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Proclivity ID
18811001
Unpublish
Citation Name
OBG Manag
Specialty Focus
Obstetrics
Gynecology
Surgery
Negative Keywords
gaming
gambling
compulsive behaviors
ammunition
assault rifle
black jack
Boko Haram
bondage
child abuse
cocaine
Daech
drug paraphernalia
explosion
gun
human trafficking
ISIL
ISIS
Islamic caliphate
Islamic state
mixed martial arts
MMA
molestation
national rifle association
NRA
nsfw
pedophile
pedophilia
poker
porn
pornography
psychedelic drug
recreational drug
sex slave rings
slot machine
terrorism
terrorist
Texas hold 'em
UFC
substance abuse
abuseed
abuseer
abusees
abuseing
abusely
abuses
aeolus
aeolused
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aholeed
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aholees
aholeing
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alcohol
alcoholed
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alcoholes
alcoholing
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allmaned
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alted
altes
alting
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analer
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anilingused
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anus
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areola
areolaed
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aryaned
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aryaning
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asiaed
asiaer
asiaes
asiaing
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asias
ass
ass hole
ass lick
ass licked
ass licker
ass lickes
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assbangedes
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asshated
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azz
azzed
azzer
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azzing
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beardedclamed
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beardedclames
beardedclaming
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beastialityed
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beastialityes
beastialitying
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beatched
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beatered
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biatched
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biatching
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biatchs
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big titsed
big titser
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bisexualed
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bitched
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bitching
bitchly
bitchs
bitchy
bitchyed
bitchyer
bitchyes
bitchying
bitchyly
bitchys
bleached
bleacher
bleaches
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bleachly
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blow job
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blow jobes
blow jobing
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boink
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boinkes
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bollock
bollocked
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bollocks
bollocksed
bollockser
bollockses
bollocksing
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bollockss
bollok
bolloked
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boner
bonered
bonerer
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bonering
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bonerser
bonerses
bonersing
bonersly
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bong
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bonges
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boob
boobed
boober
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boobies
boobiesed
boobieser
boobieses
boobiesing
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boobiess
boobing
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boobser
boobses
boobsing
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boobyes
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boogered
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boogering
boogerly
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bookie
bookieed
bookieer
bookiees
bookieing
bookiely
bookies
bootee
booteeed
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booteees
booteeing
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bootieed
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bootieing
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bootyed
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bootyes
bootying
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boozeed
boozeer
boozees
boozeing
boozely
boozer
boozered
boozerer
boozeres
boozering
boozerly
boozers
boozes
boozy
boozyed
boozyer
boozyes
boozying
boozyly
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bosomed
bosomer
bosomes
bosoming
bosomly
bosoms
bosomy
bosomyed
bosomyer
bosomyes
bosomying
bosomyly
bosomys
bugger
buggered
buggerer
buggeres
buggering
buggerly
buggers
bukkake
bukkakeed
bukkakeer
bukkakees
bukkakeing
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bukkakes
bull shit
bull shited
bull shiter
bull shites
bull shiting
bull shitly
bull shits
bullshit
bullshited
bullshiter
bullshites
bullshiting
bullshitly
bullshits
bullshitsed
bullshitser
bullshitses
bullshitsing
bullshitsly
bullshitss
bullshitted
bullshitteded
bullshitteder
bullshittedes
bullshitteding
bullshittedly
bullshitteds
bullturds
bullturdsed
bullturdser
bullturdses
bullturdsing
bullturdsly
bullturdss
bung
bunged
bunger
bunges
bunging
bungly
bungs
busty
bustyed
bustyer
bustyes
bustying
bustyly
bustys
butt
butt fuck
butt fucked
butt fucker
butt fuckes
butt fucking
butt fuckly
butt fucks
butted
buttes
buttfuck
buttfucked
buttfucker
buttfuckered
buttfuckerer
buttfuckeres
buttfuckering
buttfuckerly
buttfuckers
buttfuckes
buttfucking
buttfuckly
buttfucks
butting
buttly
buttplug
buttpluged
buttpluger
buttpluges
buttpluging
buttplugly
buttplugs
butts
caca
cacaed
cacaer
cacaes
cacaing
cacaly
cacas
cahone
cahoneed
cahoneer
cahonees
cahoneing
cahonely
cahones
cameltoe
cameltoeed
cameltoeer
cameltoees
cameltoeing
cameltoely
cameltoes
carpetmuncher
carpetmunchered
carpetmuncherer
carpetmuncheres
carpetmunchering
carpetmuncherly
carpetmunchers
cawk
cawked
cawker
cawkes
cawking
cawkly
cawks
chinc
chinced
chincer
chinces
chincing
chincly
chincs
chincsed
chincser
chincses
chincsing
chincsly
chincss
chink
chinked
chinker
chinkes
chinking
chinkly
chinks
chode
chodeed
chodeer
chodees
chodeing
chodely
chodes
chodesed
chodeser
chodeses
chodesing
chodesly
chodess
clit
clited
cliter
clites
cliting
clitly
clitoris
clitorised
clitoriser
clitorises
clitorising
clitorisly
clitoriss
clitorus
clitorused
clitoruser
clitoruses
clitorusing
clitorusly
clitoruss
clits
clitsed
clitser
clitses
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clitsly
clitss
clitty
clittyed
clittyer
clittyes
clittying
clittyly
clittys
cocain
cocaine
cocained
cocaineed
cocaineer
cocainees
cocaineing
cocainely
cocainer
cocaines
cocaining
cocainly
cocains
cock
cock sucker
cock suckered
cock suckerer
cock suckeres
cock suckering
cock suckerly
cock suckers
cockblock
cockblocked
cockblocker
cockblockes
cockblocking
cockblockly
cockblocks
cocked
cocker
cockes
cockholster
cockholstered
cockholsterer
cockholsteres
cockholstering
cockholsterly
cockholsters
cocking
cockknocker
cockknockered
cockknockerer
cockknockeres
cockknockering
cockknockerly
cockknockers
cockly
cocks
cocksed
cockser
cockses
cocksing
cocksly
cocksmoker
cocksmokered
cocksmokerer
cocksmokeres
cocksmokering
cocksmokerly
cocksmokers
cockss
cocksucker
cocksuckered
cocksuckerer
cocksuckeres
cocksuckering
cocksuckerly
cocksuckers
coital
coitaled
coitaler
coitales
coitaling
coitally
coitals
commie
commieed
commieer
commiees
commieing
commiely
commies
condomed
condomer
condomes
condoming
condomly
condoms
coon
cooned
cooner
coones
cooning
coonly
coons
coonsed
coonser
coonses
coonsing
coonsly
coonss
corksucker
corksuckered
corksuckerer
corksuckeres
corksuckering
corksuckerly
corksuckers
cracked
crackwhore
crackwhoreed
crackwhoreer
crackwhorees
crackwhoreing
crackwhorely
crackwhores
crap
craped
craper
crapes
craping
craply
crappy
crappyed
crappyer
crappyes
crappying
crappyly
crappys
cum
cumed
cumer
cumes
cuming
cumly
cummin
cummined
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cummines
cumming
cumminged
cumminger
cumminges
cumminging
cummingly
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cumminly
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cums
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cumshoted
cumshoter
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cumshoting
cumshotly
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cumshotsed
cumshotser
cumshotses
cumshotsing
cumshotsly
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cumsluted
cumsluter
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cumsluting
cumslutly
cumsluts
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cumstained
cumstainer
cumstaines
cumstaining
cumstainly
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cunilingus
cunilingused
cunilinguser
cunilinguses
cunilingusing
cunilingusly
cunilinguss
cunnilingus
cunnilingused
cunnilinguser
cunnilinguses
cunnilingusing
cunnilingusly
cunnilinguss
cunny
cunnyed
cunnyer
cunnyes
cunnying
cunnyly
cunnys
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cunted
cunter
cuntes
cuntface
cuntfaceed
cuntfaceer
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cuntfaceing
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cuntfaces
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cunthuntered
cunthunterer
cunthunteres
cunthuntering
cunthunterly
cunthunters
cunting
cuntlick
cuntlicked
cuntlicker
cuntlickered
cuntlickerer
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cuntlickerly
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cuntlickes
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cuntly
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cuntser
cuntses
cuntsing
cuntsly
cuntss
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dagoed
dagoer
dagoes
dagoing
dagoly
dagos
dagosed
dagoser
dagoses
dagosing
dagosly
dagoss
dammit
dammited
dammiter
dammites
dammiting
dammitly
dammits
damn
damned
damneded
damneder
damnedes
damneding
damnedly
damneds
damner
damnes
damning
damnit
damnited
damniter
damnites
damniting
damnitly
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damnly
damns
dick
dickbag
dickbaged
dickbager
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dickbaging
dickbagly
dickbags
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dickdippered
dickdipperer
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dickdippering
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dicker
dickes
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dickfaceed
dickfaceer
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dickfaceing
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dickheaded
dickheader
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dickheading
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dickheadsing
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dickishly
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dickly
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dicksipper
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dickweed
dickweeded
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dickweedly
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dickwhipperer
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dickzipper
dickzippered
dickzipperer
dickzipperes
dickzippering
dickzipperly
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diddle
diddleed
diddleer
diddlees
diddleing
diddlely
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dikeing
dikely
dikes
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dildoed
dildoer
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dildoing
dildoly
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dildosing
dildosly
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diligafed
diligafer
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diligafing
diligafly
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dillweed
dillweeded
dillweeder
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dillweeding
dillweedly
dillweeds
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dimwited
dimwiter
dimwites
dimwiting
dimwitly
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dingle
dingleed
dingleer
dinglees
dingleing
dinglely
dingles
dipship
dipshiped
dipshiper
dipshipes
dipshiping
dipshiply
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dizzyed
dizzyer
dizzyes
dizzying
dizzyly
dizzys
doggiestyleed
doggiestyleer
doggiestylees
doggiestyleing
doggiestylely
doggiestyles
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doggystyleer
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doggystyleing
doggystylely
doggystyles
dong
donged
donger
donges
donging
dongly
dongs
doofus
doofused
doofuser
doofuses
doofusing
doofusly
doofuss
doosh
dooshed
doosher
dooshes
dooshing
dooshly
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dopeyed
dopeyer
dopeyes
dopeying
dopeyly
dopeys
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douchebaged
douchebager
douchebages
douchebaging
douchebagly
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douchebagsed
douchebagser
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douchebagsing
douchebagsly
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doucheer
douchees
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douchely
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doucheyes
doucheying
doucheyly
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drunked
drunker
drunkes
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drunkly
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dumassed
dumasser
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dumassly
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dumbass
dumbassed
dumbasser
dumbasses
dumbassesed
dumbasseser
dumbasseses
dumbassesing
dumbassesly
dumbassess
dumbassing
dumbassly
dumbasss
dummy
dummyed
dummyer
dummyes
dummying
dummyly
dummys
dyke
dykeed
dykeer
dykees
dykeing
dykely
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dykeser
dykeses
dykesing
dykesly
dykess
erotic
eroticed
eroticer
erotices
eroticing
eroticly
erotics
extacy
extacyed
extacyer
extacyes
extacying
extacyly
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extasyed
extasyer
extasyes
extasying
extasyly
extasys
fack
facked
facker
fackes
facking
fackly
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fag
faged
fager
fages
fagg
fagged
faggeded
faggeder
faggedes
faggeding
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faggeds
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fagges
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faggited
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faggites
faggiting
faggitly
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faggly
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faggoter
faggotes
faggoting
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faggs
faging
fagly
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fagoted
fagoter
fagotes
fagoting
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fagser
fagses
fagsing
fagsly
fagss
faig
faiged
faiger
faiges
faiging
faigly
faigs
faigt
faigted
faigter
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faigting
faigtly
faigts
fannybandit
fannybandited
fannybanditer
fannybandites
fannybanditing
fannybanditly
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farter
fartes
farting
fartknocker
fartknockered
fartknockerer
fartknockeres
fartknockering
fartknockerly
fartknockers
fartly
farts
felch
felched
felcher
felchered
felcherer
felcheres
felchering
felcherly
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felches
felching
felchinged
felchinger
felchinges
felchinging
felchingly
felchings
felchly
felchs
fellate
fellateed
fellateer
fellatees
fellateing
fellately
fellates
fellatio
fellatioed
fellatioer
fellatioes
fellatioing
fellatioly
fellatios
feltch
feltched
feltcher
feltchered
feltcherer
feltcheres
feltchering
feltcherly
feltchers
feltches
feltching
feltchly
feltchs
feom
feomed
feomer
feomes
feoming
feomly
feoms
fisted
fisteded
fisteder
fistedes
fisteding
fistedly
fisteds
fisting
fistinged
fistinger
fistinges
fistinging
fistingly
fistings
fisty
fistyed
fistyer
fistyes
fistying
fistyly
fistys
floozy
floozyed
floozyer
floozyes
floozying
floozyly
floozys
foad
foaded
foader
foades
foading
foadly
foads
fondleed
fondleer
fondlees
fondleing
fondlely
fondles
foobar
foobared
foobarer
foobares
foobaring
foobarly
foobars
freex
freexed
freexer
freexes
freexing
freexly
freexs
frigg
frigga
friggaed
friggaer
friggaes
friggaing
friggaly
friggas
frigged
frigger
frigges
frigging
friggly
friggs
fubar
fubared
fubarer
fubares
fubaring
fubarly
fubars
fuck
fuckass
fuckassed
fuckasser
fuckasses
fuckassing
fuckassly
fuckasss
fucked
fuckeded
fuckeder
fuckedes
fuckeding
fuckedly
fuckeds
fucker
fuckered
fuckerer
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Moving forward with ICD-10: Capitalize on this extra time

