Abstract 1122‐000021: Delayed Vasospasm and Cerebral Ischemia Following Mild Traumatic Brain Injury

Abstract

Introduction : Post‐traumatic vasospasm (PTV) is a significant cause of morbidity and mortality following traumatic brain injury (TBI). 1 Delayed PTV is thought to occur due to inflammation from SAH. 1 The risk of symptomatic PTV is associated with the severity of TBI. 1,2,3 Treatment of PTV traditionally involves agents used in aneurysmal vasospasm such as Nimodipine. Intra‐arterial and intravenous verapamil and milrinone have been utilized to treat PTV. 4 We present a rare case of delayed cerebral ischemia caused by PTV without SAH treated with intra‐arterial milrinone and oral verapamil. Methods : This is a case report of a case of a 16‐day delay of cerebral ischemia secondary to PTV. Results : A 19‐year‐old female without significant medical history presented to the emergency room as the restrained driver in a motor vehicle collision involving a car versus a tree. The patient’s Glasgow Coma Scale score was 13 and the initial head CT did not demonstrate SAH with a Rotterdam score of 0. There were multiple fractures and soft tissue contusions noted on imaging which required surgical correction and splinting. The patient’s hospital stay was complicated by a large retroperitoneal hematoma requiring blood transfusions and surgical evacuation. 16 days after admission, the patient experienced sudden‐onset right upper extremity paralysis and weakness of the right leg. CT head demonstrated loss of gray‐white differentiation in the left middle cerebral artery (MCA) territory and CT angiography demonstrated 70% stenosis of the left supra‐clinoid internal carotid artery (ICA) and proximal left MCA. Cerebral angiography demonstrated 60% stenosis left supra‐clinoid ICA and 60% stenosis at the origin of the left MCA consistent with PTV. Left MCA stenosis improved to 20% post 10 mg intra‐arterial milrinone in the left ICA (Figure 1). The patient also received verapamil orally. Transcranial doppler demonstrated elevated peak systolic velocities at 298 cm/s in the left MCA and 276 cm/s in the left ICA. Six days later this improved to 150 cm/s in the left MCA and 151 cm/s in the left ICA. The patient continued to be unable to move her right side against gravity with dense expressive aphasia and dysarthria at discharge to inpatient rehabilitation. At follow‐up 4 weeks later, her right hemiparesis had improved significantly to being able to stand with assistance and her expressive aphasia had improved from one word to occasionally forming several word sentences. Conclusions : PTV is a potentially devastating complication of TBI. As our case demonstrates, the presence of mild TBI and absence of SAH may be falsely reassuring. 2 Additionally, our case report demonstrates that intra‐arterial milrinone causes radiographic improvement in PTV. Further studies are needed for the best screening and diagnostic exams for PTV and therapeutic interventions.