Pleural effusion: comparison of clinical judgment and Light's criteria in determining the cause.

Pleural fluid analysis is often the initial diagnostic test used to determine the cause of a pleural effusion. We prospectively studied 33 consecutive patients with pleural effusions to determine whether the fluid arose from a transudative or an exudative process. Clinical judgment by an internist before thoracentesis and both serum and pleural fluid protein and lactic dehydrogenase levels (commonly referred to as "Light's criteria") were compared to the patient's final diagnosis. The internist correctly classified 15 of 17 exudative processes and all 16 transudative processes; the presence of any one of Light's three criteria correctly classified 15 of 17 exudative processes, whereas the absence of all three criteria correctly classified 14 of 16 transudative processes. Clinical judgment and Light's criteria are comparable in their ability to predict whether an exudative or transudative process was responsible for the effusion. Both methods are associated with errors, though of different kinds; these errors occurred infrequently. Recognizing the limitations of these methods will permit the most accurate effusion categorization.

Phosphate therapy in diabetic ketoacidosis.

To determine the efficacy of phosphate replacement in the therapy for diabetic ketoacidosis (DKA), 44 patients were randomly assigned to three treatment groups: those who received no phosphate replacement, those who received 15 mmole of sodium phosphate at the fourth hour, or those who received 15 mmole of sodium phosphate at 2, 6, and 10 hours. All patients were treated with intravenous insulin injection (0.1 units/kg/hr), fluids, and potassium. Four hours after a 15-mmole sodium phosphate infusion, the serum phosphate level was 2.8 +/- 0.8 mg/dL vs 2.1 +/- 0.8 mg/dL in the control patients; however, this dose was insufficient to maintain the serum phosphate level at 16 and 24 hours. Forty-five millimoles of phosphate prevented severe hypophosphatemia in all but one patient and produced substantially higher phosphate levels at 8, 16, and 24 hours. Phosphate therapy did not affect the duration of DKA, dose of insulin required to correct the acidosis, abnormal muscle enzyme levels, glucose disappearance, or morbidity and mortality. Although theoretically appealing, phosphate therapy is not an essential part of the therapy for DKA in most patients.