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Moving forward with ICD-10: Capitalize on this extra time

Yes, we have been here before. Another day, another delay in implementing International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM). But, do not expect another postponement. If you are already conducting training sessions to move to the new system come next October, continue to do so. If you have not yet started, now is the time to start. ICD-10-CM is coming to your practice, and it will change everything.

“Why the switch?” you ask?
This change in our diagnostic coding system is required to allow coding for increased specificity in the reporting of diseases and recently recognized conditions as well as to maintain our status with respect to the rest of the world (which has been using ICD-10 for years). It also will be essential to use this coding system with the electronic medical record (EMR), so that meaningful use can be demonstrated more easily. Keep in mind that failure to show meaningful use will lead to penalties in the future. This new system offers improvements over ICD-9-CM in coding primary care encounters, external causes of injury, mental disorders, neoplasms, obstetric complications, and preventive health. It also allows physicians to demonstrate severity of illness in a way that is not possible with ICD-9-CM.

There will be 65,000 more codes than currently exist in ICD-9-CM. No physician will be able to keep all of these code numbers handy, but by making changes to clinician documentation and applying diagnostic coding guidelines correctly within the framework of the new system, the transition will not be onerous. And consider that, while the number of new codes is great, the number of codes used in the typical ObGyn practice will be a fraction of that number.

Related article: As ICD-10 conversion nears, keep these factors in mind to ensure proper reimbursements in 2014. Barbara S. Levy, MD (Audiocast, January 2014)

For ICD-10, documentation is paramount
The most important issue when considering overall coding and practice changes will be recognizing that clinician documentation will be the key to coding the highest level of specificity—and this high level of specificity may be required by most payers when ­deciding to reimburse for treatments rendered. Complete documentation sets the stage for the severity of illness and should in fact result in fewer denials for medical necessity.

For the new process to work efficiently, however, without a lot of delays due to coders and billers having to get more information from clinician offices before sending out claims, your understanding of and “buy-in” to the more clinically specific documentation will be essential.

To explain, under ICD-9-CM coding, simply documenting amenorrhea was acceptable. But when we switch to ICD-10-CM, documentation will need to specify whether the amenorrhea was primary or secondary. This more specific diagnostic coding will make a difference in the health statistics we collect. These data are used for research and to make decisions about allocation of resources—all essential components to excellent quality patient care.

The codes themselves will look different, which may be why some are resisting the change. Instead of the up to five digits required in ICD-9-CM, ICD-10-CM will require up to seven characters. All of the ICD-10-CM codes begin with a letter, may require a placeholder code of “x” as part of the code number, and the seventh character can be either a number or a letter. For instance, with some ICD-10-CM diagnoses reported by ObGyns, a seventh character might require documentation of the encounter as being initial, subsequent, or a sequel; in other cases, that seventh character will be used to identify which fetus has the problem identified by the diagnostic code.

Related article: The economics of surgical gynecology: How we can not only survive, but thrive, in the 21st Century. Q&A with Barbara S. Levy, MD (Practice Management; February 2013)

Your understanding, although not a necessity, is best for all involved
In truth, most clinicians are not familiar with code formats and code numbers within our current ICD-9-CM code set. The expectation that you will suddenly become fluent in ICD-10-CM “code speak” is not realistic. But an understanding of the new codes in relation to documentation expectations will go a long way to making this transition as smooth as possible. For instance, when a patient currently presents reporting vaginal pain that is found to be due to erosion of a previously placed mesh, the code 628.31 (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue) is  reported. But in ICD-10-CM, the documentation would need to include whether this was an initial encounter and the code would become T83.711A (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue, initial encounter).

 

 

Smart search. The good news is that most EMR products will have a “smart search” program available for clinicians to pick the correct code based on the search criteria. The bad news is that you will have to be a bit more exact in the search terms you use to make the process easy. For instance, the patient has pelvic pain but you search only on the term “pain.” That term by itself will result in about 100 codes to select from, and the order of the codes may mean that the correct code for pelvic pain is 25 codes down the list. However, if you instead search on the term “pelvic pain,” the one and only code for this condition will be listed and you can simply select it and move on.

Develop cheat sheets. Health-care professionals who are not using an EMR or some sort of computerized code search program will have a harder time, but the use of multiple paper “cheat sheets” for general gynecology, family planning, surgical cases, urology, infertility, obstetrics, etc., will ease that burden. Practice management staff can develop these forms, built on the codes that are currently being reported by the clinician. Place all of the options to replace the older code on the sheet so the correct selection can be made.

For instance, if the provider previously had reported vaginitis with one code, when we move to ICD-10-CM the code would expand to four code selections based on documentation of acute vaginitis, subacute and chronic vaginitis, acute vulvitis, or subacute and chronic vulvitis. If you only had documented vaginitis in the medical record, this gives you the opportunity to refine the documentation to something more specific that supports selection of the correct code and supports the medical need for management options.

Related article: Dos, don’ts, and dollars: Making the switch to an HER. Neil H. Baum, MD; Paul Kepper, MS. (Practice Management; November 2013)

Take advantage of the extra time
Now that we have a delay in the rollout, take this time to critically examine your documentation styles, and practice selecting ICD-10-CM codes before it counts toward payment or nonpayment of a claim. When the time comes, your practice will be fluent in the new system and there will be no delays in getting claims out the door or payment due to incorrect diagnostic coding. In other words, practice makes perfect.

In fact, some ObGyn practices that were ready for the new system have decided to switch to ICD-10-CM coding as of October 1, 2014. They will code each encounter by reporting both the ICD-9-CM code and the ICD-10-CM code on the revised CMS claim form or electronic billing format that permits dual diagnostic coding. This type of experience will ensure that all physicians and other health-care professionals in the practice have ample opportunity to improve their documentation and make any adjustments before the 2015 deadline.

Related article: The 2014 CPT and Medicare code changes affecting ObGyn practice. Melanie Witt, RN, CPC, COBGC, MA (Reimbursement Adviser; January 2014)

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Melanie Witt, RN, CPC, COBGC, MA, is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.

Ms. Witt reports that she is a coding consultant to American Medical Systems, Bladder Health Network, Boston Scientific, and CerviLenz.

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Melanie Witt, RN, CPC, COBGC, MA, is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.

Ms. Witt reports that she is a coding consultant to American Medical Systems, Bladder Health Network, Boston Scientific, and CerviLenz.

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Related Articles

Yes, we have been here before. Another day, another delay in implementing International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM). But, do not expect another postponement. If you are already conducting training sessions to move to the new system come next October, continue to do so. If you have not yet started, now is the time to start. ICD-10-CM is coming to your practice, and it will change everything.

“Why the switch?” you ask?
This change in our diagnostic coding system is required to allow coding for increased specificity in the reporting of diseases and recently recognized conditions as well as to maintain our status with respect to the rest of the world (which has been using ICD-10 for years). It also will be essential to use this coding system with the electronic medical record (EMR), so that meaningful use can be demonstrated more easily. Keep in mind that failure to show meaningful use will lead to penalties in the future. This new system offers improvements over ICD-9-CM in coding primary care encounters, external causes of injury, mental disorders, neoplasms, obstetric complications, and preventive health. It also allows physicians to demonstrate severity of illness in a way that is not possible with ICD-9-CM.

There will be 65,000 more codes than currently exist in ICD-9-CM. No physician will be able to keep all of these code numbers handy, but by making changes to clinician documentation and applying diagnostic coding guidelines correctly within the framework of the new system, the transition will not be onerous. And consider that, while the number of new codes is great, the number of codes used in the typical ObGyn practice will be a fraction of that number.

Related article: As ICD-10 conversion nears, keep these factors in mind to ensure proper reimbursements in 2014. Barbara S. Levy, MD (Audiocast, January 2014)

For ICD-10, documentation is paramount
The most important issue when considering overall coding and practice changes will be recognizing that clinician documentation will be the key to coding the highest level of specificity—and this high level of specificity may be required by most payers when ­deciding to reimburse for treatments rendered. Complete documentation sets the stage for the severity of illness and should in fact result in fewer denials for medical necessity.

For the new process to work efficiently, however, without a lot of delays due to coders and billers having to get more information from clinician offices before sending out claims, your understanding of and “buy-in” to the more clinically specific documentation will be essential.

To explain, under ICD-9-CM coding, simply documenting amenorrhea was acceptable. But when we switch to ICD-10-CM, documentation will need to specify whether the amenorrhea was primary or secondary. This more specific diagnostic coding will make a difference in the health statistics we collect. These data are used for research and to make decisions about allocation of resources—all essential components to excellent quality patient care.

The codes themselves will look different, which may be why some are resisting the change. Instead of the up to five digits required in ICD-9-CM, ICD-10-CM will require up to seven characters. All of the ICD-10-CM codes begin with a letter, may require a placeholder code of “x” as part of the code number, and the seventh character can be either a number or a letter. For instance, with some ICD-10-CM diagnoses reported by ObGyns, a seventh character might require documentation of the encounter as being initial, subsequent, or a sequel; in other cases, that seventh character will be used to identify which fetus has the problem identified by the diagnostic code.

Related article: The economics of surgical gynecology: How we can not only survive, but thrive, in the 21st Century. Q&A with Barbara S. Levy, MD (Practice Management; February 2013)

Your understanding, although not a necessity, is best for all involved
In truth, most clinicians are not familiar with code formats and code numbers within our current ICD-9-CM code set. The expectation that you will suddenly become fluent in ICD-10-CM “code speak” is not realistic. But an understanding of the new codes in relation to documentation expectations will go a long way to making this transition as smooth as possible. For instance, when a patient currently presents reporting vaginal pain that is found to be due to erosion of a previously placed mesh, the code 628.31 (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue) is  reported. But in ICD-10-CM, the documentation would need to include whether this was an initial encounter and the code would become T83.711A (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue, initial encounter).

