title: Fluid resuscitation following a burn injury: implications of a mathematical model of microvascular exchange.
abstract: A validated mathematical model of microvascular exchange in thermally injured humans has been used to predict the consequences of different forms of resuscitation and potential modes of action of pharmaceuticals on the distribution and transport of fluid and macromolecules in the body. Specially, for 10 and/or 50 per cent burn surface area injuries, predictions are presented for no resuscitation, resuscitation with the Parkland formula (a high fluid and low protein formulation) and resuscitation with the Evans formula (a low fluid and high protein formulation). As expected, Parkland formula resuscitation leads to interstitial accumulation of excess fluid, while use of the Evans formula leads to interstitial accumulation of excessive amounts of proteins. The hypothetical effects of pharmaceuticals on the transport barrier properties of the microvascular barrier and on the highly negative tissue pressure generated postburn in the injured tissue were also investigated. Simulations predict a relatively greater amelioration of the acute postburn edema through modulation of the postburn tissue pressure effects.
authors.affiliation: Department of Chemical Engineering, University of British Columbia, Vancouver, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Bert
authors.forename: C
authors.initials: C
authors.lastname: Gyenge
authors.forename: B
authors.initials: B
authors.lastname: Bowen
authors.forename: R
authors.initials: R
authors.lastname: Reed
authors.forename: T
authors.initials: T
authors.lastname: Lund
mesh_terms: D002056:Burns / Q000150:complications / Q000628:therapy*; D002463:Cell Membrane Permeability / Q000502:physiology; D005440:Fluid Therapy / Q000379:methods*; D006801:Humans; D015601:Injury Severity Score; D008833:Microcirculation / Q000502:physiology; D008954:Models, Biological; D012151:Resuscitation / Q000379:methods*; D014883:Water-Electrolyte Imbalance / Q000209:etiology / Q000628:therapy*