創(chuàng)傷與戰(zhàn)傷(英文版)

TraumaAndWarInjuryRiskfactorsTrafficaccident,industrialinjury,Naturaldisaster,warinjuryand

soon.CONTENT1.Theconceptoftrauma.2.Theclassificationoftrauma.3.Thepathphysiologyoftrauma.4.Thediagnosisoftrauma.5.Thetreatmentoftrauma.DEFINITIONTrauma

istheinjurycausedbymechanicalorchemicalfactors,whichleadstotissueintegritydamagedandlossoffunction.Chapter1ClassificationoftheTrauma1.Fortheintegrityofskin1).Theopenedinjury:Abrasion（摖傷）Laceration（撕裂傷）Incisedwoundsorcutwounds（切傷/

砍傷）Puncturewounds（刺傷）2).Thebluntinjury:Contusion（挫傷）Crushinjury（擠壓傷）Sprain（扭傷）Concussion（震蕩傷）Luxationandsemiluxation（關(guān)節(jié)脫位/半脫位）Closedbonefracture（閉合性骨折）Closedinternalinjury（閉合性內(nèi)臟傷）2.ForinjuredplaceandorganCraniocerebralinjury（顱腦傷）

:

Chestinjury（胸部傷）:hematopneumothrax

Abdomeninjury（腹部傷）:burstspleen,perforatedbowelLimbs（四肢傷）:fracture,dislocationSpinalinjury（脊柱傷）:fracture,paraplegia3.WoundcausingfactorsColdweaponwounds（冷兵器傷）:KnifeFirearmwounds（火器傷）:gun

Burns（燒傷）:HightemperatureColdinjury（冷傷）:LowtemperatureBlastinjury（沖擊傷）:爆震傷Chemicalinjury（化學(xué)傷）:chemicalweaponRadiationinjury（放射性損傷）:Electromagneticradiation，ParticulateradiationChapter2Pathophysiologyoftrauma

Trauma

cantriggeracascadeofpathologicalresponsewhichincludesinflammatory/immunereaction,neuroendocrineresponseandfunctionalchangeofvitalorgan.1.Theinflammatory/immunereaction1.Inflammatory:localtissueinflammatory2.Immunosuppressing:glucocorticoidsinhibitinmmunocytesfunction.3.Immunomodulating:Systemicinflammatoryresponsesyndrome(SIRS)Compensatoryanti-inflammatoryresponsesyndrome(CARS)ImmunomodulatingBothglucocorticoidsandcatecholaminesdirectlyinhibittheproductionoftype1cytokines,suchasIL-12,IL-2,TNF-αandINF-γ,thatenhancecellularimmunityandT-helper1(Th1)formationandconverselyfavortheproductionoftype2cytokines,suchasIL-10,IL-4,IL-13,thatinducehumoralimmunityandT-helper2(Th2)formation.Thus,duringanimmunechallenge,stresscausesanadaptiveTh1toTh2shiftinordertoprotectthetissuesfromthepotentiallydestructiveactionsofthepro-inflammatorytype1cytokinesandotherproductsofactivatedmacrophages.Thehomeostaticroleofstress-inducedTh2shiftagainstovershootingofcellularimmunityoftencomplicatespathologicconditionswhere,eithercellularimmunityisbeneficial(e.g.carcinogenesis,infections)orhumoralimmunityisdeleterious(e.g.allergy,autoimmunediseases).Schematicrepresentationoftheinteractionsbetweenthestressandtheimmunesystem.LC/NE:locusceruleus/norepinephrine-sympatheticsystem,SPGN:sympatheticpostgaglionicneurons,CRH:corticotropin-releasinghormone,AVP:argininevasopressin,ACTH:corticotrophin,PAF:plateletactivatingfactor,NE/E:norepinephrine/epinephrine,:Th1:T-helperlymphocyte1,Th2:T-helperlymphocyte2.Stimulationisrepresentedbysolidgreenlinesandinhibitionbydashedredlines.1.Sympathetic/adrenocortexsystem2.Hypothalamus/pituitarysystem3.Renin-angiotensionsystem2.NeuroendocrineresponseThepurposeofthephysicalreactionistomaintainthecirculationofthebloodandtissueperfusion

1.SNS-NeurohormonalresponseStimulatedbysympathetic/adrenocortexsystem(catecholamine)IncreasedheartrateIncreasedcontractilityVasoconstriction(SVR-Afterload)IncreasedPreload2.SNS-Hormonal:AdrenalCortexAnteriorpituitaryreleasesadrenocorticotropichormone(ACTH).StimulatesadrenalCxtoreleaseglucorticoids.Bloodsugarincreasestomeetincreasedmetabolicneeds.3.SNS-Hormonal:AntidiureticHormoneOsmoreceptorsinhypothalamusstimulatedADHreleasedbyPosteriorpituitaryglandVasopressoreffecttoincreaseBPActsonrenaltubulestoretainwater4.SNS-Hormonal:Renin-angiotensionsystemDecreaserenalperfusionReleasesrenin angiotensionIangiotensionII potentvasoconstriction&releasesaldosteroneadrenalcortexsodium&waterretention3.FunctionalchangeofvitalorganHeart:Catecholamineincreases

heartrate.

