Surgery
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Intestinal ischemia-reperfusion injury is a common and important clinical event associated with the activation of an endogenous inflammatory response. Some of the mediators of this response may be involved in the pathogenesis of multiple organ system failure. The purpose of this study was to determine whether remote organ dysfunction--specifically, acute lung injury--occurs after intestinal ischemia-reperfusion injury. ⋯ Lung microvascular permeability increased threefold after 120 minutes of intestinal ischemia and 120 minutes of reperfusion (0.10 +/- 0.01 vs. 0.35 +/- 0.05 [lung/blood counts per minute], p less than 0.05). Intestinal ischemia followed by reperfusion is associated with acute lung injury characterized by increased microvascular permeability, histologic evidence of alveolar capillary endothelial cell injury, reduced lung tissue ATP levels, and the pulmonary sequestration of neutrophils. These data confirm an acute lung injury associated with intestinal ischemia-reperfusion and suggest a possible pathogenic role for the neutrophil.
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To evaluate the significance of myocardial contusion, we evaluated 243 stable patients hospitalized for blunt chest trauma between 1982 and 1986. The groups were identified according to results of radionuclide angiography, mean injury severity score (ISS), and outcome. Group I (n = 71; mean ISS = 12.7) patients were those without myocardial contusion by radionuclide angiography. ⋯ There were no significant differences between the cardiac complication rate in the three groups, and each complication was present when the patient arrived in the emergency department. The predicted mortality rate based on ISS was 10% to 20% for patients with myocardial contusion, whereas the observed mortality rate for the groups (II and III) overall was 0.58%. We conclude that in the stable trauma patient myocardial contusion (1) does not by itself increase the risk of complication, (2) does not necessitate intensive care unit monitoring, (3) should be devalued when computing ISS scores, (4) may account for lengthy and often unnecessary hospitalization, and (5) in patients at risk for complications may be identified by ECG abnormalities on arrival to the emergency department.
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Tumor necrosis factor (TNF) is reported to cause a shock syndrome similar to that produced by endotoxin (LPS). The purpose of this study was to determine the relationship between TNF and LPS in causing shock. Eighty rats received infusions of either TNF, LPS, or TNF plus LPS, as compared with saline solution. ⋯ It was concluded that TNF does not cause hypotension or shock in the rat. TNF will cause lethal shock, however, if combined with a sublethal dose of endotoxin. This suggests that synergy between TNF and endotoxin is important in septic shock.