Open AccessEffects of Crystalloid on Lung Fluid Balance After Smoke Inhalation
Author(s) -
William R. Clark,
Gary F. Nieman,
Donna Goyette,
Daniel Gryzboski
Publication year - 1988
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198807000-00008
Subject(s) - oncotic pressure , medicine , smoke inhalation , smoke inhalation injury , pulmonary edema , lung , resuscitation , edema , anesthesia , inhalation , smoke , pulmonary surfactant , chemistry , albumin , biochemistry , organic chemistry
Inhalation injury occurs in 21% of flame burn victims who require large fluid volumes for resuscitation and have a mortality rate greater than 30%. This study was done to determine how vulnerable the smoke-injured lung is to fluid accumulation when crystalloids are infused rapidly. Mongrel dogs were exposed to smoke and 10% body-weight Ringer's lactate in three groups: (I) fluid only, (II) smoke only, and (III) smoke and fluid. The increase in wet-dry lung weight ratio was 2% in Group I, 28% in Group II, and 42% in Group III, consistent with pulmonary edema present only in Group III. The decrease in colloid oncotic pressure was similar in both of the groups that were given fluid, and the rise in the surface tension minimum of lung extracts was similar in both of the groups that were exposed to smoke. The smoke-injured lung loses the ability to protect itself when challenged with fluid. Reduced oncotic pressure is not responsible. Changes in microvascular pressure, endothelial and epithelial damage, and surfactant inactivation interact to cause this increase in extravascular lung water.