ACIDOSIS OF LOW-GLUCOSE PLEURAL EFFUSIONS

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Abstract
To clarify the relationship between pleural fluid pH and pleural fluid glucose concentration and to investigate the mechanisms responsible for these phenomena, a heterogeneous population of 21 consecutive patients with pleural effusions was studied. Simultaneous measurements of pleural fluid and blood pH, PCO2 [partial pressure of CO2], glucose, lactate, pyruvate, total protein, total leukocyte count, differential count and lactic dehydrogenase were determined. Six patients had pleural fluid acidosis (pH < 7.30) and pleural fluid glucose concentrations < 60 mg/100 ml. None of these 6 had acidemia and their mean .+-. SE pleural fluid ratio of lactate to pyruvate was 110.4 .+-. 36.2 compared with a blood ratio of 11.5 .+-. 0.8 (P < 0.05). A significant correlation between pleural fluid pH and relative glucose concentration (pleural fluid/blood glucose) was found (r = 0.88; P < 0.01). A significant inverse correlation was observed between pleural fluid pH and pleural fluid lactate (r = -0.91; P < 0.01) and between pleural fluid pH and pleural fluid PCO2 (r = 0.86; P < 0.01). Both pleural fluid lactate and pleural fluid PCO2 increased with decreases in relative glucose concentration (r = -0.85, P < 0.01; and r = -0.72, P < 0.01, respectively). Pleural fluid lactate/CO2 correlated inversely with pleural fluid pH (r = -0.60; P < 0.05) and with relative glucose concentration (r = -0.74; P < 0.01). pH and glucose parallel each other in all pleural effusions. Pleural fluid acidosis results from lactate and CO2 production by the pleura and/or pleural fluid. Because the ratio of lactate to CO2 increases as pleural fluid pH and glucose concentration decrease, lactate appears to be the major end product of glucose metabolism in the pleural space and the larger contributor to pleural fluid acidosis.

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