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HyperbaricOxygenTherapy
Author:EmiLatham,MD,FACEPChiefEditor:ZabMosenifar,MDmore... Updated:May19,2010

Overview
OverviewHyperbaricoxygentherapy(HBOT)isbreathing100%oxygenwhile underincreasedatmosphericpressure.HBOTisatreatmentthatcanbetraced backtothe1600s.ThefirstwellknownchamberwasbuiltandrunbyaBritish clergymannamedHenshaw.Hebuiltastructurecalledthedomiciliumthatwas usedtotreatamultitudeofdiseases.[1]Thechamberwaspressurizedwithairor unpressurizedusingbellows.Theideaoftreatingpatientsunderincreased pressurewascontinuedbytheFrenchsurgeonFontaine,whobuiltapressurized, mobileoperatingroomin1879.[2]Dr.OrvilleCunningham,aprofessorof anesthesia,ranwhatwasknownasthe"SteelBallHospital."Thestructure, erectedin1928,was6storieshighand64feetindiameter.Thehospitalcould reach3atmospheresofpressure.[2]Thehospitalwasclosedin1930becauseof thelackofscientificevidenceindicatingthatsuchtreatmentalleviateddisease.It wasdeconstructedduringWorldWarIIforscrap. Themilitarycontinuedworkwithhyperbaricoxygen.TheworkofPaulBert,who demonstratedthetoxiceffectsofoxygen(producinggrandmalseizures),aswell astheworkofJ.LorrainSmith,whodemonstratedpulmonaryoxygentoxicity, wereusedwithNavydivers.Exposuretimestooxygenatdifferentdepthsofwater

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(and,hence,differentlevelsofpressure)werequantifiedandtestedbasedontime toconvulsions.[2]

OxygenChambers
Whenapatientisgiven100%oxygenunderpressure,hemoglobinissaturated, butthebloodcanbehyperoxygenatedbydissolvingoxygenwithintheplasma. Thepatientcanbeadministeredsystemicoxygenvia2basicchambers:TypeA, multiplaceandTypeB,monoplace.Bothtypescanbeusedforroutinewound care,treatmentofmostdiveinjuries,andtreatmentofpatientswhoareventilated orincriticalcare.

Multiplacechamber
Multiplacechamberstreatmultiplepatientsatthesametime,generallywitha nurseoranotherinsideobserverwhomonitorsthepatientsandassistswith equipmentmanipulationoremergencies(seeimagesbelow).Patientsina multiplacechamberbreathe100%oxygenviaamaskorclosefittingplastichood. Multiplacechamberscanusuallybepressurizedtotheequivalentofabout6 atmospheresofpressure. Ifadifferentmixtureofgas(nitrogenorheliummixture)isdesired,themixturecan begiven,viathemask,toonlythepatient,nottheemployee.Allequipmentused withpatients,suchasventilatorsandintravenouslines,isputintothechamber withthepatient.Sincetheemployeeisbreathingairduringthetreatment(not usingamask),hisorhernitrogenintakemustbemonitored,asthispresentsarisk forproblemssimilartothosesometimesdevelopedbyscubadivers(eg, decompressionsickness[DCS]).

Rectangularhyperbaricchamber.

Interiorofrectangularchamber.

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Cylindricalmultiplacechamber.

Monoplacechamber
Amonoplacechambercompressesonepersonatatime,usuallyinareclining position(seeimagebelow).Thegasusedtopressurizethevesselisusually100% oxygen.Somechambershavemasksavailabletoprovideanalternatebreathing gas(suchasair).Employeestendtothepatientfromoutsideofthechamberand equipmentremainsoutsidethechamberonlycertainintravenouslinesand ventilationductspenetratethroughthehull.NewerDuoplacechamberscanhold2 peopletheiroperationissimilartothatofamonoplacechamber.

Monoplacechamber.

Otherchambers
Twoothertypesofchambersareworthmentioning,althoughtheyarenot consideredHBOT. Topicaloxygen,orTopox,isadministeredthroughasmallchamberthatisplaced overanextremityandpressurizedwithoxygen.Thepatientdoesnotbreathethe oxygen,noristheremainderofthebodypressurized.Therefore,thepatient cannotbenefitfrommostofthepositiveeffectsofHBOT,whicharesystemicor occurataleveldeeperthantopicaloxygencanpenetrate(seeHyperbaricPhysics andPhysiologysectionbelow).Topoxisbasedontheconceptthatoxygen diffusesthroughtissueatadepthof3050microns.[3]Thismethoddoesnottreat DCS,arterialgasemboli(AGE),orcarbonmonoxide(CO)poisoning. AnotherproblemwithTopoxisthedesignoftheunit.Apressuredifferentialmust becreatedbetweenthemachineandopenatmospheretocompressthemachine. Inordertokeeptheextremityfrombeingpushedoutofthepressurizedmachine,

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thecuffoftheboxmustfitverytightlyaroundtheextremity,therebycreatinga tourniquetlikeeffect.Topoxisnotcoveredbyinsurance,norisitendorsedbythe journalDiabetesCareforthetreatmentoffootulcers.[4] Theothertypeofchamberistheportable"mild"hyperbaricchamber.Thesesoft vesselscanbepressurizedto1.51.7atmospheresabsolute(ATA).Theyareonly approvedbytheFDAforthetreatmentofaltitudeillness.Thenumberofthese chambershasincreased,astheyarebeingusedmorecommonlyinofflabel indications.

HyperbaricPhysicsandPhysiology
PhysicsofHyperbaricMedicine
Thephysicsbehindhyperbaricoxygentherapy(HBOT)lieswithintheidealgas laws. TheapplicationofBoyleslaw(p1v1=p2v2)isseeninmanyaspectsof HBOT.Thiscanbeusefulwithembolicphenomenasuchasdecompression sickness(DCS)orarterialgasemboli(AGE).Asthepressureisincreased, thevolumeoftheconcerningbubbledecreases.Thisalsobecomesimportant withchamberdecompressionifapatientholdsherbreath,thevolumeofthe gastrappedinthelungsoverexpandsandcausesapneumothorax. Charleslaw([p1v1]/T1=[p2v2]/T2)explainsthetemperatureincreasewhen thevesselispressurizedandthedecreaseintemperaturewith depressurization.Thisisimportanttorememberwhentreatingchildrenor patientswhoareverysickorareintubated. Henryslawstatesthattheamountofgasdissolvedinaliquidisequaltothe partialpressureofthegasexertedonthesurfaceoftheliquid.Byincreasing theatmosphericpressureinthechamber,moreoxygencanbedissolvedinto theplasmathanwouldbeseenatsurfacepressure. Theclinicianmustbeabletocalculatehowmuchoxygenapatientisreceiving.In ordertostandardizethisamount,atmospheresabsolute(ATA)areused.Thiscan becalculatedfromthepercentageofoxygeninthegasmixture(usually100%in HBOT21%ifusingair)andmultipliedbythepressure.Thepressureisexpressed infeetofseawater(fsw),whichisthepressureexperiencedifonewere descendingtothatdepthwhileinseawater.Depthandpressurecanbemeasured inmanywayssomecommonconversionsare1atmosphere(atm)=33feetof seawater(fsw)=10metersofseawater(msw)=14.7poundspersquareinch (psi)=1.01bar.

