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PARAQUAT
POISINDEXManagements

TREATMENT
ORALEXPOSURE
6.5.1)PREVENTIONOFABSORPTION/PREHOSPITAL
A)EMESIS/NOTRECOMMENDED
1)InducingemesisisNOTrecommended.

B)ACTIVATEDCHARCOAL
1)PREHOSPITALACTIVATEDCHARCOALADMINISTRATION
a)Considerprehospitaladministrationofactivatedcharcoalasanaqueousslurryinpatients
withapotentiallytoxicingestionwhoareawakeandabletoprotecttheirairway.Activated
charcoalismosteffectivewhenadministeredwithinonehourofingestion.Administrationin
theprehospitalsettinghasthepotentialtosignificantlydecreasethetimefromtoxin
ingestiontoactivatedcharcoaladministration,althoughithasnotbeenshowntoaffect
outcome(Alaspaaetal,2005Thakore&Murphy,2002Spiller&Rogers,2002).
1)Inpatientswhoareatriskfortheabruptonsetofseizuresormentalstatusdepression,
activatedcharcoalshouldnotbeadministeredintheprehospitalsetting,duetotheriskof
aspirationintheeventofspontaneousemesis.

2)Theadditionofflavoringagents(coladrinks,chocolatemilk,cherrysyrup)toactivated
charcoalimprovesthepalatabilityforchildrenandmayfacilitatesuccessfuladministration
(GuentherSkokanetal,2001Dagnoneetal,2002).

2)CHARCOALDOSE
a)Useaminimumof240millilitersofwaterper30gramscharcoal(FDA,1985).Optimum
dosenotestablishedusualdoseis25to100gramsinadultsandadolescents25to50
gramsinchildrenaged1to12years(or0.5to1gram/kilogrambodyweight)and0.5to1
gram/kilogramininfantsupto1yearold(Chykaetal,2005).
1)RoutineuseofacatharticwithactivatedcharcoalisNOTrecommendedasthereisno
evidencethatcatharticsreducedrugabsorptionandcatharticsareknowntocauseadverse
effectssuchasnausea,vomiting,abdominalcramps,electrolyteimbalancesandoccasionally
hypotension(NoneListed,2004).

b)ADVERSEEFFECTS/CONTRAINDICATIONS
1)Complications:emesis,aspiration(Chykaetal,2005).Aspirationmaybecomplicatedby
acuterespiratoryfailure,ARDS,bronchiolitisobliteransorchroniclungdisease(Golejetal,
2001Graffetal,2002Pollacketal,1981Harris&Filandrinos,1993Elliotetal,1989
Rauetal,1988Golejetal,2001Graffetal,2002).RefertotheACTIVATED
CHARCOAL/TREATMENTmanagementforfurtherinformation.

2)Contraindications:unprotectedairway(increasesrisk/severityofaspiration),
nonfunctioninggastrointestinaltract,uncontrolledvomiting,andingestionofmost
hydrocarbons(Chykaetal,2005).

C)DERMALEXPOSURE
1)Removecontaminatedclothingandwashtheexposureareathoroughlywithsoapand
water.

6.5.2)PREVENTIONOFABSORPTION
A)GASTRICEMPTYING
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1)InducingemesisisNOTrecommended.Gastriclavagemaybeusefulwhenperformed
withinonehourofingestion,althoughsomeauthorsadvocateitsuseupto24hoursafter
ingestion(Huangetal,2005).Becauseparaquatisaliquidasmallnasogastrictubemaybe
used.Riskofbleedingorperforationmustbeweighedagainstpotentialbenefitofparaquat
removal.Administeractivatedcharcoalorclays(Fuller'sEarthBentonite).

