This Clinical Practice Guideline (CPG) addresses the topic of acute fluid resuscitation during the first 48 hours following a burn injury for adults with burns ≥20% of the total body surface area (%TBSA). The listed authors formed an investigation panel and developed clinically relevant PICO (Population, Intervention, Comparator, Outcome) questions. A systematic literature search returned 5978 titles related to this topic and after 3 levels of screening, 24 studies met criteria to address the PICO questions and were critically reviewed. We recommend that clinicians consider the use of human albumin solution, especially in patients with larger burns, to lower resuscitation volumes and improve urine output. We recommend initiating resuscitation based on providing 2 mL/kg/% TBSA burn in order to reduce resuscitation fluid volumes. We recommend selective monitoring of intra-abdominal and intraocular pressure during burn shock resuscitation. We make a weak recommendation for clinicians to consider the use of computer decision support software to guide fluid titration and lower resuscitation fluid volumes. We do not recommend the use of transpulmonary thermodilution-derived variables to guide burn shock resuscitation. We are unable to make any recommendations on the use of high-dose vitamin C (ascorbic acid), fresh frozen plasma (FFP), early continuous renal replacement therapy, or vasopressors as adjuncts during acute burn shock resuscitation. Mortality is an important outcome in burn shock resuscitation, but it was not formally included as a PICO outcome because the available scientific literature is missing studies of sufficient population size and quality to allow us to confidently make recommendations related to the outcome of survival at this time.

The Burn Care Quality Platform (BCQP) consolidates data previously collected from the National Burn Repository and the Burn Quality Improvement Program into a single registry. Its data elements and their associated definitions are tailored to create consistency across other national trauma registries, namely the National Trauma Data Bank implemented by the American College of Surgeons Trauma Quality Improvement Program (ACS TQIP). The BCQP now includes 103 participating burn centers and has captured data from 375,000 total patients as of 2021. With 12,000 patients entered under the current data dictionary, the BCQP represents the largest registry of its kind. On behalf of the American Burn Association Research Committee, the aim of this whitepaper is to provide a succinct overview of the BCQP, showcasing its unique features, strengths, limitations, and relevant statistical considerations. This whitepaper will highlight the resources available to the burn research community and offer insight on proper study design when preparing to conduct a large data set investigation for burn care. All recommendations herein were formulated through the consensus of a multidisciplinary committee and based on the available scientific evidence.

Introduction: Hematopoiesis proceeds in a tiered pattern of differentiation, beginning with hematopoietic stem cells (HSC) and culminating in erythroid, myeloid, and lymphoid lineages. Pathologically altered lineage commitment can result in inadequate leukocyte production or dysfunctional cell lines. Drivers of emergency hematopoiesis after burn injury are inadequately defined. Burn injury induces a myeloid predominance associated with infection that worsens outcomes. This study aims to further profile bone marrow HSCs following burn injury in a murine model. Methods: C57BL/6 mice received burn or sham injury with ~12% total body surface area scald burn on the dorsal surface with subsequent sacrifice at 1, 2, 3, 7, and 10 days postinjury. Bone marrow from hindlimbs was analyzed for HSC populations via flow cytometry and analyzed using FlowJo Software (version 10.6). Event counts and frequencies were analyzed with multiple unpaired t tests and linear mixed-effect regression. Real-time polymerase chain reaction performed on isolated lineage-negative bone marrow cell RNA targeted PU.1, GATA-1, and GATA-3 with subsequent analysis conducted with QuantStudio 3 software. Statistical analysis and representation were performed on GraphPad software (Prism). Results: Flow cytometry revealed significantly elevated proportions of long-term HSCs at 3 days post-injury (P < 0.05) and short-term HSCs at days 2, 3, and 10 (all P < 0.05) in burn-injured mice. There was a sustained, but not significant, increase in proportions in the multipotent progenitor (MPP) 2 and 3 subpopulations in the burn cohort compared to sham controls. The common myeloid progenitor (CMP) proportion was significantly higher on days 3 and 10 (both P < 0.01), whereas the granulocyte-macrophage progenitor (GMP) proportion increased on days 1, 2, and 10 (P < 0.05, P < 0.01, P < 0.01, respectively). Although the megakaryocyte-erythrocyte progenitor (MEP) proportion appeared consistently lower in the burn cohort, this did not reach significance. mRNA analysis resulted in a downregulation of PU.1 on day 1 (P = 0.0002) with an upregulation by day 7 (P < 0.01). GATA-1 downregulation occurred by day 7 (P < 0.05), and GATA3 showed downregulation on days 3 and 7 (P < 0.05). Discussion: Full-thickness burn results in an emergency hematopoiesis via proportional increase of long-term HSC and short-term HSC/MPP1 subpopulations beginning in the early postinjury period. Subsequent lineage commitment displays a myeloid predominance with a shift toward myeloid progenitors with mRNA analysis corroborating this finding with associated upregulation of PU.1 and downregulation of GATA-1 and GATA-3. Further studies are needed to understand how burn-induced emergency hematopoiesis may predispose to infection by pathologic lineage selection.

Background: Pneumonia contributes to post-burn morbidity and mortality. Understanding the mechanisms that predispose burn patients to pneumonia is crucial to both stratifying patients at increased risk and developing targeted interventions. Methods: A prospective observational study was conducted with 47 human patients who sustained large burn injuries with serum collected on days 2 and 3 post-burn and assessed for Angiopoietin-1 (Ang-1) and -2 (Ang-2). C57BL/6 mice were subjected to either sham injury or a 12.5% total body surface area (TBSA) scald burn injury, and plasma and lungs were assessed. Results: Patients who developed pneumonia within 30 days of injury had higher serum Ang-2 and Ang-2/1 ratio on post-injury days 2 and 3. Similar to patient findings, we observed an increase in Ang-2 in burn mice compared to sham. Within the lungs of burn mice, we found significant increases in Tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (TIE2) receptor transcript Tek, downstream mediators TNFAIP3 Interacting Protein 2 (Tnip2) and phosphoinositide-3-kinase regulatory subunit 1 (Pik3r1), in addition to endothelial adhesion molecules intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), along with neutrophil infiltration and markers compared to sham. Conclusions: These findings suggest that burn injury increases Angiopoetin-2 and downstream signaling in the lungs, which may contribute to post-burn pulmonary dysfunction. Further studies are necessary to understand if modulating the Ang–TIE2 axis can protect against pneumonia post-burn.