 

 

Smart search. The good news is that most EMR products will have a “smart search” program available for clinicians to pick the correct code based on the search criteria. The bad news is that you will have to be a bit more exact in the search terms you use to make the process easy. For instance, the patient has pelvic pain but you search only on the term “pain.” That term by itself will result in about 100 codes to select from, and the order of the codes may mean that the correct code for pelvic pain is 25 codes down the list. However, if you instead search on the term “pelvic pain,” the one and only code for this condition will be listed and you can simply select it and move on.

Develop cheat sheets. Health-care professionals who are not using an EMR or some sort of computerized code search program will have a harder time, but the use of multiple paper “cheat sheets” for general gynecology, family planning, surgical cases, urology, infertility, obstetrics, etc., will ease that burden. Practice management staff can develop these forms, built on the codes that are currently being reported by the clinician. Place all of the options to replace the older code on the sheet so the correct selection can be made.

For instance, if the provider previously had reported vaginitis with one code, when we move to ICD-10-CM the code would expand to four code selections based on documentation of acute vaginitis, subacute and chronic vaginitis, acute vulvitis, or subacute and chronic vulvitis. If you only had documented vaginitis in the medical record, this gives you the opportunity to refine the documentation to something more specific that supports selection of the correct code and supports the medical need for management options.

Related article: Dos, don’ts, and dollars: Making the switch to an HER. Neil H. Baum, MD; Paul Kepper, MS. (Practice Management; November 2013)

Take advantage of the extra time
Now that we have a delay in the rollout, take this time to critically examine your documentation styles, and practice selecting ICD-10-CM codes before it counts toward payment or nonpayment of a claim. When the time comes, your practice will be fluent in the new system and there will be no delays in getting claims out the door or payment due to incorrect diagnostic coding. In other words, practice makes perfect.

In fact, some ObGyn practices that were ready for the new system have decided to switch to ICD-10-CM coding as of October 1, 2014. They will code each encounter by reporting both the ICD-9-CM code and the ICD-10-CM code on the revised CMS claim form or electronic billing format that permits dual diagnostic coding. This type of experience will ensure that all physicians and other health-care professionals in the practice have ample opportunity to improve their documentation and make any adjustments before the 2015 deadline.

Related article: The 2014 CPT and Medicare code changes affecting ObGyn practice. Melanie Witt, RN, CPC, COBGC, MA (Reimbursement Adviser; January 2014)

WE WANT TO HEAR FROM YOU!
Drop us a line and let us know what you think about current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected]

Yes, we have been here before. Another day, another delay in implementing International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM). But, do not expect another postponement. If you are already conducting training sessions to move to the new system come next October, continue to do so. If you have not yet started, now is the time to start. ICD-10-CM is coming to your practice, and it will change everything.

“Why the switch?” you ask?
This change in our diagnostic coding system is required to allow coding for increased specificity in the reporting of diseases and recently recognized conditions as well as to maintain our status with respect to the rest of the world (which has been using ICD-10 for years). It also will be essential to use this coding system with the electronic medical record (EMR), so that meaningful use can be demonstrated more easily. Keep in mind that failure to show meaningful use will lead to penalties in the future. This new system offers improvements over ICD-9-CM in coding primary care encounters, external causes of injury, mental disorders, neoplasms, obstetric complications, and preventive health. It also allows physicians to demonstrate severity of illness in a way that is not possible with ICD-9-CM.

There will be 65,000 more codes than currently exist in ICD-9-CM. No physician will be able to keep all of these code numbers handy, but by making changes to clinician documentation and applying diagnostic coding guidelines correctly within the framework of the new system, the transition will not be onerous. And consider that, while the number of new codes is great, the number of codes used in the typical ObGyn practice will be a fraction of that number.

Related article: As ICD-10 conversion nears, keep these factors in mind to ensure proper reimbursements in 2014. Barbara S. Levy, MD (Audiocast, January 2014)

For ICD-10, documentation is paramount
The most important issue when considering overall coding and practice changes will be recognizing that clinician documentation will be the key to coding the highest level of specificity—and this high level of specificity may be required by most payers when ­deciding to reimburse for treatments rendered. Complete documentation sets the stage for the severity of illness and should in fact result in fewer denials for medical necessity.

For the new process to work efficiently, however, without a lot of delays due to coders and billers having to get more information from clinician offices before sending out claims, your understanding of and “buy-in” to the more clinically specific documentation will be essential.

To explain, under ICD-9-CM coding, simply documenting amenorrhea was acceptable. But when we switch to ICD-10-CM, documentation will need to specify whether the amenorrhea was primary or secondary. This more specific diagnostic coding will make a difference in the health statistics we collect. These data are used for research and to make decisions about allocation of resources—all essential components to excellent quality patient care.

The codes themselves will look different, which may be why some are resisting the change. Instead of the up to five digits required in ICD-9-CM, ICD-10-CM will require up to seven characters. All of the ICD-10-CM codes begin with a letter, may require a placeholder code of “x” as part of the code number, and the seventh character can be either a number or a letter. For instance, with some ICD-10-CM diagnoses reported by ObGyns, a seventh character might require documentation of the encounter as being initial, subsequent, or a sequel; in other cases, that seventh character will be used to identify which fetus has the problem identified by the diagnostic code.

Related article: The economics of surgical gynecology: How we can not only survive, but thrive, in the 21st Century. Q&A with Barbara S. Levy, MD (Practice Management; February 2013)

Your understanding, although not a necessity, is best for all involved
In truth, most clinicians are not familiar with code formats and code numbers within our current ICD-9-CM code set. The expectation that you will suddenly become fluent in ICD-10-CM “code speak” is not realistic. But an understanding of the new codes in relation to documentation expectations will go a long way to making this transition as smooth as possible. For instance, when a patient currently presents reporting vaginal pain that is found to be due to erosion of a previously placed mesh, the code 628.31 (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue) is  reported. But in ICD-10-CM, the documentation would need to include whether this was an initial encounter and the code would become T83.711A (Erosion of implanted vaginal mesh and other prosthetic materials to surrounding organ or tissue, initial encounter).

 

 

Smart search. The good news is that most EMR products will have a “smart search” program available for clinicians to pick the correct code based on the search criteria. The bad news is that you will have to be a bit more exact in the search terms you use to make the process easy. For instance, the patient has pelvic pain but you search only on the term “pain.” That term by itself will result in about 100 codes to select from, and the order of the codes may mean that the correct code for pelvic pain is 25 codes down the list. However, if you instead search on the term “pelvic pain,” the one and only code for this condition will be listed and you can simply select it and move on.

Develop cheat sheets. Health-care professionals who are not using an EMR or some sort of computerized code search program will have a harder time, but the use of multiple paper “cheat sheets” for general gynecology, family planning, surgical cases, urology, infertility, obstetrics, etc., will ease that burden. Practice management staff can develop these forms, built on the codes that are currently being reported by the clinician. Place all of the options to replace the older code on the sheet so the correct selection can be made.

For instance, if the provider previously had reported vaginitis with one code, when we move to ICD-10-CM the code would expand to four code selections based on documentation of acute vaginitis, subacute and chronic vaginitis, acute vulvitis, or subacute and chronic vulvitis. If you only had documented vaginitis in the medical record, this gives you the opportunity to refine the documentation to something more specific that supports selection of the correct code and supports the medical need for management options.

Related article: Dos, don’ts, and dollars: Making the switch to an HER. Neil H. Baum, MD; Paul Kepper, MS. (Practice Management; November 2013)

Take advantage of the extra time
Now that we have a delay in the rollout, take this time to critically examine your documentation styles, and practice selecting ICD-10-CM codes before it counts toward payment or nonpayment of a claim. When the time comes, your practice will be fluent in the new system and there will be no delays in getting claims out the door or payment due to incorrect diagnostic coding. In other words, practice makes perfect.

In fact, some ObGyn practices that were ready for the new system have decided to switch to ICD-10-CM coding as of October 1, 2014. They will code each encounter by reporting both the ICD-9-CM code and the ICD-10-CM code on the revised CMS claim form or electronic billing format that permits dual diagnostic coding. This type of experience will ensure that all physicians and other health-care professionals in the practice have ample opportunity to improve their documentation and make any adjustments before the 2015 deadline.

Related article: The 2014 CPT and Medicare code changes affecting ObGyn practice. Melanie Witt, RN, CPC, COBGC, MA (Reimbursement Adviser; January 2014)

WE WANT TO HEAR FROM YOU!
Drop us a line and let us know what you think about current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected]

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Enigmatic inconsistencies between WHI data and conclusions; Exaggerated or intentionally fabricated data?

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"In the latest report from the WHI, the data contradict the conclusions"
Holly Thacker, MD (Commentary, March 2014)

Enigmatic inconsistencies between WHI data and conclusions
The issue of the inconsistencies between the Women’s Health Initiative (WHI) data and conclusions is enigmatic because the integrity and judgment of researchers has in the past and should remain above reproach.

For those of us in the private sector of obstetrics and gynecology, the feeling that there must be information that intentionally or unintentionally has been omitted from our view remains the most comfortable and convenient explanation for the discrepancies.

The vindication of observational studies predating WHI by the reanalysis of WHI data seems to be continually suppressed in the literature, and the unreasoning exclusion of the critical issue of timing in the initiation and continued administration of estrogen therapy (ET) and hormone therapy (HT) is inexplicable. One is repeatedly tempted to consider some underlying agenda.

Elimination of sampling by Wyeth, and now exclusion from drug formularies with the attendant exorbitant increases in cost have, in addition to the absence of a defense by researchers or manufacturers, discouraged continuing use of this valuable medication, even among those in whom the safety and benefits of Premarin and Prempro have been established over years of experience and scores of studies. 

It is much like the children’s story, “The Emperor’s New Clothes.” It seems incredible that so many know­ledgeable authorities seem unable to recognize a 60% reduction in coronary artery plaque in recently menopausal women (ages 50–59 years) after 5.2 years of HT, which underscores the importance of patient selection and timing of administration.1 Wyeth’s explanation, when I inquired, was that this involved “off-label” use, although the data are from reanalysis of WHI data. I would think that a 60% reduction of arterial plaque deserves front-page coverage.

When articles about the discontinuation of WHI began to appear in 2001, stated reasons included the overwhelming predominance of new breast cancer cases in estrogen-administered subjects, but no one seems to appreciate the 47% decrease in breast cancer mortality discovered in the reanalysis, due to the chronologically earlier appearance of disease at earlier clinical stages. In my practice, we are finding in situ disease in HT and ET patients after 4 to 5 years of use.

Consequently, I am appreciative of Dr. Thacker’s mention of the ­Sarrel data2 and her expansion into the “so often” overlooked issues. I think that it’s overdue—integrity must be restored to the interpretation of NIH’s $780,000,000 expenditure of taxpayer dollars. After all, WHI was to be the statistically unimpeachable clarification of estrogen and hormone replacement.

Glenn N. Hayashi, MD
Honolulu, Hawaii

Exaggerated or intentionally fabricated data?
Thank you for publishing Dr. Holly Thacker’s commentary regarding the travesty that was and is WHI. I enthusiastically support her admonition to “look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.”

My only disagreement is Dr. Thacker’s choice of the word “exaggerated” when describing the harms linked to HT. I would have chosen instead the words “intentionally fabricated.” How? By taking data out of context, by releasing data selectively, by withholding data—all for the purpose of achieving and then protecting their frighteningly negative and destructive initial conclusions.

I wish it were the case that an independent commission might right these wrongs. Unfortunately, that cannot happen in today’s intellectual context. The fundamental error that made WHI’s multitude of errors possible was the notion that we can dispense with the difficult work of considering “the totality of the data” by placing our faith in “statistical significance” derived from a single “randomized controlled trial.” That fundamental error is too deeply entrenched, too highly remunerative, and too propitiously useful to those seeking a world concordant with their fantasies.