B)ACTIVATEDCHARCOAL
1)Paraquatirreversiblybindstoclaysandactivatedcharcoal.Activatedcharcoalshouldbe
administerediftheingestioniswithinthelast24hoursandthepatientisalertortheairway
isprotected.
2)CHARCOALADMINISTRATION
a)Consideradministrationofactivatedcharcoalafterapotentiallytoxicingestion(Chykaet
al,2005).Administercharcoalasanaqueousslurrymosteffectivewhenadministeredwithin
onehourofingestion.
3)CHARCOALDOSE
a)Useaminimumof240millilitersofwaterper30gramscharcoal(FDA,1985).Optimum
dosenotestablishedusualdoseis25to100gramsinadultsandadolescents25to50
gramsinchildrenaged1to12years(or0.5to1gram/kilogrambodyweight)and0.5to1
gram/kilogramininfantsupto1yearold(Chykaetal,2005).
1)RoutineuseofacatharticwithactivatedcharcoalisNOTrecommendedasthereisno
evidencethatcatharticsreducedrugabsorptionandcatharticsareknowntocauseadverse
effectssuchasnausea,vomiting,abdominalcramps,electrolyteimbalancesandoccasionally
hypotension(NoneListed,2004).

b)ADVERSEEFFECTS/CONTRAINDICATIONS
1)Complications:emesis,aspiration(Chykaetal,2005).Aspirationmaybecomplicatedby
acuterespiratoryfailure,ARDS,bronchiolitisobliteransorchroniclungdisease(Golejetal,
2001Graffetal,2002Pollacketal,1981Harris&Filandrinos,1993Elliotetal,1989
Rauetal,1988Golejetal,2001Graffetal,2002).RefertotheACTIVATED
CHARCOAL/TREATMENTmanagementforfurtherinformation.

2)Contraindications:unprotectedairway(increasesrisk/severityofaspiration),
nonfunctioninggastrointestinaltract,uncontrolledvomiting,andingestionofmost
hydrocarbons(Chykaetal,2005).

4)Oneanimalstudy(Gaudreaultetal,1985)demonstratedincreasedefficacyofactivated
charcoalcombinedwithmagnesiumcitrate.
C)CLAYS
1)BENTONITECLAY:DOSE:ADULT:100to150gCHILDlessthan12yearsofage:2g/kg
(7%suspension)(Bronstein,2004)
2)FULLER'SEARTH:DOSE:ADULT:100to150gCHILDlessthan12yearsofage:2g/kg
(30%suspension)(Bronstein,2004).
3)EXPERIMENTALTHERAPY:SODIUMPOLYSTYRENESULFONATE
a)CONCLUSION:AdditionalstudiesareneededbeforetheuseofSPScanberecommended.
b)ThedoseofSPSusedinthesestudieswasexcessivecomparedtothedoseusedtotreat
hyperkalemia.
c)Thesurvivaldataintheonlytrialinhumansisnotimpressive.Nodetailswereprovided
ontheactualcauseofdeathinthe16patientswhodieddespiteaggressivetreatmentwith
SPSandcathartics.
d)Sodiumpolystyrenesulfonate(SPS)(Kayexalate(R))hasbeenreportedtohavean
adsorptioncapacityforparaquat15timesgreaterthanactivatedcharcoaland6times
greaterthanadsorptioninvitro.TheLD50inratsincreasedfrom144mg/kgto296mg/kg
whensodiumpolystyrenesulfonate(1,000milligrams/kilogram)wasinstilledintothe
stomachafewminutesaftertheparaquat(Takagietal,1983).Therewereonly8ratsin
eachstudygroup.
e)Theeffectoftimebetweenparaquatandsodiumpolystyrenesulfonateadministrationwas
examinedinanotherstudyinrats.Theseanimalsweregiven2grams/kilogramofSPSat0,
0.5,1,2,3,and4hoursafter200mg/kgofparaquat.Whensurvivalwasusedasameasure2/7
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0.5,1,2,3,and4hoursafter200mg/kgofparaquat.Whensurvivalwasusedasameasure
ofefficacy,7of8ratssurvivedfor7dayswhenSPSwasadministeredimmediatelyafterthe
paraquat,however,only3of8ratssurvivedfor7dayswhenSPSadministrationwasdelayed
until4hoursafterparaquatadministration(Yamashitaetal,1987).

f)Yamashitaetal(1987)usedSPSin22patientswithparaquatpoisoningandreported
survivalinonly6of22patients.Therewerenodetailsontheseverityofpoisoninginany
patientsandthetimeelapsedbetweeningestionandtreatment.Thefollowingprotocolwas
used:

1)Gastriclavagewasperformedusing5to10litersofnormalsalinecontaining100
grams/LiterofSPS.

