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Background: Anemia in burn patients is due to surgical blood loss and anemia of critical illness. Because the commitment paradigm of common bone marrow progenitors dictates the production of erythroid, myeloid, and lymphoid cells, we hypothesized that skewed bone marrow lineage commitment decreases red cell production and causes anemia after a burn injury., Methods: After anesthesia, B(6)D(2)F(1) mice received a 15% total body surface area dorsal scald burn. The sham group did not receive scald burn. Femoral bone marrow was harvested on 2, 5, 7, 14, and 21 postburn days (PBD). Total bone marrow cells were labeled with specific antibodies to erythroid (CD71/Ter119), myeloid (CD11b), and lymphoid (CD19) lineages and analyzed by flow cytometry. To test whether erythropoietin (EPO) could increase red blood cell production, EPO was administered to sham and burn animals and their reticulocyte response was measured on PBD 2 and PBD 7., Results: Burn injury reduced the erythroid cells of the bone marrow from 35% in sham to 17% by PBD 5 and remained at similar level until PBD 21. Myeloid cells, however, increased from 42% in sham to 60% on PBD 5 and 77% on PBD 21. Burn injury reduced reticulocyte counts on PBD 2 and PBD 7 indicating that the erythroid compartment is severely depleted. This depleted compartment, however, responded to EPO but was not sufficient to change red cell production., Conclusion: Burn injury skews the bone marrow hematopoietic commitment away from erythroid and toward myeloid cells. Shrinkage of the erythroid compartment contributes to resistance to EPO and the anemia of critical illness.

Background: Critically ill patients require transfusions because of acute blood loss and the anemia of critical illness. In critically ill burn patients, typically, no distinction is made between transfusions related to acute surgical blood loss and those related to the anemia of critical illness. We sought to identify the percentage of blood transfusions due to the anemia of critical illness and the clinical characteristics associated with these transfusions in severely burned patients., Methods: Sixty adult patients with ≥20% total body surface area (TBSA) burn who were transfused at least 1 unit of packed red blood cells during their hospitalization were studied. Clinical variables including age, %TBSA burn, Acute Physiology and Chronic Health Evaluation (APACHE) II score, number of ventilator days, inhalation injury, and number of operative events were correlated with the total number of packed red blood cell units and percentage of nonsurgical transfusions in these patients. Nonsurgical transfusions were defined as transfusions occurring after postoperative day 1 for each distinct operative event and were classified as being caused by the anemia of critical illness., Results: Patients were transfused an average of 16.6 units ± 21.2 units. Nonsurgical transfusions accounted for 52% of these transfusions. APACHE II score, %TBSA burn, number of ventilator days, and number of operative events, all correlated with total transfusions. However, nonsurgical transfusions correlated with only APACHE II score (p = 0.01) and number of ventilator days (p = 0.03). There was no correlation between nonsurgical transfusions and other clinical variables., Conclusion: The anemia of critical illness is responsible for >50% of all transfusions in severely burned patients. The initial severity of critical illness (APACHE II score) and duration of the critical illness (number of ventilator days) correlated with transfusions related to anemia of critical illness. Further investigation into the specific risk factors for these transfusions may help to develop strategies to further reduce transfusion rates.

Typically, burn wound infections are classified by the organisms present in the wound within the first several days after injury or later by routine surveillance cultures. With universal acceptance of early excision and grafting, classification of burn wound colonization in unexcised burn wounds is less relevant, shifting clinical significance to open burn-related surgical wound infections (SWIs). To better characterize SWIs and their clinical relevance, the authors identified the pathogens responsible for SWIs, their impact on rates of regrafting, and the relationship between SWI and nosocomial infection (NI) pathogens. Epidemiologic and clinical data for 71 adult patients with ≥ 20% TBSA burn were collected. After excision and grafting, if a grafted site had clinical characteristics of infection, a wound culture swab was obtained and the organism identified. Surveillance cultures were not obtained. SWI pathogen, anatomic location, postburn day of occurrence, and need for regrafting were compiled. A positive culture obtained from an isolated anatomic location at any time point after excision and grafting of that location was considered a distinct infection. Pathogens responsible for NIs (urinary tract infections, pneumonia, bloodstream and catheter-related bloodstream infections, pseudomembranous colitis, and donor site infections) and their postburn day were identified. The profiles of SWI pathogens and NI pathogens were then compared. Of the 71 patients included, 2 withdrew, 6 had no excision or grafting performed, and 1 had incomplete data. Of the remaining 62 patients, 24 (39%) developed an SWI. In these 24 patients, 70 distinct infections were identified, of which 46% required regrafting. Candida species (24%), Pseudomonas aeruginosa (22%), Serratia marcescens (11%), and Staphylococcus aureus (11%) comprised the majority of pathogens. Development of an SWI with the need for regrafting increased overall length of stay, area of autograft, number of operative events, and was closely associated with the number of NIs. The %TBSA burn and depth of the burn were the main risk factors for SWI with need for regrafting. The SWI pathogen was identified as an NI pathogen 56% of the time, with no temporal correlation between shared SWI and NI pathogens. SWIs are commonly found in severely burned patients and are associated with regrafting. As a result, patients with SWIs are subjected to increased operative events, autograft placement, and increased length of hospitalization. In addition, the presence of an SWI may be a risk factor for development of NIs.