Abstract 206: Basilar Artery Entrapment Secondary to Longitudinal Clivus Fracture

• Published in: Stroke: vascular and interventional neurology 2024-11, Vol.4 (S1)
• Main Authors: Edalatpour, R, Miley, J T
• Format: Article
• Language: English
• Subjects: Fractures; Ischemia
• ISSN: 2694-5746; 2694-5746
• DOI: 10.1161/SVIN.04.suppl_1.206

IntroductionTraumatic clivus fractures are exceedingly uncommon skull base fractures that occur as a result of high‐energy craniofacial injury. The longitudinal subtype of clivus fractures are associated with a mortality rate of 67‐80%. Longitudinal clivus fracture have an exceptionally high risk of impingement and entrapment of the basilar artery and resultant ischemic infarction of the brainstem.MethodsElectronic charts of a patient with traumatic longitudinal clivus fracture and subsequent basilar artery entrapment were reviewed.ResultsWe present a 40 year old male with no past medical history who presented after a motorized scooter accident. The patient was riding a motorized scooter at a speed of 40 miles per hour without a helmet when he suddenly sustained a collision with a metal pole. The patient arrived via emergency medical services to the hospital and was minimally responsive with a GCS score of 5. The patient was intubated and underwent emergent CT imaging which revealed a longitudinal clivus fracture, right frontal depressed skull fracture, bilateral frontal sinus fractures, and a small amount of subarachnoid hemorrhage. In addition, CT angiographic imaging revealed high grade occlusion of the basilar artery. Subsequent MRI imaging of the brain revealed bilateral medial pontine ischemic infarction.ConclusionThe patient underwent emergent digital subtraction angiography which revealed entrapment of the basilar artery due to impingement from the longitudinal clivus fracture. The patient's basilar artery entrapment was not amenable to endovascular treatment. The patient was returned to the ICU for medical management and treatment of his other traumatic injuries. The patient's clinical neurologic exam remained poor over the subsequent week. Seven days after his traumatic brain injury, the patient suddenly developed a precipitous decline in clinical status. His pupils became unequal in size and minimally reactive, he became unresponsive to noxious stimuli, and his cough and gag reflex became weak. The patient became hypotensive, bradycardic and eventually suffered cardiac arrest. He was unable to be resuscitated and died. This case illustrates the fatality of a rare type of traumatic skull base fracture. All clivus fracture types can be associated with cranial nerve deficits, CSF leaks and the development of diabetes insipidus. However, the longitudinal clivus fracture subtype is highly associated with fatal injury to the vertebrobasilar system.