2)Intestinallavagewasperformedbyplacingaduodenaltubeunderxrayexaminationand
administering600to800milliliter/hourofnormalsalinesolutioncontaining100grams/Liter
ofSPS.

3)Magnesiumsulfate,magnesiumcitrate,orsorbitolwasadministeredevery4hoursto
inducecatharsis.

D)WHOLEBOWELIRRIGATION(WBI)
1)WholebowelirrigationhasNOTbeenshowntobeofanybenefitinparaquatpoisoning
(Meredith&Vale,1995).

6.5.3)TREATMENT
A)AIRWAYMANAGEMENT
1)AirwaymanagementshouldbeconsideredforpatientswithsevereCNSdepressionor
thoseatriskofaspiration.

2)OXYGENTHERAPY:DoNOTadministersupplementaloxygen(Rhodesetal,1976).Some
cliniciansadvocatehypoxic(10%to12%)atmospheres.Allowadditionaloxygenonlyin
victimsconsideredbeyondrescuetorelieveairhungerandterminaldisease.

B)MONITORINGOFPATIENT
1)Afulllaboratoryanalysis,includingliverfunctiontests,basicmetabolicpanel,complete
bloodcount,chestxrayandurinalysis,shouldbeperformedonanyoneingestingparaquat.
Arterialbloodgasanalysisshouldbeperformedonthosewithalatepresentationorthose
withhypoxia.Thosewithchronicdermalexposuresandsystemicsymptomsorthosewith
hypoxia.Thosewithchronicdermalexposuresandsystemicsymptomsshouldhavethesame
testingasthoseacuteingestions.Notestingisindicatedinpatientswithacutedermal
exposureswithoutsystemicsymptoms.

2)Bedsidetestingcanbeperformedusinga1%aqueoussodiumdithionitein0.1normal
sodiumhydroxidetoformastableblueradicalintheurine.Ifparaquatispresent,theurine
willappearbluecomparedwiththecontrol(anotherurinesample).

3)Serumparaquatconcentrations(informationavailable24hoursaday7daysaweek
throughZenecaEmergencyInformationNetwork,18003278633,
ctltestkitsupply@syngenta.com)canbeusefulforprognosis.

C)FLUID/ELECTROLYTEBALANCEREGULATION
1)Replacefluidandelectrolyteslostfromvomitingorcatharsis.

D)ACUTETUBULARNECROSIS
1)Acutetubularnecrosisisalmostalwaysreversible.Adequatefluidresuscitationisprimary
therapytolimitsecondaryrenalinjury.Hemodialysisforoliguricrenalfailureisoccasionally
neededasatemporizingmeasureuntilrenalfunctionimproves.

E)IMMUNOSUPPRESSIVETHERAPY
1)SUMMARY
a)Thecombinationofcorticosteroidsandcyclophosphamidehavebeenshownin2,small,
randomizedcontrolledstudiestoreducemortalityinsevereparaquatpoisoning(Linetal,
2006Afzali&Gholyaf,2008).

b)COCHRANEREVIEW:Inasystematicreview,patientswithparaquatinducedlungfibrosis
givenstandardtherapy(eg,decontamination,hemoperfusion)andsteroidsand
cyclophosphamidehadareducedriskofdeathof28%(range:11%to41%reductionin
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cyclophosphamidehadareducedriskofdeathof28%(range:11%to41%reductionin
deathsRR0.7295%ConfidenceInterval(CI)0.59to0.89)comparedtopatientstreated
withstandardtherapyalone.Thereviewwasbasedon3smallrandomizedcontroltrials
(RCTs)andincluded164patientswithmoderatetosevereparaquatpoisoning.Thefindings
shouldbeinterpretedwithcautionbecausethestudiesweresmallandonewasofpoor
methodologicalquality.Furtherrandomizedcontrolledtrialsweresuggestedbytheauthors
(Lietal,2012).

c)Theuseofimmunosuppressivetherapyislimitedandlarge,adequatelycontrolled
randomizedtrialshavenotbeenconducted.Inoneuncontrolledstudy,nosurvivalbenefit
wasobservedwiththeuseofcyclophosphamideanddexamethasone(Gunawardenaetal,
2007).

