HYPOVOLEMIA, PULMONARY-EDEMA AND PROTEIN-CHANGES IN SEVERE SALICYLATE POISONING

Two patients are described with severe salicylate intoxication in which perfusion failure and pulmonary edema supervened. In both instances the clinical course was complicated by hypovolemia, hypotension, lactacidemia and hypoproteinemia. Proteinuria was a prominent early finding. Pulmonary edema developed several hours after the ingestion of aspirin, when the levels of salicylate in the serum were declining. Cardiac filling pressures were low at the onset of pulmonary edema. Samples of fluid from the airway during florid pulmonary edema contained essentially identical protein and electrolyte composition as samples of plasma obtained simultaneously. This finding supports the concept that pulmonary edema associated with salicylate intoxication is related to an increase in pulmonary vascular permeability to protein. Clinical deterioration followed the infusion of crystalloidal fluids. In contrast, pulmonary edema, hypoproteinemia and hypovolemia were corrected, and hemodynamic competence was restored after infusion of colloidal fluids. The results indicate that cautious infusion of colloidal agents may be useful in the management of severe salicylate intoxication. The data on an additional 32 patients with salicylate intoxication were reviewed. In each instance, when serum salicylate exceeded 30 mg/dl, more than 100 mg/dl of urinary protein were excreted. These observations suggest that proteinuria corroborates increased membrane permeability and may, therefore, be useful for the early detection of patients suspected of salicylate intoxication. © 1979.