Basilar Artery Thrombosis Treatment & Management

  • Author: Salvador Cruz-Flores, MD, MPH, FAHA, FCCM; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: May 10, 2012
 

Approach Considerations

All patients should be admitted to a stroke unit. Patients with unstable or fluctuating neurologic 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 neurologic intensive care unit (ICU).

Recanalization of the basilar artery is key to the successful treatment of basilar artery thrombosis and to improving its prognosis. Some unresolved issues need further clarification, such as the best method of recanalization (intra-arterial thrombolysis, mechanical thrombolysis, or a combination), the time window for the treatment, and patient selection.

In the absence of clear evidence, treating patients with basilar artery thrombosis in the context of a clinical trial seems most reasonable. If this option is not available (and given the limited time window), IV thrombolysis within 3 hours seems to be a reasonable alternative. In institutions in which the service is available, intra-arterial pharmacologic or mechanical thrombolysis can be considered.

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.

Stroke-related therapy

Treatment of patients with basilar artery thrombosis includes the following:

  • Hemodynamic management
  • Respiratory management
  • Thrombolysis
  • Intra-arterial thrombolysis
  • Combination therapy - The combination of IV thrombolysis with consecutive, on-demand, mechanical endovascular 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[13]

Sedation and paralysis

Sedation and paralysis should be avoided because they interfere with neurologic assessment of the patient. However, sedation alone can and should be used to maintain comfort. Under certain circumstances, such as the occurrence of neurogenic hyperventilation, the use of sedation and paralysis may be required to avoid hypocarbia, which can worsen the ischemic process.

Consultations

Physical 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 his or her 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.

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Hemodynamic Management

The goal of hemodynamic management 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).

Hypertension

If the patient has a fluctuating neurologic condition and his or her blood pressure requires close monitoring, an arterial catheter should be placed.

No evidence from randomized trials indicates that treating hypertension is better than not treating it. However, currently available guidelines for the management of acute stroke recommend the use of antihypertensives to lower blood pressure to a systolic value of less than 185 mm Hg or a diastolic value of less than 110 mm Hg if thrombolysis is being considered. (Some evidence, however, suggests that in selected cases, induced hypertension may be beneficial for limiting ischemic injury.)

Hypertension should also be treated if 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. Otherwise, treatment is indicated only when the diastolic blood pressure is greater than 120 mm Hg or the systolic blood pressure is greater than 220 mm Hg.

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.

Hypotension

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.

Unknown intravascular volume status

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.

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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.

Ventilation

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.

Synchronized, intermittent, mandatory ventilation may be a better mode for patients with poor respiratory drive. This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with the patient's inspiratory effort but allows the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort during the extra breaths.

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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 basilar artery occlusion. Moreover, the trial did not systematically study vascular anatomy in all patients.

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Intra-Arterial Thrombolysis

This has emerged as a therapeutic strategy despite the absence of randomized, controlled clinical trials examining its use in vertebrobasilar occlusion.

Several case series have been published on intra-arterial thrombolysis, with the average time to treatment ranging from 8-48 hours. Overall mortality rates have decreased from 46-75% to 26-60%.

The rate of hemorrhagic transformation is approximately 8%, which is a little higher than that for IV thrombolysis in anterior circulation, confirmed by a study in animal models. Indeed, a systematic analysis demonstrated that the morbidity and mortality of patients treated with intra-arterial thrombolysis are not all that different from those associated with IV thrombolysis, although recanalization was achieved more frequently with intra-arterial thrombolysis.[10]

The patient's condition at presentation appears to be the major prognostic factor for intra-arterial thrombolysis; patients with quadriplegia and/or coma have worse outcomes than do other patients.

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 described below and with recognition of the absence of evidence from randomized trials.

Thrombolytic agents

Thrombolytic agents include urokinase, pro-urokinase, streptokinase, and tPA. Urokinase is not on the market in the United States because of concerns regarding its production. Streptokinase has been discontinued by the manufacturer.

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 IV and intra-arterial thrombolysis; the dosage used is 0.3 mg/kg, up to a maximum of 10-20 mg intra-arterially.

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.

Guidelines

Some general guidelines should be followed when treating a patient with IV or intra-arterial thrombolysis.