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HyperbaricPhysiology
Table1belowsummarizesthephysiologicmechanismsofHBOT.Eachoftheseis discussedinthecontextoftheindicationsforHBOTlaterinthisarticle. Table1.PhysiologicMechanismsofHyperbaricOxygenTherapy(OpenTableina newwindow) Mechanism Hyperoxygenation* References ClinicalApplication

BoeremaI[5] DCS/AGE

BassettBE[6] COpoisoning

BirdAD[7]

Centralretinalarteryocclusion

Crushinjury/compartment syndrome

Compromisedgraftsandflaps

Severebloodlossanemia

Decreasegasbubblesize Vasoconstriction

Boyle'slaw

Airorgasembolism

NylanderG[8] Crushinjury/compartment syndrome

SukoffMH[9]

Thermalburns

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Angiogenesis

Knighton DR[10]

Problemwounds

Compromisedgraftsandflaps

Delayedradiationinjury

Fibroblastproliferation/collagen synthesis

HuntTK[11]

Problemwounds

Delayedradiationinjury

Leukocyteoxidativekilling

MaderJT[12] Necrotizingsofttissue infections

ParkMK[13]

Refractoryosteomyelitis

Mandell GL[14]

Problemwounds

Reducesintravascularleukocyte adherence

Zamboni WA[15]

Crushinjury/compartment syndrome

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ThomSR[16,
17]

Reduceslipidperoxidation

ThomSR[18] COpoisoning

Crushinjury/compartment syndrome

Toxininhibition Antibioticsynergy

VanUnnik A[19]

Clostridialmyonecrosis

MirhijNJ[20] Necrotizingsofttissue infections

KeckPE[21]

Refractoryosteomyelitis

MendelV[22]

Muhvich KH[23]

*Mostoxygencarriedinthebloodisboundtohemoglobin,whichis97% saturatedatstandardpressure.Someoxygen,however,iscarriedinsolution, andthisportionisincreasedunderhyperbaricconditionsduetoHenry'slaw. Tissuesatrestextract56mLofoxygenperdeciliterofblood,assumingnormal perfusion.Administering100%oxygenatnormobaricpressureincreasesthe amountofoxygendissolvedinthebloodto1.5mL/dLat3atmospheres,the dissolvedoxygencontentisapproximately6mL/dL,whichismorethanenough tomeetrestingcellularrequirementswithoutanycontributionfromhemoglobin.

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Becausetheoxygenisinsolution,itcanreachareaswhereredbloodcellsmay notbeabletopassandcanalsoprovidetissueoxygenationinthesettingof impairedhemoglobinconcentrationorfunction.

Hyperoxiainnormaltissuescausesvasoconstriction,butthisiscompensated byincreasedplasmaoxygencontentandmicrovascularbloodflow.This vasoconstrictiveeffectdoes,however,reduceposttraumatictissueedema,which contributestothetreatmentofcrushinjuries,compartmentsyndromes,and burns.

HBOTincreasesthegenerationofoxygenfreeradicals,whichoxidizeproteins andmembranelipids,damageDNA,andinhibitbacterialmetabolicfunctions. HBOisparticularlyeffectiveagainstanaerobesandfacilitatestheoxygen dependentperoxidasesystembywhichleukocyteskillbacteria.

Additionally,evidenceisgrowingthatHBOTaltersthelevelsofproinflammatory mediatorsandmayblunttheinflammatorycascade.Morestudiesareneededto furtherelucidatethiscomplexinteraction. AsHBOTisknowntodecreaseheartratewhilemaintainingstrokevolume,ithas thepotentialtodecreasecardiacoutput.Atthesametime,throughsystemic vasoconstriction,HBOTincreasesafterload.Thiscombinedeffectcanexacerbate congestiveheartfailureinpatientswithseverediseasehowever,clinically significantworseningofcongestiveheartfailureisrare.

Contraindications
Aswithmostmedicaltreatments,absoluteandrelativecontraindicationsexistwith theuseofhyperbaricoxygentherapy(HBOT).[2] Table2.AbsoluteContraindicationstoHyperbaricOxygenTherapy(OpenTablein anewwindow) Absolute Contraindications Untreated ReasonContraindicated Gasemboli NecessaryConditions PriortoHBOT Thoracostomy

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pneumothorax

Tensionpneumothorax

Pneumomediastinum

Bleomycin

Interstitialpneumonitis

Notreatmentforextended timefromuseof medication Notreatmentforextended timefromuseof medication

Cisplatin

Impairedwoundhealing

Disulfiram

Blockssuperoxidedismutase, Discontinuemedication whichisprotectiveagainstoxygen toxicity Cardiotoxicity Impairedwoundhealing Discontinuemedication Discontinueandremove medication

Doxorubicin Sulfamylon

Table3.RelativeContraindicationstoHyperbaricOxygenTherapy(OpenTablein anewwindow) Relative Contraindications Asthma Claustrophobia Congenital spherocytosis ReasonContraindicated Airtrappinguponascent leadingtopneumothorax Anxiety Severehemolysis NecessaryConditions PriortoHBOT Mustbewellcontrolledwith medications Treatmentwith benzodiazepines NoneHBOTfor emergenciesonly

Chronic Lossofhypoxicdrivetobreathe Observationinchamber obstructive pulmonarydisease (COPD) Eustachiantube Barotraumatotympanic Training,PEtubes

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dysfunction Highfever

membrane Higherriskofseizures

Provideantipyretic Ensurecompanyhas pressuretesteddeviceand learntowhatdepth None,butHBOTmaybe usedinemergencies Shouldbestableon medicationsmaybetreated withbenzodiazepines Resolutionofsymptomsor decongestants

Pacemakersor Malfunctionordeformationof epiduralpainpump deviceunderpressure Pregnancy Unknowneffectonfetus (PreviousstudiesfromRussia suggestHBOTissafe.) Mayhavelowerseizure threshold Barotrauma

Seizures

Upperrespiratory infection(URI)

DecompressionSicknessandAirEmbolism
DecompressionSicknessDecompressionsickness(DCS)referstosymptoms causedbyblockedbloodsupply,damagefromdirectmechanicaleffects,orlater biochemicalactionsfromsuspectedbubblesevolvingfrominertgasdissolvedin bloodortissueswhenatmosphericpressuredecreasestoorapidly.[24,25]DCScan occurafterscubadiving,ascentwithflying,orhypobaricorhyperbaricexposure. DCScanbebrokendownintothefollowing3types: TypeIinvolvesmusculoskeletal,skin,andlymphatictissue,andoftenhas accompanyingfatigue. TypeIIincludesneurologicsystems(eitherCNSorperipheral), cardiorespiratory,audiovestibular,andshock.[25] TypeIIIDCSdescribesasyndromethatpresentswithsymptomsthat progresstoaspinaldeficitthatmayberefractorytorecompression. ThebubblescausingDCSalsocaninjurevesselendothelium,whichleadsto plateletaggregation,denaturedlipoproteins,andactivationofleukocytes,causing capillaryleaksandproinflammatoryevents.[26,27] Hyperbaricoxygentherapy(HBOT)isusedtodiminishthesizeofthebubbles,not simplythroughpressure,butalsobyusinganoxygengradient.Accordingto Boyleslaw,thevolumeofthebubblebecomessmalleraspressureincreases. Withachangein1.8ATA,thisisonlyabout30%.ThebubblecausingDCSis thoughttobecomposedofnitrogen.Whenatissuecompartmentisatequilibrium