Reality demands that we account for every fact and will in time put an end to this deadly conceit. 

Geoffrey C. Kincaid, MD
Knoxville, Tennessee

TELL US WHAT YOU THINK! Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state. Stay in touch! Your feedback is important to us!

References

1. Manson JE, Allison MA, Rossouw JE, et al; WHI and WHI-CACS Investigators. Estrogen therapy and coronary-artery calcification. N Engl J Med. 2007;356(25):2591–2602.

2. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.

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"In the latest report from the WHI, the data contradict the conclusions"
Holly Thacker, MD (Commentary, March 2014)

Enigmatic inconsistencies between WHI data and conclusions
The issue of the inconsistencies between the Women’s Health Initiative (WHI) data and conclusions is enigmatic because the integrity and judgment of researchers has in the past and should remain above reproach.

For those of us in the private sector of obstetrics and gynecology, the feeling that there must be information that intentionally or unintentionally has been omitted from our view remains the most comfortable and convenient explanation for the discrepancies.

The vindication of observational studies predating WHI by the reanalysis of WHI data seems to be continually suppressed in the literature, and the unreasoning exclusion of the critical issue of timing in the initiation and continued administration of estrogen therapy (ET) and hormone therapy (HT) is inexplicable. One is repeatedly tempted to consider some underlying agenda.

Elimination of sampling by Wyeth, and now exclusion from drug formularies with the attendant exorbitant increases in cost have, in addition to the absence of a defense by researchers or manufacturers, discouraged continuing use of this valuable medication, even among those in whom the safety and benefits of Premarin and Prempro have been established over years of experience and scores of studies. 

It is much like the children’s story, “The Emperor’s New Clothes.” It seems incredible that so many know­ledgeable authorities seem unable to recognize a 60% reduction in coronary artery plaque in recently menopausal women (ages 50–59 years) after 5.2 years of HT, which underscores the importance of patient selection and timing of administration.1 Wyeth’s explanation, when I inquired, was that this involved “off-label” use, although the data are from reanalysis of WHI data. I would think that a 60% reduction of arterial plaque deserves front-page coverage.

When articles about the discontinuation of WHI began to appear in 2001, stated reasons included the overwhelming predominance of new breast cancer cases in estrogen-administered subjects, but no one seems to appreciate the 47% decrease in breast cancer mortality discovered in the reanalysis, due to the chronologically earlier appearance of disease at earlier clinical stages. In my practice, we are finding in situ disease in HT and ET patients after 4 to 5 years of use.

Consequently, I am appreciative of Dr. Thacker’s mention of the ­Sarrel data2 and her expansion into the “so often” overlooked issues. I think that it’s overdue—integrity must be restored to the interpretation of NIH’s $780,000,000 expenditure of taxpayer dollars. After all, WHI was to be the statistically unimpeachable clarification of estrogen and hormone replacement.

Glenn N. Hayashi, MD
Honolulu, Hawaii

Exaggerated or intentionally fabricated data?
Thank you for publishing Dr. Holly Thacker’s commentary regarding the travesty that was and is WHI. I enthusiastically support her admonition to “look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.”

My only disagreement is Dr. Thacker’s choice of the word “exaggerated” when describing the harms linked to HT. I would have chosen instead the words “intentionally fabricated.” How? By taking data out of context, by releasing data selectively, by withholding data—all for the purpose of achieving and then protecting their frighteningly negative and destructive initial conclusions.

I wish it were the case that an independent commission might right these wrongs. Unfortunately, that cannot happen in today’s intellectual context. The fundamental error that made WHI’s multitude of errors possible was the notion that we can dispense with the difficult work of considering “the totality of the data” by placing our faith in “statistical significance” derived from a single “randomized controlled trial.” That fundamental error is too deeply entrenched, too highly remunerative, and too propitiously useful to those seeking a world concordant with their fantasies.

Reality demands that we account for every fact and will in time put an end to this deadly conceit. 

Geoffrey C. Kincaid, MD
Knoxville, Tennessee

TELL US WHAT YOU THINK! Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state. Stay in touch! Your feedback is important to us!

"In the latest report from the WHI, the data contradict the conclusions"
Holly Thacker, MD (Commentary, March 2014)

Enigmatic inconsistencies between WHI data and conclusions
The issue of the inconsistencies between the Women’s Health Initiative (WHI) data and conclusions is enigmatic because the integrity and judgment of researchers has in the past and should remain above reproach.

For those of us in the private sector of obstetrics and gynecology, the feeling that there must be information that intentionally or unintentionally has been omitted from our view remains the most comfortable and convenient explanation for the discrepancies.

The vindication of observational studies predating WHI by the reanalysis of WHI data seems to be continually suppressed in the literature, and the unreasoning exclusion of the critical issue of timing in the initiation and continued administration of estrogen therapy (ET) and hormone therapy (HT) is inexplicable. One is repeatedly tempted to consider some underlying agenda.

Elimination of sampling by Wyeth, and now exclusion from drug formularies with the attendant exorbitant increases in cost have, in addition to the absence of a defense by researchers or manufacturers, discouraged continuing use of this valuable medication, even among those in whom the safety and benefits of Premarin and Prempro have been established over years of experience and scores of studies. 

It is much like the children’s story, “The Emperor’s New Clothes.” It seems incredible that so many know­ledgeable authorities seem unable to recognize a 60% reduction in coronary artery plaque in recently menopausal women (ages 50–59 years) after 5.2 years of HT, which underscores the importance of patient selection and timing of administration.1 Wyeth’s explanation, when I inquired, was that this involved “off-label” use, although the data are from reanalysis of WHI data. I would think that a 60% reduction of arterial plaque deserves front-page coverage.

When articles about the discontinuation of WHI began to appear in 2001, stated reasons included the overwhelming predominance of new breast cancer cases in estrogen-administered subjects, but no one seems to appreciate the 47% decrease in breast cancer mortality discovered in the reanalysis, due to the chronologically earlier appearance of disease at earlier clinical stages. In my practice, we are finding in situ disease in HT and ET patients after 4 to 5 years of use.

Consequently, I am appreciative of Dr. Thacker’s mention of the ­Sarrel data2 and her expansion into the “so often” overlooked issues. I think that it’s overdue—integrity must be restored to the interpretation of NIH’s $780,000,000 expenditure of taxpayer dollars. After all, WHI was to be the statistically unimpeachable clarification of estrogen and hormone replacement.

Glenn N. Hayashi, MD
Honolulu, Hawaii

Exaggerated or intentionally fabricated data?
Thank you for publishing Dr. Holly Thacker’s commentary regarding the travesty that was and is WHI. I enthusiastically support her admonition to “look at the totality of the data on menopausal HT, evaluate our patients individually, treat those who are truly hormonally deficient and suffering, and counsel them that many of the harms linked to HT have been exaggerated.”

My only disagreement is Dr. Thacker’s choice of the word “exaggerated” when describing the harms linked to HT. I would have chosen instead the words “intentionally fabricated.” How? By taking data out of context, by releasing data selectively, by withholding data—all for the purpose of achieving and then protecting their frighteningly negative and destructive initial conclusions.

I wish it were the case that an independent commission might right these wrongs. Unfortunately, that cannot happen in today’s intellectual context. The fundamental error that made WHI’s multitude of errors possible was the notion that we can dispense with the difficult work of considering “the totality of the data” by placing our faith in “statistical significance” derived from a single “randomized controlled trial.” That fundamental error is too deeply entrenched, too highly remunerative, and too propitiously useful to those seeking a world concordant with their fantasies.

Reality demands that we account for every fact and will in time put an end to this deadly conceit. 

Geoffrey C. Kincaid, MD
Knoxville, Tennessee

TELL US WHAT YOU THINK! Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state. Stay in touch! Your feedback is important to us!

References

1. Manson JE, Allison MA, Rossouw JE, et al; WHI and WHI-CACS Investigators. Estrogen therapy and coronary-artery calcification. N Engl J Med. 2007;356(25):2591–2602.

2. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.

References

1. Manson JE, Allison MA, Rossouw JE, et al; WHI and WHI-CACS Investigators. Estrogen therapy and coronary-artery calcification. N Engl J Med. 2007;356(25):2591–2602.

2. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59. Am J Pub Health. 2013;103(9):1583–1588.

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Blue towel left in abdomen: $7.2M verdict

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Blue towel left in abdomen: $7.2M verdict
When a 61-year-old woman underwent
laparoscopic hysterectomy, her gynecologist, Dr. A, was assisted by another gynecologist (Dr. B), a nurse, and a technician. When Dr. A noted that the uterine artery had been injured, he converted to an open procedure, retracted the bowel, repaired the artery, and completed the operation.

Postdischarge, the patient was febrile and developed abdominal pain and an odorous vaginal discharge. A month later, exploratory surgery revealed a retained blue towel that had been used for bowel retraction. The patient required open healing of the surgical wound and a temporary colostomy. She developed an incisional hernia after colostomy reversal, and hernia repair required resection of a small portion of the bowel.

PATIENT’S CLAIM It was negligent to use a blue towel to retract the bowel. The towel should have been removed from her abdomen before closure.

DEFENDANTS’ DEFENSE The technician claimed that she did not provide the towel, did not see the towel used, and that she was not told that the towel had to be tracked. She noted that its color indicated that it lacked a radiopaque tag, and that hospital policy forbade use of untagged towels in an open wound.

Dr. A claimed that he specifically requested a blue towel because it was absorbent, that the technician provided the towel, and that the towel’s use prevented the patient from bleeding to death.

VERDICT A $7.2 million New York verdict was returned against both gynecologists and the hospital as the technician’s employer.

MISCARRIAGE AFTER D&C
A few days after a woman thought she miscarried, her family practi-tioner (FP) performed a dilation and curettage (D&C). 

The patient was at work 12 days later when she expelled a fully formed 14-week fetus into a toilet. She was taken to the emergency department (ED), where the cord was cut. Later that day, she passed placental tissue; a repeat D&C was performed the next day.

PATIENT'S CLAIM The FP did not properly perform the first D&C. Although the pathology report was available to the FP prior to the patient’s postoperative visit, the FP failed to inform the patient that no fetal parts had been extracted.

PHYSICIAN’S DEFENSE Because the FP thought that the fetus had been passed prior to the D&C, she believed the pathology report was appropriate.

The patient had been informed of the possibility of retained products of conception after the D&C. The FP had ordered a blood pregnancy test that would have revealed the presence of retained products of conception, but the patient did not have the test. The patient did not contact the FP to report symptoms that felt like labor pains on the day that she passed the fetus.

VERDICT A bench trial resulted in a $51,000 California verdict.

PREGNANT WOMAN COMPLAINS OF LEG PAIN; DIES OF DVT
A 23-year-old woman went to the ED with pain and swelling in her lower left leg and calf. The symptoms were reported to her ObGyn, who examined and then discharged her within a few hours, with instructions to come for her regularly scheduled prenatal visit.

The patient died 2 weeks later. The cause of death was determined to be a pulmonary embolus from a thrombus of the left popliteal vein.

ESTATE’S CLAIM The ObGyn was negligent in failing to test the patient for thrombosis in her left leg when she was in the ED or several days later at the office, when she continued to report leg pain.

PHYSICIAN’S DEFENSE The patient did not have signs of thrombosis at the ED or at the subsequent office visit. The pathologist reported that the clot that caused the embolus appeared fresh. The ObGyn surmised that it had formed after the patient’s last appointment.

VERDICT A Texas defense verdict was returned.

 

Mother took topiramate; child born with cleft lip and palate: $3M verdict
When a woman learned she was pregnant
in December 2007, she was taking topiramate (Topamax) to treat migraine headaches. She discussed tapering off but not discontinuing topiramate usage with her neurologist. The patient’s ObGyn told her that topiramate was safe to take during pregnancy. The child was born with a cleft lip and palate.

