Perfluorocarbons cause thrombocytopenia, changes in RBC morphology and death in a baboon model of systemic inflammation.

A perfluorocarbon (PFC) investigated for treatment of traumatic brain injury (TBI) delivers oxygen to support brain function, but causes transient thrombocytopenia. TBI can cause acute inflammation with resulting thrombocytopenia; an interaction between the PFC effects and TBI inflammation might exacerbate thrombocytopenia. Therefore, PFC effects on platelet (PLT) function and hemostasis in a lipopolysaccharide (LPS) model of inflammation in the baboon were studied. Animals were randomized to receive saline ±LPS, and ± one of two doses of PFC. PLT count, transmission electron microscopy, and microparticle populations were quantified at baseline (BL) and at 2, 24, 48, 72, and 96 hours; hemostatic parameters for aggregometry and for blood clotting were measured at baseline (BL) and days 3 and 4. Injection of vehicle and LPS caused thrombocytopenia within hours; PFCs caused delayed thrombocytopenia beginning 48 hours post-infusion. LPS+PFC produced a more prolonged PLT decline and decreased clot strength. LPS+PFC increased ADP-stimulated aggregation, but PFC alone did not. Microparticle abundance was greatest in the LPS+PFC groups. LPS+PFC caused diffuse microvascular hemorrhage and death in 2 of 5 baboons in the low dose LPS-PFC group and 2 of 2 in the high dose LPS-PFC group. Necropsy and histology suggested death was caused by shock associated with hemorrhage in multiple organs. Abnormal morphology of platelets and red blood cells were notable for PFC inclusions. In summary, PFC infusion caused clinically significant thrombocytopenia and exacerbated LPS-induced platelet activation. The interaction between these effects resulted in decreased hemostatic capacity, diffuse bleeding, shock and death.

Analgesic use in contemporary burn practice: Applications to burn mass casualty incident planning.

BACKGROUND: Determining the amount of analgesics required will help burn centers improve their ability to plan for a burn mass casualty incident (BMCI). We sought to quantify the amount of analgesics needed in an inpatient burn population. We hoped that assessing the analgesic use in daily burn care practice will potentially help estimate opioid needs in a burn mass casualty incident (BMCI). METHODS: We included patients with burns covering equal to or less than 30% total body surface area (TBSA), admitted from spring 2013 to spring 2015. Patient records were reviewed for analgesics and adjuncts, pain scores, age and TBSA. The doses of the different opioids administered were converted into morphine equivalent doses (MED). RESULTS: We enrolled 141 acute burn survivors with a mean TBSA of 8.2±0.6%. The lowest daily average MED per person was 24.6±2.0mg MED, recorded on the day of injury. The daily average MED per person increased until it peaked at 52.5±5.6mg MED at day 8 post-burn. Then, it declined to 24.6±3.4mg MED by day 14. Bivariate regression analysis of average MED by TBSA showed a significant positive correlation (p<0.001). The analysis of average MED by age showed a significant negative correlation (p<0001). CONCLUSION: Our study quantified opioid requirements in an inpatient burn population and identified TBSA (positively) and age (negatively) as significant predictors.