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FLUID AND ELECTROLYTE ALTERATIONS IN BURNED MONKEYS *
Author(s) -
Fox Charles L.,
Lasker Sigmund E.
Publication year - 1968
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1968.tb14713.x
Subject(s) - medicine , total body surface area , fluid compartments , edema , anesthesia , metabolic acidosis , shock (circulatory) , third degree burn , acidosis , resuscitation , blood volume , vasoconstriction , hyponatremia , oncotic pressure , surgery , physiology , extracellular fluid , chemistry , biochemistry , extracellular , albumin
Summary and Conclusions These studies with monkeys demonstrate the difficulty of using the minimal thermal trauma that produced a localized full‐thickness injury to cause reproducible death in burn shock so that fluid therapy could be evaluated. Scalds that caused a full‐thickness injury were lethal in twelve hr when 55% of body surface was involved. In contrast, flash burns were lethal in 1–2 days when only 25% of body surface was involved. Fluid therapy which prolonged survival after scalds did not prolong survival after flash burns. The addition of whole blood or dextran to Ringer's lactate solution given in a total volume of 150 cc/kg body weight did not improve the results of therapy. Tissue analyses demonstrated that scald is an edema‐forming injury but flash burns cause huge influx of sodium without water into muscle under burned skin. These differences may explain in part the different response to fluid therapy. The rise in venous pressure post‐burn suggests the early onset of circulatory depression. The blood chemistry data demonstrate the metabolic acidosis with fall in plasma bicarbonate. Hyponatremia and renal shutdown did not occur in control or treated monkeys. The dangers of excessive fluid administration in man are being detected more frequently, together with the previously unrecognized findings of a high incidence of thrombo‐embolic phenomena and pulmonary edema. These findings may be related to the increased viscosity of the blood in burns and vasoconstriction. These comparative studies emphasize the fallacy of the often stated opinion that burns cause an influx of plasma or circulating fluid into tissues resulting in the reduction of plasma volume and that fluid therapy compensates for these changes and results in recovery. The “fluid loss,” particularly in flash or flame burns, is less than alleged and the recommended schedules of fluid therapy are less effective than is believed. The metabolic disturbances, such as acidosis and fall in body temperature, highlight the profound physiologic alterations which follow deep burns; more effective therapy awaits discovery in this direction.