Benefit of extracorporeal membrane oxygenation in major burns after stun grenade explosion: Experience from a single military medical center.

INTRODUCTION: Explosion injury is very common on the battlefield and is associated with major burn and inhalation injuries and subsequent high mortality and morbidity rates. Here we report six victims who suffered from explosion injuries caused by stun grenade; all were treated with extracorporeal membrane oxygenation (ECMO) as salvage therapy. This study was aimed to evaluate the indications and efficacy of ECMO in acute and critically ill major burn patients. METHODS: This was a retrospective analysis of six patients from Tri-Service General Hospital, National Defense Medical Center in Taiwan. All suffered from major burns with 89.0±19.1% average of total body surface area over second degree (TBSA; range, 50-99%). ECMO was used due to inhalation injury in five patients and cardiogenic shock in one patient. The average interval to start ECMO was 26.5±19.0h (range, 14-63h). Venoarterial ECMO was used on in four patients due to unstable hemodynamic status, whereas venovenous ECMO was used in two patients for sustained hypoxemia. RESULTS: All patients had rhabdomyolysis with acute renal failure. The average duration of ECMO was 169.6±180.9h (range, 27-401h). All patients developed coagulopathy and needed debridement surgery during ECMO support, and five underwent torso escharotomy due to inspiratory compromise. Only one patient whose second and third degree burns covered 50% TBSA was successfully weaned from ECMO and survived; he was discharged after 221 hospital days. All patients who died had second and third degree burns covering over 90% of their TBSA. Three patients died of multiple organ failure, one died of septic shock, and the other died of cardiogenic shock. Overall survival rate was 16.7%. CONCLUSIONS: In acute and critically ill major burn patients, ECMO could be considered as a salvage therapy, particularly in those with inhalation injury and burn-related acute respiratory distress syndrome. However, ECMO does not seem to provide benefits for circulatory support in those with hemodynamic compromise. The use of ECMO in these patients is still investigational, as our data provided no benefit in terms of the outcomes or survival, particularly in those with more than 90% TBSA burns.

Exposure in utero to 2,2',3,3',4,6'-hexachlorobiphenyl (PCB 132) impairs sperm function and alters testicular apoptosis-related gene expression in rat offspring.

Toxicity of the polychlorinated biphenyls (PCBs) depends on their molecular structure. Mechanisms by prenatal exposure to a non-dioxin-like PCB, 2,2',3,4',5',6-hexachlorobiphenyl (PCB 132) that may act on reproductive pathways in male offspring are relatively unknown. The purpose was to determine whether epididymal sperm function and expression of apoptosis-related genes were induced or inhibited by prenatal exposure to PCB 132. Pregnant rats were treated with a single dose of PCB 132 at 1 or 10 mg/kg on gestational day 15. Male offspring were killed and the epididymal sperm counts, motility, velocity, reactive oxygen species (ROS) generation, sperm-oocyte penetration rate (SOPR), testicular histopathology, apoptosis-related gene expression and caspase activation were assessed on postnatal day 84. Prenatal exposure to PCB 132 with a single dose of 1 or 10 mg/kg decreased cauda epididymal weight, epididymal sperm count and motile epididymal sperm count in adult offspring. The spermatozoa of PCB 132-exposed offspring produced significantly higher levels of ROS than the controls; ROS induction and SOPR reduction were dose-related. In the low-dose PCB 132 group, p53 was significantly induced and caspase-3 was inhibited. In the high-dose group, activation of caspase-3 and -9 was significantly increased, while the expressions of Fas, Bax, bcl-2, and p53 genes were significantly decreased. Gene expression and caspase activation data may provide insight into the mechanisms by which exposure to low-dose or high-dose PCB 132 affects reproduction in male offspring in rats. Because the doses of PCB 132 administered to the dams were approximately 625-fold in low-dose group and 6250-fold higher in high-dose group than the concentration in human tissue levels, the concentrations are not biologically or environmentally relevant. Further studies using environmentally relevant doses are needed for hazard identification.

Sperm DNA damage correlates with polycyclic aromatic hydrocarbons biomarker in coke-oven workers.

OBJECTIVES: The aim was to determine whether occupational exposure to polycyclic aromatic hydrocarbons (PAHs) in men has adverse effect on semen quality. METHODS: Forty-eight coke-oven workers, including 16 topside-oven (TO) workers and 32 sideoven (SO) workers, were studied. Ambient PAHs exposure, urinary 1-hydroxypyrene (1-OHP) levels, and parameters of semen quality were determined. RESULTS: TO workers had significantly higher ambient PAHs exposure (3,436.1+/-3,411.0 vs. 1,123.1+/-1,829.3 ng/m3, P < 0.01), urinary 1-OHP levels (207.8+/-176.4 vs. 54.0+/-44.8 microg/g, P < 0.001), frequency of oligospermia (18.8 vs. 0%, P < 0.05), and morphological abnormality in sperm (32.3 vs. 14.6%, P < 0.01) than SO workers. Among cigarette smokers, TO workers had significantly higher rates of DNA denaturation in spermatozoa (alphaT) and percentage of sperm with increased DNA denaturation (COMP alphaT) levels than SO workers (246.2+/-49.5 vs. 198.1+/-30.3 for alphaT; 34.8+/-14.4 vs. 19.3+/-13.9% for COMP alphaT, P < 0.05). There was a positive correlation between urinary 1-OHP and alphaT, COMP alphaT, and abnormal sperm morphology and a tenfold increase in urinary 1-OHP associated with a 2.35-fold increase in alphaT, as well as a 1.07-fold increase in percentage of sperm with abnormal morphology. CONCLUSIONS: A potential risk of sperm dysfunction should be considered for workers occupationally exposed to high levels of PAHs. Cigarette smoking may aggravate this risk. Urinary 1-OHP can be used as a biomarker predicting sperm dysfunction.