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andthenascendstoadecreasedatmosphericpressure,nitrogenseepsoutof blood,tissue,orboth,causingabubble.DuringHBOT,thepatientbreathes100% oxygen,creatingoxygenrich,nitrogenpoorblood.Thiscreatesagradientof nitrogenbetweenthebloodandthebubble,causingnitrogentoeffluxfromthe bubbleintothebloodstream,which,ineffect,makesthebubblesmaller.[25] Thetreatmentofchoiceisrecompression.Althoughtreatmentassoonaspossible hasthegreatestsuccess,recompressionisstillthedefinitivetreatment,andno exclusionarytimefromsymptomonsethasbeenestablished.[25,26]DCSTypeI canbetreatedusingtheUSNavyTreatmentTable5:60fswfortwo20min periods,withaslowdecompressionto30fswforanother20minutes.ForDCS typesI,II,andIII,theUSNavyTreatmentTable6isarecommendedtreatment protocol.Patientsareplacedat60fsw(2.8ATA)foratleastthree20minintervals andthenareslowlydecompressedto30fsw.Theyremainthereforatleast another2.5hours.Thetimeapatientiskeptat60or30fswcanbeextended dependingonthepatientssymptomresponsetotherapy.[28]

AirEmbolism
Airembolismreferstobubblesinthearterialorvenouscirculation.Venous bubblescanresultfromcompressedgasdiving(suchasscuba)[29]butareoften filteredthroughthepulmonarycapillarybed.Ifalargevolumeofbubblesisnoted, theymayoverwhelmthepulmonaryfilterandenterthearterialcirculation.[30] Arterialgasemboli(AGE)canalsoresultfrompulmonarybarotrauma[25]or accidentalintravenousairinjectionorsomesurgicalprocedures.[31,32,33,34,35] Symptomsusuallyoccurwithinsecondstominutesoftheeventandcaninclude lossofconsciousness,confusion,neurologicaldeficits,cardiacarrhythmias,or cardiacarrest. Thetreatmentofchoiceisrecompressiontherapy.Gasembolismusedtobe treatedwithUSNavyTreatmentTable6A,whichrequiredapressureof6ATA. Therationalewasthatthelargervolumeofgaswarrantedincreasedpressureto forcebubbleredistributionorelimination.Noconclusiveevidenceshowsthatthis offerssuperiortreatmenttotheUSNavyTreatmentTable6formostcases however,ifcompletereliefisnotachievedafterinitialrecompression,deeper recompressionmaybeneeded.[25]

CarbonMonoxidePoisoning
Carbonmonoxide(CO)poisoning,whetherintentionaloraccidental,occurswhen oneinhalesthecolorlessandodorlesscarbonmonoxidegas.Despiteimproved awarenessandsensoryalarms,multipledeathsoccureachyear.

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CObindstohemoglobinwith200timestheaffinityofoxygen.COalsoshiftsthe oxygendissociationcurvetotheleft(theHaldaneeffect),whichdecreasesoxygen releasetotissues.COcanalsobindcytochromeoxidaseaa3/Candmyoglobin. Reperfusioninjurycanoccurwhenfreeradicalsandlipidperoxidationare produced. ThetreatmentofCOpoisoningwithhyperbaricoxygentherapy(HBOT)isbased uponthetheorythatoxygencompetitivelydisplacesCOfromhemoglobin.While breathingroomair,thisprocesstakesabout300minutes.Whileona100% oxygennonrebreathermask,thistimeisreducedtoabout90minuteswithHBOT, thetimeisshortenedto32minutes.HBOT(butnotnormobaricoxygen)restores cytochromeoxidaseaa3/C[36]andhelpstopreventlipidperoxidation.[37]HBOTis alsousedtohelppreventthedelayedneurologicsequelae(DNS)treatment institutedsoonerismoreeffective.[38]Multiplepapersdescribecontroversial methodsandconclusionsabouttheuseofHBOTforCOpoisoning.[39,37,40,41,42] PatientswithCOpoisoningcanpresentwithmyriadsymptomsthattheymaynot initiallyattributetoCOpoisoning,asCOisconsideredthegreatimitatorofother illnesses.[18,43,44]Presentationcanincludeflulikesymptomssuchasheadache, visualchanges,dizziness,andnausea.Moreseriousmanifestationsincludeloss ofconsciousness,seizures,chestpain,ECGchanges,tachycardia,andmildto severeacidosis. CandidatesforHBOTarethosewhopresentwithmorbidityandmortalityrisksthat includepregnancyandcardiovasculardysfunctionandthosewhomanifestsignsof seriousintoxication,suchasunconsciousness(nomatterhowlongaperiod), neurologicsigns,orsevereacidosis.COhemoglobin(Hgb)levelusuallydoesnot correlatewellwithsymptomsoroutcome[45,37,46]manypatientswithCOHgb levelsof2530%aretreated. PregnantfemalesoftenhaveaCOlevelthatis1015%lowerthanthefetus.Fetal HgbnotonlyhasahigheraffinityforCObutalsohasaleftshiftedoxygen dissociationcurvecomparedwithadulthemoglobin.ExposuretoCOcausesan evenfartherleftwardshift,inbothadultandfetalhemoglobin,anddecreased oxygenreleasefrommaternalbloodtofetalbloodandfromfetalbloodtofetal tissues.PregnantpatientswithCOHgblevelsgreaterthan10%shouldbetreated withHBOT.[2] HBOTisadministeredat2.53ATAforperiodsof60100minutes.Dependingon patientpresentationandresponse,15treatmentsarerecommended.[3]

EnhancementofHealinginSelectedProblem Wounds
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Normalwoundhealingproceedsthroughstagesofhemostasis,removalof infectiousagents,resolutionoftheinflammatoryresponse,reestablishmentofa connectivetissuematrix,angiogenesis,andresurfacing.Problem(orchronic) woundsarethosewhichdonotproceedcompletelythroughthisprocessbecause ofanynumberoflocalandsystemichostfactors.Forthisreason,chronicwounds areoftencategorizedasdiabeticwounds,venousstasisulcers,arterialulcers,or pressureulcers. Woundsthatfailtohealaretypicallyhypoxic.[47]Multiplecomponentsofthewound healingprocessareaffectedbyoxygenconcentrationorgradients,whichexplains whyhyperbaricoxygentherapy(HBOT)canbeaneffectivetherapytotreat chronicwounds.Angiogenesisoccursinresponsetohighoxygen concentration.[10]ThisislikelyamultifactorialeffectofHBOT.First,fibroblast proliferationandcollagensynthesisareoxygendependent,[11]andcollagenisthe foundationalmatrixforangiogenesis.Inaddition,HBOTlikelystimulatesgrowth factorsinvolvingangiogenesisandothermediatorsofthewoundhealing process.[48]Hyperbaricoxygenalsohasbeenshowntohavedirectandindirect antimicrobialactivityinparticular,itincreasesintracellularleukocytekilling.[13,14,
12]

