New horizons (Baltimore, Md.)最新文献

Sepsis and septic shock are common problems in the ICU and carry a very high mortality. Myocardial depression is a common finding in patients with sepsis, and is usually reversible as the patient recovers. Both exogenous mediators, such as endotoxin, and endogenous cytokines, including tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6, have been implicated as important factors in the pathophysiology of septic shock and the development of myocardial depression in sepsis. Nitric oxide has also been implicated in the pathophysiology of the cardiovascular response to sepsis. Better understanding of the roles and interactions of these substances will be necessary to develop more effective therapies without increasing morbidity and mortality.

Contemporary wound infection surveillance is inexact. Tracking down suspicious incisions with maximal accuracy to isolate the subset of healing failures attributable to established tissue invasion by infecting pathogens has a solitary purpose: to learn how to improve one aspect of surgical practice. Wound infection is always the result of complex, probabilistic interplay of numerous concealed variables. A wound infection rate, whether determined for a hospital, a specialty, a risk class, an operation type, or a surgeon, only approximates a degree of failure to achieve one kind of surgical perfection. Interpretation of any rate will be flawed if issues of accuracy and meaning are suppressed. Gathering and revealing circumstances of individual infections may heuristically affect surgical teams. Interpretation of surveillance wound infection rates, infection rate comparisons to standards as a means of performance measurement, and particularly the meaning of rate changes over time in a hospital are matters of more than academic importance. Given current health care reform and a widespread fascination with industrial process-improvement philosophy, wound infection surveillance programs may be natural test platforms for probing surgical relevance of several quality-improvement methodologies. It is not a trivial fact that wound infection shares important prototypical features with most contemporary surgical care process flaws: rare, random, multifactorial in cause, costly, and impossible to uniformly preclude or predict.

The most important risk factor in patients suffering from acute necrotizing pancreatitis is pancreatic infection, a factor that determines the course of the disease, its therapeutic management, and its outcome. The bacterial infection route is very likely via the colon. In patients with acute pancreatitis, the infection rate is about 40 to 70% within the first 3 wks. Bacteria most frequently found are those from the gastrointestinal tract: Escherichia coli, Pseudomonas species, Streptococcus fecalis, Enterococcus, and Staphylococcus aureus. Screening methods for infected necrotizing pancreatitis include fine needle puncture by ultrasonography or computed tomographic guidance with Gram staining and culture of the aspirate. We previously investigated different broad-spectrum antibiotics with regard to their efficacy at preventing infection. This analysis indicated that antibiotics have different efficacy factors based on pharmacodynamic properties. Imipenem and quinolones, in combination with metronidazole, are the drugs of choice for treating or preventing pancreatic infection, whereas aminoglycosides do not enter the pancreas and therefore are not indicated. Based on increasing evidence that patients with acute necrotizing pancreatitis will benefit by early and appropriate antibiotic therapy, we altered the approach in such patients with an immediate start of antibiotic therapy continued for at least 14 days. We have found a reduction of the infection rate to 33% (11/32) in the third week after the onset of the disease. This treatment of the infection and the possibility of delaying operative intervention resulted in optimal surgical conditions. However, further prospective, controlled, and randomized studies are necessary to determine which antibiotics and antimycotic therapeutic regimens should be chosen.

In the sequelae of massive traumatic stress, substantial impairment of immunologic reactivity has been demonstrated to correlate clinically with increased susceptibility to serious infection. Posttraumatic immune abnormalities consist basically of two coexistent mechanisms: Hyperinflammation and depression of cell-mediated immune responses. It is our understanding that the endogenous ability of the organism to survive overwhelming trauma is insufficient and requires exogenous support to prevent the conversion from systemic inflammatory response syndrome to bacterial sepsis and septic shock. The objectives of immunomodulatory interventions, which should be started as early as possible after tissue destruction, include a) prevention of excessive macrophage stimulation via neutralization of circulating endotoxins and exotoxins with high doses of polyvalent immunoglobulin and soluble complement receptors, b) global short-term (<72 hrs) down-regulation of inflammatory monocyte/macrophage and polymorphonuclear neutrophil activity, and c) restoration of cell-mediated immune performance to overcome posttraumatic functional paralysis. Among recent promising strategies, the use of granulocyte-macrophage colony-stimulating factor, pentoxifylline, and recombinant human interleukin-13 has been suggested, all of them predominantly down-regulating the Mphi (monocyte/macrophage) inflammatory potential. Cyclooxygenase inhibitors such as indomethacin and thymomimetic peptides can help normalize the immunoreactivity by restoring the forward-regulatory pathway of cell-mediated immunity responses. The efficacy of interferon to reduce infection and deaths in severely injured patients has been assessed in clinical trials. Still other compounds, i.e., CNI-1493, interleukin-11, tissue factor pathway inhibitors, and PGG-Glucan represent auspicious immunomodulatory approaches for control of posttraumatic or postoperative infections.

Ventilator-associated pneumonia (VAP) is a common infection in intensive care unit patients that results in high mortality and morbidity and increased duration of hospital stay. Clinical diagnostic methods are sensitive, but lack specificity. Quantitative analysis of specimens from the lower respiratory tract increases specificity. Bacteria causing VAP may originate from the patient's endogenous flora, other patients or hospital personnel, or from environmental sources. Aspiration or direct inoculation are the major routes of bacterial entry into the lower respiratory tract. The bacterial inoculum and host response in the lung are important factors for pathogenesis. Late-onset nosocomial pneumonia is often caused by Pseudomonas aeruginosa, Acinetobacter species, and Staphylococcus aureus. Streptococcus pneumoniae and Haemophilus influenzae, however, are the more common pathogens in early-onset disease. Oropharyngeal and gastric colonization with bacteria, cross-infection, as well as the indiscriminate use of antibiotics or invasive devices substantially increase the risk of VAP. An understanding of the epidemiology and pathogenesis of VAP, along with implementation of appropriate preventive measures, are needed to decrease the incidence, morbidity, and mortality associated with VAP.