PARENTS’ CLAIM Janssen Pharmaceuticals, manufacturer of Topamax, failed to provide adequate warnings about the potential risks associated with Topamax until labeling was changed in March 2011. Janssen knew of potential birth defects associated with Topamax use during pregnancy more than a decade before the labeling change; Janssen’s associate director of regulatory affairs had testified in an earlier hearing that there was knowledge of related birth defects as early as 1996.

 

 

DEFENDANTS’ DEFENSE There is uncertainty as to whether exposure to Topamax during pregnancy causes birth defects. The neurologist had warned the patient of possible risks associated with taking Topamax during pregnancy, but the patient had refused to discontinue the drug.

VERDICT A $3 million Pennsylvania verdict was returned.

Related articles:
• Is it time to rethink the use of oral contraceptives in premenopausal women with migraine? Anne H. Calhoun, MD (Audiocast; October 2013)
• How to choose a contraceptive for a patient who has headaches.
Kristina M. Tocce, MD; Stephanie B. Teal, MD, MPH (February 2011)
• The gynecologist’s role in managing menstrual migraine.
Anne H. Calhoun, MD (April 2010)

WAS MOTHER’S HISTORY OF INCOMPETENT CERVIX IGNORED?
Early in her second pregnancy
, a woman told her ObGyn that she had previously miscarried due to an incompetent cervix.

At 24 weeks’ gestation, the patient was admitted to the hospital with back and pelvic pain and vaginal bleeding. Shortly after admission, the ObGyn performed a vaginal examination and ordered ultrasonography (US), which showed that the fetus was in the transverse position and the membranes were bulging.

The ObGyn performed an emergency cesarean delivery, but the premature infant died within 2 hours.

PARENTS’ CLAIM The ObGyn should have performed a cervical cerclage because of the mother’s history of an incompetent cervix. The mother should have been placed on bed rest and monitored every 2 weeks for cervical dilation.

PHYSICIAN’S DEFENSE The patient underwent regular prenatal evaluations for an incompetent cervix, and the findings were always normal.

VERDICT A Florida defense verdict was returned.


Related article:
A stepwise approach to cervical cerclage. Katrin Karl, MD; Michael Katz, MD (Surgical Technique; June 2012)

ObGyn unresponsive to patient’s postsurgical phone calls
In 2009, a 50-year-old woman
reported occasional right lower quadrant pain to her ObGyn. US results were normal. The menopausal patient’s history included three cesarean deliveries, a total abdominal hysterectomy, and a laparoscopic ovarian cystectomy. 

When the patient saw her ObGyn in December 2010, she reported intermittent, progressive right lower quadrant pain that radiated down her right leg. She also reported urine loss with coughing or sneezing, and slight pain on intercourse. The ObGyn prescribed oxybutynin chloride (Ditropan) to treat the patient’s incontinence.

Three weeks later, the patient reported bilateral lower quadrant pain to her ObGyn, with minor improvement in incontinence.

The ObGyn performed bilateral salpingo-oophorectomy (BSO) in January 2011. Surgery took 3.5 hours due to extensive adhesiolysis.

After discharge, the patient felt ill and vomited. She attempted to reach the ObGyn by phone several times. That evening, the ObGyn prescribed a suppository to treat nausea and vomiting.

The patient went to the ED later that night and was found to have a perforated colon. Emergency surgery to repair the injury included creation of a colostomy, which was repaired 20 months later.

PATIENT’S CLAIM A proper workup of her symptoms was not performed; BSO was unnecessary. The ObGyn was negligent for failing to respond in a timely manner to her post-discharge phone calls, and did not properly evaluate her postoperative symptoms.

PHYSICIAN’S DEFENSE BSO was warranted. Colon injury is a known complication of the procedure.

VERDICT A $716,976 California verdict was returned, but was reduced to $591,967 under the state cap.


Who delayed delivery? $32.8M verdict for child with CP
An 18-year-old woman at 38 weeks’ gestation went to the hospital in labor. After 3.5 hours, the fetal heart rate dropped to 60 bpm. A nurse repositioned the patient, administered oxygen, and increased intravenous fluids. When the nurse rang the emergency call bell, a second nurse responded. Eighteen minutes after the fetal heart rate first dropped, a nurse rang the call bell again and the on-call ObGyn appeared.

The ObGyn performed a vaginal examination and repositioned the patient. She noted that the fetal heart-rate monitor was not working correctly, and called for an emergency cesarean delivery. The baby was born 42 minutes after the fetal heart rate initially dropped.

The child received a diagnosis of spastic-quadriplegia cerebral palsy (CP). She requires a wheelchair and has severe speech deficits and developmental delays.

PARENT’S CLAIM Cesarean delivery was not performed in a timely manner; the delivery delay was responsible for the injury that caused CP. The ObGyn was negligent in not responding to the initial emergency call. The nurses should have summoned the ObGyn earlier.

DEFENDANTS’ DEFENSE The hospital argued that the nurses followed proper protocol. Furthermore, the hospital noted that the ObGyn did not respond to the first call, and did not request a cesarean delivery for 17 minutes.

 

 

The ObGyn claimed that she made the decision to perform cesarean delivery within 5 minutes of her arrival, but it took another 15 minutes to gather the surgical team.

VERDICT A $32,882,860 Pennsylvania verdict was returned against the hospital. The ObGyn was vindicated. 

DIFFICULT DELIVERY: ZAVANELLI MANEUVER
At 38 5/7 weeks’ gestation, a woman went to the hospital for induction of labor. Twenty-four hours later, she began to push. After an hour of pushing, the mother was exhausted and had a low-grade fever, and the fetal heart rate was slowing. Her ObGyn, Dr. A, attempted vacuum extraction and performed a midline episiotomy. Shoulder dystocia was encountered and maneuvers were used, but without success. Another ObGyn, Dr. B, arrived to assist and also attempted the maneuvers.

The physicians agreed to try the Zavanelli maneuver, which involves pushing the baby’s head back inside the vagina and performing a cesarean delivery.

The baby was sent to the neonatal intensive care unit, where her breathing quickly normalized without supplemental oxygen. The child has a brachial plexus injury.

PARENTS’ CLAIM Dr. A should have performed an earlier cesarean delivery. Excessive traction was used when shoulder dystocia maneuvers were attempted.

PHYSICIANS’ DEFENSE The ObGyns’ actions saved the baby’s life and prevented serious injury to both mother and baby. 

VERDICT An Alabama defense verdict was returned.


Related article:
You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; May 2013)

PLACENTA PREVIA FOUND EARLY, BUT FETUS DIES
A woman's first pregnancy was complicated by complete placenta previa. A cesarean delivery was scheduled at 36 weeks’ gestation. However, before that date, the mother developed vaginal bleeding and was taken to the ED. The covering ObGyn was notified of the mother’s arrival within 15 minutes, but did not come to the hospital for 2.5 hours. After examining her, the ObGyn ordered US evaluation and transferred the mother to the obstetric floor. Nursing notes indicate that the fetal heart rate was 120 bpm at that time.

There are no notes from the ObGyn between 5:30 am and mid-afternoon. There is no record of the fetal heart rate when the mother was taken for US in the afternoon, which revealed fetal demise and a large extraovular hematoma. A cesarean delivery was performed. It was determined that the fetus died from placental abruption.

PARENTS’ CLAIM The mother was not adequately evaluated and monitored, which led to fetal demise. Delivery could have proceeded while the fetus was still alive.

PHYSICIAN’S DEFENSE The case was settled during the trial.

VERDICT A $495,000 Massachusetts settlement was reached.


Related articles:

• What is the optimal time to deliver a woman who has placenta previa?
John T. Repke, MD (Examining the Evidence; April 2011)
• Act fast when confronted by a coagulopathy postpartum.
Robert L. Barbieri, MD (Editorial; March 2012)

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

TELL US WHAT YOU THINK! Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state. Stay in touch! Your feedback is important to us!

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Blue towel left in abdomen: $7.2M verdict
When a 61-year-old woman underwent
laparoscopic hysterectomy, her gynecologist, Dr. A, was assisted by another gynecologist (Dr. B), a nurse, and a technician. When Dr. A noted that the uterine artery had been injured, he converted to an open procedure, retracted the bowel, repaired the artery, and completed the operation.

Postdischarge, the patient was febrile and developed abdominal pain and an odorous vaginal discharge. A month later, exploratory surgery revealed a retained blue towel that had been used for bowel retraction. The patient required open healing of the surgical wound and a temporary colostomy. She developed an incisional hernia after colostomy reversal, and hernia repair required resection of a small portion of the bowel.

PATIENT’S CLAIM It was negligent to use a blue towel to retract the bowel. The towel should have been removed from her abdomen before closure.

DEFENDANTS’ DEFENSE The technician claimed that she did not provide the towel, did not see the towel used, and that she was not told that the towel had to be tracked. She noted that its color indicated that it lacked a radiopaque tag, and that hospital policy forbade use of untagged towels in an open wound.

Dr. A claimed that he specifically requested a blue towel because it was absorbent, that the technician provided the towel, and that the towel’s use prevented the patient from bleeding to death.

VERDICT A $7.2 million New York verdict was returned against both gynecologists and the hospital as the technician’s employer.

MISCARRIAGE AFTER D&C
A few days after a woman thought she miscarried, her family practi-tioner (FP) performed a dilation and curettage (D&C). 

The patient was at work 12 days later when she expelled a fully formed 14-week fetus into a toilet. She was taken to the emergency department (ED), where the cord was cut. Later that day, she passed placental tissue; a repeat D&C was performed the next day.

PATIENT'S CLAIM The FP did not properly perform the first D&C. Although the pathology report was available to the FP prior to the patient’s postoperative visit, the FP failed to inform the patient that no fetal parts had been extracted.

PHYSICIAN’S DEFENSE Because the FP thought that the fetus had been passed prior to the D&C, she believed the pathology report was appropriate.

The patient had been informed of the possibility of retained products of conception after the D&C. The FP had ordered a blood pregnancy test that would have revealed the presence of retained products of conception, but the patient did not have the test. The patient did not contact the FP to report symptoms that felt like labor pains on the day that she passed the fetus.

VERDICT A bench trial resulted in a $51,000 California verdict.

PREGNANT WOMAN COMPLAINS OF LEG PAIN; DIES OF DVT
A 23-year-old woman went to the ED with pain and swelling in her lower left leg and calf. The symptoms were reported to her ObGyn, who examined and then discharged her within a few hours, with instructions to come for her regularly scheduled prenatal visit.

The patient died 2 weeks later. The cause of death was determined to be a pulmonary embolus from a thrombus of the left popliteal vein.

ESTATE’S CLAIM The ObGyn was negligent in failing to test the patient for thrombosis in her left leg when she was in the ED or several days later at the office, when she continued to report leg pain.

PHYSICIAN’S DEFENSE The patient did not have signs of thrombosis at the ED or at the subsequent office visit. The pathologist reported that the clot that caused the embolus appeared fresh. The ObGyn surmised that it had formed after the patient’s last appointment.

VERDICT A Texas defense verdict was returned.

 

Mother took topiramate; child born with cleft lip and palate: $3M verdict
When a woman learned she was pregnant
in December 2007, she was taking topiramate (Topamax) to treat migraine headaches. She discussed tapering off but not discontinuing topiramate usage with her neurologist. The patient’s ObGyn told her that topiramate was safe to take during pregnancy. The child was born with a cleft lip and palate.

PARENTS’ CLAIM Janssen Pharmaceuticals, manufacturer of Topamax, failed to provide adequate warnings about the potential risks associated with Topamax until labeling was changed in March 2011. Janssen knew of potential birth defects associated with Topamax use during pregnancy more than a decade before the labeling change; Janssen’s associate director of regulatory affairs had testified in an earlier hearing that there was knowledge of related birth defects as early as 1996.

