Joseph J. Lopez

Minimally invasive surgery (MIS) for trauma in pediatric cases remains controversial. Recent studies have shown the validity of using minimally invasive techniques to decrease the rate of negative and nontherapeutic laparotomy and thoracotomy. The purpose of this study was to evaluate the diagnostic accuracy and therapeutic options of MIS in pediatric trauma at a level I pediatric trauma center. We reviewed cases of patients aged 15 years and younger who had undergone laparoscopy or thoracoscopy for trauma in our institution over the past 20 years. Each case was evaluated for mechanism of injury, computed tomographic (CT) scan findings, operative management, and patient outcomes. There were 23 patients in the study (16 boys and 7 girls). Twenty-one had undergone diagnostic laparoscopy and 2 had had diagnostic thoracoscopy. In 16, there were positive findings in diagnostic laparoscopy. Laparoscopic therapeutic interventions were performed in 6 patients; the remaining 10 required conversion to laparotomy. Both patients who underwent diagnostic thoracoscopy had positive findings. One had a thoracoscopic repair, and the other underwent conversion to thoracotomy. There were 5 negative diagnostic laparoscopies. There was no mortality among the 23 patients. The use of laparoscopy and thoracoscopy in pediatric trauma helps to reduce unnecessary laparotomy and thoracotomy. Some injuries can be repaired by a minimally invasive approach. When conversion is necessary, the use of these techniques can guide the placement and size of surgical incisions. The goal is to shift the paradigm in favor of using MIS in the treatment of pediatric trauma as the first-choice modality in stable patients.

Repeated, intense contractile activity compromises the ability of skeletal muscle to generate force and velocity, resulting in fatigue. The decrease in velocity is thought to be due, in part, to the intracellular build-up of acidosis inhibiting the function of the contractile proteins myosin and troponin; however, the underlying molecular basis of this process remains poorly understood. We sought to gain novel insight into the decrease in velocity by determining whether the depressive effect of acidosis could be altered by 1) introducing Ca⁺⁺-sensitizing mutations into troponin (Tn) or 2) by agents that directly affect myosin function, including inorganic phosphate (P_i) and 2-deoxy-ATP (dATP) in an in vitro motility assay. Acidosis reduced regulated thin-filament velocity ( V_RTF) at both maximal and submaximal Ca⁺⁺levels in a pH-dependent manner. A truncated construct of the inhibitory subunit of Tn (TnI) and a Ca⁺⁺-sensitizing mutation in the Ca⁺⁺-binding subunit of Tn (TnC) increased V_RTFat submaximal Ca⁺⁺under acidic conditions but had no effect on V_RTFat maximal Ca⁺⁺levels. In contrast, both P_iand replacement of ATP with dATP reversed much of the acidosis-induced depression of V_RTFat saturating Ca⁺⁺. Interestingly, despite producing similar magnitude increases in V_RTF, the combined effects of P_iand dATP were additive, suggesting different underlying mechanisms of action. These findings suggest that acidosis depresses velocity by slowing the detachment rate from actin but also by possibly slowing the attachment rate.