Diabeticlowerextremityulcershavebeenthefocusofmostwoundresearchin hyperbaricmedicine,sincetheetiologyofthesewoundsismultifactorial,and HBOTcanaddressmanyofthesefactors.Severalrandomizedcontrolledclinical trialshavestudiedHBOTforthetreatmentofdiabeticlowerextremitywounds.[49, 50,51,52]Additionally,manymoreprospective,noncontrolledclinicaltrialsand retrospectivetrialshavebeencompleted.Basedonthebodyofevidence,major insurancecarriersaroundtheworldnowendorsetheuseofHBOTforthe treatmentofdiabeticlowerextremitywoundsthatshowevidenceofdeepsoft tissueinfection,osteomyelitis,organgrene.HBOThasbeenshowntoreducethe amputationrateinpatientswithdiabeticulcersaswell.[49,50,52] InanefforttoselectpatientsappropriatelyforHBOT,variousobjectivevascular evaluationmethodshavebeenused,includingtranscutaneousoximetry,capillary perfusionpressure,laserDoppler,andothertypesofvascularstudies.Debateis ongoingregardingwhichmethodprovidesthemostreliabledataandwhether thesemethodsaremoreusefulthanotherclinicalmarkersofwoundfailure. NotethatHBOTshouldbeusedinconjunctionwithacompletewoundhealing careplan.Aswithallchronicwounds,otherunderlyinghostfactors(eg,large vesseldisease,glycemiccontrol,nutrition,infection,presenceofnecrotictissue, offloading)mustbesimultaneouslyaddressedinordertohavethehighestchance ofsuccessfulhealingandfunctionalcapacity. BecausethegoalsofHBOTforwoundhealingincludecellularproliferationand
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angiogenesis,HBOTisgenerallyperformeddailyforaminimumof30treatments. Treatmentisgenerallyat2to2.4ATAforatotalof90minutesof100%oxygen breathingtime.Basedontheresponsetotherapy,extendedcoursesoftherapy maybeindicated.

CompromisedSkinGraftsandFlaps
Mostskingraftsandflapsinnormalhostshealwell.Inpatientswithcompromised circulation,thismaynotbethecase.Patientswithdiabetesorvasculopathyfrom anotheretiologyandpatientswhohaveirradiatedtissueareparticularlysubjectto flaporgraftcompromise.Inthesepatients,hyperbaricoxygentherapy(HBOT)has beenshowntobeuseful.Unfortunately,ifpatientsarenotidentifiedearly,the initialflaporgraftmaybelost.Eveninsuchcases,patientscansignificantly benefitfromHBOTtopreparethewoundbedforanothergraftorflapprocedure theprocedurethenhasahigherchanceofsuccessfollowingHBOT. Over30animalstudieshaveshownefficacyofHBOTinpreservingbothpedicled andfreeflapsinmultiplemodels.Thesemodelslookedatarterial,venous,and combinedinsultsinadditiontoirradiatedtissues.Whileimprovementwas observedregardlessofthetypeofvasculardefect,thosewitharterialinsufficiency andradiationinjuryshowedthegreatestimprovement. Humancasestudiesshowingbenefitofhyperbarictreatmentforflapsurvivalwere firstreportedin1966.Acontrolledclinicaltrialshowingimprovedsurvivalofsplit skingraftsfollowedshortlythereafter.[53]Thiswascorroboratedbyalaterclinical trial.[54]Additionally,evidenceexistsofbenefitforflapsinpostirradiatedtissuein humansubjects.[55] Astheunderlyingpathophysiologyofallcompromisedgraftsandflapsishypoxia, HBOTbenefitspatientsbyreducingtheoxygendeficit.Auniquemechanismof actionofHBOTforpreservingcompromisedflapsisthepossibilityofclosing arteriovenousshunts.[56]Additionally,thesamemechanismsofactionthatimprove woundhealing,namely,improvedfibroblastandcollagensynthesis[11]and angiogenesis,[10]alsoarelikelytobenefitacompromisedgraftorflap. ThecurrentstandardforHBOTtotreatacompromisedgraftorflapincludestwice dailytreatmentuntilthegraftorflapappearsviableandthenonceperdayuntil completelyhealed.TheinitiationofHBOTshouldbeexpedited.Ingeneral,benefit shouldbeseenby20treatmentsifitisnot,continuationoftherapyshouldbe reviewed.However,thecostofcreatingacomplexflapishigh,whichmakes HBOTcosteffectiveforthisdiagnosis.Ofcourse,patientswithcompromisedflaps needsurgicalattentiontothearterialandvenoussupply,appropriatelocal management,andmaximizationofmedicalsupport.

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CrushInjuryandCompartmentSyndrome
Acuteperipheraltraumaticischemiaincludesthoseinjuriesthatarecausedby traumathatleadstoischemiaandedemaagradientofinjuryexists.Thiscategory containscrushinjuriesaswellascompartmentsyndrome.Crushinjuriesoften resultinpooroutcomebecauseofthebodysattempttomanagetheprimary injury.Thebodythendevelopsmoreinjuryduetothereperfusionresponse. Injuriesaregradedusingdefinitepointsonaseverityscale.Thecommonly referencedsystemistheGustiloclassification,[57]butotherclassificationscales areavailable. Thebenefitsofhyperbaricoxygentherapy(HBOT)forthisindicationinclude hyperoxygenationbyincreasingoxygenwithintheplasma.HBOTalsoinducesa reductioninbloodflow[58,59]thatallowscapillariestoresorbextrafluid,resultingin decreasededema.Asagradientofoxygenationisbasedonbloodflow,oxygen tissuetensionscanbereturned,allowingforthehostdefensestoproperly function.[11]Animalstudiessuggestthatadecreasedneutrophiladherenceto ischemicvenulesisobservedwithelevatedoxygenpressures(2.5ATA).[15,16] Reperfusioninjuryisdiminished,asHBOTgeneratesscavengerstodestroy oxygenradicals.[60] Compartmentsyndromealsoisacontinuumofinjurythatoccurswhen compartmentpressuresexceedthecapillaryperfusionpressures.Theextentto whichtheinjuryhasaffectedtissuesisunclear,evenaftersurgicalintervention.[61, 58,62]HBOTisnotrecommendedduringthesuspectedstageofinjury,when compartmentsyndromeisnotyetpresentbutmaybeimpending.HBOTis beneficialduringtheimpendingstage,whenobjectivesignsarenoted(pain, weakness,painwithpassivestretch,tensecompartment).Withthesesigns,even ifsurgeryisnotelectedbecauseofcompartmentpressuresorpatientstability, HBOTisindicated.Oncethepatienthasundergonefasciotomy,HBOTcanbe usedtohelpdecreasemorbidity.[3] HBOTshouldbestartedassoonasisfeasible,ideallywithin46hoursfromtime ofinjury.Afteremergentsurgicalintervention,thepatientshouldundergoHBOTat 22.5ATAfor6090minutes.Forthenext23days,performHBOT3timesdaily, thentwicedailyfor23days,andthendailyforthenext23days.[2]

