, bed rest is advised until the symptoms have stabilized. In some patients, the severity of the deficits is such that free ambulation is not possible; however, patients should be mobilized out of bed and be actively involved with physical and occupational therapy.

Medication

The medications used in the treatment of patients with basilar artery thrombosis include thrombolytic agents, anticoagulants, antihypertensive agents, and antiplatelet agents. Some patients, particularly those with severe and active comorbid conditions, such as an acute myocardial infarction, require inotropic agents and vasopressors.

Several new oral anticoagulant medications 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.

Antihypertensive Agents

Control severe hypertension. Recommended for patients considered candidates for thrombolytic therapy who have a systolic blood pressure >185 mm Hg and/or a diastolic blood pressure >110 mm Hg.


Nicardipine (Cardene)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Adult

IV continuous drip: Start drip at 5 mg/h and titrate by 2.5 mg/h to target blood pressure q15min, not to exceed 15 mg/h; once target blood pressure reached, consider decreasing rate to 3 mg/h

Pediatric

Not established

Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)

Documented hypersensitivity; advanced aortic stenosis (reduction of diastolic pressure in these patients may worsen rather than improve myocardial oxygen balance)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Because nicardipine decreases peripheral resistance, monitoring of blood pressure during administration required; may occasionally produce symptomatic hypotension; caution advised to avoid systemic hypotension when administering drug to patients who have sustained acute cerebral infarction or hemorrhage
Adjust dose in renal/hepatic impairment; may cause lower extremity edema; allergic hepatitis has occurred but is rare
At high IV doses (5 mg/20 min), reported to increase hepatic venous pressure gradient by 4 mm Hg in cirrhotic patients (use with caution in patients with portal hypertension)
Careful dose titration advised when treating renally impaired patients


Labetalol (Normodyne, Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Adult

Initial dose: 5-10 mg IV bolus over 2 min; repeated doses can be given in escalating fashion from 20-80 mg IV push at 10-min intervals until desired blood pressure achieved or total of 300 mg has been administered
Alternatively, may give drip at rate of 2 mg/min

Pediatric

Not established

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia that results from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes

Documented hypersensitivity; heart failure; chronic obstructive pulmonary disease; bronchial asthma; second- or third-degree heart block; cardiogenic shock; severe bradycardia; hepatic failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy upon signs of liver dysfunction; in elderly patients, response rate may be lower and incidence of toxicity may be higher than in other patients


Nitroprusside sodium (Nitropress)

Produces vasodilation and increases inotropic activity of heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Adult

0.5-10 mcg/kg/min IV until blood pressure controlled

Pediatric

Not established

Documented hypersensitivity; compensatory hypertension; aortic coarctation; heart failure; congenital optic atrophy; tobacco-induced amblyopia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; sodium nitroprusside has ability to lower blood pressure and, thus, should be used only in patients with MAP >70 mm Hg


Enalapril (Vasotec)

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

Adult

0.650-1.25 mg IV q6h

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; diuretics may increase hypotensive effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe congestive heart failure

Thrombolytic Agents

Potential benefits of thrombolytic therapy for the treatment of thrombosis include fast dissolution of physiologically compromising pulmonary emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.


Alteplase (Activase)

This is a tPA. Safety and efficacy with concomitant heparin or aspirin during first 24 h after symptom onset have not been investigated. Only drug approved for use in patients within 3 h of onset of acute ischemic stroke.

Adult

IV: 0.9 mg/kg; not to exceed 90 mg; 10% of dose to be administered over 2-3 min and the rest over 1 h
Intra-arterial: 0.3 mg/kg; not to exceed 10-20 mg

Pediatric

Not established

Drugs that alter platelet function (eg, aspirin, dipyridamole, abciximab) may increase risk of bleeding prior to, during, or after therapy; current guidelines prohibit use of any anticoagulant or antiplatelet agents for 24 h after IV tPA; interventionalists who use intra-arterial tPA empirically give heparin afterward to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications

Documented hypersensitivity; active systemic or intracranial bleeding; intracranial neoplasm; AVM; concurrent heparin with aPTT >1.5 times control or concurrent warfarin with INR >1.6; coagulopathies; recent major surgery; head injury or stroke in previous 3 mo; history of ICH

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke (doses >0.9 mg/kg may cause ICH)

Anticoagulant agents

Rationale for use of these agents is to prevent recurrent embolism or extension of the thrombosis.


Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Adult

Although no nomogram exists for its use, authors do not regularly administer IV bolus; usually start IV drip at 1000 U/h; aPTT checked at 4 h, and infusion adjusted accordingly until aPTT of 1.5-2 times control achieved; drip also can be started at dose of 18 U/kg/h
Prophylaxis of deep vein thrombosis: 5000 U q12h SC

Pediatric

Not established

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Documented hypersensitivity; active systemic or intracranial bleeding; severe thrombocytopenia or blood dyscrasias; hypersensitivity during or after eye, brain, or spinal cord surgery

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

In neonates, preservative-free heparin recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as a preservative; caution in severe hypotension and shock; monitor for bleeding in peptic ulcer disease, menstruation, increased capillary permeability, and with IM injections


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.
Tailor dose to maintain INR in range of 2-3. Used for long-term stroke prophylaxis.

Adult

Adjust PO dose to maintain INR between 2-3 for most indications and 2.5-3.5 for patients with prosthetic heart valves

Pediatric

Not established

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 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

X - Contraindicated; benefit does not outweigh risk

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Antiplatelet agents

Inhibit cyclooxygenase system, decreasing the level of thromboxane A2, a potent platelet activator.


Aspirin (Bayer Aspirin, Ascriptin, Anacin)

Inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low doses to inhibit platelet aggregation and improve complications of venous stasis and thrombosis. Used for long-term stroke prophylaxis.

Adult

81-1300 mg PO qd

Pediatric

Not established

Antacids and urinary alkalinizers may decrease effects; corticosteroids decrease serum levels; anticoagulants may cause additive hypoprothrombinemic effects and increase bleeding time; 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 studies in humans; may use if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid in patients with severe anemia, with history of blood coagulation defects, or who are taking anticoagulants


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; warfarin safety 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 studies 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 (eg, ulcers) with propensity to bleed


Aspirin 25 mg/dipyridamole 200 mg (Aggrenox)

Drug combination with antithrombotic action.
Aspirin inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low doses to inhibit platelet aggregation and to improve complications of venous stasis and thrombosis.
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 cAMP within platelets and formation of potent platelet activator thromboxane A2.

Adult

1 tab PO bid

Pediatric

Not established

Theophylline may decrease hypotensive effects of dipyridamole; antiplatelet activity of dipyridamole may increase heparin toxicity; antacids and urinary alkalinizers may decrease aspirin effects; corticosteroids decrease salicylate serum levels; anticoagulants may increase additive hypoprothrombinemic effects and bleeding time; 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 studies in humans; may use 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 who are taking anticoagulants; caution in hypotension; dipyridamole has peripheral vasodilating effects

More on Basilar Artery Thrombosis

Overview: Basilar Artery Thrombosis
Differential Diagnoses & Workup: Basilar Artery Thrombosis
Treatment & Medication: Basilar Artery Thrombosis
Follow-up: Basilar Artery Thrombosis
Multimedia: Basilar Artery Thrombosis
References
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Further Reading

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Keywords

basilar artery occlusion, anterior inferior cerebellar artery, AICA, posterior cerebral artery, PCA, atherothrombosis, embolism, arterial dissection, atherosclerotic occlusion, vertebrobasilar insufficiency, VBI, stroke, hypertension, partial basilar artery occlusion, intravenous thrombolysis, atherosclerotic basilar artery stenosis, occlusion of the distal basilar artery, pontine ischemia, locked-in syndrome, top-of-the-basilar syndrome, stroke, neck injury, chiropractic manipulation, atrial fibrillation.

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Contributor Information and Disclosures

Author

Salvador Cruz-Flores, MD, MPH, Professor of Neurology, Director of Souers Stroke Institute, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Mid-America Stroke Network and Neuroscience Critical Care Unit, St Louis University Hospital
Salvador Cruz-Flores, MD, MPH is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Neurology, American College of Physicians, American Heart Association, American Medical Association, American Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine
Disclosure: NovoNordisk Grant/research funds clinical trial; Photothera INC Grant/research funds clinical trial; IMRX therapeutics Inc Grant/research funds clinical trial; Coaxia Inc Grant/research funds clinical trial; Neurobiological Technologies Inc Grant/research funds clinical trial

Coauthor(s)

Sombat Muengtaweepongsa, MD, Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand
Disclosure: Nothing to disclose.

Medical Editor

Draga Jichici, BSc, MD, FRCP, Associate Clinical Professor, Department of Medicine, Division of Neurology and Critical Care Medicine, McMaster University, Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; Associate Director, Oregon Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association
Disclosure: Co-Axia Consulting fee Review panel membership; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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