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Development of Carotid Cavernous Fistula After Traumatic Brain Injury

Tseng, Chih-Hung MD; Wu, Kun-Lin MD; Tsai, Su-Ju MD; Lew, Henry L. MD, PhD

American Journal of Physical Medicine & Rehabilitation: February 2013 - Volume 92 - Issue 2 - p 187–188
doi: 10.1097/PHM.0b013e318246648c
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From the Department of Physical Medicine and Rehabilitation, Tungs’ Taichung MetroHarbor Hospital, Taichung City, Taiwan (C-HT, K-LW); Department of Physical Medicine and Rehabilitation, School of Medicine, Chung Shan Medical University, and Department of Physical Medicine and Rehabilitation, Chung Shan Medical University Hospital, Taichung City, Taiwan (S-JT); Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University School of Medicine, Richmond, Virginia (HLL); and John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii (HLL).

All correspondence and requests for reprints should be addressed to: Su-Ju Tsai, MD, Department of Physical Medicine and Rehabilitation, School of Medicine, Chung Shan Medical University, No. 110, Section 1, Jianguo N. Road, Taichung City 402, Taiwan.

Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.

A 24-yr-old previously healthy man suffered a severe traumatic brain injury (TBI) secondary to a motorcycle accident. On initial examination, he had a Glasgow Coma Score of 7, in addition to multiple lacerations involving his head, face, and right thigh. Computed tomographic scan revealed an epidural hemorrhage over the left temporo-parieto-occipital region, contusion hemorrhage of right frontal and parietal lobes, and multiple fractures involving the skull base and facial bones (Figs. 1 A, B). After craniotomy and repair surgery for maxillary and mandibular fractures, he gradually regained consciousness (Glasgow Coma Score, 15). However, he had residual cognitive dysfunction in addition to weakness of his left limbs (strength, 3/5). During the following 2 mos, he participated in a comprehensive rehabilitation program and became able to ambulate with a quad cane.



Five months after the initial TBI, he returned, complaining of right orbital pain, intermittent diplopia and difficulty in writing. Ophthalmologic consultation revealed normal intraocular pressure and normal movement of extraocular eye muscles. However, a significant left homonymous hemianopia was identified. Immediate follow-up computed tomography showed a high-density lesion over the right parasellar region (Fig. 1 C). Confirmatory magnetic resonance imaging and angiography demonstrated a right carotid cavernous fistula (CCF) (Fig. 1 D). A week later, he presented with headache and the classic triad of CCF: exophthalmos, conjunctival injection, and an audible orbital bruit. Transarterial embolization surgery was performed with complete closure of the CCF. One month after the procedure, the patient recovered from all the symptoms and signs of CCF.

Carotid cavernous fistula is a rare but potentially fatal complication of TBI, occurring in 0.2% to 0.3% of craniofacial trauma cases.1,2 It typically occurs several days to several weeks after TBI. The abnormal shunting of high-flow arterial blood can cause vascular congestion around the cavernous sinus, leading to a number of ophthalmologic and neurologic symptoms, including blindness and intracranial hemorrhage.2,3 Diagnosis of CCF may be a challenge in patients with TBI and cognitive impairment, especially if the presentation is delayed. Clinicians treating patients with TBI (especially in cases involving a basilar skull fracture) should have a high index of suspicion regarding CCF, particularly if they notice the classical triad of exophthalmos, conjunctival injection, and an audible orbital bruit. Prompt diagnosis and early intervention may significantly improve patient outcome.1,4

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