Historical Background

Reconstruction of the subclavian arteries via thromboendarterectomy was first described by Cate and Scott in 1957 and a year later, Crawford, DeBakey, and Fields described the technique of transsubclavian endarterectomy of the vertebral artery. In 1964 Parrott introduced the technique of transposition of the second portion of the subclavian artery to the common carotid artery. Transposition of the proximal vertebral artery to the common carotid artery was described by Clark and Perry in 1966 through a similar approach.

During the 1970s the saphenous vein was used to bypass vertebral artery origin stenoses. Eventually it was recognized that transposition techniques were superior solutions for proximal subclavian and vertebral disease. These have supplanted endarterectomy and bypass as the reconstruction options of choice. The approach to the distal vertebral artery was first described by Matas and later by Henry and was used for the treatment of traumatic injury. During the late 1970s, venous bypass and skull base transposition procedures to revascularize the distal vertebral artery were developed using a similar approach.

Indications

The most common disease affecting the vertebral artery is atherosclerosis. Less common pathologic processes include trauma, fibromuscular dysplasia, Takayasu disease, osteophyte compression, dissections, aneurysms and other arteritides.

Disease involving the vertebrobasilar arteries can lead to symptoms of posterior circulation ischemia. Approximately 25% of all ischemic strokes occur in the vertebrobasilar territory. One half of patients present initially with stroke, and 26% of patients present with transient ischemic symptoms rapidly followed by stroke. For patients who experience vertebrobasilar transient ischemic attacks, disease in the vertebral arteries portends a 22% to 35% risk of stroke over 5 years. The mortality associated with a posterior circulation stroke is 20% to 30%, which is higher than that for an anterior circulation event.

Ischemia affecting the temporooccipital areas of the cerebral hemispheres or segments of the brainstem and cerebellum characteristically produces bilateral symptoms. The classic symptoms of vertebrobasilar ischemia include dizziness, vertigo, drop attacks, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria and ataxia. Box 10-1 gives a complete list of symptoms. When patients present with two or more of these symptoms, the likelihood of vertebrobasilar ischemia is high.

In general, the ischemic mechanisms can be broken down into those that are hemodynamic and those that are embolic. Hemodynamic symptoms occur as a result of transient “end organ” (brainstem, cerebellum, occipital lobes, or all a combination of these) hypoperfusion and can be precipitated by postural changes or transient reduction in cardiac output. Ischemia from hemodynamic mechanisms rarely results in infarction; rather, symptoms are short lived, repetitive, and more of a nuisance than a danger. For hemodynamic symptoms to occur in direct relation to the vertebrobasilar arteries, significant occlusive pathology must be present in both of the paired vertebral vessels or in the basilar artery. In addition compensatory contribution from the carotid circulation via the circle of Willis must be incomplete. Alternatively, hemodynamic ischemic symptoms may follow proximal subclavian artery occlusion and the syndrome of subclavian or vertebral artery steal. In the later years of life, vertebral artery stenosis is a common arteriographic finding and dizziness is a common complaint. The presence of both cannot necessarily be assumed to have a cause-effect relationship. Surgical reconstruction is not indicated in an asymptomatic patient with stenotic or occlusive vertebral lesions, because these patients are well compensated from the carotid circulation through the posterior communicating vessels. The minimal anatomic requirement to justify vertebral artery reconstruction for hemodynamic symptoms is (1) stenosis greater than 60% diameter in both vertebral arteries if both are patent and complete or (2) the same degree of stenosis in the dominant vertebral artery if the opposite vertebral artery is hypoplastic, ends in a posteroinferior cerebellar artery, or is occluded. A single, normal vertebral artery is sufficient to adequately perfuse the basilar artery, regardless of the patency status of the contralateral vertebral artery.

It is estimated that up to one third of vertebrobasilar ischemic episodes are caused by distal embolization from plaques or mural lesions of the subclavian, vertebral, or basilar arteries or some combination of them. Arterial to arterial emboli can arise from atherosclerotic lesions, from intimal defects caused by extrinsic compression or repetitive trauma, and rarely from fibromuscular dysplasia, aneurysms, or dissections. Although fewer patients suffer from embolic phenomena than do those with hemodynamic mechanisms, actual infarctions in the vertebrobasilar distribution are most often the result of embolic events. Patients with embolic ischemia often develop multiple and multifocal infarcts in the brainstem, cerebellum, and occasionally, posterior cerebral artery territory. For patients with posterior circulation ischemia secondary to microembolism and appropriate lesions in a vertebral artery, the potential source of the embolus needs to be eliminated regardless of the status of the contralateral vertebral artery. Patients with symptomatic vertebrobasilar ischemia because of emboli are candidates for surgical correction of the offending lesion regardless of the condition of the contralateral vertebral artery. Surgical intervention is not indicated in asymptomatic patients who harbor suspicious radiographic findings.

