Correspondence  |   October 2007
Abducens Nerve Palsy after Thyroidectomy with Unilateral Modified Neck Dissection
Author Notes
  • Tokushima Municipal Hospital, Tokushima City, Japan.
Article Information
Correspondence   |   October 2007
Abducens Nerve Palsy after Thyroidectomy with Unilateral Modified Neck Dissection
Anesthesiology 10 2007, Vol.107, 679-680. doi:10.1097/
Anesthesiology 10 2007, Vol.107, 679-680. doi:10.1097/
To the Editor:—
A 48-yr-old patient with right-sided thyroid carcinoma underwent subtotal thyroidectomy with right unilateral modified neck dissection (MND). MND involves removal of lymph node groups I–III while preserving all three of the functional structures, i.e.  , the internal jugular vein (IJV), the spinal accessory nerve, and the sternocleidomastoid muscle. Standard subtotal thyroidectomy was performed by two thyroid specialists. The patient was not reconstructed with any flaps and did not have postoperative radiation treatment or any findings of infection.1–3 On postoperative day (POD) 1, the patient's recovery was unremarkable, and his appetite was good. On POD 2, he developed nausea and lost his appetite. On POD 4, he reported severe headache and nausea. However, the surgeon in charge considered these complications to be induced by cervicogenic factors because of the typical neck-extended position, and prescribed antiemetics and analgesics. The patient was discharged from the hospital. On POD 7, he developed diplopia, transient visual obscuration, and continuous visual blurring. Cranial computed tomography and magnetic resonance imaging scans were normal. On POD 24, clinical examination revealed binocular papilledema, reduced visual acuity, and left abducens nerve palsy. The patient was hospitalized again, but the etiology could not be diagnosed. Only symptomatic treatment was given. The ophthalmologist consulted me about this case; pseudotumor cerebri was suspected (POD 36). Therapy was started with oral prednisolone (20 mg/day), acetazolamide (500 mg/day), and mecobalamin (1.5 mg/day). On POD 49, the clinical symptoms resolved. Ultrasonography showed that the right-side IJV had no flow, whereas the flow of the left-side IJV was normal (POD 57). In addition, cerebral angiography ruled out left transverse sinus thrombosis. On POD 80, the papilledema improved little by little.
This is the first report of a patient with pseudotumor cerebri undergoing unilateral MND. This case illustrates that severe neurologic complications after unilateral MND may develop, even in the presence of a prominent contralateral IJV, if the remaining venous collateral network, comprising the intraspinal and extraspinal vertebral system and the deep neck veins, is inadequate.
It is difficult to distinguish these common symptoms (headache, nausea and vomiting) after thyroid surgery from the almost identical symptoms caused by intracranial hypertension. This delayed a diagnosis of a right IJV thrombosis and subsequently pseudotumor cerebri. The most important and atypical finding in this case was the onset of the clinical symptoms. From January 2004 to February 2007, 354 patients underwent thyroid surgery at our hospital. Forty-eight hours postoperatively, 58% of these patients reported headache and/or head fullness. Postoperative nausea and vomiting (PONV) occurred in 45%. Headache occurred in 95.8% of patients and PONV occurred in 95.6% of patients within 24 h postoperatively, and the severity of these complications was decresaed 48 h postoperatively. There were no patients except the current one who reported no symptoms during the first postoperative 24 h followed by onset of severe headache and PONV after 36 h. Retrospectively, the time delay of more than 36 h between surgery and the onset of severe headache and PONV and the more difficult complications 48 h postoperatively were distinctive in this case. The blood loss volume was only 26 ml, the urinary volume was 250 ml, and the total infusion was 1,350 ml during the intraoperative period. For 24 h postoperatively, the patient had no PONV, and his appetite was good. It is therefore difficult to imagine that circulatory changes, including dehydration, were the main cause of thrombosis. The patient was given a percutaneous drain (OD = 3.3 mm) via  the front of the trachea to the front of the right IJV under the sternocleidomastoid muscle for 24 h postoperatively. The position of the drainage of the thyroid space is important because it is suspected to have induced mechanical compression of the right IJV in the current case.
Serious neurologic complications are extremely rare in patients undergoing unilateral radical neck dissection.4 Few patients with pseudotumor cerebri after unilateral radical neck dissection have been reported previously.5,6 In all cases, insufficient venous outflow via  the opposite transverse sinus and IJV was postulated. In the current case, cerebral angiography demonstrated occlusion of the right IJV and the left transverse sinus without extension of the cerebral venous circulation time. Some authors suggest a retrograde thrombosis of the sigmoid sinus with a subsequently compromised collateral flow via  emissary veins as a possible explanation for pseudotumor cerebri.7,8 In patients with cerebral venous outflow obstruction, resistance to venous drainage generates elevated venous back pressure.8 Elevated sinus pressure increases the resistance to cerebrospinal fluid absorption. In addition, lower flow is found consistently in the left IJV with little compensatory increase in flow after resection of the right IJV.9 In the current case, ultrasonography demonstrated that the flow in the left IJV remained within the normal range, and there was no compensatory increase in flow. Right IJV thrombosis, left transverse sinus occlusion, and a small compensatory increase in flow of the left IJV are thought to explain the pseudotumor cerebri in the current case. Previously, only intracranial involvement in the pathogenesis of pseudotumor cerebri was reported, but this case provides evidence for the involvement of extracranial vasculature. The restriction of venous outflow in the IJVs was associated with increased intracranial pressure, probably due to cerebral venous congestion. Abducens nerve palsy caused by elevated intracranial pressure is most likely a consequence of prolonged increased extracranial resistance to venous outflow.
In summary, the current case illustrates that a critical increase in intracranial hypertension after unilateral MND may develop, even in the presence of a contralateral IJV, if complete IJV thrombosis occurs after MND. The fact that the patency of the IJV cannot always be preserved, even after MND, is important when clinicians find atypical headache and PONV.
Tokushima Municipal Hospital, Tokushima City, Japan.
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