BACKGROUND: During hemorrhagic shock blood flow to vital organs is maintained by the diversion of blood from both the splanchnic organs and skeletal muscle. In this swine study, we tested the hypotheses that (1). liver and muscle pH are correlated during both shock and resuscitation and (2). muscle pH during shock is an indicator of potential liver injury after resuscitation. MATERIALS AND METHODS: Hemorrhagic shock was induced over 15 min to lower systolic blood pressure to 40 mm Hg and was maintained for 60 (n = 5) or 90 (n = 5) min. Resuscitation was achieved with shed blood and warm saline to maintain mean pressure >60 mm Hg for 120 min. Liver and muscle pH were measured with microelectrodes throughout the entire shock and resuscitation periods, along with hepatic venous oxygen saturation. Arterial lactate and aspartate aminotransferase were measured at baseline, end of shock, and resuscitation. Correlation between muscle and liver pH was determined. The ability of muscle pH to predict liver injury (40% increase in arterial aspartate aminotransferase) was compared with other predictors: liver pH, arterial lactate, and tonometric-arterial PCO(2) gap. RESULTS: pH values and rates of change were similar in both muscle and liver tissue. Liver pH was well correlated with muscle pH during both shock and resuscitation, R(2) = 0.84. Muscle pH predicts potential liver injury with the same sensitivity as blood lactate in this swine shock model. CONCLUSIONS: Minimally invasive measurement of muscle pH warrants further study as a method to assess splanchnic hypoperfusion and resultant injury.

OBJECTIVES: To determine whether the simultaneous measurement of tissue pH, Pco2, and Po2 with a multiple-parameter fiberoptic sensor can be used to indicate the onset of hepatic dysoxia, to determine critical values, and to assess their use in predicting negative outcomes. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Fourteen Yorkshire swine. INTERVENTIONS: Hemorrhagic shock (n = 11) was induced over 15 mins to lower systolic blood pressure to 40 mm Hg and was maintained for 30, 60, or 90 mins. Resuscitation was achieved with shed blood and warm saline to maintain mean pressure >60 mm Hg for 120 mins. Sham animals (n = 3) were subjected to 90 mins of sham shock, followed by a 120-min recovery period. MEASUREMENTS AND MAIN RESULTS: The multiple-parameter sensor continuously measured tissue pH, Pco2, and Po2. pH and Pco2, indicators of anaerobic metabolism, were plotted against tissue Po2. All shocked animals, but no sham animals, showed a biphasic relationship between Po2 and both pH and Pco2. Curves were fit to both an exponential and a dual-line linear function to determine critical values for Po2, pH, and Pco2. The length of time the animal was dysoxic was evaluated as a predictor of negative outcome. Critical values determined from the exponential models were more sensitive indicators of negative outcome than values determined from the linear model and more sensitive than arterial lactate and tonometric intramucosal pH and Pco2. CONCLUSIONS: The multiple-parameter sensor offers the unique opportunity to study solid as well as hollow organ dysoxia through the simultaneous measurement of interstitial pH, Pco2, and Po2 in a small tissue region. The gradual transition from sufficient oxygen availability to dysoxia as a result of hemorrhage was better described by an exponential equation. The length of time that pH was below or Pco2 was above the critical value determined from the exponential model was predictive of a negative outcome.

The purpose of this study was to investigate the feasibility of using near infrared (NIR) spectroscopy of the liver to simultaneously assess oxygen content in combination with tissue pH, an indicator of anaerobic metabolism. Six anesthetized swine were subjected to 45 min of hemorrhagic shock followed by resuscitation with blood and crystalloid. Calibration models between NIR spectra and reference measurements of tissue pH, hepatic venous oxygen saturation (S(V)O2), and blood hemoglobin concentration (Hb) were developed using partial least-squares regression. Model accuracy was assessed using cross validation. The average correlation (R2) between NIR and reference measurements was 0.87, 0.68, and 0.93, respectively for pH, Hb, and S(V)O2. Estimated accuracy, the root mean squared deviation between spectral, and reference measurements was 0.03 pH units, 0.3 g/dL, and 6%. NIR determination of hepatic oxygen content and tissue pH during shock and resuscitation demonstrated that there can be a variance between hepatic venous oxygenation and regional tissue acidosis. NIR spectroscopy provides a technique to explore the implications of post-shock depression of tissue pH and evaluate new methods of resuscitation.

