Articles: sepsis.
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Septic shock is one of the leading causes of death in intensive care units, and its incidence is increasing. Mortality rates as high as 95% are reported, with rates of 60% or more even when diagnosed and treated promptly. This review examines the definition of septic shock, its pathogenesis, and supportive therapy, with particular attention to intervention during the septic shock cascade.
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Multicenter Study Clinical Trial
Role of calcium channel blockers in diabetic renal transplant patients: preliminary observations on protection from sepsis.
Diabetic recipients of kidney transplants have an excessively high risk of allograft loss, infectious complications with sepsis, cardiovascular events and early death. This study was designed in order to determine whether post-transplantation medical management influenced long-term results. ⋯ Allograft success and patient survivals may be improved and sepsis related events diminished when diabetic renal allograft recipients are treated with calcium channel blocking agents, plus or minus beta blockers. Considerable savings can be accomplished and graft results with these drugs can approach non-diabetic and live-related transplant results.
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Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi · Sep 1995
Hypothermia and sepsis: the major causes of mortality in gastroschisis.
From 1984 to 1993, 25 neonates with gastroschisis were treated at Chianghua Christian Hospital (CCH). Twenty-one patients were outborn, and only four were inborn babies. Eighteen patients were treated by primary fascial closure of the abdominal wall defect and seven, by the silastic sac technique. ⋯ Six patients (24%) developed sepsis and only one survived. Metabolic acidosis related to hypothermia and sepsis were the major causes of death in this study (P values of 0.024 and 0.01 respectively). It is no doubt that an experienced pediatrician is essential for immediate neonatal care to prevent unnecessary insults.
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Clin. Diagn. Lab. Immunol. · Sep 1995
Comparative StudyPattern of cytokines and pharmacomodulation in sepsis induced by cecal ligation and puncture compared with that induced by endotoxin.
The production of tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 and their pharmacomodulation were evaluated in a model of polymicrobial sepsis induced in mice by cecal ligation and puncture (CLP) and were compared with the effects of endotoxin (lipopolysaccharide [LPS]) treatment. LPS levels rose as early as 1 h after CLP and increased further after 2 and 21 h. TNF-alpha was detectable in serum, spleen, liver, and lungs during the first 4 h, with a peak 2 h after CLP. ⋯ However, CPZ and DEX protected the mice from LPS mortality. On inhibiting TNF-alpha with DEX, CPZ, or pentoxifylline, survival was reduced, unchanged, and increased, respectively, and on increasing TNF-alpha with IBU and TNF, survival was decreased or unchanged, respectively, suggesting that the modulation of this cytokine does not play a significant role in sepsis induced by CLP, unlike treatment with LPS. The negative effects of IBU and N(G)-nitro-L-arginine suggest a protective role by prostaglandins and nitric oxide in sepsis induced by CLP.
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Clinical endocrinology · Aug 1995
Temperature-induced down-regulation of the glucocorticoid receptor in peripheral blood mononuclear leucocyte in patients with sepsis or septic shock.
Activation of the hypothalamic-pituitary-adrenal axis is of vital importance during critical illness. We have studied the adaptive mechanisms which occur at the level of the glucocorticoid receptor in glucocorticoid target tissues in patients with sepsis or septic shock. ⋯ There is no obvious regulation of the number of glucocorticoid receptors by plasma cortisol concentrations in vivo. The decreased affinity of the glucocorticoid receptor together with the negative correlation between hyperthermia and the number of glucocorticoid receptors in patients with sepsis or septic shock suggest that hypothalamic-pituitary-adrenal axis activation during critical illness is accompanied by peripheral adaptation in glucocorticoid receptor number and affinity.