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 being 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 brainstem infarcts, is even less clear than for other individuals with this type of occlusion

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Additional Pharmacologic and Mechanical Therapies

Anticoagulant and antiplatelet agents

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 antiplatelets, such as clopidogrel and the combination of aspirin and dipyridamole, in the treatment of acute basilar artery occlusion is not known.

Angioplasty

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 excellent and quick anatomic 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.

Embolectomy

Only one case report has described successful endovascular embolectomy in basilar artery thrombosis.[11] In the Mechanical Embolus Removal in Cerebral Ischemia (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 did those without recanalization.[12]

Thrombus retrieval

Thrombus retrieval has been 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 neurologic outcome is not known.

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Rehabilitation

Patients with brainstem, cerebellar, diencephalic, or occipital infarcts secondary to basilar artery occlusion have a significant degree of disability because of weakness, ataxia, swallowing difficulties, or other cranial neuropathies or due to a combination of these.

Patients with dysphagia are at significant risk for aspiration and pneumonia. Evaluation of these patients should be thorough and should include videofluoroscopy with modified barium swallow to assess for silent aspiration. Interventions for prevention of aspiration include compensatory strategies such as oromotor exercises, postural changes while swallowing, and facilitative strategies (including modification of bolus consistency, volume, and delivery).

Patients also need training on balance and gait. Using a patch on 1 eye or prisms can help diplopia.

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Stroke Prevention

Prevention strategies for basilar artery thrombosis, in addition to risk factor control, depend pharmacologically on the cause of the occlusion. For example, patients with a definite cardioembolic source, such as atrial fibrillation, should be treated with warfarin to maintain an INR of between 2 and 3.

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) can be used for stroke prophylaxis. No trials have been reported that directly compare clopidogrel with aspirin/dipyridamole. Secondary prevention trials showed that these agents are marginally better than aspirin alone; 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.

No definite indication currently exists for long-term anticoagulation in patients with noncardioembolic stroke.

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Contributor Information and Disclosures
Author

Salvador Cruz-Flores, MD, MPH, FAHA, FCCM  Professor of Neurology and Epidemiology, Sidney W Souers Endowed Chair, Director of Souers Stroke Institute, Cerebrovascular and Neurointensive Care Section, Director, Vascular Neurology Fellowship Training Program, Interim Chairman, Department of Neurology and Psychiatry, St Louis University School of Medicine; Director, Neuroscience Intensive Care Unit (5ICU), St Louis University Hospital

Salvador Cruz-Flores, MD, MPH, FAHA, FCCM 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 Society of Neuroimaging, American Stroke Association, National Stroke Association, Neurocritical Care Society, and Society of Critical Care Medicine

Disclosure: Axio inc Honoraria Review panel membership; Roche Honoraria Review panel membership; Lilly Honoraria Review panel membership

Coauthor(s)

Sombat Muengtaweepongsa, MD  Faculty, Department of Neurology, Thammasat University, Pathumthani, Thailand

Sombat Muengtaweepongsa, MD is a member of the following medical societies: American Academy of Neurology and Royal College of Physicians of Thailand

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; 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; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Additional Contributors

Draga Jichici, MD, FRCP, FAHA Associate Clinical Professor, Department of Neurology and Critical Care Medicine, McMaster University School of Medicine, Canada

Draga Jichici, MD, FRCP, FAHA is a member of the following medical societies: American Academy of Neurology, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Congress of Neurological Sciences, Canadian Critical Care Society, Canadian Medical Protective Association, Canadian Neurocritical Care Society, Neurocritical Care Society, Royal College of Physicians and Surgeons of Canada, and Society of Critical Care Medicine (USA)

Disclosure: Nothing to disclose.

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: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Diffusion-weighted MRI images showing a right cerebellar infarct.
Magnetic resonance angiography demonstrating the absence of flow in the vertebrobasilar system.
Right vertebral artery angiography showing an occlusion with no flow in the basilar artery.
Angiography performed after intra-arterial thrombolysis and angioplasty showing recanalization and perfusion of the basilar artery and its branches.
Hyperdense basilar artery (arrow).
Spiral CT angiography showing occluded basilar artery.
 
 
 
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