NecrotizingSoftTissueInfections
Theseinfectionsmaybesingleaerobicoranaerobicbutaremoreoftenmixed infectionsthatoftenoccurasaresultoftrauma,surgicalwounds,orforeign bodies,includingsubcutaneousandmuscularinjectionofcontaminatedstreet

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drugs.Theyareoftenseenincompromisedhostswhohavediabetesora vasculopathyofanothertype.Theseinfectionsarenamedbasedontheirclinical presentationandincludenecrotizingfasciitis,clostridialandnonclostridial myonecrosis,andFourniergangrene. Regardlessofthedepthofthetissueinvasion,theseinfectionshavesimilar pathophysiologythatincludeslocaltissuehypoxia,whichisexacerbatedbya secondaryocclusiveendarteritis.[63]Intravascularsequestrationofleukocytesis commoninthesetypesofinfections,mediatedbytoxinsfromspecific organisms.[64]Clostridialthetatoxinappearstobeonesuchmediator.Allofthese factorstogetherfosteranenvironmentforfacultativeorganismstocontinueto consumeremainingoxygen,andthispromotesgrowthofanaerobes. Thecornerstonesoftherapyarewidesurgicaldebridementandaggressive antibiotictherapy.Hyperbaricoxygentherapy(HBOT)isusedadjunctivelywith thesemeasures,asitoffersseveralmechanismsofactiontocontroltheinfection andreducetissueloss.First,HBOTistoxictoanaerobicbacteria.[65]Next,HBOT improvespolymorphonuclearfunctionandbacterialclearance.[12,66]Basedon resultsofworkrelatedtoCOpoisoning,HBOTmaydecreaseneutrophil adherencebasedoninhibitionofbeta2integrinfunction.[17,16]Further investigationisneededtoseeifthismechanismisatworkinnecrotizinginfections aswell.Inthecaseofclostridialmyonecrosis,HBOTcanstoptheproductionof thealphatoxin.[19,67]Finally,limitedevidenceindicatesthatHBOTmayfacilitate antibioticpenetrationoractioninseveralclassesofantibiotics,including aminoglycosides,[20]cephalosporins,[22]sulfonamides[21]andamphotericin.[23] MultipleclinicalstudiessuggestthatHBOTisefficaciousinthetreatmentof necrotizingsofttissueinfections.Theseincludecaseseries,retrospectiveand prospectivestudies,andnonrandomizedclinicaltrials.Theysuggestsignificant reductionsinmortalityandmorbidity.Thereductioninmortalitywasremarkably similarin2studies:34%(untreated)vs.11.9%(treated)inonestudy[68]38% (untreated)vs.12.5%(treated)intheother.[69]Inanotherstudy,[70]thetreated grouphadmorepatientswithdiabetesandmorepatientsinshockandstillhad significantlylessmortality(23%)thantheuntreatedgroup(66%).Clinicalstudies involvingpatientswithFourniergangrenetreatedwithHBOTbearsimilarresults. InitialHBOTisaggressivelyperformedatleasttwiceperdayincoordinationwith surgicaldebridement.Typically,atreatmentpressurerangingfrom2.02.5ATAis adequate.However,inthespecificcaseofclostridialmyonecrosis,3ATAisoften usedtoensureadequatetissueoxygentensionstostopalphatoxinproduction. Forthesamereason,HBOTshouldbeinitiatedasquicklyaspossibleinthis circumstanceandperformed3timesinthefirst24hifatallfeasible.

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Intracranialabscess
Thedisordersconsideredintreatmentofintracranialabscesses(ICA)include subduralandepiduralempyemaaswellascerebralabscess.[2]Studiesfrom aroundtheworldhavereviewedmortalityfromICAwitharesultingmortalityof about20%.[71]HBOThasmultiplemechanismsthatmakeitusefulasan adjunctivetherapyforICA. HBOTinduceshighoxygentensionsintissue,whichhelpstopreventanaerobic bacterialgrowth,includingorganismscommonlyfoundinICA.[72,73,74,75]HBOT canalsohelpreduceincreasedintracranialpressure(ICP)anditseffectsare proposedtobemorepronouncedwithperifocalbrainswelling.[9,76,77]As discussedearlier,HBOTcanenhancehostimmunesystemsandthetreatmentof osteomyelitis.[78]CandidatesforadjunctiveHBOTarepatientswhohavemultiple abscesses,whohaveanabscessthatisinadeepordominantlocation,whose immunesystemsarecompromised,inwhomsurgeryiscontraindicated,whoare poorcandidatesforsurgery,andwhoexhibitinadequateresponsedespite standardsurgicalandantibiotictreatment.[3] HBOTisadministeredat2.02.5ATAfor6090minutespertreatment.HBOTmay be12sessionsperday.Theoptimizednumberoftreatmentshasnotbeen determined.[3]

DelayedRadiationInjury
Radiationtherapycausesacute,subacute,anddelayedinjuries.Acuteand subacuteinjuriesaregenerallyselflimited.However,delayedinjuriesareoften muchmoredifficulttotreatandmayappearanywherefrom6monthstoyearsafter treatment.Theygenerallyareseenafteraminimumdoseof6000cGy.While uncommon,theseinjuriescancausedevastatingchronicdebilitationtopatients. Notably,theycanbequiescentuntilaninvasiveprocedureisperformedinthe radiationfield.Injuriesaregenerallydividedintosofttissueversushardtissue injury(osteoradionecrosis[ORN]). Whiletheexactmechanismofdelayedradiationinjuryisstillbeingelucidated,the generallyacceptedexplanationisthatanobliterativeendarteritisandtissue hypoxialeadtosecondaryfibrosis.[79]Hyperbaricoxygentherapy(HBOT)wasfirst usedtotreatORNofthemandible.Basedonthefoundationalclinicalresearchof Marx,[80]multiplesubsequentstudiessupporteditsuse.ThesuccessofHBOTin treatingORNthenledtoitsuseinsofttissueradionecrosisaswell.

