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Spinal accessory neuropathy and internal jugular thrombosis after carotid endarterectomy
  1. GEORGE WOODWARD,
  2. RAM VENKATESH
  1. Department of Neurology, University of Kansas, and Neurology Section, VA Eastern Kansas Health Care System, VA, USA
  1. Dr George Woodward, Neurology Section (111), VA Medical Centre, Leavenworth, Kansas 66048, USA. Telephone 001 913 682 2000 extension 2441; fax 001 913 758 4225.

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Spinal accessory neuropathy is a rare complication of carotid endarterectomy (CEA).1 Internal jugular venous thrombosis after CEA has also been reported rarely, but is likely more common; as internal jugular venous thrombosis is often asymptomatic, or presents with non-specific pain, it is probably unrecognised in many cases.2 Concurrent ipsilateral spinal accessory neuropathy and internal jugular venous thrombosis after CEA is expected to be rare, and this is underscored by the lack of published cases. Despite this apparent rarity, a common pathogenetic mechanism for postoperative spinal accessory neuropathy and internal jugular venous thrombosis may well be present, at least in some cases, which may lead to the consideration of the possibility of both when either is discovered.

We report on a patient who developed right spinal accessory neuropathy and internal jugular venous thrombosis after right CEA.

A 59 year old man underwent right CEA for possibly symptomatic stenosis. Angiography had shown 90% stenosis of the right internal carotid. The operation was done under general anaesthesia. The carotid bifurcation was unusually distal, necessitating a long dissection and high retraction. No immediate postoperative complications were evident. The next day, the patient complained of mild pain at the operative site, but he did not notice any weakness. The pain spread into his right shoulder within several days; at that time, he also noted difficulty raising his right arm. His symptoms worsened further a few weeks later. The symptoms persisted, and he presented for neurological evaluation 4 months after CEA. At that time, he had some induration along the incision site and a palpable cord within the right supraclavicular fossa. There was moderate atrophy of the right sternocleidomastoid and trapezius, with right shoulder drooping and minor right scapular winging. Right arm abduction produced more prominent scapular winging and was limited to 90 degrees due to pain and weakness. Electrodiagnostic studies were consistent with partial right accessory neuropathy with minor denervation of the right trapezius. Cervical ultrasonography and MRI demonstrated right internal jugular venous thrombosis. The patient was treated with a shoulder support, analgesics, and low dose aspirin. There was no significant clinical change 1 year after CEA. Repeat electrodiagnostic studies were consistent with severe chronic right spinal accessory neuropathy, and repeat ultrasonography showed persistent right internal jugular venous thrombosis.

Spinal accessory neuropathy was first reported as a complication of CEA in 1982.3 Since then, there have been several case reports and small series.1 4 A 1996 review of reports of cranial neuropathy after CEA disclosed only one patient with spinal accessory neuropathy in over 3000 cases.1 Although the authors did not include several other reports3 4 which, taken together, may seem to suggest a somewhat higher incidence, the overall small number of reported cases in proportion to the hundreds of thousands of CEAs that have been done worldwide suggests that clinically significant spinal accessory neuropathy is a rare complication. Minor or transient spinal accessory neuropathy after CEA may be more frequent. The cause of spinal accessory neuropathy after CEA is usually not well established, but intraoperative nerve stretching or compression from retraction is most often invoked.4 Delayed onset (after 3 weeks) has been noted in some; for these patients, postoperative inflammation and scarring seem more likely causes. Spinal accessory nerve transection or ischaemia/infarction (arterial or venous) are other possibilities. As in our patient, high carotid dissection and retraction have been reported to precede spinal accessory neuropathy.1 4

The spinal accessory nerve courses along the internal jugular vein and near the internal carotid artery, typically well above the carotid bifurcation. It stands to reason that a high incision and retraction resulting from a high carotid bifurcation would place the nerve at risk. Whether this realisation may lead to any technical modification to decrease the risk of spinal accessory neuropathy in those with a high bifurcation is unclear.

From our search, internal jugular venous thrombosis after CEA has been reported in only one case.2 As Southcottet al noted, retraction of the internal jugular during CEA may cause complete occlusion, leading to thrombosis from venous stasis or endothelial injury. Other causes of internal jugular venous thrombosis include jugular cannulation, blunt cervical trauma, and a hypercoagulable state. Internal jugular venous thrombosis may occur within a week after neck dissection, often with recanalisation after several months.5

The presence of induration about the incision site and a palpable supraclavicular cord in our patient led us to suspect venous thrombosis. Internal jugular venous thrombosis may often be asymptomatic. Potential symptoms of internal jugular venous thrombosis include headache, dysphagia, and anterolateral neck pain, tenderness, and swelling. In addition to perivenous induration, fever and leukocytosis may occur.2

Common pathogenetic mechanisms for spinal accessory neuropathy and internal jugular venous thrombosis may include intraoperative traction, haematoma, and postoperative inflammation and scarring.

Although the onset of either spinal accessory neuropathy or internal jugular venous thrombosis in our patient cannot be determined precisely, it is likely that both developed at about the same time. The delayed worsening of spinal accessory neuropathy in this case suggests postoperative scarring or inflammation. The lack of improvement after a year, as in some other cases of spinal accessory neuropathy after CEA, implies considerable axonal injury, but does not clarify the manner of injury.

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