2)PULSETHERAPY
a)PULSETHERAPYPROTOCOL:Theprotocolusedinonestudywasasfollows(Linetal,
2006):

b)Gastriclavagefollowedbyadministrationof1gram/kilogramofactivatedcharcoalin250
millilitersofmagnesiumcitrateinpatientspresentingwithin24hoursofingestion.

c)Two8hourscoursesofactivatedcharcoalhemoperfusionwithin24hoursofparaquat
ingestion.

d)Afterhemoperfusion,administerintravenouscyclophosphamide15
milligrams/kilogram/dayin200mlD5NSinfusedover2hoursfortwoconsecutivedays.Also
administer1grammethylprednisolonein200millilitersD5NSinfusedover2hoursdailyfor3
consecutivedays.

e)Aftertheinitialpulsetherapy,administerdexamethasone5milligramsintravenouslyevery
6hoursuntilPaO2is80mmHg(11.5kPa)orgreater.

f)IfPaO2<60mmHg(8.64kPa),repeatintravenousmethylprednisolone1gramin200
millilitersD5NSinfusedover2hoursdailyfor3consecutivedays.IfWBC>3000/m(3)andit
hasbeen2weekssincetheinitialpulseofcyclophosphamide,repeatintravenousinfusionof
cyclophosphamide15milligrams/kilogramin200millilitersD5NSinfusedover2hoursasa
singledose.

g)Thencontinueintravenousdexamethasone5milligramsevery6hoursuntilPaO2is80
mmHg(kPa11.5)orgreater.Thenreducedexamethasonedosegradually.

3)ALTERNATIVETHERAPIES
a)Othertreatmentmethodshaveincludedthefollowing:
1)Highdosetherapyincludesthesameinitialtreatment(activatedcharcoaland
hemoperfusion)aspulsetherapyalongwithhighdosecyclophosphamide(5mg/kg/d)and
dexamethasone24mg/dfor14days.However,thistreatmentremainscontroversialdueto
alackofprovenefficacy(Linetal,1999).Anotherstudyusedaslightlydifferenthighdose
therapyusingcyclophosphamide100mg/dayorallyand15mg/dayofIVdexamethasonefor
14days(Hsuetal,2003).

2)Anothermethodincludesearlydecontaminationand15mg/kgofcyclophosphamidein
D5NSin200mLinfusedover2hrsfor2daysandmethylprednisolone1gin200mLD5NS
IVinfusedover4hrsandrepeatedfor3consecutivedays.Mesna(15mg/kg)wasalso
administeredover4daystoavoidsideeffectstocyclophosphamide(Lietal,2012).

4)EVIDENCE
a)POSITIVESTUDY:Aprospectiverandomizedcontrolledtrialevaluated23paraquat
poisonedpatientswithgreaterthan50%andlessthan90%predictivemortality.Thecontrol
group(n=7)receivedconventionaltherapyandthestudygroup(n=16)receivedthenovel
repeatedpulsetreatmentwithlongtermsteroidtherapy[methylprednisolone1g/dayfor3
days,cyclophosphamide15mg/kg/dayfor2days,andthendexamethasone20mg/dayuntil
PaO2wasgreaterthan11.5kPa(80mmHg)andrepeatedpulsetherapywith
methylprednisolone1g/dayfor3daysandcyclophosphamide15mg/kg/dayfor1day,
repeatedifPaO2waslessthan8.64kPa(60mmHg)].Themortalityrateofthestudygroup
waslowerthanthatofthecontrolgroup(5of16,31.3%ofstudygroupvs6of7,85.7%of
controlgroupp=0.0272)(Linetal,2006).

b)POSITIVESTUDY:Adramaticfall(68%:41/61casescomparedto28%:20/72cases)in
mortalityofparaquatpoisoningwasindicatedbythecombinationtherapyortreatmentfor24/7
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mortalityofparaquatpoisoningwasindicatedbythecombinationtherapyortreatmentfor2
weekswithhighdosesoftwoimmunosuppressants,dexamethasoneandcyclophosphamide,
andstandardtherapytoinactivateandeliminatethepoisonfromgutandblood.Notallcases
wereconfirmedbyserumparaquatlevels(Addo&PoonKing,1986).

