Subject(s)
Cysts/diagnostic imaging , Cysts/etiology , Lung Diseases/diagnostic imaging , Lung Diseases/etiology , Thoracic Injuries/complications , Wounds, Nonpenetrating/complications , Child , Diagnosis, Differential , Dyspnea/etiology , Female , Humans , Hypoxia/etiology , Tomography, X-Ray ComputedABSTRACT
Empyema rarely complicates pneumonia. In a 361-bed regional pediatric hospital, 50 pleural empyemas were identified from 1988 through 1994; 17 (34%) occurred in the last 12 months of this period, for which the incidence was 3.3 per 100,000 of the population aged < or = 18 years (P < .05, chi 2 test). A significant seasonal prevalence was observed: 50% of cases occurred in the winter (P < .001, chi 2 test). In contrast with the findings of previous studies, in which empyemas predominantly occurred in infants, the median age of our patients was 7 years; underlying illnesses were present in only 10%, and all had community-acquired disease. Eighty-two percent had chest tubes inserted, 56% required a thoracotomy with pleural decortication, and 2% had a lobectomy. There were no deaths. Streptococcus pneumoniae was isolated in 40% of the cases; specimens in 44% of the cases were sterile. None of the empyemas were associated with Staphylococcus aureus or Haemophilus influenzae type b, and only one was caused by group A streptococcus. Among 13 S. pneumoniae isolates, the rate of resistance to penicillin was 15%; to erythromycin, 15%; to chloramphenicol, 31%; and to cefotaxime, 23%. The penicillin-resistance rate among blood and cerebrospinal fluid pneumococcal isolates was 17% during 1993-1994. Drug-resistant S. pneumoniae is now a recognized cause of pleural empyemas in children.
Subject(s)
Empyema, Pleural/microbiology , Pneumococcal Infections/microbiology , Adolescent , Adult , Age Factors , Anti-Bacterial Agents/therapeutic use , Child , Child, Preschool , Community-Acquired Infections/diagnosis , Community-Acquired Infections/drug therapy , Community-Acquired Infections/epidemiology , Drug Resistance, Microbial , Empyema, Pleural/diagnosis , Empyema, Pleural/epidemiology , Empyema, Pleural/therapy , Female , Humans , Infant , Male , Pneumococcal Infections/diagnosis , Pneumococcal Infections/epidemiology , Pneumococcal Infections/therapy , Seasons , Serotyping , Streptococcus pneumoniae/drug effects , Streptococcus pneumoniae/isolation & purification , Treatment OutcomeABSTRACT
Interstitial lung disease in children is a heterogeneous group of disorders of both known and unknown causes that share a common histologic characteristic (i.e., inflammation of the pulmonary interstitium that may resolve completely, partially, or progress to derangement of alveolar structures with varying degrees of fibrosis). The inflammatory process, evoked as a result of injury to alveolar epithelium and/or the endothelium, is responsible for alveolar wall thickening that is the histologic marker of ILD. This article extrapolates some of the known pathogenic mechanisms of ILD from adult and animal models and applies this information for a better understanding of the pathogenesis of ILD in children. The clinical manifestations vary and are often subtle and nonspecific. There is no consensus on specific criteria for the clinical diagnosis of ILD in children. There are no pathognomonic laboratory criteria for the diagnosis of ILD in children other than the characteristic findings on histologic examination of the lung. It is important to make the diagnosis early to minimize lung damage. Therapy is directed toward the reduction of the inflammatory response to minimize or prevent the progression to fibrosis. ILD suffers from lack of uniform guidelines for diagnostic evaluation, therapy, and prognostic indicators essential for critical monitoring of disease activity. No one medical center has enough cases of ILD in children to allow objective evaluation of a significant number of cases with adequate longitudinal follow-up to determine guidelines for optimal management and to identify accurate prognostic indicators. The organization of a multicenter approach will guide us towards a better understanding of ILD in children.
Subject(s)
Lung Diseases, Interstitial/diagnosis , Adrenal Cortex Hormones/administration & dosage , Adrenal Cortex Hormones/classification , Adrenal Cortex Hormones/therapeutic use , Biopsy , Bronchoalveolar Lavage Fluid/chemistry , Child , Child, Preschool , Humans , Infant , Infant, Newborn , Lung Diseases, Interstitial/drug therapy , Lung Diseases, Interstitial/etiology , Oxygen/therapeutic use , Respiratory Function TestsABSTRACT
Tumor necrosis factor, a mononuclear phagocyte-derived peptide produced in response to lipopolysaccharide, has been shown to mediate certain aspects of septic shock and multiple organ failure resulting from gram-negative septicemia. In the present investigation, pretreatment of animals with pentoxifylline inhibited lipopolysaccharide-induced serum tumor necrosis factor in a dose-dependent fashion. Pentoxifylline prevented the sequestration of neutrophils seen in animals given intravenous lipopolysaccharide. Furthermore, pentoxifylline protected animals from the lethal effects of an intravenous challenge with lipopolysaccharide. These data indicate that pentoxifylline inhibits lipopolysaccharide-induced tumor necrosis factor and may be an effective agent in mitigating the lethal consequences of sepsis and other disease processes mediated by this cytokine.
