Surgical infections
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Surgical infections · Jan 2004
Predictors of outcome for children with perforated appendicitis initially treated with non-operative management.
Initial non-operative therapy for children with perforated appendicitis has become increasingly popular with the advent of powerful broad-spectrum antibiotics. However, there is no consensus regarding which patients may be managed effectively with this strategy. We reviewed all children with perforated appendicitis who were treated initially with non-operative therapy to determine those characteristics that may predict a successful outcome. ⋯ Children with perforated appendicitis can be managed effectively with nonoperative therapy, even in the presence of intra-abdominal abscesses. However, the need for abscess drainage increases the failure rate, perhaps due to inadequate source control. Those patients with a phlegmon on CT scan as opposed to an abscess, are most likely to respond to non-operative management. Initial non-operative therapy of perforated appendicitis in children is appropriate under certain clinical circumstances, especially when the body itself or interventional radiology can achieve adequate source control.
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Surgical infections · Jan 2004
Comparative StudyInfluence of enteral and parenteral nutrition on splanchnic hemodynamics in septic patients.
Enteral nutrition is believed to augment splanchnic perfusion, thereby preserving splanchnic integrity, whereas parenteral nutrition does not offer this benefit. In an effort to study this, we compared splanchnic oxygen exchange and blood flow in critically ill, septic patients to normal controls during enteral or total parenteral nutrition. ⋯ Critically ill patients exhibited a hyperdynamic splanchnic state as indicated by the marked increase in HBFI and SplVO(2)I. However, neither nutrient regimen at clinically relevant rates altered splanchnic hemodynamics over the course of study. Thus, enteral nutrients do not appear to offer hemodynamic protection to the splanchnic system in critically ill patients.
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Surgical infections · Jan 2004
Longitudinal outcomes of intra-abdominal infection complicated by critical illness.
Critically ill surgical patients remain at high risk of adverse outcomes as a result of intra-abdominal infections, including prolonged length of stay, organ dysfunction, and death despite advances in critical care and innovations in management of the peritoneal cavity. We evaluated the causes and consequences of intra-abdominal infections among critically ill surgical patients in a single tertiary-care intensive care unit (ICU) over a decade. ⋯ Although outcomes are improving, generalized peritonitis still causes high organ dysfunction-related mortality among critically ill surgical patients. Further improvements in resuscitation, surgical technique, and pharmacotherapy of severe intra-abdominal infections are needed.
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Surgical infections · Jan 2004
Allogenic blood transfusion in the first 24 hours after trauma is associated with increased systemic inflammatory response syndrome (SIRS) and death.
Previous studies have documented that blood transfusion incites a substantial inflammatory response with the systemic release of cytokines. Furthermore, blood transfusion is a significant independent predictor of multiple organ failure in trauma. The objective of this study was to assess the risk of systemic inflammatory response syndrome (SIRS) and intensive care unit (ICU) admission, length of stay (LOS), and mortality in trauma patients who require blood transfusion. ⋯ Blood transfusion within the first 24 h was an independent predictor of mortality, SIRS, ICU admission, and ICU LOS in trauma patients. The use of blood substitutes and alternative agents to increase serum hemoglobin concentration in the post-injury period warrants further investigation.
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Surgical infections · Jan 2004
Sepsis-induced changes in macrophage co-stimulatory molecule expression: CD86 as a regulator of anti-inflammatory IL-10 response.
Sepsis remains a substantial risk after surgery or other trauma. Macrophage dysfunction, as a component of immune suppression seen during trauma and sepsis, appears to be one of the contributing factors to morbidity and mortality. However, whereas it is known that the ability of macrophages to present antigen and express major histocompatibility complex MHC class II molecules is decreased during sepsis, it is not known to what extent this is associated with the loss of co-stimulatory receptor expression. Our objectives in this study were, therefore, to determine if the expression of co-stimulatory molecules, such as CD40, CD80, or CD86, on peritoneal/splenic/liver macrophages were altered by sepsis (cecal ligation [CL] and puncture [CLP] or necrotic tissue injury (CL) alone; and to establish the contribution of such changes to the response to septic challenge using mice that are deficient in these receptors. ⋯ Together, these data suggest a potential role for the co-stimulatory receptor CD86/B7-2 beyond that of simply promoting competent antigen presentation to T-cells, but also as a regulator of the anti-inflammatory IL-10 response. Such a role may implicate the latter response in the development of sepsis-induced immune dysfunction.