Hydrogen peroxide (H2O2) levels are increased in the exhaled breath of patients with the acute respiratory distress syndrome (ARDS). Because liposome-encapsulated prostaglandin E1 (PGE1) downregulates the CD11/CD18 receptor of the neutrophil, thereby limiting endothelial adhesion, the use of this drug should decrease the excretion of H2O2 in the expiratory condensate of patients with ARDS. Patients > 11 yr of age with ARDS (diffuse, patchy infiltrates by chest radiograph; Pao2/fraction of inspired oxygen [P/F] ratio < or = 200 mm Hg; pulmonary capillary wedge pressure < or = 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 micrograms/kg) of liposomal PGE1 (n = 14) every 6 h for up to 7 days. Condensate was collected every morning from the expiratory tubing that was submerged in an ice saltwater bath (-5 degrees C). H2O2 levels were measured by using a horseradish peroxidase assay. Other data collected included white blood cell count and P/F ratios. There was no significant difference in the concentration of H2O2 in the expiratory condensate between the liposomal PGE1 group and the control group either before (0.99 +/- 0.52 vs 0.93 +/- 0.48 mumol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mumol/L). Liposomal PGE1 treatment improved the P/F ratio and decreased the white blood cell count over time. Despite its ability to downregulate the CD11/CD18 neutrophil receptor, liposomal PGE1 did not reduce exhaled H2O2 excretion. Implications: White blood cells (WBC) are thought to be part of the cause of the acute respiratory distress syndrome, a lung disease. WBC in the lung produce hydrogen peroxide, which is exhaled. Liposomal PGE1 inhibits WBC function but was found to have no effect in decreasing exhaled hydrogen peroxide in patients with the acute respiratory distress syndrome.

OBJECTIVE: To evaluate the efficacy of triple-lumen central venous catheters coated with a combination product of chlorhexidine and silver sulfadiazine (CSS) in reducing the incidence of local catheter infection and catheter-related bacteremia. DESIGN: Randomized, controlled trial. SETTING: The surgical intensive care units in a university hospital. PATIENTS: All patients who needed central venous catheterization were randomized to receive either an uncoated triple-lumen catheter (n = 157) or a catheter coated with CSS (n = 151). MAIN OUTCOME MEASURE: Catheters were removed when no longer needed or suspected as a cause of infection. The tip and a 5-cm segment of the intradermal portion of the catheter were cultured semiquantitatively. Blood cultures were obtained when clinically indicated. The remaining segment of catheters coated with CSS were cut and incubated on an agar plate with strains of Staphylococcus aureus and Enterococcus. Zone of inhibition was determined 24 hours later. Data were analyzed by survival and logistic multivariate regression methods. RESULTS: Catheters coated with CSS were effective in reducing the rate of significant bacterial growth on either the tip or intradermal segment (40%) compared with control catheters (52%; P = .04). However, there was no difference in the incidence of catheter-related bacteremia (3.8% [uncoated] vs 3.3% [coated]; P = .81). In vitro activity of catheters with CSS against S aureus was evident up to 25 days but activity against Enterococcus dissipated more quickly over time and was absent by day 4. The most common colonizing organisms were coagulase-negative staphylococcus and enterococcus. Variables that were associated with a significant amount of growth on the tip or intradermal segment were a duration of catheterization of longer than 7 days, jugular insertion site, and the absence of a CSS coating. The use of a guidewire when the catheter was removed was associated with a lower risk of significant bacterial growth. CONCLUSIONS: The use of CSS reduces the incidence of significant bacterial growth on either the tip or intradermal segments of coated triple-lumen catheters but has no effect on the incidence of catheter-related bacteremia. In this patient population, catheters coated with CSS provide no additional benefit over uncoated catheters.