A full-thickness burn produces total destruction of the epidermis and dermis, including the dermal appendages that harbor cells needed for epithelial regeneration. Both thirdand fourth-degree burns are in this category. In partial-thickness burns, at least the deeper portions of the dermal appendages are spared. Partial-thickness burns include first-degree burns (epithelial involvement only) and second-degree burns (involving both the epidermis and the superficial dermis).
MORPHOLOGYOngrossinspection,full-thickness burns arewhiteorcharred,dry,andanesthetic(asaresultofthedestructionofnerveendings),whereaspartial-thickness burns, dependingonthedepth,arepinkormottled,blistered,andpainful.Histologicexaminationofdevitalizedtissueshowscoagulativenecrosisadjacenttovitaltissue,whichquicklyaccumulatesinflammatorycellsandmarkedexudation.
Despitecontinuousimprovementintherapy,anyburnexceeding50%ofthetotalbodysurface,whethersuperficialordeep,isgraveandpotentiallyfatal.Withburnsofmorethan20%ofthebodysurface,thereisarapidshiftofbodyfluidsintotheinterstitialcompartments,bothattheburnsiteandsystemically,whichcanresultinhypovolemic shock (Chapter4).Becauseproteinfromthebloodislostintointerstitialtissue,generalizededema,includingpulmonary edema, maybecomesevere.
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Anotherimportantconsiderationisthedegreeofinjurytotheairwaysandlungs.Inhalation injury isfrequentinpersonstrappedinburningbuildingsandmayresultfromthedirecteffectofheatonthemouth,nose,andupperairwaysorfromtheinhalationofheatedairandgasesinthesmoke.Water-solublegases,suchaschlorine,sulfuroxides,andammonia,mayreactwithwatertoformacidsoralkalis,particularlyintheupperairways,resultingininflammationandswelling,whichmayleadtopartialorcompleteairwayobstruction.Lipid-solublegases,suchasnitrousoxideandproductsofburningplastics,aremorelikelytoreachdeeperairways,producingpneumonitis.Unlikeinshock,whichdevelopswithinhours,pulmonarymanifestationsmaynotdevelopfor24to48hours.
Organ system failure resultingfromsepsis continuestobetheleadingcauseofdeathinburnedpatients.Theburnsiteisidealforthegrowthofmicroorganisms;theserumanddebrisprovidenutrients,andtheburninjurycompromisesbloodflow,blockingeffectiveinflammatoryresponses.ThemostcommonoffenderistheopportunistPseudomonas aeruginosa, butantibiotic-resistantstrainsofothercommonhospital-acquiredbacteria,suchasS. aureus andfungi,particularlyCandida spp.,alsomaybeinvolved.Furthermore,cellularandhumoraldefensesagainstinfectionsarecompromised,andbothlymphocyteandphagocytefunctionsareimpaired.Directbacteremicspreadandreleaseoftoxicsubstancessuchasendotoxinfromthelocalsitehavedireconsequences.Pneumonia orseptic shock, accompaniedbyrenal failure and/ortheacuterespiratorydistresssyndrome(ARDS)(Chapter13),arethemostcommonserioussequelae.
Anotherveryimportantpathophysiologiceffectofburnsisthedevelopmentofahypermetabolicstate,withexcessheatlossandanincreasedneedfornutritionalsupport.Itisestimatedthatwhenmorethan40%ofthebodysurfaceisburned,therestingmetabolicratemayapproachtwicenormal.