c)POSITIVESTUDY:Inaretrospectivestudyof29casesofparaquatpoisoning,therapy
withcyclophosphamide,dexamethasone,furosemideandvitaminsBandCwasassociated
withsurvivalof1outof11patientsingesting<45millilitersof20%paraquatwhile
conventionaltherapy(gastricdecontaminationandsupportivecare)wasassociatedwith
survivalin0of6patients(BotelladeMagila&Tarin,2000).

d)POSITIVESTUDY:Inaprospectivestudyofparaquatpoisoning,useofcyclophosphamide
andcorticosteroidswasassociatedwithsurvivalin18of22patientswithmoderatepoisoning
comparedwith12of28controlswithmoderatepoisoning(Linetal,1999).Nopatients
presentingwithfulminantpoisoningsurvivedineithertreatmentgroup.Whenthesedataare
reanalyzedonanintentiontotreatbasis,thiseffectlosesstatisticalsignificance(18survivors
of56patientsinthetreatmentgroupvs12survivorsof65controlpatients)(Buckley,2001).

e)NEGATIVESTUDY:Aprospective,nonrandomizedstudyofparaquatpoisoningtreated
withstandardtherapy(lavage,bentonite,magnesiumsulfate,metoclopramide14cases)or
standardtherapyplusdexamethasone/cyclophosphamide(33cases)foundnodifferencein
survivalbetweengroups.Complicationsofimmunosuppressanttherapyincludedsepticemia
(2cases),alopecia(9cases),andacne(8cases)(Perriensetal,1992).

f)METAANALYSIS:Ametaanalysisof10clinicalstudies(1randomizedclinicaltrialand9
nonrandomizedstudies)wasconductedtodeterminetheeffectivenessofimmunosuppressive
therapyfortreatmentofparaquatinducedlungfibrosis.Theresultsofthemetaanalysis
wereinconclusiveduetovariousconfoundingfactorsofeachstudy(Eddlestonetal,2003).

F)ACETYLCYSTEINE
1)Cotgreaveetal(1987)demonstratedthatthecombinationofEbselen(PZ51:2phenyl1,2
benzoisoselenazol3(H)one)andNacetylcysteinemayprovideaneffectiveantidoteincases
ofoverexposuretoparaquatthroughaninvitrostudyusingisolatedhepatocytes,butthishas
NOTbeenestablishedclinically.

2)Draultetal(1999)reportedapatientwhosurvivedtheingestionof60gofparaquatafter
treatmentwithIVNacetylcysteineandearlyhemodialysis(within4hoursofingestion).
G)TRANSPLANT
1)LUNGTRANSPLANTATION:Lungtransplants,bothsingleandbilateral,havebeen
performedinseveralpatientswhoingestedtoxicamountsofparaquat.Manypatientsdied
despitetransplant(TorontoLungTransplantGroup,1985Kamholzetal,1984Cookeetal,
1973).Occasionalsurvivalhassincebeenreported(Lickeretal,1998Walderetal,1997).

H)EXTRACORPOREALMEMBRANEOXYGENATION
1)CASEREPORT:A23yearoldmanpresentedtoalocalEDafterinadvertentlyingestinga
mouthfulofparaquat20%(about6to10g).Heimmediatelyinducedvomitingafter
ingestion.Onadmission,hisparaquatconcentrationsinserumandurinewere2.12mg/Land
350mg/L,respectively,indicatingalethaldose.Despitedecontaminationwithagastric
lavageandactivatedcharcoal,hedevelopedacutenonoligurickidneyinjurywithin48hours
andwastransferredtoatertiarycarecenter.Hisphysicalexaminationshowedmildjaundice
andswellingandrednessofthethroatwhilehislaryngoscopyrevealedrednessandnecroses
ofthehypopharynx,epiglottis,andvocalcords.Laboratoryresultsrevealedelevatedliver
enzymes,mildlyelevatedinflammatorymarkersandacutekidneyinjury.Heunderwent
hemodialysisandreceivedIVmethylprednisoloneandcyclophosphamidetodelaythe
developmentofpulmonaryfibrosis.Inaddition,hereceivedtamoxifen(3x20mgorally)due
toitsantiproliferativeandantiinflammatoryeffectsinretroperitonealfibrosis.About72hours
postingestion,hisconditiondeterioratedandhedevelopedrespiratoryfailure,necessitating
oxygensupplementation.Onday9,invasiveventilationwasrequiredduetotheprogression
ofpulmonaryfibrosis.Hewasplacedonahighurgencylungtransplantationlisthowever,his
conditioncontinuedtodeterioratewiththeonsetofsystemicinflammatoryresponse
syndrome.Onday12,anextracorporealmembraneoxygenation(ECMO)wasimplemented,
butdespitefurthersupportivecare,hedevelopedhemodynamicinstabilityandseptic
multiorgandysfunctionwithkidney,liver,andhemodynamicfailure.Thepatientdied32days5/7
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multiorgandysfunctionwithkidney,liver,andhemodynamicfailure.Thepatientdied32days
postingestionfromcardiacfailurewithpulselesselectricalactivity(Bertrametal,2013).

