eMedicine Specialties > Emergency Medicine > Neurology
Vertebrobasilar Atherothrombotic Disease: Treatment & Medication
Updated: Jun 3, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Emergency Department Care
Vertebrobasilar atherothrombotic disease (VBATD) management in the emergency department (ED) varies on the basis of the patient's symptoms and condition.
- For patients with VBATD who have experienced ischemic infarcts, management falls into 2 major categories: supportive measures and interventions to reestablish patency in the infarct-related artery or to prevent occlusion of a vessel at risk for atherothrombotic or embolic occlusion.
- Airway issues must be addressed in patients with brainstem infarction resulting from VBATD.
- Compromise of ninth and tenth cranial nerves can blunt the gag reflex and inhibit even a conscious or awake patient from handling secretions effectively.
- Secure the airway of patient with an unstable course or severe deficits before starting prolonged diagnostic imaging studies.
- Patients who present to the ED with ischemic stroke are often hypertensive, even in the absence of premorbid blood pressure elevations.
- Given the autoregulatory curve's tendency to shift to the right during hypertension, most authors caution against lowering the blood pressure in the first 24-48 hours after onset of stroke.
- A precipitous drop in blood pressure can have a significant impact on cerebral perfusion pressure.
- Consider antihypertensive medication only in cases of concomitant hypertensive emergency (ongoing end-organ damage), mean arterial pressure (MAP) greater than 130 mm Hg, or systolic blood pressure greater than 220 mm Hg.
- Because most patients with significant neurologic symptoms are denied oral intake until swallowing mechanisms are evaluated, goals of intravenous fluid therapy are to provide isotonic hydration and to avoid hyperglycemia, which appears to exacerbate neuronal injury in stroke.
- Treat vomiting with antiemetics; vomiting may be severe in some brainstem infarctions.
- If a hemorrhagic lesion has been excluded, patients with VBATD are treated with antiplatelet agents or, in certain circumstances, an anticoagulant such as warfarin (see Medication).3 Reperfuse the infarct-related artery by intraarterial thrombolysis or percutaneous transluminal angioplasty (see Consultations).
Consultations
- Neurologist
- Neurosurgeon: Consultation with a neurosurgeon is indicated for surgical evacuation of cerebellar hemorrhages and to manage cerebellar infarction complicated by hydrocephalus.
- Interventional neuroradiologist
- Intraarterial thrombolysis: The high mortality rate associated with basilar artery occlusion and resulting brainstem infarction has prompted research into reperfusion therapy via intraarterial infusion of thrombolytic agents (see Medication). Several case series and small randomized controlled trials have shown promise with regards to recanalization and improved clinical outcomes in basilar artery occlusion and vertebrobasilar stroke.4
- Percutaneous transluminal cerebral angioplasty: Increasingly, investigators have described successful dilation of high-grade vertebral artery stenoses in patients with VBATD who did not respond to medical therapy. Although this approach is not without risk (rate of stroke as high as 40% in some series), other studies have described 80% success rates in restoring flow and eliminating symptoms.
Medication
Antiplatelet medications constitute first-line treatment for patients with vertebrobasilar atherothrombotic disease (VBATD). This approach is supported by a large body of clinical research in the secondary prevention of strokes, but its application to posterior circulation events is not well established.
Despite this, important inferences can be drawn from the European Stroke Prevention Study, which examined the efficacy of a daily regimen of 225 mg of dipyridamole and 990 mg of aspirin in 2500 patients randomized to receive drug therapy or placebo.5 All participants had a history of TIA or stroke. Fully one third had diseases classified as vertebrobasilar. During a 2-year follow-up study, combined incidences of stroke or death in patients with VBATD were 14% among those receiving treatment and 14% among those receiving placebos.
No randomized clinical trials have been conducted to determine antiplatelet therapy's efficacy in treating VBATD. Antiplatelet therapy's widely perceived benefits for cerebrovascular disease may prevent an ethically acceptable trial with a placebo arm.
Data from the International Stroke Trial (IST) revealed a small but real clinical benefit of antiplatelet therapy in patients who experienced a completed stroke.6 The IST results suggest that only 1% of patients may benefit from aspirin therapy.
Arguments for anticoagulant therapy in VBATD are much more tenuous. A nonrandomized, concurrent, cohort study suggested that anticoagulation provided superior stroke protection for patients with vertebrobasilar TIAs than for patients with carotid TIAs.7 No randomized clinical trials involving patients with vertebrobasilar TIAs have compared anticoagulants to antiplatelet therapy or to placebos.
A strong argument favoring use of anticoagulants in VBATD includes settings in which the embolic source of thrombi is known or suspected (eg, atrial fibrillation).