Anoxia,acidosis→theinjuriesofcardiacmuscle.Lungs:Theventilation-perfusionimbalance→ARDS.Kidneys:Renalfailure,oliguria(<400ml/d),anuria(<100ml/d).Brain:Edema,Theencephalicpressureincreases.Gastrointestine:theintestinalmucosabarrierwasdamaged→shiftofbacteriaandtoxin→MODS.Liver:Theendotoxicemia→metabolicdisturbanceandacidosisaggravated.Chapter3Repairofinjuredtissue

Traumadirectlystimulateslocaltissueandtriggersacascadeoftissuerepairprocesswhichincludes:A.Inflammation.B.Proliferationanddifferentiationofmanytypesofcell—granulationformation.C.Woundshealingandcarformation.Theconceptofinflammation

Inflammationcanbedefinedasalocalizedprotectivetissueresponseelicitedbyinjuryordestructionoftissues,whichservestodestroy,diluteorwalloffboththeinjuriousagentandtheinjuredtissues.Theinflammationisoftencharacterizedbyinjuredtissueshowingredness,swelling,heat,painandlossoffunction.

NewTissueFormation(granulation)

Followingtheinflammation--proliferationandmigrationofcellsatthewoundsite.Thisdensepopulationofmacrophages,fibroblastsandendothelialcells,etc.,embeddedinaloosematrix.Granulationformation–fillthegapofinjuredtissuebeforetheircoveragebyepidermalcells.MatrixFormationandRemodeling

Remodelingoftheimmaturetissuematrixcommencessimultaneouslywithgranulationtissueformation.Forclarity,however,itisnormallyregardedasformingthethirdandfinalphaseofwoundhealingduetoitscontinuationformanymonthsoryearsaftergranulationtissuehasbeenresolved.Duringthisphasethehighlycellularandhighlyvasculargranulationtissueisgraduallyreplacedandremodeled,formingscartissue.AngiogenesisTissuehealingThewoundhealing

1.Thefirstintention:mainlycomposedoftheoriginalcells,withlittlefibroustissue,e.g.epithelialcell--skin,mucosa,osteoblast--bones,endothelialcell--wallofvesselswithoutloseoffunctionThewoundhealing

2.Thesecondintention:mainlycomposedoffibroustissue,owningapoorfunctionafterhealing,notonlylackingtheoriginalfunction,butowningthescarcontractionorhyperplasia,whichresultinmalformationanddysfunction.

Thedisadvantageousfactorsforheal1.Infection.2.Foreignbody.3.Inadequatebloodsupply.4.Improperlocalfixation.5.Thesystemicfactorse.g.malnutrition,improperuseofmedicine,poorimmunity.Chapter4DiagnosisofTraumaThesystemicexamination1.Thevitalsigns:1)Temperature2)R,BP,P3)Others:oliguria,thirsty,sleeplessness,anorexia,etc.2.Traumaevaluation:1)CRAMS2)ISS(injuryseverityscore)3)AIS(abbreviatedinjuryscore)

ClinicalManifestationsLocalManifestations:(1)Pain(2)Swelling(3)Dysfunction

1.Thehistory:(1)Thecause,thewoundedpositionandtheposture.

(2)Thesymptomsandtheevolvementafterthewound.(3)Thelocaldisposal.(4)Thepasthealth.

2.PE:

(1)R,P,BP,theconsciousness,theface,theposture,shockedornot.(2)Accordingtothehistory,examiningthelocalwoundcarefully.(3)Fortheopenedwound,examiningthesize,shape,depth,contamination,bleedingofwoundandforeignbodyinwound.Theaccessoryexaminations

(1)Thetests--B-R,U-R,S-R,HCT,electrolytes,CO2CP,BUN,enzymology,etc.

(2)Puncture,PipeExamination1.Thecavumsofthorax,abdomenandjoints.2.Todraintheurine,intubation.3.CVP--thecentralveinpressure.

(3)TheimagingexaminationX-ray,CT,MRI,ultrasonictest,etc.Complications(1)Thepurulentinfection--openedfracture,largewound(2)Shock(3)MODS—e.g.:Theadultrespiratorydistresssyndrome,acuterenalfailure,thestressulcer.Chapter5TreatmentoftraumaFirstaidEmergencytreatment1.Theaimforthetreatmentistorepairthewoundedtissuesandtheorgans,andrecoverphysiologicalfunctions.2.Thecriticalcasesshouldbetreatedfirstly,suchasstopofheartbeat,asphyxia,massivehaemorrhage,openedpneumothorax,shock,etc.3.Thebasicstepsforsavetheseverecase“A,B,C”--AirwayBreathingCirculationThegeneraldisposal1.Thepostureandthelocalfixation.2.Topreventandtreattheinfection.3.Tomaintainthebalanceofbodyfluidandthenutritiousmetabolism.4.Toceasepain,usingcalmandthe