Critical care medicine
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Critical care medicine · Aug 2000
A myocardial cytotoxic process is involved in the cardiac dysfunction of meningococcal septic shock.
Myocardial dysfunction is a characteristic component of meningococcal septic shock and contributes to the persisting high mortality from the disease. Specific treatment of the myocardial failure has been hampered by the lack of understanding of its pathophysiology. We were interested to determine whether myocardial cell death was occurring in the presence of meningococcal septicemia and whether it correlated with the degree of left ventricular dysfunction and disease severity. We therefore investigated the release of cardiac troponin I (cTnI), a sensitive and specific marker of myocardial cell death, and related this to the severity of disease and cardiac dysfunction. ⋯ The elevated serum concentrations of cTnI indicate that myocardial cell death is occurring in meningococcal septicemia. The relationship between cTnI and markers of myocardial function suggest that the cell death may have a role in the pathogenesis of myocardial dysfunction in meningococcal septicemia. Elucidation of the mechanism responsible for myocardial injury may lead to the development of therapeutic interventions to prevent or limit this cardiac damage.
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Critical care medicine · Aug 2000
Randomized Controlled Trial Clinical TrialA lipid A analog, E5531, blocks the endotoxin response in human volunteers with experimental endotoxemia.
Endotoxin (lipopolysaccharide [LPS]) has been associated with sepsis and the high mortality rate seen in septic shock. The administration of a small amount of LPS to healthy subjects produces a mild syndrome qualitatively similar to that seen in clinical sepsis. We used this model to test the efficacy of an endotoxin antagonist, E5531, in blocking this LPS-induced syndrome. ⋯ E5531 blocks the symptoms and signs and cytokine, white blood cell count, C-reactive protein, and cardiovascular response seen in experimental endotoxemia. This agent is a potent inhibitor of endotoxin challenge in humans and may be of benefit in the prevention or treatment of sepsis and septic shock.
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Critical care medicine · Aug 2000
Clinical TrialIndicators of postpyloric feeding tube placement in children.
To determine the validity of five indicators (color, pH, and concentrations of bilirubin, pepsin, and trypsin in aspirated gastrointestinal secretions) in predicting postpyloric placement of feeding tubes in critically ill children. ⋯ Simple bedside assessment of gastrointestinal aspirate color, pH, and bilirubin concentration is useful for predicting feeding tube position. Use of these tests may reduce the number of radiographic studies needed to confirm postpyloric positioning. Laboratory-determined pepsin and trypsin concentrations predict tube position with a high degree of accuracy. Development of simple and inexpensive bedside tests for the detection of gastrointestinal enzymes may be useful.
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Critical care medicine · Aug 2000
Clinical TrialEffects of helium-oxygen on intrinsic positive end-expiratory pressure in intubated and mechanically ventilated patients with severe chronic obstructive pulmonary disease.
To test the hypothesis that replacing 70:30 nitrogen: oxygen (Air-O2) with 70:30 helium:oxygen (He-O2) can decrease dynamic hyperinflation ("intrinsic" positive end-expiratory pressure) in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD), and to document the consequences of such an effect on arterial blood gases and hemodynamics. ⋯ In mechanically ventilated COPD patients with intrinsic positive end-expiratory pressure, the use of He-O2 can markedly reduce trapped lung volume, intrinsic positive end-expiratory pressure, and peak and mean airway pressures. No effect was noted on hemodynamics or arterial blood gases. He-O2 might prove beneficial in this setting to reduce the risk of barotrauma, as well as to improve hemodynamics and gas exchange in patients with very high levels of intrinsic positive end-expiratory pressure.
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Critical care medicine · Aug 2000
Clinical TrialEffect of norepinephrine on the outcome of septic shock.
Despite increasingly sophisticated critical care, the mortality of septic shock remains elevated. Accordingly, care remains supportive. Volume resuscitation combined with vasopressor support remains the standard of care as adjuvant therapy, and many consider dopamine to be the pressor of choice. Because of fear of excessive vasoconstriction, norepinephrine is considered to be deleterious. The present study was designed to identify factors associated with outcome in a cohort of septic shock patients. Special attention was paid to hemodynamic management and to the choice of vasopressor used, to determine whether the use of norepinephrine was associated with increased mortality. ⋯ Our results indicate that the use of norepinephrine as part of hemodynamic management may influence outcome favorably in septic shock patients. The data contradict the notion that norepinephrine potentiates end-organ hypoperfusion, thereby contributing to increased mortality. However, the present study suffers from some limitation because of its nonrandomized, open-label, observational design. Hence, a randomized clinical trial is needed to clearly establish that norepinephrine improves mortality of patients with septic shock, as compared with high-dose dopamine or epinephrine. Pneumonia as the cause of septic shock, high blood lactate concentration, and low urine output on admission are strong indicators of a poor prognosis. Multiple organ failure is confirmed as a reliable predictor of mortality in septic patients.