Use of low-molecular-weight heparins has shown no significant improvement in outcome over conventional treatments.
No clinical evidence supports using intravenous administered thrombolytics to patients with posterior circulation infarcts, let alone VBI. No published subgroup analyses of trials studying thrombolysis in the general stroke population suggest a beneficial role for thrombolytics in treating brainstem or cerebellar infarction. All thrombolytics are plasminogen activators and act either directly (urokinase, alteplase) or indirectly (streptokinase).
The scientific literature describes 5 case series totalling 150 patients with acute brainstem infarction who received intra-arterial thrombolysis. Recanalization of the infarcted artery was achieved in only 50-75% of patients in this limited sample; however, patients who experienced reperfusion had a mortality rate of 40-50%, which compares favorably with the 75-85% mortality rate associated with historical controls.
The incidence of intracerebral hemorrhage as a complication of treatment was apparently 10%, similar to rates seen in stroke trials using systemic thrombolysis.
Anticoagulants
These agents prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation.
Heparin
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse yet is able to inhibit further thrombogenesis. Prevents reaccumulation of clots after spontaneous fibrinolysis.
Adult
Loading dose: 40-170 U/kg IV
Maintenance infusion: 18 U/kg/h IV
Alternatively, start with 50 U/kg/h IV, followed by continuous infusion of 15-25 U/kg/h IV; increase dosage by 5 U/kg/h q4h prn using aPTT results
Pediatric
Loading dose: 50 U/kg/h IV
Maintenance infusion: 15-25 U/kg/h IV
Increase dosage by 2-4 U/kg/h IV q6-8h prn using aPTT results
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; conversely, NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity
Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia
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
In neonates, preservative-free heparin recommended to avoid possible toxicity (ie, gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock
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.
Adult
5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR
Pediatric
0.05-0.34 mg/kg/d PO; adjust dose according to desired INR (infants may require doses at or near high end of this range)
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
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes mellitus; patients with protein C or S deficiency are at risk of developing skin necrosis
Antiplatelet agents
These agents inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.
Aspirin (Anacin, Ascriptin, Bayer aspirin)
Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Studies report 300 mg/d dose as effective as larger dose and may be associated with fewer adverse effects.
Adult
650 mg PO divided bid/qid; not to exceed 1.3 g/d
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
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
Ticlopidine (Ticlid)
Second-line antiplatelet therapy for patients who cannot tolerate aspirin or in whom aspirin is ineffective.
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 decreases to <1.2 x 109/L or if platelet count falls to <80 x 109/L
Clopidogrel (Plavix)
Inhibits platelet aggregation by inhibiting binding of ADP to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex. Rapidly absorbed from GI tract. Used as second-line therapy for patients with TIA crescendo symptoms who are already taking aspirin.
Adult
75 mg PO qd with or without food
Pediatric
Not recommended
Evening primrose oil, garlic, ginger, ginkgo biloba, grapeseed extract increase effects; warfarin increases risk of bleeding
Documented hypersensitivity; lactation; active bleeding from peptic ulcer; intracranial hemorrhage
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in patients at increased risk of bleeding from trauma, surgery, or other pathologic conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)
Thrombolytics
These agents restore perfusion in the infarct-related artery.
Alteplase (Activase)
Tissue plasminogen activator exerts effect on fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. Serum half-life is 4-6 min but half-life lengthened when bound to fibrin in clot. Used in management of acute myocardial infarction (MI), acute ischemic stroke, and pulmonary embolism (PE). Heparin and aspirin are not given for 24 h after tPA. Must be given within 3 h of stroke onset. Exclude hemorrhage by CT scan. If hypertensive, lower BP with labetalol, 10 mg IV. Safety and efficacy of concomitant administration with aspirin and heparin during first 24 h after onset of symptoms have not been investigated.
Adult
0.9 mg/kg IV over 60 min; not to exceed 90 mg; 10% of total dose administered as initial IV bolus over 1 min; administer only within 3 h of onset of stroke symptoms
Pediatric
Not established
Anticoagulants and antiplatelets may increase risk of bleeding; may give heparin with and after alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications
Documented hypersensitivity; active internal bleeding, cerebrovascular accident or stroke within last 2 mo, intracranial or intraspinal surgery or trauma, intracranial hemorrhage on pretreatment evaluation, suspicion of subarachnoid hemorrhage, intracranial neoplasm, arteriovenous malformation or aneurysm, bleeding diathesis, or severe uncontrolled hypertension
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
Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase 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
More on Vertebrobasilar Atherothrombotic Disease |
| Overview: Vertebrobasilar Atherothrombotic Disease |
| Differential Diagnoses & Workup: Vertebrobasilar Atherothrombotic Disease |
 Treatment & Medication: Vertebrobasilar Atherothrombotic Disease |
| Follow-up: Vertebrobasilar Atherothrombotic Disease |
| References |
| « Previous Page | Next Page » |
References
Flossmann E, Rothwell PM. Prognosis of vertebrobasilar transient ischaemic attack and minor stroke. Brain. Sep 2003;126(Pt 9):1940-54. [Medline].
