Lap-belt syndrome: management of aortic intimal dissection in a 7-year-old child with a constellation of injuries.

We present a case of lap-belt motor vehicle injury in a 7-year-old male who was admitted with abdominal ecchymoses and pain with associated aortic intimal flap, bowel injury, hemoperitoneum, and retroperitoneal hematoma at initial imaging with CT. Most of these findings were confirmed at subsequent laparotomy, and the patient underwent operative repair of bowel injuries. His aortic intimal flap was followed with US and color Doppler imaging during which time he was treated conservatively until there was sonographic evidence of intimal healing. This patient illustrates a multimodality approach to imaging and conservative management.

The use of extracorporeal membrane oxygenation in infants with congenital diaphragmatic hernia.

The use of extracorporeal membrane oxygenation (ECMO) has revolutionized the care of the critical infant born with a congenital diaphragmatic hernia (CDH). In some respects, this is surprising given our current lack of understanding regarding optimal preoperative ventilation strategy, identification of patients most likely to benefit from ECMO, and the correct timing of hernia repair for the infant treated with ECMO. Historically, repair of CDH was considered one of the few true pediatric surgical emergencies. Mortality, however, was high. In the 1970s, ECMO was first utilized as a rescue therapy following repair of CDH when conventional methods failed. In the 1980s, advancements in neonatal intensive care and an understanding of the pathophysiology of pulmonary hypertension associated with CDH led to a strategy involving preoperative stabilization and delayed surgical intervention. Historical reviews demonstrate an improvement of survival in infants treated with ECMO from 56% to 71%. This paper will outline the advances in the care of the CDH patient and the approach used for treatment with ECMO.

Recombinant plasma gelsolin infusion attenuates burn-induced pulmonary microvascular dysfunction.

Reduced plasma concentrations of the extracellular actin-binding proteins gelsolin and Gc-globulin correlate with pulmonary failure and death in humans after injury. The purpose of this study was to investigate the role of plasma gelsolin in the pathophysiology of inflammation-induced lung injury. We postulated that plasma gelsolin levels decrease at an early time point after burn injury and that the intravenous infusion of gelsolin prevents burn-induced pulmonary microvascular dysfunction. Adult Sprague-Dawley rats were randomized to undergo a 40% body surface area thermal injury (Burn) or manipulation without burn (Sham). Plasma gelsolin and Gc-globulin concentrations were determined at various times during the first 6 days of injury by Western blotting. Other animals were randomized to receive either recombinant human gelsolin (0.078, 0.78, or 7.8 mg) or albumin (7.8 mg) before and 8 h after Burn or Sham. Twenty-four hours later, pulmonary microvascular permeability was assessed by measuring the capillary filtration by use of an isolated, perfused lung model. We found that plasma gelsolin levels of burn-injured rats decreased to 10% of normal levels within 12 h and remained below normal levels for up to 6 days postinjury. Gc-globulin values also fall, but to a lesser extent and only transiently. Treatment of burned animals with intravenous infusions of recombinant human gelsolin prevented the increase in pulmonary microvascular permeability that accompanies this injury. Our findings are consistent with the hypothesis that plasma gelsolin depletion contributes to the pathophysiology of pulmonary microvascular dysfunction during inflammation.

Rho inhibition decreases TNF-induced endothelial MAPK activation and monolayer permeability.

Our laboratory previously demonstrated that MAPK activation is an important signal during cytokine-induced endothelial permeability (Nwariaku FE, Liu Z, Terada L, Duffy S, Sarosi G, and Turnage R. Shock 18: 82-85, 2002). Because GTP-binding proteins have been implicated in MAPK activation, we now hypothesize that the GTP-binding protein Rho is a mediator of TNF-induced MAPK activation and increased endothelial permeability. Transmonolayer permeability was assessed in human lung microvascular cells by measuring transmonolayer electrical resistance. MAPK activity was assessed by using a phospho-specific immunoprecipitation kinase assay and by comparing Western blots for phospho-MAPK with total MAPK. MAPK inhibitors used were SB-202190 and PD-098059, whereas Clostridium botulinum C3 transferase was used as a Rho inactivator. Rho-associated coiled-coil kinase was inhibited with Y-27632. TNF increased pulmonary endothelial permeability in vitro and caused a rapid, sustained increase in endothelial p38 and extracellular signal-regulated kinase MAPK activity. Inhibition of p38 and extracellular signal-regulated kinase MAPK with SB-202190 and PD-098059, respectively, decreased TNF-induced endothelial permeability. C3 transferase attenuated TNF-induced MAPK activation and blocked TNF-induced endothelial permeability. Finally, inhibition of Rho-associated coiled-coil kinase with Y-27632 prevented both MAPK activation and TNF-induced decreases in transmonolayer resistance. Rho acts upstream of mitogen-activated protein kinases in mediating TNF-induced pulmonary endothelial leak.