Treatment of Chronic Hypertrophic Burn Scars With a Fractional CO 2 Laser Is Well Tolerated in an Outpatient Clinic Setting.

INTRODUCTION: The necessity of treating hypertrophic burn scars has expanded significantly with increased burn survivorship. Ablative lasers, such as carbon dioxide (CO 2 ) lasers, have been the most common nonoperative option for improving functional outcomes in severe recalcitrant hypertrophic burn scars. However, the overwhelming majority of ablative lasers used for this indication require a combination of systemic analgesia, sedation, and/or general anesthesia due to the painful nature of the procedure. More recently, the technology of ablative lasers has advanced and is more tolerable than their first-generation counterparts. Herein, we hypothesized that refractory hypertrophic burn scars can be treated by a CO 2 laser in an outpatient clinic. METHODS: We enrolled 17 consecutive patients with chronic hypertrophic burn scars that were treated with a CO 2 laser. All patients were treated in the outpatient clinic with a combination of a topical solution (23% lidocaine and 7% tetracaine) applied to the scar 30 minutes before the procedure, Cryo 6 air chiller by Zimmer, and some patients received a mixture of N 2 O/O 2 . Laser treatments were repeated every 4 to 8 weeks until the patient's goals were met. Each patient completed a standardized questionnaire to assess tolerability and patient satisfaction of functional results. RESULTS: All patients tolerated the laser well in the outpatient clinic setting, with 0% indicating "not tolerable," 70.6% "tolerable," and 29.4% "very tolerable." Each patient received more than 1 laser treatment for the following complaints: decreased range of motion (n = 16, 94.1%), pain (n = 11, 64.7%), or pruritis (n = 12, 70.6%). Patients were also satisfied with the results of the laser treatments ("no improvement or worsened" = 0%, "improved" = 47.1%, and "significant improvement" = 52.9%). The age of patient, type of burn, location of burn, presence of skin graft, or age of scar did not significantly affect the tolerability of treatment or satisfaction of outcome. CONCLUSIONS: The treatment of chronic hypertrophic burn scars with a CO 2 laser is well tolerated in an outpatient clinic setting in select patients. Patients reported a high level of satisfaction with notable improvement in functional and cosmetic outcomes.

Association Between Adverse Childhood Experiences and Posttraumatic Stress Disorder Symptoms in Adults With Injury.

This case-control study examines the risk factors associated with acute stress disorder in patients with severe injury.

Potential contribution of mitochondrial DNA damage associated molecular patterns in transfusion products to the development of acute respiratory distress syndrome after multiple transfusions.

BACKGROUND: Massive transfusions are accompanied by an increased incidence of a particularly aggressive and lethal form of acute lung injury (delayed transfusion-related acute lung injury) which occurs longer than 24 hours after transfusions. In light of recent reports showing that mitochondrial (mt)DNA damage-associated molecular patterns (DAMPs) are potent proinflammatory mediators, and that their abundance in the sera of severely injured or septic patients is predictive of clinical outcomes, we explored the idea that mtDNA DAMPs are present in transfusion products and are associated with the occurrence of delayed transfusion-related acute lung injury. METHODS: We prospectively enrolled fourteen consecutive severely injured patients that received greater than three units of blood transfusion products and determined if the total amount of mtDNA DAMPs delivered during transfusion correlated with serum mtDNA DAMPs measured after the last transfusion, and whether the quantity of mtDNA DAMPs in the serum-predicted development of acute respiratory distress syndrome (ARDS). RESULTS: We found detectable levels of mtDNA DAMPs in packed red blood cells (3 ± 0.4 ng/mL), fresh frozen plasma (213.7 ± 65 ng/mL), and platelets (94.8 ± 69.2), with the latter two transfusion products containing significant amounts of mtDNA fragments. There was a linear relationship between the mtDNA DAMPs given during transfusion and the serum concentration of mtDNA fragments (R = 0.0.74, p < 0.01). The quantity of mtDNA DAMPs in serum measured at 24 hours after transfusion predicted the occurrence of ARDS (9.9 ± 1.4 vs. 3.3 ± 0.9, p < 0.01). CONCLUSION: These data show that fresh frozen plasma and platelets contain large amounts of extracellular mtDNA, that the amount of mtDNA DAMPs administered during transfusion may be a determinant of serum mtDNA DAMP levels, and that serum levels of mtDNA DAMPs after multiple transfusions may predict the development of ARDS. Collectively, these findings support the idea that mtDNA DAMPs in transfusion products significantly contribute to the incidence of ARDS after massive transfusions. LEVEL OF EVIDENCE: Prognostic study, level II; therapeutic study, level II.

Mitochondrial DNA damage associated molecular patterns in ventilator-associated pneumonia: Prevention and reversal by intratracheal DNase I.

BACKGROUND: Previous studies in isolated perfused rat lungs have revealed that endothelial barrier disruption after intratracheal administration of Pseudomonas aeruginosa (strain 103; PA103) only occurs after accumulation of extracellular mitochondrial DNA (mtDNA) damage-associated molecular patterns (DAMPs) in the perfusate and is suppressed by addition of DNase to the perfusion medium. Herein, we tested the hypothesis that intratracheal DNase-a route of administration readily translatable to patient with ventilator-associated pneumonia (VAP)-also enhances degradation of mtDNA and prevents bacteria-induced lung injury. METHODS: Intratracheal DNase was administered to isolated rat lungs either before or after intratracheal challenge with PA103 to determine if bacteria-induced mtDNA DAMP-dependent lung injury could be prevented or reversed by enhanced mtDNA degradation. To explore whether this concept is translatable to patients with VAP, consecutive patients suspected of VAP were prospectively enrolled. All patients suspected of VAP received a bronchoalveolar lavage (BAL) with quantitative culture for the diagnosis of VAP. Mitochondrial and nuclear DNAs were measured from the BAL. MtDNA DAMPs (i.e., ND6) were measured from serum at time of suspected diagnosis and at 24 to 48 hours afterward. RESULTS: Intratracheal PA103 caused significantly increased the vascular filtration coefficient (Kf) and perfusate mtDNA DAMPs. In contrast, lungs pretreated or posttreated with intratracheal DNase were protected from increases in Kf and mtDNA DAMPs. Patients with the diagnosis of VAP had significantly higher mtDNA DAMPs in the BAL (248.70 ± 109.7 vs. 43.91 ± 16.61, p < 0.05, respectively) and in the serum at 24 hours (159.60 ± 77.37 vs. 10.43 ± 4.36, p < 0.05; respectively) when compared with patients that did not have VAP. CONCLUSION: These findings in isolated perfused rat lungs and a cohort of severely injured patients reveal an association between bacterial pneumonia and accumulation of mtDNA DAMPs in the lung and serum. Furthermore, administration of intratracheal DNase I prevented and reversed pulmonary endothelial dysfunction evoked by PA103.