Osteoradionecrosis

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MarxdemonstratedconclusivelythatORNisprimarilyanavascularaseptic necrosisratherthantheresultofinfection.[80]Hedevelopedastagingsystemfor classifyingandplanningtreatment,[81]whichislargelyacceptedthroughoutthe oromaxillofacialsurgerycommunity. StageIExposedalveolarbone:Thepatientreceives30HBOTtreatments andthenisreassessedforboneexposure,granulation,andresorptionof nonviablebone.Ifresponseisfavorable,anadditional10treatmentsmaybe considered. StageIIApatientwhoformerlywasStageIwithincompleteresponseor failuretorespond:Performtransoralsequestrectomywithprimarywound closurefollowedbyanadditional10treatments. StageIIIApatientwhofailsstageIIorhasanorocutaneousfistula, pathologicfracture,orresorptiontotheinferiorborderofthemandible:The patientreceives30treatments,transcutaneousmandibularresection,wound closure,andmandibularfixation,followedbyanadditional10postoperative treatments. StageIIIRMandibularreconstruction10weeksaftersuccessfulresolutionof mandibularORN:Thepatientreceives10additionalpostoperativeHBOT treatments. Thecornerstoneoftherapyistobeginandcomplete(ifpossible)HBOTpriorto anysurgicalinterventionandthentoresumeHBOTassoonaspossibleafter surgery.Onlyinthiswayisadequatetimeallowedforangiogenesistosupport postoperativehealing.Forpatientswithahistoryofsignificantradiationexposure, butnoexposedbone,whorequireoralsurgery,manypractitionerssuggest20 HBOTtreatmentspriortosurgeryand10treatmentsimmediatelyfollowing surgery.Feldmeierhaspublishedanexcellentreviewofthisliterature.[82]

Softtissueradionecrosis
Whilesofttissueradionecrosisalsoisrare,itcausessignificantmorbidity, dependingonthesiteofinjury.Alloftheseinjuriesleadtosignificantlocalpain. Bothradiationcystitisandradiationproctitiscanresultinseverebloodlosswith symptomaticanemia,andradiationcystitismaycauseobstructiveuropathy secondarytofibrosisandbloodclotformation.Radionecrosisoftheneckand larynxcanleadtodysphagiaandrespiratoryobstruction.Irradiatedskindevelops painful,necroticwoundsthatdonothealwithstandardwoundhealingcareplans. Foreachofthesesubpopulationsofsofttissueradionecrosis,publishedcase seriesandprospective,nonrandomizedclinicaltrialscorroborateoneanother, providingadegreeofexternalvalidity.Largerstudiesarewarranted.Anational registryiscurrentlybeingevaluated,fromwhichmorepowerfulconclusionsmay

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beforthcoming.Currently,thelargestgroupofreportedpatientstreatedwithHBOT forsofttissueradionecrosisarethosewithradiationcystitis.Atleast15 publications,representingalmost200patients,reportacombinedsuccessratein the80%range.The2largeststudieswerepublishedbyBevers[83]andChong.[84]

HBOTandcarcinogenesis
PractitionersandpatientsareoftenconcernedthatHBOTmayfosterrecurrenceof malignancyorpromotethegrowthofanexistingtumor.Thisislargelybecauseof theknownangiogeniceffectiveofHBOT.Feldmeierhasreviewedthissubject extensively.Malignantangiogenesisappearstofollowadifferentpathwaythan angiogenesisrelatedtowoundhealing.Hisreviewoftheliteraturesuggeststhat theriskislow.[85]

RefractoryOsteomyelitis
Refractoryosteomyelitisisdefinedasacuteorchronicosteomyelitisthatisnot curedafterappropriateinterventions.Moreoftenthannot,refractoryosteomyelitis isseeninpatientswhosesystemsarecompromised.Thisconditionoftenresultsin nonhealingwounds,sinustracts,and,intheworstcase,moreaggressive infectionsthatrequireamputation. MaderandNiinikoskishowedthathyperbaricoxygentherapy(HBOT)iscapableof elevatingoxygentensionininfectedbonetonormalorabovenormallevels.[86,12] Sincepolymorphonuclear(PMN)functionrequiresadequateoxygenconcentration, thisisasignificantmechanismbywhichHBOThelpstocontrolosteomyelitis,as demonstratedbyMaderinthesamestudy.[12] AuniquemechanismbywhichHBOTisbeneficialinosteomyelitisisinpromoting osteoclastfunction.Theresorptionofnecroticbonebyosteoclastsisoxygen dependent.Thishasbestbeendemonstratedinanimalmodelsofosteomyelitis.[87] Additionally,aspreviouslymentioned,HBOTfacilitatesthepenetrationorfunction ofantibioticdrugs.OtherpropertiesofHBOTpreviouslydiscussed,suchas neovascularizationandbluntingtheinflammatoryresponse,likelyprovide additionalbenefit. ConvincinganimalevidencesupportstheuseofHBOTinthetreatmentof osteomyelitis.Clinicalstudiesaresomewhatproblematic,however,because osteomyelitishassomanydifferentpresentationsthatcomparisonsbecome difficult.Thisiscompoundedbythesmallstudysizesfoundintheliterature however,thesedosuggestbenefitofHBOTforrefractoryosteomyelitisinhumans. Onespecificsubsetofosteomyelitisthatmeritsspecialattentionismalignantotitis
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externa.Thisprogressivepseudomonalosteomyelitisoftheearcanalcanspread totheskullbaseandbecomefatal.Davisetalpublishedastudyof17patients withmalignantotitisexterna,allofwhomshoweddramaticimprovementwiththe additionofHBOTtostandardsurgicaldebridementandantibiotictherapy.[88]

ThermalBurns
Thermalburnspresentamultifactorialtissueinjurythatculminatesinamarked inflammatoryresponsewithvascularderangementfromactivatedplateletsand whitecelladhesionwithresultantedema,hypoxia,andvulnerabilitytosevere infection.Poorwhitecellfunctioncausedbythelocalenvironmentexacerbates thisproblem.Hyperbaricoxygentherapy(HBOT)addresseseachofthese pathophysiologicalderangements,andcan,therefore,makeasignificant differenceinpatientoutcomes.Thesemechanismsofactionhavebeendiscussed above. MultipleanimalstudiessupporttheutilityofHBOTfortreatmentofthermalburns. Humanstudiesrangingfromcaseseriestorandomizedclinicaltrialshave supportedthepotentialbenefitofHBOTinburntreatment.Theseincludeasmall randomizedstudybyHart[89]thatdemonstratedimprovedhealinganddecreased mortality.Niezgoda[90]showedincreasedhealinginastandardizedhumanburn model.Inaseriesofpublications,Cianci[91,92]suggestssignificantreductionin lengthofhospitalstay,needforsurgery,andcost. Becauseofthegoalsoftherapy,HBOTisbegunassoonaspossibleafterinjury, withagoalof3treatmentswithinthefirst24hoursandthentwicedaily.Lengthof treatmentdependsontheclinicalimpairmentofthepatientandtheextentofand responsetografting.Specialattentionmustbegiventofluidmanagementand chamberandpatienttemperaturetoavoidunduephysiologicstresstothepatient aswellaspotentialcomplicationsoftreatment(ie,oxygentoxicity).