 

 

DEFENDANTS’ DEFENSE There is uncertainty as to whether exposure to Topamax during pregnancy causes birth defects. The neurologist had warned the patient of possible risks associated with taking Topamax during pregnancy, but the patient had refused to discontinue the drug.

VERDICT A $3 million Pennsylvania verdict was returned.

Related articles:
• Is it time to rethink the use of oral contraceptives in premenopausal women with migraine? Anne H. Calhoun, MD (Audiocast; October 2013)
• How to choose a contraceptive for a patient who has headaches.
Kristina M. Tocce, MD; Stephanie B. Teal, MD, MPH (February 2011)
• The gynecologist’s role in managing menstrual migraine.
Anne H. Calhoun, MD (April 2010)

WAS MOTHER’S HISTORY OF INCOMPETENT CERVIX IGNORED?
Early in her second pregnancy
, a woman told her ObGyn that she had previously miscarried due to an incompetent cervix.

At 24 weeks’ gestation, the patient was admitted to the hospital with back and pelvic pain and vaginal bleeding. Shortly after admission, the ObGyn performed a vaginal examination and ordered ultrasonography (US), which showed that the fetus was in the transverse position and the membranes were bulging.

The ObGyn performed an emergency cesarean delivery, but the premature infant died within 2 hours.

PARENTS’ CLAIM The ObGyn should have performed a cervical cerclage because of the mother’s history of an incompetent cervix. The mother should have been placed on bed rest and monitored every 2 weeks for cervical dilation.

PHYSICIAN’S DEFENSE The patient underwent regular prenatal evaluations for an incompetent cervix, and the findings were always normal.

VERDICT A Florida defense verdict was returned.


Related article:
A stepwise approach to cervical cerclage. Katrin Karl, MD; Michael Katz, MD (Surgical Technique; June 2012)

ObGyn unresponsive to patient’s postsurgical phone calls
In 2009, a 50-year-old woman
reported occasional right lower quadrant pain to her ObGyn. US results were normal. The menopausal patient’s history included three cesarean deliveries, a total abdominal hysterectomy, and a laparoscopic ovarian cystectomy. 

When the patient saw her ObGyn in December 2010, she reported intermittent, progressive right lower quadrant pain that radiated down her right leg. She also reported urine loss with coughing or sneezing, and slight pain on intercourse. The ObGyn prescribed oxybutynin chloride (Ditropan) to treat the patient’s incontinence.

Three weeks later, the patient reported bilateral lower quadrant pain to her ObGyn, with minor improvement in incontinence.

The ObGyn performed bilateral salpingo-oophorectomy (BSO) in January 2011. Surgery took 3.5 hours due to extensive adhesiolysis.

After discharge, the patient felt ill and vomited. She attempted to reach the ObGyn by phone several times. That evening, the ObGyn prescribed a suppository to treat nausea and vomiting.

The patient went to the ED later that night and was found to have a perforated colon. Emergency surgery to repair the injury included creation of a colostomy, which was repaired 20 months later.

PATIENT’S CLAIM A proper workup of her symptoms was not performed; BSO was unnecessary. The ObGyn was negligent for failing to respond in a timely manner to her post-discharge phone calls, and did not properly evaluate her postoperative symptoms.

PHYSICIAN’S DEFENSE BSO was warranted. Colon injury is a known complication of the procedure.

VERDICT A $716,976 California verdict was returned, but was reduced to $591,967 under the state cap.


Who delayed delivery? $32.8M verdict for child with CP
An 18-year-old woman at 38 weeks’ gestation went to the hospital in labor. After 3.5 hours, the fetal heart rate dropped to 60 bpm. A nurse repositioned the patient, administered oxygen, and increased intravenous fluids. When the nurse rang the emergency call bell, a second nurse responded. Eighteen minutes after the fetal heart rate first dropped, a nurse rang the call bell again and the on-call ObGyn appeared.

The ObGyn performed a vaginal examination and repositioned the patient. She noted that the fetal heart-rate monitor was not working correctly, and called for an emergency cesarean delivery. The baby was born 42 minutes after the fetal heart rate initially dropped.

The child received a diagnosis of spastic-quadriplegia cerebral palsy (CP). She requires a wheelchair and has severe speech deficits and developmental delays.

PARENT’S CLAIM Cesarean delivery was not performed in a timely manner; the delivery delay was responsible for the injury that caused CP. The ObGyn was negligent in not responding to the initial emergency call. The nurses should have summoned the ObGyn earlier.

DEFENDANTS’ DEFENSE The hospital argued that the nurses followed proper protocol. Furthermore, the hospital noted that the ObGyn did not respond to the first call, and did not request a cesarean delivery for 17 minutes.

 

 

The ObGyn claimed that she made the decision to perform cesarean delivery within 5 minutes of her arrival, but it took another 15 minutes to gather the surgical team.

VERDICT A $32,882,860 Pennsylvania verdict was returned against the hospital. The ObGyn was vindicated. 

DIFFICULT DELIVERY: ZAVANELLI MANEUVER
At 38 5/7 weeks’ gestation, a woman went to the hospital for induction of labor. Twenty-four hours later, she began to push. After an hour of pushing, the mother was exhausted and had a low-grade fever, and the fetal heart rate was slowing. Her ObGyn, Dr. A, attempted vacuum extraction and performed a midline episiotomy. Shoulder dystocia was encountered and maneuvers were used, but without success. Another ObGyn, Dr. B, arrived to assist and also attempted the maneuvers.

The physicians agreed to try the Zavanelli maneuver, which involves pushing the baby’s head back inside the vagina and performing a cesarean delivery.

The baby was sent to the neonatal intensive care unit, where her breathing quickly normalized without supplemental oxygen. The child has a brachial plexus injury.

PARENTS’ CLAIM Dr. A should have performed an earlier cesarean delivery. Excessive traction was used when shoulder dystocia maneuvers were attempted.

PHYSICIANS’ DEFENSE The ObGyns’ actions saved the baby’s life and prevented serious injury to both mother and baby. 

VERDICT An Alabama defense verdict was returned.


Related article:
You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; May 2013)

PLACENTA PREVIA FOUND EARLY, BUT FETUS DIES
A woman's first pregnancy was complicated by complete placenta previa. A cesarean delivery was scheduled at 36 weeks’ gestation. However, before that date, the mother developed vaginal bleeding and was taken to the ED. The covering ObGyn was notified of the mother’s arrival within 15 minutes, but did not come to the hospital for 2.5 hours. After examining her, the ObGyn ordered US evaluation and transferred the mother to the obstetric floor. Nursing notes indicate that the fetal heart rate was 120 bpm at that time.

There are no notes from the ObGyn between 5:30 am and mid-afternoon. There is no record of the fetal heart rate when the mother was taken for US in the afternoon, which revealed fetal demise and a large extraovular hematoma. A cesarean delivery was performed. It was determined that the fetus died from placental abruption.

PARENTS’ CLAIM The mother was not adequately evaluated and monitored, which led to fetal demise. Delivery could have proceeded while the fetus was still alive.

PHYSICIAN’S DEFENSE The case was settled during the trial.

VERDICT A $495,000 Massachusetts settlement was reached.


Related articles:

• What is the optimal time to deliver a woman who has placenta previa?
John T. Repke, MD (Examining the Evidence; April 2011)
• Act fast when confronted by a coagulopathy postpartum.
Robert L. Barbieri, MD (Editorial; March 2012)

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

TELL US WHAT YOU THINK! Drop us a line and let us know what you think about this or other current articles, which topics you'd like to see covered in future issues, and what challenges you face in daily practice. Tell us what you think by emailing us at: [email protected] Please include your name, city and state. Stay in touch! Your feedback is important to us!



Blue towel left in abdomen: $7.2M verdict
When a 61-year-old woman underwent
laparoscopic hysterectomy, her gynecologist, Dr. A, was assisted by another gynecologist (Dr. B), a nurse, and a technician. When Dr. A noted that the uterine artery had been injured, he converted to an open procedure, retracted the bowel, repaired the artery, and completed the operation.

Postdischarge, the patient was febrile and developed abdominal pain and an odorous vaginal discharge. A month later, exploratory surgery revealed a retained blue towel that had been used for bowel retraction. The patient required open healing of the surgical wound and a temporary colostomy. She developed an incisional hernia after colostomy reversal, and hernia repair required resection of a small portion of the bowel.

PATIENT’S CLAIM It was negligent to use a blue towel to retract the bowel. The towel should have been removed from her abdomen before closure.

DEFENDANTS’ DEFENSE The technician claimed that she did not provide the towel, did not see the towel used, and that she was not told that the towel had to be tracked. She noted that its color indicated that it lacked a radiopaque tag, and that hospital policy forbade use of untagged towels in an open wound.

Dr. A claimed that he specifically requested a blue towel because it was absorbent, that the technician provided the towel, and that the towel’s use prevented the patient from bleeding to death.

VERDICT A $7.2 million New York verdict was returned against both gynecologists and the hospital as the technician’s employer.

MISCARRIAGE AFTER D&C
A few days after a woman thought she miscarried, her family practi-tioner (FP) performed a dilation and curettage (D&C). 

The patient was at work 12 days later when she expelled a fully formed 14-week fetus into a toilet. She was taken to the emergency department (ED), where the cord was cut. Later that day, she passed placental tissue; a repeat D&C was performed the next day.

PATIENT'S CLAIM The FP did not properly perform the first D&C. Although the pathology report was available to the FP prior to the patient’s postoperative visit, the FP failed to inform the patient that no fetal parts had been extracted.

PHYSICIAN’S DEFENSE Because the FP thought that the fetus had been passed prior to the D&C, she believed the pathology report was appropriate.

The patient had been informed of the possibility of retained products of conception after the D&C. The FP had ordered a blood pregnancy test that would have revealed the presence of retained products of conception, but the patient did not have the test. The patient did not contact the FP to report symptoms that felt like labor pains on the day that she passed the fetus.

VERDICT A bench trial resulted in a $51,000 California verdict.

PREGNANT WOMAN COMPLAINS OF LEG PAIN; DIES OF DVT
A 23-year-old woman went to the ED with pain and swelling in her lower left leg and calf. The symptoms were reported to her ObGyn, who examined and then discharged her within a few hours, with instructions to come for her regularly scheduled prenatal visit.

The patient died 2 weeks later. The cause of death was determined to be a pulmonary embolus from a thrombus of the left popliteal vein.

ESTATE’S CLAIM The ObGyn was negligent in failing to test the patient for thrombosis in her left leg when she was in the ED or several days later at the office, when she continued to report leg pain.

PHYSICIAN’S DEFENSE The patient did not have signs of thrombosis at the ED or at the subsequent office visit. The pathologist reported that the clot that caused the embolus appeared fresh. The ObGyn surmised that it had formed after the patient’s last appointment.

VERDICT A Texas defense verdict was returned.

 

Mother took topiramate; child born with cleft lip and palate: $3M verdict
When a woman learned she was pregnant
in December 2007, she was taking topiramate (Topamax) to treat migraine headaches. She discussed tapering off but not discontinuing topiramate usage with her neurologist. The patient’s ObGyn told her that topiramate was safe to take during pregnancy. The child was born with a cleft lip and palate.

PARENTS’ CLAIM Janssen Pharmaceuticals, manufacturer of Topamax, failed to provide adequate warnings about the potential risks associated with Topamax until labeling was changed in March 2011. Janssen knew of potential birth defects associated with Topamax use during pregnancy more than a decade before the labeling change; Janssen’s associate director of regulatory affairs had testified in an earlier hearing that there was knowledge of related birth defects as early as 1996.

 

 

DEFENDANTS’ DEFENSE There is uncertainty as to whether exposure to Topamax during pregnancy causes birth defects. The neurologist had warned the patient of possible risks associated with taking Topamax during pregnancy, but the patient had refused to discontinue the drug.

