A Review of Electrolyte, Mineral, and Vitamin Changes After Traumatic Brain Injury.

INTRODUCTION: Despite the prevalence of traumatic brain injury (TBI) in both civilian and military populations, the management guidelines developed by the Joint Trauma System involve minimal recommendations for electrolyte physiology optimization during the acute phase of TBI recovery. This narrative review aims to assess the current state of the science for electrolyte and mineral derangements found after TBI. MATERIALS AND METHODS: We used Google Scholar and PubMed to identify literature on electrolyte derangements caused by TBI and supplements that may mitigate secondary injuries after TBI between 1991 and 2022. RESULTS: We screened 94 sources, of which 26 met all inclusion criteria. Most were retrospective studies (n = 9), followed by clinical trials (n = 7), observational studies (n = 7), and case reports (n = 2). Of those, 29% covered the use of some type of supplement to support recovery after TBI, 28% covered electrolyte or mineral derangements after TBI, 16% covered the mechanisms of secondary injury after TBI and how they are related to mineral and electrolyte derangements, 14% covered current management of TBI, and 13% covered the potential toxic effects of the supplements during TBI recovery. CONCLUSIONS: Knowledge of mechanisms and subsequent derangements of electrolyte, mineral, and vitamin physiology after TBI remains incomplete. Sodium and potassium tended to be the most well-studied derangements after TBI. Overall, data involving human subjects were limited and mostly involved observational studies. The data on vitamin and mineral effects were limited, and targeted research is needed before further recommendations can be made. Data on electrolyte derangements were stronger, but interventional studies are needed to assess causation.

A prospective assessment of the medic autologous blood transfusion skills for field transfusion preparation.

BACKGROUND: Data demonstrate the benefit of blood product administration near point-of-injury (POI). Fresh whole blood transfusion from a pre-screened donor provides a source of blood at the POI when resources are constrained. We captured transfusion skills data for medics performing autologous blood transfusion training. METHODS: We conducted a prospective, observational study of medics with varying levels of experience. Inexperienced medics were those with minimal or no reported experience learning the autologous transfusion procedures, versus reported experience among special operations medics. When available, medics were debriefed after the procedure for qualitative feedback. We followed them for up to 7 days for adverse events. RESULTS: The median number of attempts for inexperienced and experienced medics was 1 versus 1 (interquartile range 1-1 for both, p = .260). The inexperienced medics had a slower median time to needle venipuncture access for the donation of 7.3 versus 1.5 min, needle removal after clamping time of 0.3 versus 0.2 min, time to bag preparation of 1.9 versus 1.0 min, time to IV access for reinfusion of 6.0 versus 3.0 min, time to transfusion completion of 17.3 versus 11.0 min, and time to IV removal of 0.9 versus 0.3 min (all p < .05). We noted one administrative safety event in which an allogeneic transfusion occurred. No major adverse events occurred. Qualitative data saturated around the need for quarterly training. CONCLUSIONS: Inexperienced medics have longer procedure times when training autologous whole blood transfusion skills. This data will help establish training measures of performance for skills optimization when learning this procedure.

Intense Light Pretreatment Improves Hemodynamics, Barrier Function and Inflammation in a Murine Model of Hemorrhagic Shock Lung.

INTRODUCTION: Hemorrhagic shock is a primary injury amongst combat casualties. Hemorrhagic shock can lead to acute lung injury, which has a high mortality rate. Based on studies showing the role of intense light for organ-protection, we sought to evaluate if intense light pretreatment would be protective in a murine model of hemorrhagic shock lung. MATERIALS AND METHODS: After exposure to standard room light or to intense light (10 000 LUX), mice were hemorrhaged for 90 minutes to maintain a mean arterial pressure (MAP) of 30-35 mmHg. Mice were then resuscitated with their blood and a NaCl infusion at a rate of 0.2 ml/h over a 3-hour period. During resuscitation, blood pressure was recorded. At the end of resuscitation, bronchoalveolar lavage was analyzed for alveolar epithelial barrier function and inflammation. To get insight into the relevance of intense light for humans, we performed a proteomics screen for lung injury biomarkers in plasma from healthy volunteers following intense light therapy. RESULTS: We found that intense light pretreated mice had improved hemodynamics and significantly lower albumin, IL-6, and IL-8 levels in their bronchoalveolar lavage than controls. We further discovered that intense light therapy in humans significantly downregulated proinflammatory plasma proteins that are known to cause acute lung injury. CONCLUSIONS: Our data demonstrate that mice exposed to intense light before hemorrhagic shock lung have less lung inflammation and improved alveolar epithelial barrier function. We further show that intense light therapy downregulates lung injury promoting proteins in human plasma. Together, these data suggest intense light as a possible strategy to ameliorate the consequences of a hemorrhagic shock on lung injury.