ExceptionalAnemia
Patientswhodevelopexceptionalanemiahavelostsignificantoxygencarrying capacityintheblood.Thesepatientsbecomecandidatesforhyperbaricoxygen therapy(HBOT)whentheyareunabletoreceivebloodproductsbecauseof religiousormedicalreasons.Themajoroxygencarrierinhumanbloodis hemoglobin,transporting1.34mLofoxygenpergram.Boremaperformedan experimentinthe1960sinwhichexsanguinatedpigs(whohadonlyplasmain theirvasculature)wereabletosustainlifeunderhyperbaricconditions.[5] Thebodygenerallyuses56vol%(mLofO2per100mLofblood)[93]under3

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ATA,6vol%ofmolecularoxygencanbedissolvedintotheplasma.[94]TheCNS andcardiovascularsystemsarethetwomostoxygensensitivesystemsinthe humanbody.[93,95]Oxygendebtisonewayofdeterminingapatientsneedtostart orcontinueHBOT.Acumulativeoxygendebtisthetimeintegralofthevolumeof oxygenconsumption(VO2)measuredduringandaftershockinsultminusthe baselineVO2requiredduringthesametimeinterval.[3]Patientswhohaveadebt >33L/m2donotsurvive,whereaspatientswithdebts9usuallyrecover.[2] HBOTisadministeredat23ATAforperiodsofupto4hourspertreatment.As manyas34sessionsadaymaybenecessary,dependingonapatientsclinical picture.Treatmentsshouldcontinueuntilthepatientcanreceivebloodproducts, nolongerdemonstratesendstageorganfailure,ornolongerhasacalculated oxygendebt.[3]

CentralRetinalArteryOcclusion
Centralretinalarteryocclusion(CRAO)isasudden,painlesslossofvisionthisis themostrecentlyapprovedindicationbytheUnderseaandHyperbaricMedicine Society(UHMS)forHBOT.[96]CRAOiscausedbytheobstructionofthecentral retinalarteryand,althoughaninfrequentcauseofvisualloss,[97]leadsto permanentvisualloss.CurrenttreatmentforCRAOconsistsofattemptstolower intraocularpressureandmovementofapotentialembolusdownstream,ocular massage,anteriorchamberparacentesis,andmedications(botheyedropsand oral)mostmodalitieshaveproveninefficacious.[98] AsmallstudybyHertzogetalevaluatedHBOTwithCRAO.Patientsweredivided intogroupsbasedontimeofonsetofCRAOtoHBOT.ThestudynotedthatHBOT wasmostusefulinpreservingvisionifinstitutedwithin8hours.[99]Another retrospectivestudypublishedbyBeirancomparedpatientsfromafacilitywhere HBOTwasavailabletoafacilitythatdidnothaveHBOT.Thepatientswho receivedHBOTdemonstratedvisualimprovement(82%HBOTvs29.7% control).[100] PatientselectionforHBOTshouldmeetthefollowingcriteria:<24hoursof painlessvisionlossnohistoryofflashesorfloaterspriortovisionlossvisual acuity20/200orworse,evenwithpinholetestingage>40yearsandnorecent eyesurgeryortrauma.[96]Visualimprovementhasbeenreportedevenwithdelay ofHBOT.[101] HBOTisadministeredat2ATAon100%oxygen.Ifnoresponseisnoted, pressureshouldbeincreasedto2.8ATA.Ifvisionisstillnotimprovedafter20 minutes,USNavytreatmentTable6isindicated.Ifvisionisimproved,continueat

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treatmentdepthfor90minutesbid.Continuedailybidcompressionuntilresulting in3dayswithoutvisualimprovement.Ifthepatientrespondsto100%oxygenvia nonrebreather(NRB)maskitself,HBOTisnotneeded,andthepatientshouldbe maintainedonsurface100%oxygenfor12hours.[96]

ComplicationsandSpecialConcerns
Aswithanymedicaltherapy,treatmentbringsbothrisksandbenefits.Oneofthe morefrequentlyseeninjuriescausedbyhyperbaricoxygentherapy(HBOT)is barotrauma(ie,injuriescausedbypressureasaresultofaninabilitytoequalize pressurefromanaircontainingspaceandthesurroundingenvironment).[2,3] Table4.ComplicationstoHyperbaricOxygenTherapy(OpenTableinanew window) Complication Barotrauma Middleear(URI, Eustachiantube dysfunction) Earpain,fullness Autoinflationtechnique Presentation Treatment

Muffledhearing

Pseudoephedrine/oxymetazoline

Tympanostomytubes

WaitforURIresolution

Sinus

Sinuspainorbleeding Oxymetazoline/pseudoephedrine

Antihistamines

Steroidnasalspray
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Dental

Toothpain

Replacementoffillingorcrown (allowstrappedairbubbleto escape) Nobreathholding

Pulmonary

Drycough

Chestpainorburning

Thoracostomy(ifpneumothorax)

Decreasedvital capacity

Increasedecompressiontime

Roundoroval windowblowout

Immediatedeafness

DiscontinueValsalva

Tinnitus

RefertoENT

Nystagmus,vertigo,or both

Visualrefractionchange Lensmorphology Progressivemyopia Mostresolvespontaneously withprolongednumber whentreatmentfinished oftreatments Cloudingofvision Prescreenforexistingcataracts

Cataracts

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HBOTdoesnotinfluence cataractformation

Oxygentoxicity CNS(Incidence0.7 Seizure per10,000treatments at2.4ATA) Removalfromoxygensource

ResumeHBOTwithshorter oxygentreatmentperiods

Doesnotrequiremedication

Treathypoglycemiaifpresent

Treatfeverifpresent

Pulmonary

Drycough

Decreasetotaloxygenexposure time(includingoutsideHBOT)

Chestpainorburning

Decreasedvital capacity

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Pediatricconsiderations
Pediatricpatientsalsohavespecialconcerns.Theproportionofsurfaceareato bodymassismuchgreaterinchildrenthaninadults.Astemperatureinthe chambercanfluctuate,caremustbetakentoensurethechildremainswarm withoutcausinghyperthermia.Thiscanbemoredifficultinamonoplacechamber becausethepatientcannotbephysicallyreachedfromoutsidethechamberto provideblanketsorwarmedwaterasheatsources.Unlesschildrencanfocusand equalizetheirears,considerationforplacementoftympanostomytubesshouldbe discussedwiththeparentstopreventmiddleearbarotrauma. Oxygenadministrationiseasyinamonoplacechamberbecausethechamberis pressurizedwithoxygen.Multiplacechamberscanfashionequipmenttofitthe child.Aneckringcanbefittedoverthechildstorso,or,ifthechildissmall enough,2hoodscanbeplacedtogethertoformacapsulearoundthechild.Care mustbetakenwhentreatingpatientswithductaldependentlesions,asoxygenisa signalforductusarteriosusclosure.Thishasnotbeenadocumentedproblemin pregnancy.Bronchopulmonarydysplasiainapreterminfant,asisassociatedwith mechanicalventilationandelevatedoxygentensions,canbeacceleratedwith HBOT.[2]

PotentialNewIndicationsforHyperbaricOxygen Therapy
SuddenDeafnessSuddensensorineuralhearingloss(SSHL)isarelativelyrare causeoftotalsensorineuralhearinglosscases.SSHLhasmanycauses,but idiopathicSSHLstillpredominates.Theconditionisthoughttoberelatedtoinner earhypoxia,andHBOTincreasesthepartialpressureofoxygen(pO2)intheinner ear. TheeffectivenessofHBOTinSSHLaseitherprimaryoradjunctivetherapyhas notbeenconclusivelyestablished.Althoughsomestudieshaveshown improvementinhearingafterHBOT,othershavenot.Becausetwothirdsormore ofthesepatientshavespontaneousrecovery,selectionofpatientsandevaluation ofresultsiseasilyconfounded.HBOThasbeenadoptedfortreatmentofSSHLin somecountriesbuthasnotgainedwidespreadacceptanceintheUnitedStates andisnotanapprovedindicationbytheUHMS.

