Airbag Associated Bilateral Internal Carotid Artery Dissection with Hyperdense Middle Cerebral Artery Sign - A Case Report

摘要

Although an uncommon injury, bilateral dissection of the internal carotid arteries can have devastating consequences. Awareness and diagnosis has risen since it was described in 1967 by Yamada et al. However, given the vague presentation and difficulty in diagnosis, it is important to identify all associated signs and symptoms. We present a previously unreported finding of bilateral hyperdense middle cerebral arteries in the absence of previously described contributing factors. Knowledge of this highly specific sign in patients involved in airbag-associated motor vehicle accidents can contribute to the early diagnosis and treatment of such patients. Introduction Traumatic bilateral dissection of the internal carotid artery is a devastating injury. Although it leads to serious consequences, it remains underreported because it is overlooked. The mechanisms that cause this injury vary widely. Horseback riding, 1rollercoasters,2 strangulation,3 softballs4 and airbags,5 to name a few, have been named as culprits in the literature. As illustrated by our case, airbag deployment can result in injury as serious as bilateral carotid dissection and can be associated with a grim outcome. It is our intention to raise awareness to such presentations in order to facilitate diagnosis, since full recovery requires prompt recognition and treatment. Case Report A 29-year-old female was involved in an early evening motor vehicle accident in which her airbag deployed. According to paramedics, she briefly lost consciousness at the scene. She was transferred to our hospital from another primary center, where a non-contrast computed tomography (CT) had been performed. In the ER, her Glasgow Coma Scale (GCS) was 14, her pupils were 2.5mm and equally reactive, and she moved all four extremities spontaneously. The patient was admitted to the trauma service for observation. Her vital signs were normal, and a complete blood count showed all values to be normal, including hematocrit. Although neurologically intact, our patient was consistently agitated and no explanation could be provided at the time. A head CT at admission was unremarkable. Several hours later, the patient became increasingly agitated and confused. A repeat head CT at 1:00 am showed mild cerebral edema and a bilateral hyperdense middle cerebral artery (MCA) that was originally attributed to contrast administration (figure 1). By 6:00 am the patient was comatose and a head CT performed at that time showed loss of the gray-white matter interface in both hemispheres (figure 2). An angiogram performed following the CT revealed bilateral carotid dissection (figures 3-6); several hours later, the patient expired from a massive bilateral stroke despite aggressive medical treatment.