Preoperative Preparation

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  A number of medical conditions may mimic vertebrobasilar ischemia. A precise diagnosis of vertebrobasilar ischemia begins with an accurate assessment of the manifesting symptom complex. An important aspect of the history is identifying triggering events such as positional or postural changes. This must be followed by efforts to exclude other causes for patient symptoms ( Box 10-2 ).

  
  
  
  

  Box 10-2

  
  

  
  

  
  

  
  

  
  
  
  
  
  

  Cardiac arrhythmia Pacemaker malfunction Cardioemboli Labyrinthine dysfunction CPA tumors

  Antihypertensives Cerebellar degeneration Myxedema Electrolyte imbalance Hypoglycemia

   

  
  

  
  

  CPA, Cerebellopontine angle.

  
  

  NONVASCULAR AND CARDIAC CONDITIONS THAT CAUSE OR MIMIC VERTEBROBASILAR ISCHEMIA
  
  
  
  
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  Duplex ultrasound is an excellent tool for detecting lesions in the carotid artery, but it has significant limitations when used to detect vertebral artery pathology. The usefulness of duplex ultrasound lies in its ability to confirm reversal of flow within the vertebral arteries and detect flow velocity changes consistent with a proximal stenosis.

  
  
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  Contrast-enhanced magnetic resonance angiography with three-dimensional reconstruction and maximum image intensity techniques provide full imaging of the vessels, including the supraaortic trunks and the carotid and vertebral arteries ( Fig. 10-1 ). Transaxial magnetic resonance images can readily diagnose both acute and chronic posterior fossa infarcts. Brainstem infarctions are often missed by computed tomography (CT) scan because they tend to be small and the resolution of the CT scan in the brainstem is poor. In patients who are candidates for vertebral artery reconstruction, magnetic resonance brain scans are performed preoperatively to ascertain whether infarctions have taken place in the vertebrobasilar territory.

  
  

  
  

  
  

  

  
  

  
  

  Four vessel cerebral magnetic resonance angiogram.

  
  
  
  
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  Selective subclavian and vertebral angiography remains the gold standard for preoperative evaluation of patients with vertebrobasilar ischemia. The most common site of disease, the vertebral artery origin, may not be well imaged with ultrasound or magnetic resonance angiography and often can only be displayed with oblique projections that are not part of standard arch evaluation. Patients with suspected vertebral artery compression should undergo dynamic angiography, which incorporates provocative positioning. Lastly, delayed imaging should be performed in order to demonstrate reconstitution of the extracranial vertebral arteries through cervical collaterals, such as the occipital artery ( Fig. 10-2 ) or via collaterals from the ipsilateral subclavian artery via branches of the thyrocervical trunk ( Fig. 10-3 ). Because of this collateral network, the distal vertebral and basilar arteries usually remain patent despite a proximal vertebral artery occlusion. A patent V3 segment can be exploited as a distal target for reconstruction.

  
  

  
  

  
  

  

  
  

  
  

  The distal vertebral artery being fed (black arrows) by an occipital collateral from the external carotid artery in a patient with distal vertebral artery occlusion. Retrograde filling of the distal vertebral artery is demonstrated (white arrow).

  
  

  
  

  
  

  

  
  

  
  

  The distal vertebral artery (double arrow) and basilar artery (single arrow) fed by thyrocervical collateral in a patient with proximal vertebral artery occlusion.

  
  
  
  
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  Preoperative aspirin is indicated.

  
  
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  Evaluation of cardiac risk is recommended by clinical profiling or in select patients through use of noninvasive stress testing.

  
  
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  Evaluation of vocal cord function should be performed in patients with a history of prior carotid surgery.

  
  
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  Prophylactic antibiotics should be administered within an hour of surgery.

  
  
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  Intraoperative arterial line monitoring of blood pressure is recommended.

Pitfalls and Danger Points

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  Proximal Vertebral Reconstruction

  
  
  
  
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    Low (C7) entry to the transverse spine process

    
    
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    Horner syndrome

    
    
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    Vagus nerve injury

    
    
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    Thoracic duct or lymph leak

  
  
  
  
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  Distal Vertebral Reconstruction

  
  
  
  
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    Spinal accessory nerve injury

    
    
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    Vagus nerve injury

    
    
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    Venous plexus bleeding

    
    
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    Carotid clamp injury and embolization