Following burn injury, the host is susceptible to bacterial infections normally cleared by healthy patients. We hypothesized that during the systemic immune response that follows scald injury, the host's altered immune status increases infection susceptibility. Using a murine model of scald injury under inhaled anesthesia followed by intraperitoneal infection, we observed increased neutrophil numbers and function at postburn day (PBD) 1 compared with sham-burned and PBD4 mice. Further, increased mortality, bacteremia, and serum IL-6 were observed in PBD1 mice after Pseudomonas aeruginosa (PA) infection compared with sham-burned and PBD4 mice infected with PA. To examine these disparate responses, we investigated neutrophils isolated at 5 and 24 h following PA infection from PBD1 and sham-burned mice. Five hours after infection, there was no significant difference in number of recruited neutrophils; however, neutrophils from injured mice had decreased activation, active-p38, and oxidative burst compared with sham-burned mice. In direct contrast, 24 h after infection, we observed increased numbers, active-p38, and oxidative burst of neutrophils from PBD1 mice. Finally, we demonstrated that in neutrophils isolated from PBD1 mice, the observed increase in oxidative burst was p38 dependent. Altogether, neutrophil activation and function from thermally injured mice are initially delayed and later exacerbated by a p38-dependent mechanism. This mechanism is likely key to the observed increase in bacterial load and mortality of PBD1 mice infected with PA.

Objective. To describe a profoundly immunocompromised (panleukopenia) child with septic shock who developed abdominal compartment syndrome (ACS) and was successfully treated with surgical decompression. Design. Individual case report. Setting. Pediatric intensive care unit of a tertiary children's hospital. Patient. A 32-month-old male with Fanconi anemia who underwent bone marrow transplantation (BMT) 5 days prior to developing septic shock secondary to Streptococcus viridans and Escherichia coli ACS developed after massive fluid resuscitation, leading to cardiopulmonary instability. Interventions. Emergent surgical bedside laparotomy and silo placement. Measurements and Main Results. The patient's cardiopulmonary status stabilized after decompressive laparotomy. The abdomen was closed and the patient survived to hospital discharge without cardiac, respiratory, or renal dysfunction. Conclusions. The use of laparotomy and silo placement in an unengrafted BMT patient with ACS and septic shock did not result in additional complications. Surgical intervention for ACS is a reasonable option for high risk, profoundly immunocompromised patients.

The clinical spectrum of infectious causes of upper airway obstruction has changed dramatically in the last few decades, especially after the introduction of vaccines against diphtheria and Haemophilus influenzae. Nevertheless, infectious causes of upper airway obstruction remain an important source of morbidity and potential mortality in the pediatric age group. Physicians caring for children need to be cognizant of the clinical presentation of this group of disorders because prompt recognition and early appropriate treatment are lifesaving. Epiglottitis, or supraglottitis as some authors prefer, is a potentially life-threatening bacterial infection of the epiglottis and surrounding tissues, including the aryepiglottic folds, the arytenoids, and the supraglottic larynx. Despite the virtual elimination of invasive H. influenzae type B infection, it is important for physicians caring for children to understand the management issues surrounding patients with supraglottitis to avoid disastrous outcomes. As illustrated in the following case, these children may not always present with classic features of supraglottitis.