Effect of inhalation injury on lung water accumulation.

Fourteen thermally injured patients with severe inhalation injury were sequentially studied with the thermal-green dye double indicator dilution technique of extravascular lung water (EVLW) measurement. Eight females and six males (average age, 49 years, and average thermal burn, 37% body surface) were studied for 2–31 days postinjury. All were burned in a closed space, had facial burns, soot in their sputum, and a mean carboxyhemoglobin level of 30%. Nine patients died, six of sepsis, one each of acute renal failure, hepatorenal syndrome, and anoxic brain damage. Mean EVLW on admission was 7.0±2.9 ml/kg and remained normal in the five survivors and in the patients dying of acute renal failure and anoxic brain damage. Six patients had increases in EVLW, caused by altered pulmonary capillary permeability in five and by elevation of hydrostatic pressures in one patient (hepatorenal death). Of the five patients with permeability edema, one appeared to result from a direct early effect of inhalation injury resulting in an EVLW of 13.3 ml/kg on admission. The other four patients had EVLW increases after the onset of sepsis, resulting in a mean EVLW of 23.2±7.2 ml/kg at death (p We thus conclude that increases in EVLW after thermal and inhalational injury are primarily caused by systemic or pulmonary sepsis, and have a delayed onset. Early increases in EVLW may be a result of the chemical toxicity of inhaled gases but are very uncommon, moderate in degree, and are seen only with the severest cases of inhalation injury.