Articles: sepsis.
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Schweiz Med Wochenschr Suppl · Jan 1996
Review[Treatment of severe infections: should one always administer an aminoglycoside?].
Until recently, aminoglycoside antibiotics were the cornerstone for the treatment of severe infections. The rationale for using combination therapy containing beta-lactams and aminoglycosides was not only to broaden the antimicrobial spectrum but also to achieve enhanced bacterial killing by synergism and to prevent the emergence of antibiotic resistance. ⋯ A review of the literature suggests that the addition of an aminoglycoside to a broad-spectrum beta-lactam does not improve the outcome in nosocomial pneumonia and severe diffuse peritonitis. However, the lack of large prospective studies in severe sepsis or septic shock makes it impossible to draw any conclusion about the addition of an aminoglycoside, and the administration of these agents must be decided on an individual basis.
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While hyperoxia is commonly used for treating carbon monoxide poisoning, chronic nonhealing ulcers, acute traumatic and chronically ischemic wounds, and refractory osteomyelitis, its efficacy is unproven in numerous clinical situations, including treatment during severe sepsis. ⋯ Tissue pO2 may be an important regulator of gut barrier function. Hyperoxia treatment appears to play a major role in preserving gut barrier function.
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Despite recent advances in antibiotic therapy, aggressive operative intervention and intravenous hyperalimentation, sepsis, and multiple organ failure are still reported to contribute to significant morbidity and mortality in the surgical intensive care unit. In light of this, it is essential to determine the mechanism underlying the pathophysiology of sepsis so that better therapeutic interventions can be designed. Experimental studies indicate that murine polymicrobial sepsis induces a marked suppression in both lymphocytic and macrophage function associated with decreased cellular adenosine triphosphate levels and increased Ca2+. ⋯ We have presented evidence of marked changes in the rate of Ao in immune cells after the onset of sepsis. These data suggest the possibility that mediators released in response to septic insult contribute to the observed changes in immune cell function through the induction of Ao. Inasmuch, understanding the contribution of PCD to the pathophysiology of sepsis, should provide a better basis from which to develop more effective therapy for the septic patient.