P027: COAGULAPATHY AFTER TRAUMATIC BRAIN INJURY
Irieon K Walker, MD, Ramachandran Ramani, MD; University of Florida
An approximately 16-year-old male who was a pedestrian struck by a car at 45 MPH found comatose at the scene arrived to the ED with GCS 3 and non-reactive pupils bilaterally being bagged by EMS. He was intubated by the ED with etomidate and succinylcholine. Chest x-ray showed appropriate endotracheal tube positioning and no obvious pneumothorax. The patient’s pelvis appeared wide on pelvic x-ray so a pelvic binder was placed. FAST exam was negative. The patient was taken hemodynamically stable to the CT scanner. Trauma CT scans were obtained, which demonstrated diffuse cerebral edema, traumatic subarachnoid hemorrhage, bilateral subdural hematomas with compression of the brain leading to left-to-right subfalcine herniation, central incisural herniation, and tonsillar herniation, and complete obliteration of all basal cisterns and cortical sulci. CT scans also later confirmed a volume expanding pelvic ring injury with likely disruption of the bilateral sacroiliac joints. Initial formal neurologic evaluation in the ICU showed the patient had severe traumatic brain injury, GCS 3T, fixed non-dilated pupils, no movement to noxious stimulus in all extremities, 4/4 twitches, and absent corneal, cough, gag, and vestibulo-ocular reflex. The neurosurgical team felt it conceivable that emergent surgical decompression may save the patient’s life given his young age, recent intubation, and non-dilated pupils. The patient was then taken emergently for left decompressive hemicraniectomy. Intraoperatively, the patient was hyperventilated and resuscitated with 3 units of packed red blood cells, 1 liter 5% albumin, 2 liters plasmalyte, and 500 mL of 3% normal saline. At closing intraoperative ABG showed hemoglobin 10.9 and hematocrit 30.4. The surgeons noted the patient seemed oozy but were able to proceed with closing their incisions. Coagulation labs were sent and FFP requested from the blood bank. As closing concluded, the patient became increasingly more hemodynamically unstable requiring phenylephrine infusion, vasopressin boluses, and transfusion of another unit of packed red blood cells. Report was called, and the patient was quickly transported to intensive care unit. The patient arrived to the ICU with extreme hemodynamic instability and required multiple titrations of phenylephrine infusion as well as IV boluses of vasopressin and epinephrine to maintain physiologically normal values. The patient's surgical drains were also filling with bloody output relatively rapidly, and patient appeared to oozing from all surgical incisions. Initial hemoglobin and hematocrit were 2.9/9.2 and the first thromboelastogram was consistent with DIC. Massive transfusion protocol was initiated and the patient was given multiple units of packed red blood cells, FFP, platelets, and cryoprecipitate. Despite hyperventilation and aggressive medical management, the patient had sustained elevated intracranial pressures in the 80s. Once the patient was hemodynamically stable, neurologic examination was conducted and met criteria to proceed with formal brain death exam which did not show any evidence of cortical or brainstem activity. Coagulopathy after traumatic brain injury has been described in the literature. This case provides an opportunity to discuss the pathophysiology of coagulopathy after traumatic brain injury and discuss the challenging complexity of perioperative care for these patients for the anesthesiologist.