2)CASEREPORT:A24yearoldwomanwithahistoryofchronichepatitisBanddepression
presentedtoalocalEDabout2hourafteringestingabout50mLof20%ofparaquat(about
188mg/kg).Despitesupportivecare,includinggastriclavage,activatedcharcoal,
cyclophosphamide,methylprednisolone,andhemoperfusion(3sessions),hersymptomsdid
notimprovesignificantly.Onday2,shedevelopedelevatedliverenzymes,renalinsufficiency,
pulmonaryfibrosis,andsevererespiratoryfailure.Herconditiongraduallydeterioratedandon
day44,sheunderwentvenovenousextracorporealmembraneoxygenation(ECMO)asa
bridgetolungtransplantation.Shereceivedabilateralsequentiallungtransplantationonday
56.Followingfurthersupportivecare,includingrespiratoryandphysicalrehabilitation,her
conditiongraduallyimprovedandshewasdischargedonday80(Tangetal,2015).

I)PROLONGEDQTINTERVAL
1)Inaretrospectivestudy,theprognosticvalueofQTcprolongationinseverelyparaquat
poisonedpatientswasevaluated.Overall,53nonsurvivorsand7survivorswereincludedin
thestudy.QTcintervalsrangedfrom0.35to0.48secondsand0.32to0.63secondsinthe
survivorandnonsurvivorgroups,respectively.One(14.3%)survivorand32(60.4%)non
survivorshadaQTcof0.45secondsorhigher,withamediansurvivaltimeof26hours50%
ofthesepatientsdiedwithin1day.QTcoflessthan0.45secondswasobservedin6(85.7%)
survivorsand21(39.6%)nonsurvivors,withamediansurvivaltimeof95hours.Itwas
concludedthatQTcprolongationcanbeausefulprognosticfactorforpredictingtheseverity
ofpoisoningandmortalityriskinacuteparaquatpoisonedpatients.Inaddition,QTc
prolongationofgreaterthan45msecpredictedmortalityregardlessofpotassium
concentration(Linetal,2014).