VERDICT A $3 million Pennsylvania verdict was returned.

Related articles:
• Is it time to rethink the use of oral contraceptives in premenopausal women with migraine? Anne H. Calhoun, MD (Audiocast; October 2013)
• How to choose a contraceptive for a patient who has headaches.
Kristina M. Tocce, MD; Stephanie B. Teal, MD, MPH (February 2011)
• The gynecologist’s role in managing menstrual migraine.
Anne H. Calhoun, MD (April 2010)

WAS MOTHER’S HISTORY OF INCOMPETENT CERVIX IGNORED?
Early in her second pregnancy
, a woman told her ObGyn that she had previously miscarried due to an incompetent cervix.

At 24 weeks’ gestation, the patient was admitted to the hospital with back and pelvic pain and vaginal bleeding. Shortly after admission, the ObGyn performed a vaginal examination and ordered ultrasonography (US), which showed that the fetus was in the transverse position and the membranes were bulging.

The ObGyn performed an emergency cesarean delivery, but the premature infant died within 2 hours.

PARENTS’ CLAIM The ObGyn should have performed a cervical cerclage because of the mother’s history of an incompetent cervix. The mother should have been placed on bed rest and monitored every 2 weeks for cervical dilation.

PHYSICIAN’S DEFENSE The patient underwent regular prenatal evaluations for an incompetent cervix, and the findings were always normal.

VERDICT A Florida defense verdict was returned.


Related article:
A stepwise approach to cervical cerclage. Katrin Karl, MD; Michael Katz, MD (Surgical Technique; June 2012)

ObGyn unresponsive to patient’s postsurgical phone calls
In 2009, a 50-year-old woman
reported occasional right lower quadrant pain to her ObGyn. US results were normal. The menopausal patient’s history included three cesarean deliveries, a total abdominal hysterectomy, and a laparoscopic ovarian cystectomy. 

When the patient saw her ObGyn in December 2010, she reported intermittent, progressive right lower quadrant pain that radiated down her right leg. She also reported urine loss with coughing or sneezing, and slight pain on intercourse. The ObGyn prescribed oxybutynin chloride (Ditropan) to treat the patient’s incontinence.

Three weeks later, the patient reported bilateral lower quadrant pain to her ObGyn, with minor improvement in incontinence.

The ObGyn performed bilateral salpingo-oophorectomy (BSO) in January 2011. Surgery took 3.5 hours due to extensive adhesiolysis.

After discharge, the patient felt ill and vomited. She attempted to reach the ObGyn by phone several times. That evening, the ObGyn prescribed a suppository to treat nausea and vomiting.

The patient went to the ED later that night and was found to have a perforated colon. Emergency surgery to repair the injury included creation of a colostomy, which was repaired 20 months later.

PATIENT’S CLAIM A proper workup of her symptoms was not performed; BSO was unnecessary. The ObGyn was negligent for failing to respond in a timely manner to her post-discharge phone calls, and did not properly evaluate her postoperative symptoms.

PHYSICIAN’S DEFENSE BSO was warranted. Colon injury is a known complication of the procedure.

VERDICT A $716,976 California verdict was returned, but was reduced to $591,967 under the state cap.


Who delayed delivery? $32.8M verdict for child with CP
An 18-year-old woman at 38 weeks’ gestation went to the hospital in labor. After 3.5 hours, the fetal heart rate dropped to 60 bpm. A nurse repositioned the patient, administered oxygen, and increased intravenous fluids. When the nurse rang the emergency call bell, a second nurse responded. Eighteen minutes after the fetal heart rate first dropped, a nurse rang the call bell again and the on-call ObGyn appeared.

The ObGyn performed a vaginal examination and repositioned the patient. She noted that the fetal heart-rate monitor was not working correctly, and called for an emergency cesarean delivery. The baby was born 42 minutes after the fetal heart rate initially dropped.

The child received a diagnosis of spastic-quadriplegia cerebral palsy (CP). She requires a wheelchair and has severe speech deficits and developmental delays.

PARENT’S CLAIM Cesarean delivery was not performed in a timely manner; the delivery delay was responsible for the injury that caused CP. The ObGyn was negligent in not responding to the initial emergency call. The nurses should have summoned the ObGyn earlier.

DEFENDANTS’ DEFENSE The hospital argued that the nurses followed proper protocol. Furthermore, the hospital noted that the ObGyn did not respond to the first call, and did not request a cesarean delivery for 17 minutes.

 

 

The ObGyn claimed that she made the decision to perform cesarean delivery within 5 minutes of her arrival, but it took another 15 minutes to gather the surgical team.

VERDICT A $32,882,860 Pennsylvania verdict was returned against the hospital. The ObGyn was vindicated. 

DIFFICULT DELIVERY: ZAVANELLI MANEUVER
At 38 5/7 weeks’ gestation, a woman went to the hospital for induction of labor. Twenty-four hours later, she began to push. After an hour of pushing, the mother was exhausted and had a low-grade fever, and the fetal heart rate was slowing. Her ObGyn, Dr. A, attempted vacuum extraction and performed a midline episiotomy. Shoulder dystocia was encountered and maneuvers were used, but without success. Another ObGyn, Dr. B, arrived to assist and also attempted the maneuvers.

The physicians agreed to try the Zavanelli maneuver, which involves pushing the baby’s head back inside the vagina and performing a cesarean delivery.

The baby was sent to the neonatal intensive care unit, where her breathing quickly normalized without supplemental oxygen. The child has a brachial plexus injury.

PARENTS’ CLAIM Dr. A should have performed an earlier cesarean delivery. Excessive traction was used when shoulder dystocia maneuvers were attempted.

PHYSICIANS’ DEFENSE The ObGyns’ actions saved the baby’s life and prevented serious injury to both mother and baby. 

VERDICT An Alabama defense verdict was returned.


Related article:
You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; May 2013)

PLACENTA PREVIA FOUND EARLY, BUT FETUS DIES
A woman's first pregnancy was complicated by complete placenta previa. A cesarean delivery was scheduled at 36 weeks’ gestation. However, before that date, the mother developed vaginal bleeding and was taken to the ED. The covering ObGyn was notified of the mother’s arrival within 15 minutes, but did not come to the hospital for 2.5 hours. After examining her, the ObGyn ordered US evaluation and transferred the mother to the obstetric floor. Nursing notes indicate that the fetal heart rate was 120 bpm at that time.

There are no notes from the ObGyn between 5:30 am and mid-afternoon. There is no record of the fetal heart rate when the mother was taken for US in the afternoon, which revealed fetal demise and a large extraovular hematoma. A cesarean delivery was performed. It was determined that the fetus died from placental abruption.

PARENTS’ CLAIM The mother was not adequately evaluated and monitored, which led to fetal demise. Delivery could have proceeded while the fetus was still alive.

PHYSICIAN’S DEFENSE The case was settled during the trial.

VERDICT A $495,000 Massachusetts settlement was reached.


Related articles:

• What is the optimal time to deliver a woman who has placenta previa?
John T. Repke, MD (Examining the Evidence; April 2011)
• Act fast when confronted by a coagulopathy postpartum.
Robert L. Barbieri, MD (Editorial; March 2012)

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

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Paroxetine mesylate 7.5 mg found to be a safe alternative to hormone therapy for menopausal women with hot flashes

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The US Food and Drug Administration (FDA) recently approved paroxetine mesylate 7.5 mg (Brisdelle) for the treatment of moderate to severe menopausal vasomotor symptoms (VMS). Paroxetine, formerly known as low-dose mesylate salt of paroxetine (LDMP), is a nonhormonal agent, which makes it an alternative hot flash therapy for menopausal women who cannot or do not want to use hormones. Paroxetine mesylate (Pexeva, Brisdelle) and paroxetine hydrochloride (Paxil, and generics) are two salts of the same active compound (paroxetine). They may have somewhat different metabolism.

The efficacy and safety of paroxetine mesylate, a selective serotonin-reuptake inhibitor (SSRI), were evaluated individually in three Phase 2 or 3 multicenter, double-blind, randomized, placebo-controlled trials, published by James Simon, MD, from George Washington University School of Medicine, and colleagues,1 and Joffe and colleagues.2 Most treatment-emergent adverse events (TEAEs) in the individual studies were mild or moderate in severity, with minimal acute discontinuation symptoms reported on treatment cessation.

In a study3 presented April 29, at the 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG) in Chicago, Illinois, Simon and colleagues further reported on the overall tolerability and safety profile of paroxetine mesylate 7.5 mg using pooled data from the three randomized trials. In their post-hoc analyses, they specifically examined the emergence of adverse events linked to the use of SSRIs when prescribed for psychiatric disorders at therapeutically higher doses than 7.5 mg. The adverse events focused on included weight gain, decreased libido, and sleep disturbance, as well as suicidality, abnormal bleeding, and bone fracture.

Study details. A total of 1,276 postmenopausal women (approximately 70% white) aged 40 years or older (median age, 54 years) with moderate to severe VMS (7−8 hot flashes/day; 50−60 hot flashes/wk) received either paroxetine mesylate or placebo at bedtime for 8 (Phase 2), 12 (Phase 3), or 24 (Phase 3) weeks. The study was sponsored by Noven Therapeutics, LLC.

Treatment-emergent adverse events and discontinuation
About half (50.4%) of the 635 women in the paroxetine group and 47.0% of the 641 women in the placebo group reported at least one TEAE. Most commonly reported TEAEs in the paroxetine group (reported in ≥2% of patients and with a twofold or higher frequency than in the placebo group) were nausea, fatigue, and dizziness.

TEAEs that were determined to be related to the study drug were reported in 19.5% in the paroxetine group and in 17.6% in the placebo group. These most frequent TEAEs were fatigue, nausea, dizziness, and diarrhea.

Severe AEs were reported in 3.9% and 3.6% of women in the paroxetine and placebo groups, respectively, although the investigator determined that less than 1% were related to paroxetine treatment.

TEAEs that led to discontinuation occurred in 4.7% of paroxetine-treated women and in 3.7% of placebo-treated women, although the incidence of study drug interruptions from TEAEs was similar (0.9%) between treatments. The most frequent adverse reactions leading to discontinuation in the paroxetine arm were abdominal pain (0.3%), attention disturbances (0.3%), headache (0.3%), and suicidal ideation (0.3%).

Of the most common AEs, nausea occurred mainly within the first 4 weeks of treatment; fatigue occurred primarily within the first week of treatment and decreased in frequency with continued therapy. Incidences and types of AEs that began after 12 weeks were similar to those that began during the first 12 weeks of treatment.

AEs related to SSRIs not found to be problematic
No differences were found between groups with regard to TEAEs related to weight, libido, or sleep. No clinically meaningful changes in laboratory values, vital signs, or ECGs were observed with either group. No clinically important findings on abnormal bleeding, bone fracture, or suicidality were evident in the paroxetine arm.

In the Phase 3 studies:

  • One suicide attempt was reported in the paroxetine group in the 24-week study, but was determined by investigators to be unrelated to treatment

  • Incidence rates of gastrointestinal and other bleeding events were similar between groups

  • Five bone fractures were reported: One in the paroxetine group and four among three participants in the placebo group.

One death occurred in the 12-week Phase 3 study due to acute respiratory failure with evidence of hypertension-mediated pulmonary edema and hypertensive cardiovascular disease. The investigator did not consider the death to be related to the study drug.

Study conclusion
The authors concluded that paroxetine 7.5 mg had favorable tolerability in menopausal women with moderate to severe VMS.

“Paroxetine 7.5 mg offers a nonhormonal treatment option for women who seek treatment for moderate to severe hot flashes associated with menopause,” said Dr. Simon.

