Relationships between pleural fluid pH, PCO2 to pleural fluid PO2, amylase, protein, glucose and white cells in tuberculous and malignant effusions.

The relationships between pleural fluid pH and PO2 to pleural fluid PO2, amylase, protein, glucose, white cell count were examined in 110 cases of tuberculous and 140 cases of malignant pleural effusions. Pleural fluid amylase concentrations of 200 or more units/ml indicated malignant effusions rather than tuberculous effusions with a specificity of 92.7 per cent and sensitivity of 27.1 per cent. There was evidence which suggested that the increasing pleural fluid amylase concentrations were due to the excessive leakage of serum amylase into the pleural cavity secondary to the break-down of capillaries by tuberculosis and malignancy as well as the production of amylase by tumor cells invading the pleura. The decreasing pleural fluid pH and increasing pleural fluid PCO2 had a significant linear relationship with decreasing fluid PO2, increasing pleural fluid protein and decreasing fluid glucose. These indicated a leakage of serum protein into the pleural cavity and the over-utilization of glucose relative to the transport defect of low pleural fluid glucose concentrations in the acidotic fluid of tuberculous and malignant effusions. No relationship between pleural fluid pH and PCO2 to pleural fluid and white cell count was found in the present study.

Amikacin pharmacokinetics in plasma and pleural fluid.

The pharmacokinetics of amikacin in plasma and pleural fluid were studied in nine adult patients with pleural effusions. After a single intravenous bolus of 7.5 mg of amikacin per kg, concentrations in plasma and pleural fluid were measured by fluorescence polarization immunoassays. Pleural fluid pH and PCO2 were also measured. The plasma pharmacokinetics was similar to other studies. However, in the present study the central compartment was significantly greater than the peripheral compartment. Our study suggested that there might be a significant binding of amikacin to the inflamed and/or damaged pleural as suggested by the significant correlations between the apparent volumes of distributions of central and total compartments with pleural fluid pH and PCO2. In pleural fluid, amikacin kinetics followed a large reservoir model with maximum concentration, 4.34 +/- 0.50 mg/L, occurring at 5.64 +/- 0.67 hours post-dose and its half-life was 13.50 +/- 2.93 hours. This concentration was lower than the minimal inhibitory concentration (MIC) for most of the sensitive strains of Gram-negative bacilli and therefore the antibiotics should be given as early as possible for gram-negative pneumonia.