Feinberg WM, Albers GW, Barnett HJ. Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. Circulation. Jun 1994;89(6):2950-65. [Medline].
Coull BM, Williams LB, Goldstein LS. Anticoagulants and antiplatelet agents in acute ischemic stroke. Report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a Division of the American Heart Association). Neurology. 2002;59 (1):13-22. [Medline].
Brandt T, von Kummer R, Muller-Kuppers M. Thrombolytic therapy of acute basilar artery occlusion. Variables affecting recanalization and outcome. Stroke. May 1996;27(5):875-81. [Medline].
Sivenius J, Riekkinen PJ, Smets P. The European Stroke Prevention Study (ESPS): results by arterial distribution. Ann Neurol. Jun 1991;29(6):596-600. [Medline].
International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet. May 31 1997;349(9065):1569-81. [Medline].
Whisnant JP, Cartlidge NE, Elveback LR. Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study. Ann Neurol. Feb 1978;3(2):107-15. [Medline].
Becker KJ, Purcell LL, Hacke W. Vertebrobasilar thrombosis: diagnosis, management, and the use of intra- arterial thrombolytics. Crit Care Med. Oct 1996;24(10):1729-42. [Medline].
Caplan LR. Vertebrobasilar occlusive disease. In: Stroke: Pathophysiology, Diagnosis and Management. Vol 1. 1992:549-619.
Culebras A, Kase CS, Masdeu JC. Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke. A report of the Stroke Council, American Heart Association. Stroke. Jul 1997;28(7):1480-97. [Medline].
Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med. Dec 2003;10(12):1388-95. [Medline].
Froehling DA, Silverstein MD, Mohr DN. The rational clinical examination. Does this dizzy patient have a serious form of vertigo?. JAMA. Feb 2 1994;271(5):385-8. [Medline].
Libman RB, Kwiatkowski TG, Hansen MD. Differences between anterior and posterior circulation stroke in TOAST. Cerebrovasc Dis. 2001;11(4):311-6. [Medline].
Lipinski CA, Swanson ER. Vertebrobasilar distribution stroke mimicking transtentorial herniation. Ann Emerg Med. May 1998;31(5):640-2. [Medline].
Macleod MR, Davis SM, Mitchell PJ. Results of a multicentre, randomised controlled trial of intra-arterial urokinase in the treatment of acute posterior circulation ischaemic stroke. Cerebrovasc Dis. 2005;20(1):12-7. [Medline].
Ois A, Gomis M, Rodriguez-Campello A, et al. Factors associated with a high risk of recurrence in patients with transient ischemic attack or minor stroke. Stroke. Jun 2008;39(6):1717-21. [Medline]. [Full Text].
Phan TG, Wijdicks EF. Intra-arterial thrombolysis for vertebrobasilar circulation ischemia. Crit Care Clin. Oct 1999;15(4):719-42, vi. [Medline].
Piechowski-Jozwiak B, Bogousslavsky J. Basilar occlusive disease: the descent of the feared foe?. Arch Neurol. Apr 2004;61(4):471-2. [Medline].
Sauvaget E, Kici S, Petelle B. Vertebrobasilar occlusive disorders presenting as sudden sensorineural hearing loss. Laryngoscope. Feb 2004;114(2):327-32. [Medline].
Terada T, Higashida RT, Halbach VV. Transluminal angioplasty for arteriosclerotic disease of the distal vertebral and basilar arteries. J Neurol Neurosurg Psychiatry. Apr 1996;60(4):377-81. [Medline].
Voetsch B, DeWitt LD, Pessin MS. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol. Apr 2004;61(4):496-504. [Medline].
Further Reading
Keywords
vertebrobasilar atherothrombotic disease, VBATD, vertebrobasilar insufficiency, basilar artery occlusion, lateral medullary infarction, Wallenberg syndrome, stroke, transient ischemic attacks, TIA, vertebrobasilar atherothrombotic disease, vertebrobasilar insufficiency, VBI, labyrinthitis, vestibular neuronitis, benign paroxysmal positional vertigo, brainstem infarction, atherosclerosis, syncope, medial medullary infarct, basilar artery syndrome, subclavian steal syndrome, Horner syndrome, hypertension, diabetes mellitus, smoking, fibromuscular dysplasia, rotational occlusion, Bow hunter's stroke, vertebral artery dissection, vertebrobasilar aneurysm
