Dural composite hemangioendothelioma: The first intracranial case.

Background: Composite hemangioendothelioma (CHE) is a rare, locally aggressive neoplasm of intermediate malignant potential. It is composed of a mixture of vascular tumors with a predilection for the dermis and subcutis of the extremities. Case Description: In this report, we describe a 41-year-old man who presented with a 2-month history of headache, dizziness, and intermittent seizures. Magnetic resonance imaging showed a hemorrhagic, multilobulated, and dural-based mass with extension into the calvarium. The mass measured 10.3 × 4.8 × 4 cm along the interhemispheric fissure and encased the superior sagittal sinus. Excision was performed, and histopathologic examination revealed a heterogeneous mixture of vascular components consisting of epithelioid hemangioendothelioma, retiform hemangioendothelioma, and hemangioma. This is the first report of a primary intracranial CHE. Conclusion: The spectrum of mesenchymal neoplasms within the cranium expands to encompass CHE.

Use of Aspirin and P2Y12 Response Assays in Detecting Reversal of Platelet Inhibition With Platelet Transfusion in Patients With Traumatic Brain Injury on Antiplatelet Therapy.

BACKGROUND: At present, guidelines are lacking on platelet transfusion in patients with a traumatic intracranial bleed and history of antiplatelet therapy. The aspirin and P2Y 12 response unit (ARU and PRU, respectively) assays detect the effect of aspirin and P2Y 12 inhibitors in the cardiac population. OBJECTIVE: To describe the reversal of platelet inhibition after platelet transfusion using the ARU and PRU assays in patients with traumatic brain injury. METHODS: Between 2010 and 2015, we conducted a prospective comparative cohort study of patients presenting with a positive head computed tomography and a history of antiplatelet therapy. ARU and PRU assays were performed on admission and 6 hours after transfusion, with a primary end point of detection of disinhibition after platelet transfusion. RESULTS: One hundred seven patients were available for analysis. Seven percent of patients taking aspirin and 27% of patients taking clopidogrel were not therapeutic on admission per the ARU and PRU, respectively. After platelet transfusion, 51% of patients on any aspirin and 67% of patients on any clopidogrel failed to be reversed. ARU increased by 71 ± 76 per unit of apheresis platelets for patients taking any aspirin, and PRU increased by 48 ± 46 per unit of apheresis platelets for patients taking any clopidogrel. CONCLUSION: A significant percentage of patients taking aspirin or clopidogrel were not therapeutic and thus would be unlikely to benefit from a platelet transfusion. In patients with measured platelet inhibition, a single platelet transfusion was not sufficient to reverse platelet inhibition in almost half.

Utility of the Aspirin and P2Y12 Response Assays to Determine the Effect of Antiplatelet Agents on Platelet Reactivity in Traumatic Brain Injury.

BACKGROUND: Premorbid antithrombotic medication may worsen intracranial injury and outcome after traumatic brain injury (TBI). Routine laboratory tests are insufficient to evaluate platelet activity. OBJECTIVE: To profile the spectrum of platelet inhibition, as measured by aspirin and P2Y12 response unit assays, in a TBI population on antiplatelet therapy. METHODS: This single-center, prospective cohort study included patients presenting to our institution between November 2010 and January 2015 with a clinical history of TBI. Serum platelet reactivity levels were determined immediately on admission and analyzed using the aspirin and P2Y12 response unit assays; test results were reported as aspirin response units and P2Y12 response units. We report congruence between assay results and clinical history as well as differences in assay results between types of antiplatelet therapy. RESULTS: A sample of 317 patients was available for analysis, of which 87% had experienced mild TBI, 7% moderate, and 6% severe; the mean age was 71.5 years. The mean aspirin response units in patients with a history of any aspirin use was 456 ± 67 (range, 350-659), with 88% demonstrating therapeutic platelet inhibition. For clopidogrel, the mean P2Y12 response unit was 191 ± 70 (range, 51-351); 77% showed therapeutic response. CONCLUSION: Rapid measurement of antiplatelet function using the aspirin and P2Y12 response assays indicated as many as one fourth of patients on antiplatelet therapy do not have platelet dysfunction. Further research is required to develop guidelines for the use of these assays to guide platelet transfusion in the setting of TBI.

Prospective independent validation of IMPACT modeling as a prognostic tool in severe traumatic brain injury.

Clinical trials in traumatic brain injury (TBI) have been fraught with failure due in part to heterogeneity in pathology and insensitive outcome measurements. The International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) prognostic model has been purposed as a means of risk adjustment and outcome prediction for use in trial design and analysis. The purpose of this study was to evaluate the performance of the IMPACT model in predicting 6-month functional outcome and mortality using prospectively collected data at a large, Level 1 neurotrauma center. This population-based cohort study included all TBI patients ≥14 years of age admitted with a Glasgow Coma Scale (GCS) score of ≤8 (severe TBI) to the University of Pittsburgh Medical Center between July 1994 and May 2009. Clinical data were prospectively collected and linked to 6-month functional outcome (Glasgow Outcome Scale [GOS]) and mortality. The discriminatory power and calibration of the three iterations of the IMPACT model (core, extended, and lab) were assessed using multiple regression analyses and indicated by the area under the receiver operating characteristic curve (AUC). A sample of 587 patients was available for analysis; the mean age was 37.8±17 years. The median 6-month GOS was 3 (IQR 3); 6-month mortality was 41%. The prognostic models were composed of age, motor score, and pupillary reactivity (core model), Marshall grade on head CT and secondary insults (extended), and laboratory values (lab); all of these displayed good prediction ability for unfavorable outcome and mortality (unfavorable outcome AUC=0.76, 0.79, 0.76; mortality AUC=0.78, 0.83, 0.83, respectively). All model iterations displayed adequate calibration for predicting unfavorable outcome and mortality. Prospective, independent validation supports the IMPACT prognostic model's prediction of patient 6-month functional status and mortality after severe TBI. The IMPACT prognostic model is an effective instrument to assist TBI study design and analysis.