Journal of critical care
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Journal of critical care · Jun 1996
ReviewOrgan-specific therapy in critical illness: interfacing molecular mechanisms with physiological interventions.
Sepsis and SIRS is the outward manifestation of a generalized uncontrolled inflammatory response, which, if sustained, induces widespread endothelial damage and MODS. Immunomodulating therapies, at present, have proven ineffective in reducing morbidity and mortality, presumably because of the heterogeneous nature of sepsis and septic shock and the reciprocating and redundant nature of this inflammatory cascade. Organ-specific therapies can support life but impair both organ-specific function and remote organ function. Novel therapies aimed at minimizing further organ dysfunction may improve outcome in a cost-effective fashion by preventing both further primary organ dysfunction or remote organ dysfunction secondary to the subsequent activation of the inflammatory response.
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Journal of critical care · Jun 1996
ReviewApplications of molecular biology and biotechnology: antibody therapy of sepsis.
The use of antibody therapy for the treatment of infections and inflammatory disease is well established. Unfortunately, clinical studies of antiendotoxin and anti-TNF monoclonal antibodies have failed to show clear physiological or survival benefit. ⋯ Although both monoclonal and polyclonal antibodies have the potential to protect septic humans, at this time it is the polyclonal antibodies that have shown the greatest promise. Each type of antibody possesses specific advantages and limitations, the ultimate effectiveness of which will need to be proven in large randomized clinical trials.
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Journal of critical care · Jun 1996
Tissue-arterial PCO2 difference is a better marker of ischemia than intramural pH (pHi) or arterial pH-pHi difference.
Gastric intramucosal pH (pHi) is often calculated by the Henderson-Hasselbalch equation, using arterial plasma [HCO3-]ap and PCO2 measured in saline obtained from a silastic balloon tonometer after equilibration in the lumen of the stomach. A pHi value less than approximately 7.3 pH units is often taken as evidence of intestinal ischemia. An alternative measure is tissue PCO2 (PtCO2)-PaCO2 difference [P(t-a)CO2]. ⋯ Using the Van Slyke version of the arterial whole blood [standard base excess] ([SBE]aWB) equation, it was found that a change in [SBE]aWB at constant PaCO2 and constant PtCO2 produces a change in calculated pHi (P = 0), such that the relation between changing [SBE]aWB and changing pHi is predictable by a single polyomial equation (R2 = .999). pH(ap-i) avoids this confounding influence of [SBE]aWB. However, it was further shown that pH(ap-i) can be associated with a wide range of P(t-a)CO2, depending on the magnitude of pH(ap-i), and on the PaCO2 at which P(t-a)CO2 is measured. We conclude that P(t-a)CO2 is a more reliable index of gastric oxygenation than is pHi alone or pH(ap-i).
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Journal of critical care · Mar 1996
Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey.
In an attempt to identify the range of opinions influencing the diagnosis and therapy of patients with the adult respiratory distress syndrome (ARDS), a postal survey was mailed to 3,164 physician members of the American Thoracic Society Critical Care Assembly. The questionnaire asked opinions regarding the factors important in the diagnosis of ARDS and its treatment. Thirty-one percent of physicians surveyed responded within 4 weeks, the vast majority of which were board certified or eligible in Internal Medicine, Pulmonary Disease, and/or Critical Care Medicine. ⋯ It was reported that modest levels of positive end-expiratory pressure (PEEP) were used in incremental fashion as FiO2 requirements increased. Perceived indications for insertion of pulmonary artery catheters and compensation of the effects of PEEP on the pulmonary artery occlusion pressure varied widely among the responders. We conclude that reported practice patterns regarding the care of ARDS patients vary widely even within a relatively homogenous group of critical care practitioners.
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Journal of critical care · Mar 1996
Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome.
Elevated arterial lactate concentrations in patients with sepsis have been interpreted as evidence of peripheral, nonpulmonary tissue hypoxia. These patients often develop pulmonary failure manifested by the acute respiratory distress syndrome (ARDS). As the result of tissue hypoxia or inflammation, the lungs of patients with sepsis and ARDS may become a source of lactate release into the circulation. ⋯ The lungs of patients with sepsis and ARDS may produce lactate. Pulmonary lactate release correlates with the severity of lung injury. The contribution of pulmonary lactate release should be considered when interpreting arterial lactate concentration as an index of systemic hypoxia.