BACKGROUND: The first use of HBOC-201 in severe traumatic brain injury (TBI) is presented. The use of noninvasive cerebral oximetric devices to follow clinical progress in a patient infused with HBOC-201 is reported and the literature of hemoglobin-based oxygen carriers (HBOCs) in brain injury is reported. CASE REPORT: A 21-year-old Jehovah's Witness who was hit and dragged by a motor vehicle was admitted to the University of New Mexico Hospital Level 1 Trauma Center Trauma Surgical Intensive Care Unit with severe TBI and extensive soft tissue loss resulting in profound anemia. The patient received infusion of HBOC-201 with regional and global oximetric monitoring. RESULTS: Chart abstraction was performed to identify clinically relevant physiologic markers of patient progress. We observed a marked increase in brain tissue oxygen saturations, central venous oxygen saturation, and hemodynamic variables after administration of HBOC-201. The patient subsequently suffered massive cerebral edema and died. CONCLUSIONS: Major HBOC trials to date have excluded severe TBI. We report the first use of an HBOC in severe TBI to correct profound anemia. The HBOC-201 rapidly corrected cerebral venous and central venous oxygen saturations. The patient's death may have been due to massive reperfusion injury from delayed repayment of cerebral oxygen debt in a severely ischemic brain.
BACKGROUND: The first use of HBOC-201 in severe traumatic brain injury (TBI) is presented. The use of noninvasive cerebral oximetric devices to follow clinical progress in a patient infused with HBOC-201 is reported and the literature of hemoglobin-based oxygen carriers (HBOCs) in brain injury is reported. CASE REPORT: A 21-year-old Jehovah's Witness who was hit and dragged by a motor vehicle was admitted to the University of New Mexico Hospital Level 1 Trauma Center Trauma Surgical Intensive Care Unit with severe TBI and extensive soft tissue loss resulting in profound anemia. The patient received infusion of HBOC-201 with regional and global oximetric monitoring. RESULTS: Chart abstraction was performed to identify clinically relevant physiologic markers of patient progress. We observed a marked increase in brain tissue oxygen saturations, central venous oxygen saturation, and hemodynamic variables after administration of HBOC-201. The patient subsequently suffered massive cerebral edema and died. CONCLUSIONS: Major HBOC trials to date have excluded severe TBI. We report the first use of an HBOC in severe TBI to correct profound anemia. The HBOC-201 rapidly corrected cerebral venous and central venous oxygen saturations. The patient's death may have been due to massive reperfusion injury from delayed repayment of cerebral oxygen debt in a severely ischemic brain.
Authors: Paul W Buehler; Yipin Zhou; Pedro Cabrales; Yiping Jia; Guoyong Sun; David R Harris; Amy G Tsai; Marcos Intaglietta; Andre F Palmer Journal: Biomaterials Date: 2010-02-10 Impact factor: 12.479