J)EXPERIMENTALTHERAPY
1)Nonsteroidalantiinflammatoryagents,colchicine,collagensynthesisinhibitors,
deferoxamine,ortotalexclusionfromexternalrespirationmaypreventlungfibrosis.However,
theefficacyofthesetreatmentshasyettobeestablishedinthetreatmentofhumanparaquat
poisonings(Bismuthetal,1990Shaharetal,1989Akahori&Oehme,1983Vinckenetal,
1981Pasi,1978Fogt&Zilker,1989Jaegeretal,1995Pond,1990).
2)GLUCOCORTICOIDWITHCYCLOPHOSPHAMIDE:In3smallrandomizedcontrolledtrialsof
patients(n=164)withmoderateorsevereparaquatpoisoning,theuseofglucocorticoidand
cyclophosphamidewithstandardcarewasbeneficialintreatingpatientswithparaquat
inducedlungfibrosis.Overall,theriskofdeathinpatientsreceivingthiscombinationwas
reducedby28%(statisticallyestimatedlikelyrangeofreduceddeathsfrom41%to11%)as
comparedwithpatientsreceivingjuststandardcare(Lietal,2012).
3)L'Heureuxetal(1995)reportedthesurvivalofamanwhoingested50to60mLofa
paraquatcontainingsolutionandbenzodiazepinetablets.Treatmentincludedearly
decontamination,hemodialysis,100mgdeferoxamine/kgin24hours,and300mg
acetylcysteine/kg/dayfora3weekperiod.Reversible,acuterenalfailureandmildhepatic
enzymeelevationoccurred.Pulmonaryeffectswerelimited.Fibrosisdidnotoccur(L'Heureux
etal,1995).
4)ParaquatspecificIgGandFabfragmentshavereducedcellularuptakeofparaquatby
isolateratalveolartypeIIcells(Chenetal,1994).
5)Highmolecularweightpolyvinylsulfate(PVP)orpolyvinylsulfonate(PVS),aswellaslow
molecularweightalkylsulfonates,resultedin100%survivalofmicegivenparaquatdichloride
at200mg/kg(Tsuchiyaetal,1995).
a)Themechanismoftheirprotectionappearstobepreventionofparaquatabsorptionfrom
theintestine.Thelowmolecularweightalkyldisulfonatesalsoinhibitedtheformationof
pulmonarylipidperoxides.

6)NITRICOXIDEINHALATION:NitricOxide(NO)isavasodilatinggasthathasbeenused
successfullytoincreasethepO2inpatientswithadultrespiratorydistresssyndrome(ARDS)
(Bismuth,1995).
a)NOinhalationdidimprovethepO2andstabilizedthepulmonarystatusforthreedaysin
onepatientwithacuteparaquatpoisoning(Koppeletal,1994).

b)Whilestillexperimental,inseriousparaquatpoisoningcases,NOinhalationtomaintain
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b)Whilestillexperimental,inseriousparaquatpoisoningcases,NOinhalationtomaintain
tissueoxygenationinanticipationoflungtransplantationonceallabsorbedparaquathas
beeneliminateddeservesfurtherstudy.

7)SIROLIMUS:Amaningestedapproximately120mLofGramoxoneInteon(R)and
developeddiffusepulmonaryfibrosisandpneumomediastinumabout12daysafterexposure
andwasstartedonsirolimustolimitfurtherpulmonaryfibrosis.Therapywascontinuedfor15
days.Sirolimus,atrienemacrolideimmunosuppressant,hasantiproliferativeeffectson
fibroblastsandonlymphoidandnonlymphoidtumorcells.Otheragentsincluded
cyclophosphamide,methylprednisoloneanddexamethasone.Thepatientgraduallyimproved
andhisoxygensaturationincreasedto90%on2litersofoxygenbyhospitalday39
(Barruetoetal,2008).Theauthorssuggestedthatsirolimusalongwiththeotherconcomitant
therapieswereresponsibleforhaltingtheprogressionofparaquatinducedpulmonary
fibrosis.
8)SURFACTANTTHERAPY:Exogenoussurfactantdidimprovelungfunctionforseveralhours
inparaquatpoisonedrats(Soetal,1998).Nohumandatawaslocatedatthetimeofthis
revision.
9)HIGHDOSEVITAMINC:Inonestudy,theadministrationofhighdosevitaminC,in
combinationwithantiinflammatoryandimmunosuppressantagents,waseffectivein
preventingacuterenalinjuryinpatientswithparaquatpoisoning(anaverageingestionof
134.1+/126.3mLof24.5%liquidparaquatserumparaquatconcentrationof30.8+/45.5
mcg/mL).Fiftysevenpatientsreceivedpulsetherapy(cyclophosphamideand
methylprednisolone,thendexamethasone)for2weeksand77patientsreceivedthesame
pulsetherapywithhighdosevitaminCfor2weeks.Asignificantdecreaseintheincidenceof
paraquatinducedacuterenalinjurywasobservedinthehighdosevitaminCgroup.In
addition,theuseofvitaminCwithpulsetherapywassignificantlyassociatedwithan
increasedsurvivalofthepatients(Moon&Chun,2010).

LastModified:April12,2016
2016TruvenHealthAnalyticsInc.

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