title: Effect of graded increases in smoke inhalation injury on the early systemic response to a body burn.
abstract: OBJECTIVE
  To study the early (first 24 hrs) effect of increasing lung exposure to smoke on the hemodynamic response to a modest body burn.
  
  
  METHODS
  A prospective randomized study.
  
  
  METHODS
  Laboratory at a university medical center.
  
  
  METHODS
  Thirty-two adult yearling female sheep.
  
  
  METHODS
  Adult sheep (n = 32) were given an 18% of body surface burn; 24 sheep were then exposed to cotton toweling smoke using 12 breaths of a tidal volume of 5, 10, or 20 mL/kg. Animals were awakened, resuscitated to baseline oxygen delivery, and then killed at 24 hrs.
  
  
  RESULTS
  Vascular pressure, cardiac output, and oxygen consumption and delivery were measured, as well as blood gases, lung and soft tissue lymph flow, and fluid balance. We found that a 5-mL/kg tidal volume smoke exposure x 12 breaths did not produce significant airway inflammation or alter the cardiopulmonary response to a burn alone. Oxygen consumption (VO2) remained at baseline and the net 24-hr positive fluid balance of 1.5 L was comparable to a burn alone. Increasing the smoke exposure to 10 mL/kg tidal volume, which produced a moderate airway injury, resulted in a significant increase in early fluid requirements, a 40% early increase in VO2, a doubling of positive fluid balance, as well as a marked increase in burn edema. However, gas exchange was not impaired. The 20-mL/kg tidal volume exposure resulted in an early 100% increase in VO2, a three-fold increase in fluid requirements at 1 to 4 hrs, compared with burn alone, in addition to a severe airway inflammation with mucosal slough and resulting impaired gas exchange.
  
  
  CONCLUSIONS
  The addition of a smoke exposure which produces airway inflammation and injury significantly increases early post burn systemic metabolic demands and fluid requirements, as well as the degree of burn edema and positive fluid balance compared with a burn alone. The magnitude of the accentuated response appears to correspond with the degree of airway inflammation and not with alveolar dysfunction.
authors.affiliation: Longwood Area Trauma Center (Dr. Demling), Brigham and Women's Hospital, Boston, MA.
authors.forename: R
authors.initials: R
authors.lastname: Demling
authors.forename: C
authors.initials: C
authors.lastname: Lalonde
authors.forename: Y K
authors.initials: YK
authors.lastname: Youn
authors.forename: L
authors.initials: L
authors.lastname: Picard
mesh_terms: D000818:Animals; D002056:Burns / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics; D008168:Lung / Q000473:pathology; D008170:Lung Compliance; D010101:Oxygen Consumption; D011446:Prospective Studies; D011659:Pulmonary Gas Exchange; D011897:Random Allocation; D012756:Sheep; D015208:Smoke Inhalation Injury / Q000473:pathology / Q000503:physiopathology*; D013990:Tidal Volume