The management of pediatric appendicitis: a survey of North American Pediatric Surgeons.

BACKGROUND/PURPOSE: Variation exists among pediatric surgeons in the management of pediatric appendicitis. The goal of this study was to determine current practice patterns and provide a foundation for evidence-based outcome studies that would standardize patient care. METHODS: Members of the American Pediatric Surgical Association (APSA) were surveyed. Data included preference of imaging, timing of operation, and opinions on interval appendectomy. Intraoperative principles surveyed included use of cultures, antibiotic irrigation, transperitoneal drains, and method of wound closure. Spectrum and duration of antibiotic coverage were assessed, as were discharge criteria. RESULTS: Survey response was 70%. A majority prefers computerized tomographic (CT) imaging and favors interval appendectomy in appropriate candidates. Seventy percent indicate a stable child with suspected appendicitis would be operated on in a semiurgent manner rather than emergently in their practice. Discrepancy exists in the type and duration of antibiotic coverage, impact of clinical parameters on antibiotic use, and utility of discharge criteria. CONCLUSIONS: This study consolidates current opinions on appropriate management of pediatric appendicitis, providing a foundation for evidence-based outcome studies capable of bringing conformity to the management of this surgical disease. Such studies would establish clinical practice guidelines that optimize resource utilization while maintaining quality care.

Systemic and pulmonary effector cell function after injury.

OBJECTIVE: Traumatic injury initiates a complex inflammatory response that is associated with end-organ dysfunction, immunosuppression, and the development of nosocomial infection. We hypothesize that the lungs of injured patients experience a unique inflammatory response to traumatic injury in which the ability of alveolar effector cells to respond to a bacterial challenge is impaired. DESIGN: Prospective, longitudinal comparative study. SETTING: The surgical intensive care unit of an ACS level I trauma center. PATIENTS: Forty consecutive multiple trauma patients requiring mechanical ventilation. MEASUREMENT: Blood and bronchoalveolar lavage fluid were collected on admission, 24, and 48 hrs postinjury. Interleukin (IL)-6, IL-8, and IL-10 were measured in each sample initially and after lipopolysaccharide stimulation by using an ex vivo model of whole blood and bronchoalveolar lavage fluid cellular contents. Five patients who underwent elective surgery formed a control group. MAIN RESULTS: Systemic and alveolar levels of IL-6, IL-8, and IL-10 increase dramatically after severe injury. Levels of IL-6 and IL-8 in trauma bronchoalveolar lavage fluid are significantly greater than those of the systemic circulation. Whereas whole blood up-regulates production of IL-6 and IL-8 in response to lipopolysaccharide, bronchoalveolar lavage fluid cellular contents do not. In contrast, bronchoalveolar lavage fluid and whole blood from injured patients contain similar amounts of IL-10 and both up-regulate IL-10 production in response to lipopolysaccharide. CONCLUSION: The lungs of injured patients experience a profound proinflammatory response to injury more severe than that of the systemic circulation. Within this setting, the ability of alveolar effector cells to respond to a bacterial challenge is diminished compared with that of systemic cells. As such, alveolar effector cell function after injury seems to be impaired, possibly explaining the high frequency of pulmonary infection among these patients.

Increased IL-10 production and HLA-DR suppression in the lungs of injured patients precede the development of nosocomial pneumonia.

The incidence of nosocomial pneumonia (NP) among injured patients is substantial. We hypothesize that traumatic injury induces alterations in local organ effector cell function that may predispose the lungs of injured patients to infection. It is the objective of this study to compare the systemic and alveolar effector cell response to injury and assess the relationship these have to the development of NP. Peripheral blood and bronchoalveolar lavage fluid (BAL) were collected from 10 elective surgery patients (controls) and 16 multitrauma patients at 12, 36, and 60 h post-injury. Systemic and alveolar levels of IL-8 and IL-10 were measured. CD11b expression on peripheral blood neutrophils (PBN) and alveolar neutrophils (AN) and HLA-DR expression on peripheral blood monocytes (PBM) and alveolar macrophages (AM) were measured. Alveolar levels of IL-8 and IL-10 were significantly higher than systemic levels after injury. HLA-DR expression was reduced on both PBM and AM after injury but was lowest on the AM. Six of 16 patients (38%) developed NP (NP+). There were no differences in cytokine levels (IL-8 and IL-10) or effector cell phenotype (CD11b and HLA-DR expression) within the systemic circulation of NP+ and NP- patients. In contrast, NP+ and NP- patients differed significantly in alveolar cytokine levels and alveolar effector cell phenotype. IL-8 was significantly higher in BAL form NP+ patients at all time points after injury. Furthermore, alveolar levels of IL-10 decreased in NP- patients but increased in NP+ patients. In all patients, AM HLA-DR expression was significantly reduced from normal controls 12 h post-injury. In NP-patients, AM HLA-DR expression returned to normal 60 h post-injury, whereas in NP+ patients, expression remained suppressed. These findings identify distinct trends in local organ cytokine production and alterations in effector cell phenotype that precede NP. The persistence of reduced HLA-DR expression amidst increasing levels of IL-10 in NP+ patients suggest that cell-mediated immune function is being suppressed. As such, local organ immunosuppression may be responsible for the development of nosocomial pneumonia in injured patients.