BisphosphonateAssociatedOsteonecrosis
Bisphosphonatesareusedwidelyforthemanagementofmetastaticcancerin bone,osteoporosis,Pagetdiseaseofbone,andacutehypercalcemia.Theexact

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mechanismofthepathophysiologythatleadtoosteonecrosisisunknown. However,bisphosphonatesbindtoboneandincorporateintheosseousmatrix. Duringboneremodeling,theyaretakenupbyosteoclasts,whichinducescell death.Theyalsoinhibitosteoblastmediatedosteoclasticresorptionandhave antiangiogenicproperties.Asaresult,boneturnoverissuppressedtherefore,little physiologicremodelingoccurs.Themostvulnerablesiteappearstobethejaw. Noreliabletreatmentforthisconditioniscurrentlyavailable.Casestudiesusing HBOTtotreatbisphosphonateassociatedosteonecrosispromptedapilotstudy withfavorableresults.Therefore,arandomizedclinicaltrialiscurrentlyunderway toevaluatetheefficacyofHBOTforthiscondition.

ContributorInformationandDisclosures
Author EmiLatham,MD,FACEPAssistantClinicalProfessorofEmergencyand HyperbaricMedicine,UniversityofCaliforniaatSanDiego EmiLatham,MD,FACEPisamemberofthefollowingmedicalsocieties: AmericanAcademyofEmergencyMedicine,AmericanCollegeofEmergency Physicians,andUnderseaandHyperbaricMedicalSociety Disclosure:Nothingtodisclose. Coauthor(s) MarcAHare,MDAssistantClinicalProfessorofMedicine,Departmentof EmergencyMedicine,UniversityofCaliforniaSanDiegoMedicalCenter MedicalDirector,CenterforWoundHealingandHyperbaricMedicine,Paradise ValleyHospital MarcAHare,MDisamemberofthefollowingmedicalsocieties:American CollegeofEmergencyPhysiciansandUnderseaandHyperbaricMedicalSociety Disclosure:Nothingtodisclose. MichaelNeumeister,MD,FRCSC,FRCSC,FACSChairman,Professor, DivisionofPlasticSurgery,DirectorofHand/MicrosurgeryFellowshipProgram, ChiefofMicrosurgeryandResearch,InstituteofPlasticandReconstructive Surgery,SouthernIllinoisUniversitySchoolofMedicine MichaelNeumeister,MD,FRCSC,FRCSC,FACSisamemberofthefollowing medicalsocieties:AmericanAssociationforHandSurgery,American AssociationofPlasticSurgeons,AmericanBurnAssociation,AmericanCollege ofSurgeons,AmericanMedicalAssociation,AmericanSocietyfor ReconstructiveMicrosurgery,AmericanSocietyforSurgeryoftheHand,
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AmericanSocietyofPlasticSurgeons,AssociationofAcademicChairmenof PlasticSurgery,CanadianSocietyofPlasticSurgeons,IllinoisStateMedical Society,IllinoisStateMedicalSociety,OntarioMedicalAssociation,Plastic SurgeryResearchCouncil,RoyalCollegeofPhysiciansandSurgeonsof Canada,andSocietyofUniversitySurgeons Disclosure:Nothingtodisclose. SpecialtyEditorBoard ErikDSchraga,MDStaffPhysician,DepartmentofEmergencyMedicine,Mills PeninsulaEmergencyMedicalAssociates Disclosure:Nothingtodisclose. MaryLWindle,PharmDAdjunctAssociateProfessor,UniversityofNebraska MedicalCenterCollegeofPharmacyEditorinChief,MedscapeDrugReference Disclosure:Nothingtodisclose. ChiefEditor ZabMosenifar,MDDirector,DivisionofPulmonaryandCriticalCareMedicine, Director,Women'sGuildPulmonaryDiseaseInstitute,ProfessorandExecutive ViceChair,DepartmentofMedicine,CedarsSinaiMedicalCenter,Universityof California,LosAngeles,DavidGeffenSchoolofMedicine ZabMosenifar,MDisamemberofthefollowingmedicalsocieties:American CollegeofChestPhysicians,AmericanCollegeofPhysicians,American FederationforMedicalResearch,andAmericanThoracicSociety Disclosure:Nothingtodisclose. Acknowledgments MultiplacehyperbaricchamberphotoscourtesyofOxyHealHealthGroup,Inc. MonoplacehyperbaricchamberphotoscourtesyofSechristIndustries,Inc.

References
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oxygentherapyonaxialpatternskinflapsurvivalwhenadministeredduring andaftertotalischemia.JReconstrMicrosurg.Oct19895(4):3437 discussion34950.[Medline]. 16. ThomSR.Effectsofhyperoxiaonneutrophiladhesion.UnderseaHyperb Med.Spring200431(1):12331.[Medline]. 17. ThomSR.FunctionalinhibitionofleukocyteB2integrinsbyhyperbaric oxygenincarbonmonoxidemediatedbraininjuryinrats.ToxicolAppl Pharmacol.Dec1993123(2):24856.[Medline]. 18. ThomSR.Antagonismofcarbonmonoxidemediatedbrainlipidperoxidation byhyperbaricoxygen.ToxicolApplPharmacol.Sep11990105(2):3404. [Medline]. 19. VanUnnika.InhibitionoftoxinProductioninClostridiumPerfringensinVitro byHyperbaricOxygen.AntonieVanLeeuwenhoek.196531:1816. [Medline]. 20. MirhijNJ,RobertsRJ,MyersMG.Effectsofhypoxemiaupon aminoglycosideserumpharmacokineticsinanimals.AntimicrobAgents Chemother.Sep197814(3):3447.[Medline]. 21. KeckPE,GottliebSF,ConleyJ.Interactionofincreasedpressuresof oxygenandsulfonamidesontheinvitroandinvivogrowthofpathogenic bacteria.UnderseaBiomedRes.Jun19807(2):95106.[Medline]. 22. MendelV,ReichertB,SimanowskiHJ,etal.Therapywithhyperbaric oxygenandcefazolinforexperimentalosteomyelitisduetoStaphylococcus aureusinrats.UnderseaHyperbMed.Fall199926(3):16974.[Medline]. 23. MuhvichKH,AndersonLH,CriswellDW,etal.Hyperbarichyperoxia enhancesthelethaleffectsofamphotericinBinLeishmaniabraziliensis panamensis.UnderseaHyperbMed.Dec199320(4):3218.[Medline]. 24. HarveyEN.Decompressionsicknessandbubbleformationinbloodand tissues.BullNYAcadMed.194521:50536. 25. BrubakkA,NeumanT.BennettandElliott'sPhysiologyandMedicineof Diving.5thed.GreatBritain:ElsevierScienceLimited2003:chap10. 26. BoveA.BoveandDavis'DivingMedicine.4thed.ElsevierInc.2004:chap8, 10. 27. NeumanTS.Arterialgasembolismanddecompressionsickness.News PhysiolSci.Apr200217:7781.[Medline].

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