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Background: Ever since the introduction of invasive hemodynamic monitoring to major burn care, its utility remains controversial. Besides complications, invasive monitoring as a guideline for burn shock resuscitation is often associated with significant excessive fluid burden. This study was to summarize the clinical experiences of noninvasive esophageal echo-Doppler (ED) monitoring in burn shock resuscitation and discuss the significance of hemodynamic variables in assessment of fluid therapeutic goal., Methods: Twenty-one burn patients with an average total body surface area of 78.86% +/- 7.75% (62-92%) was enrolled in this retrospective study. Fluid therapy was guided according to Chinese general formula and adjusted with urinary output 1 mL/kg/hr as resuscitation goal. Hemodynamic parameters using ED was obtained, including cardiac output (CO), stroke volume (SV), myocardial contractility parameter--maximum acceleration at onset of systole (Acc), afterload parameter--total systemic vascular resistance (TSVR), preload parameter SV/Acc., Results: All patients were clinically diagnosed with a relatively stable condition during early shock stage. There existed inherent and dynamic tendency of hemodynamics during burn shock resuscitation with low CO, Acc, SV/Acc, and high TSVR at first followed by a continuous trend of increase in CO, Acc and SV/Acc and decrease in TSVR. Significant correlations could be seen between CO and Acc, CO and TSVR, CO and SV/Acc. The Standardized Regression Coefficients of Acc, TSVR, and SV/Acc with CO as dependent variable were 0.343, -0.670, and 0.053, respectively demonstrating that myocardial contractility and angiotasis played more important role than blood volume did in hemodynamic variation., Conclusions: Hemodynamic variables cannot routinely substitute traditional variables as the burn shock resuscitation goal. Because of its noninvasiveness, ability to real-timely provide complete profile of hemodynamics, ED monitoring is a good adjunctive method for clinical judgment.

Objective: Stress ulceration is a common complication in critically ill patients, but the mechanisms involved are poorly understood. In this study we investigated the temporal activation of the redox-sensitive transcription factor nuclear factor-kappaB and its roles in an experimental model of cold immobilization stress-induced gastric mucosal lesions., Design: Prospective, controlled, and randomized animal study., Setting: University research laboratory., Subjects: Male Sprague-Dawley rats., Interventions: The rats were subjected to cold immobilization stress for a total of 6 hrs. The temporal profiles of nuclear factor-kappaB activation and expression of tumor necrosis factor-alpha, interleukin-1beta, cytokine-induced neutrophil chemoattractant-1 (CINC-1), intercellular adhesion molecule-1 (ICAM-1), and inducible nitric oxide synthase (iNOS) were determined in the gastric corpus mucosa of stressed rats. To study the roles of nuclear factor-kappaB activation, rats received an intravenous bolus of a specific nuclear factor-kappaB inhibitor Bay 11-7082 (20 mg/kg) 1 hr before stress. For antioxidant administration, rats were treated with intravenous injection of a free radical scavenger pyrrolidine dithiocarbamate (50, 100, and 200 mg/kg) 1 hr before stress., Measurements and Main Results: Exposure of rats to 6 hrs of stress led to a rapid and persistent activation of nuclear factor-kappaB, which was associated with transient degradation of inhibitory protein IkappaBalpha and slower but sustained degradation of IkappaBbeta. Nuclear factor-kappaB activation preceded the induction of tumor necrosis factor-alpha, interleukin-1beta, CINC-1, ICAM-1, and iNOS messenger RNAs, all of which were linearly increased with the duration of stress. Bay 11-7082 selectively blocked the stress-induced nuclear factor-kappaB activation and up-regulation of tumor necrosis factor-alpha, interleukin-1beta, CINC-1, ICAM-1, and iNOS messenger RNAs. Inhibition of expression of these proinflammatory genes prevented the increases in myeloperoxidase activity (an indicator of neutrophil infiltration) in gastric mucosa and the development of gastric damage. Pyrrolidine dithiocarbamate dose-dependently inhibited the stress-induced nuclear factor-kappaB pathway activation and consequential proinflammatory gene expression, neutrophil infiltration, and gastric damage, suggesting the involvement of reactive oxygen species in these processes., Conclusions: Sustained activation of nuclear factor-kappaB by reactive oxygen species is an important in vivo mechanism mediating stress-induced gastric inflammatory damage in rats.