The Feasibility of Venovenous ECMO at Role-2 Facilities in Austere Military Environments.

INTRODUCTION: Venovenous extracorporeal membrane oxygenation (VV-ECMO) has been gaining use to bridge the recovery from acute respiratory distress syndrome (ARDS) refractory to conventional treatment. However, these interventions are often limited to higher echelons of military care. We present a case of lung salvage from severe ARDS in an Afghani soldier with VV-ECMO at a Role-2 (R2) facility in an austere military environment in Afghanistan. CASE: A 25-year-old Afghani soldier presented to an R2 facility with blast lung injury and multiple penetrating injuries following an explosion. The patient underwent immediate damage control laparotomy. The abdomen was left open for subsequent washouts and ongoing resuscitation. Due to his ineligibility for evacuation and worsening ARDS, despite 5 d of conventional ventilation strategies, he was started on VV-ECMO. The patient had immediate improvements in oxygenation, which continued for 10 d. Moreover, he underwent three transportations to the operating room without accidental decannulation or disruption of the VV-ECMO device. Despite significant improvements, the patient expired on postoperative day 15, due to an overwhelming intra-abdominal sepsis. CONCLUSION: As future advancements are sought, VV-ECMO may become a consideration for casualties with severe ARDS at the point of injury and at lower echelons of military care.

Non-hispanic whites have higher risk for pulmonary impairment from pulmonary tuberculosis.

BACKGROUND: Disparities in outcomes associated with race and ethnicity are well documented for many diseases and patient populations. Tuberculosis (TB) disproportionately affects economically disadvantaged, racial and ethnic minority populations. Pulmonary impairment after tuberculosis (PIAT) contributes heavily to the societal burden of TB. Individual impacts associated with PIAT may vary by race/ethnicity or socioeconomic status. METHODS: We analyzed the pulmonary function of 320 prospectively identified patients with pulmonary tuberculosis who had completed at least 20 weeks standard anti-TB regimes by directly observed therapy. We compared frequency and severity of spirometry-defined PIAT in groups stratified by demographics, pulmonary risk factors, and race/ethnicity, and examined clinical correlates to pulmonary function deficits. RESULTS: Pulmonary impairment after tuberculosis was identified in 71% of non-Hispanic Whites, 58% of non-Hispanic Blacks, 49% of Asians and 32% of Hispanics (p < 0.001). Predictors for PIAT varied between race/ethnicity. PIAT was evenly distributed across all levels of socioeconomic status suggesting that PIAT and socioeconomic status are not related. PIAT and its severity were significantly associated with abnormal chest x-ray, p < 0.0001. There was no association between race/ethnicity and time to beginning TB treatment, p = 0.978. CONCLUSIONS: Despite controlling for cigarette smoking, socioeconomic status and time to beginning TB treatment, non-Hispanic White race/ethnicity remained an independent predictor for disproportionately frequent and severe pulmonary impairment after tuberculosis relative to other race/ethnic groups. Since race/ethnicity was self reported and that race is not a biological construct: these findings must be interpreted with caution. However, because race/ethnicity is a proxy for several other unmeasured host, pathogen or environment factors that may contribute to disparate health outcomes, these results are meant to suggest hypotheses for further research.

Genetic variation in MYLK and lung injury in children and adults with community-acquired pneumonia.

OBJECTIVE: To investigate whether selected single nucleotide polymorphisms in the myosin light chain kinase gene are associated with more severe lung injury in children and adults with community-acquired pneumonia. Previous studies have demonstrated an association between single nucleotide polymorphisms in the myosin light chain kinase gene and increased severity of acute lung injury in adults. DESIGN: Prospective, case-control genetic association study. SETTING: Three tertiary children's hospitals and one adult healthcare system. PATIENTS: A total of 800 pediatric patients and 393 adult patients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Genetic variation in the myosin light chain kinase gene was examined. The pediatric cohort was predominantly composed of African American (n = 443) and Caucasian (n = 253) children. A total of 393 patients made up the adult cohort. Within the pediatric cohort, single nucleotide polymorphisms rs16834493, rs820463, and rs9840993 were genotyped in the African American patients, whereas single nucleotide polymorphisms rs960224, rs33264, rs11718105, and rs9289225 were genotyped in the Caucasian patients. One single nucleotide polymorphism (rs820336) was genotyped in both groups. Genotyping in the adult cohort included rs820336, rs860224, rs33264, and rs11718105. Genotyping was performed using the Taqman Assay. Data were analyzed separately for African Americans and Caucasians and for children and adults. No associations were observed between the myosin light chain kinase gene single nucleotide polymorphisms genotyped in children with community-acquired pneumonia and increased severity of lung injury. Similarly, no associations were observed between myosin light chain kinase gene single nucleotide polymorphisms genotyped in adults with community-acquired pneumonia and increased severity of lung injury. CONCLUSIONS: No association between the selected single nucleotide polymorphisms in the myosin light chain kinase gene and either the need for positive-pressure ventilation or the development of acute lung injury/acute respiratory distress syndrome was observed in children with community-acquired pneumonia. This suggests that variation in this gene may play less of a role in lung injury in children or adults with community-acquired pneumonia than in adults with sepsis or trauma.