Clark W R, Nieman G F, Goyette D, Gryzboski D
Department of Surgery, State University of New York, Syracuse.
Ann Surg. 1988 Jul;208(1):56-64. doi: 10.1097/00000658-198807000-00008.
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.
21%的火焰烧伤患者会发生吸入性损伤,这些患者需要大量液体进行复苏,死亡率超过30%。本研究旨在确定当快速输注晶体液时,烟雾损伤的肺对液体蓄积的易感性如何。将杂种犬分为三组,使其暴露于烟雾中并给予10%体重的乳酸林格液:(I)仅给予液体,(II)仅暴露于烟雾,(III)暴露于烟雾并给予液体。I组肺湿重与干重之比增加2%,II组增加28%,III组增加42%,这与仅III组出现肺水肿一致。给予液体的两组中胶体渗透压的降低相似,暴露于烟雾的两组中肺提取物表面张力最小值的升高相似。当受到液体挑战时,烟雾损伤的肺失去了自我保护能力。胶体渗透压降低并非其原因。微血管压力变化、内皮和上皮损伤以及表面活性剂失活相互作用,导致肺血管外水分增加。