Review of this case and presentation in this format was approved by the Institutional Review Board of Nationwide Children's Hospital. Informed consent for publication was obtained from the patient's mother and the patient was unable to assent given the residual effects of his TBI. The patient was a 15-year-old male who was admitted to the Pediatric Intensive Care Unit (PICU) with a severe TBI following a motor vehicle collision. He was a previously healthy teenager with a medical history significant only for attention deficit hyperactive disorder. His other injuries at the time of admission included bilateral pelvic fractures and a left internal carotid artery dissection. Following admission, a right femoral central venous catheter was placed for access during the management of his increased intracranial pressure (ICP). Due to the internal carotid artery dissection, a heparin infusion was started at 20 units/kg/hour with a low anti-Xa goal of 0.3-0.5 IU/mL. Full anticoagulation with a higher anti-Xa was deemed contraindicated due to the cerebral contusions associated with his TBI and concerns for intracranial bleeding. His hospital course was unremarkable and there was gradual resolution of the increased ICP related to his TBI. Due to clinical concern for thrombus formation, an ultrasound of the right leg was performed, revealing a non-occlusive catheter associated thrombosis in the right femoral vein. In consultation with neurosurgery, it was determined that anticoagulation was appropriate and therapeutic enoxaparin (40 mg twice a day) was started and the heparin infusion was discontinued. An anti-Xa level was obtained following the initiation of enoxaparin with a peak level of 0.55 IU/mL, within the desired therapeutic goal for our patient (0.35-0.7 IU/mL). Platelet count trends before, during and after enoxaparin therapy are presented in Figure 1. Following the initiation of enoxaparin, on day 13 of hospitalization, there was an increase in platelet count and hematology consultation was obtained. The increasing platelet count continued from hospital day 13 to 20. As other possible causes for the thrombocytosis were ruled out including anemia, infection and inflammation, medication causes were considered. It was at this time, day 19, that enoxaparin was discontinued. After the discontinuation of enoxaparin his platelet count continued to rise for one subsequent day followed by a gradual return of the platelet count to normal values. Due to a continued need to provide some level of anticoagulation for this patient's internal carotid artery dissection aspirin (81 mg daily) was started on hospital day 19 following the discontinuation of enoxaparin. As his acute medical concerns began to resolve the patient was transferred to an inpatient rehabilitation facility to continue working on mobility, self-care, cognition, and oral intake. He was able to be discharged home from inpatient rehabilitation approximately 2 months after his initial TBI.