 

 

Tell us what you think! Send your Letter to the Editor: [email protected]

References

1. Simon JA, et al. Low dose paroxetine 7.5 mg for menopausal vasomotor symptoms: two randomized controlled trials. Menopause. 2013;20(10):1027–1035.

2. Joffe H et al. Low-dose mesylate salt of paroxetine (LDMP) in treatment of vasomotor symptoms (VMS) in menopause. Presented at: 2012 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists; May 7, 2012; San Diego, CA. Poster 43.

3. Simon JA, Portman DJ, Kazempour K, Mekonnen H, Bhaskar S, Lippman J. Safety profile of paroxetine 7.5 mg in women with moderate to severe vasomotor symptoms. Poster presented at: 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG); April 26–30, 2014; Chicago, IL.

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The US Food and Drug Administration (FDA) recently approved paroxetine mesylate 7.5 mg (Brisdelle) for the treatment of moderate to severe menopausal vasomotor symptoms (VMS). Paroxetine, formerly known as low-dose mesylate salt of paroxetine (LDMP), is a nonhormonal agent, which makes it an alternative hot flash therapy for menopausal women who cannot or do not want to use hormones. Paroxetine mesylate (Pexeva, Brisdelle) and paroxetine hydrochloride (Paxil, and generics) are two salts of the same active compound (paroxetine). They may have somewhat different metabolism.

The efficacy and safety of paroxetine mesylate, a selective serotonin-reuptake inhibitor (SSRI), were evaluated individually in three Phase 2 or 3 multicenter, double-blind, randomized, placebo-controlled trials, published by James Simon, MD, from George Washington University School of Medicine, and colleagues,1 and Joffe and colleagues.2 Most treatment-emergent adverse events (TEAEs) in the individual studies were mild or moderate in severity, with minimal acute discontinuation symptoms reported on treatment cessation.

In a study3 presented April 29, at the 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG) in Chicago, Illinois, Simon and colleagues further reported on the overall tolerability and safety profile of paroxetine mesylate 7.5 mg using pooled data from the three randomized trials. In their post-hoc analyses, they specifically examined the emergence of adverse events linked to the use of SSRIs when prescribed for psychiatric disorders at therapeutically higher doses than 7.5 mg. The adverse events focused on included weight gain, decreased libido, and sleep disturbance, as well as suicidality, abnormal bleeding, and bone fracture.

Study details. A total of 1,276 postmenopausal women (approximately 70% white) aged 40 years or older (median age, 54 years) with moderate to severe VMS (7−8 hot flashes/day; 50−60 hot flashes/wk) received either paroxetine mesylate or placebo at bedtime for 8 (Phase 2), 12 (Phase 3), or 24 (Phase 3) weeks. The study was sponsored by Noven Therapeutics, LLC.

Treatment-emergent adverse events and discontinuation
About half (50.4%) of the 635 women in the paroxetine group and 47.0% of the 641 women in the placebo group reported at least one TEAE. Most commonly reported TEAEs in the paroxetine group (reported in ≥2% of patients and with a twofold or higher frequency than in the placebo group) were nausea, fatigue, and dizziness.

TEAEs that were determined to be related to the study drug were reported in 19.5% in the paroxetine group and in 17.6% in the placebo group. These most frequent TEAEs were fatigue, nausea, dizziness, and diarrhea.

Severe AEs were reported in 3.9% and 3.6% of women in the paroxetine and placebo groups, respectively, although the investigator determined that less than 1% were related to paroxetine treatment.

TEAEs that led to discontinuation occurred in 4.7% of paroxetine-treated women and in 3.7% of placebo-treated women, although the incidence of study drug interruptions from TEAEs was similar (0.9%) between treatments. The most frequent adverse reactions leading to discontinuation in the paroxetine arm were abdominal pain (0.3%), attention disturbances (0.3%), headache (0.3%), and suicidal ideation (0.3%).

Of the most common AEs, nausea occurred mainly within the first 4 weeks of treatment; fatigue occurred primarily within the first week of treatment and decreased in frequency with continued therapy. Incidences and types of AEs that began after 12 weeks were similar to those that began during the first 12 weeks of treatment.

AEs related to SSRIs not found to be problematic
No differences were found between groups with regard to TEAEs related to weight, libido, or sleep. No clinically meaningful changes in laboratory values, vital signs, or ECGs were observed with either group. No clinically important findings on abnormal bleeding, bone fracture, or suicidality were evident in the paroxetine arm.

In the Phase 3 studies:

  • One suicide attempt was reported in the paroxetine group in the 24-week study, but was determined by investigators to be unrelated to treatment

  • Incidence rates of gastrointestinal and other bleeding events were similar between groups

  • Five bone fractures were reported: One in the paroxetine group and four among three participants in the placebo group.

One death occurred in the 12-week Phase 3 study due to acute respiratory failure with evidence of hypertension-mediated pulmonary edema and hypertensive cardiovascular disease. The investigator did not consider the death to be related to the study drug.

Study conclusion
The authors concluded that paroxetine 7.5 mg had favorable tolerability in menopausal women with moderate to severe VMS.

“Paroxetine 7.5 mg offers a nonhormonal treatment option for women who seek treatment for moderate to severe hot flashes associated with menopause,” said Dr. Simon.

 

 

Tell us what you think! Send your Letter to the Editor: [email protected]

The US Food and Drug Administration (FDA) recently approved paroxetine mesylate 7.5 mg (Brisdelle) for the treatment of moderate to severe menopausal vasomotor symptoms (VMS). Paroxetine, formerly known as low-dose mesylate salt of paroxetine (LDMP), is a nonhormonal agent, which makes it an alternative hot flash therapy for menopausal women who cannot or do not want to use hormones. Paroxetine mesylate (Pexeva, Brisdelle) and paroxetine hydrochloride (Paxil, and generics) are two salts of the same active compound (paroxetine). They may have somewhat different metabolism.

The efficacy and safety of paroxetine mesylate, a selective serotonin-reuptake inhibitor (SSRI), were evaluated individually in three Phase 2 or 3 multicenter, double-blind, randomized, placebo-controlled trials, published by James Simon, MD, from George Washington University School of Medicine, and colleagues,1 and Joffe and colleagues.2 Most treatment-emergent adverse events (TEAEs) in the individual studies were mild or moderate in severity, with minimal acute discontinuation symptoms reported on treatment cessation.

In a study3 presented April 29, at the 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG) in Chicago, Illinois, Simon and colleagues further reported on the overall tolerability and safety profile of paroxetine mesylate 7.5 mg using pooled data from the three randomized trials. In their post-hoc analyses, they specifically examined the emergence of adverse events linked to the use of SSRIs when prescribed for psychiatric disorders at therapeutically higher doses than 7.5 mg. The adverse events focused on included weight gain, decreased libido, and sleep disturbance, as well as suicidality, abnormal bleeding, and bone fracture.

Study details. A total of 1,276 postmenopausal women (approximately 70% white) aged 40 years or older (median age, 54 years) with moderate to severe VMS (7−8 hot flashes/day; 50−60 hot flashes/wk) received either paroxetine mesylate or placebo at bedtime for 8 (Phase 2), 12 (Phase 3), or 24 (Phase 3) weeks. The study was sponsored by Noven Therapeutics, LLC.

Treatment-emergent adverse events and discontinuation
About half (50.4%) of the 635 women in the paroxetine group and 47.0% of the 641 women in the placebo group reported at least one TEAE. Most commonly reported TEAEs in the paroxetine group (reported in ≥2% of patients and with a twofold or higher frequency than in the placebo group) were nausea, fatigue, and dizziness.

TEAEs that were determined to be related to the study drug were reported in 19.5% in the paroxetine group and in 17.6% in the placebo group. These most frequent TEAEs were fatigue, nausea, dizziness, and diarrhea.

Severe AEs were reported in 3.9% and 3.6% of women in the paroxetine and placebo groups, respectively, although the investigator determined that less than 1% were related to paroxetine treatment.

TEAEs that led to discontinuation occurred in 4.7% of paroxetine-treated women and in 3.7% of placebo-treated women, although the incidence of study drug interruptions from TEAEs was similar (0.9%) between treatments. The most frequent adverse reactions leading to discontinuation in the paroxetine arm were abdominal pain (0.3%), attention disturbances (0.3%), headache (0.3%), and suicidal ideation (0.3%).

Of the most common AEs, nausea occurred mainly within the first 4 weeks of treatment; fatigue occurred primarily within the first week of treatment and decreased in frequency with continued therapy. Incidences and types of AEs that began after 12 weeks were similar to those that began during the first 12 weeks of treatment.

AEs related to SSRIs not found to be problematic
No differences were found between groups with regard to TEAEs related to weight, libido, or sleep. No clinically meaningful changes in laboratory values, vital signs, or ECGs were observed with either group. No clinically important findings on abnormal bleeding, bone fracture, or suicidality were evident in the paroxetine arm.

In the Phase 3 studies:

  • One suicide attempt was reported in the paroxetine group in the 24-week study, but was determined by investigators to be unrelated to treatment

  • Incidence rates of gastrointestinal and other bleeding events were similar between groups

  • Five bone fractures were reported: One in the paroxetine group and four among three participants in the placebo group.

One death occurred in the 12-week Phase 3 study due to acute respiratory failure with evidence of hypertension-mediated pulmonary edema and hypertensive cardiovascular disease. The investigator did not consider the death to be related to the study drug.

Study conclusion
The authors concluded that paroxetine 7.5 mg had favorable tolerability in menopausal women with moderate to severe VMS.

“Paroxetine 7.5 mg offers a nonhormonal treatment option for women who seek treatment for moderate to severe hot flashes associated with menopause,” said Dr. Simon.

 

 

Tell us what you think! Send your Letter to the Editor: [email protected]

References

1. Simon JA, et al. Low dose paroxetine 7.5 mg for menopausal vasomotor symptoms: two randomized controlled trials. Menopause. 2013;20(10):1027–1035.

2. Joffe H et al. Low-dose mesylate salt of paroxetine (LDMP) in treatment of vasomotor symptoms (VMS) in menopause. Presented at: 2012 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists; May 7, 2012; San Diego, CA. Poster 43.

3. Simon JA, Portman DJ, Kazempour K, Mekonnen H, Bhaskar S, Lippman J. Safety profile of paroxetine 7.5 mg in women with moderate to severe vasomotor symptoms. Poster presented at: 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG); April 26–30, 2014; Chicago, IL.

References

1. Simon JA, et al. Low dose paroxetine 7.5 mg for menopausal vasomotor symptoms: two randomized controlled trials. Menopause. 2013;20(10):1027–1035.

2. Joffe H et al. Low-dose mesylate salt of paroxetine (LDMP) in treatment of vasomotor symptoms (VMS) in menopause. Presented at: 2012 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists; May 7, 2012; San Diego, CA. Poster 43.

3. Simon JA, Portman DJ, Kazempour K, Mekonnen H, Bhaskar S, Lippman J. Safety profile of paroxetine 7.5 mg in women with moderate to severe vasomotor symptoms. Poster presented at: 2014 Annual Clinical Meeting of The American College of Obstetricians and Gynecologists (ACOG); April 26–30, 2014; Chicago, IL.

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Uterine adenomyosis: Noninvasive diagnosis

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INTRODUCTION

Steven R. Goldstein, MD, CCD, NCMP
Professor, Department of Obstetrics and Gynecology, New York University School of Medicine; Director, Gynecologic Ultrasound; and Co-Director, Bone Densitometry, New York University Medical Center, New York

In this month’s installment of Images in GYN Ultrasound, Drs. Stalnaker and Kaunitz have done an excellent job of describing what adenomyosis will look like on transvaginal ultrasound

In my first book, entitled Endovaginal Ultrasound,1 I coined the phrase “sonomicoscopy.” I maintain that we are seeing things with transvaginal ultrasound that you could not see with your naked eye if you could hold the structure at arms length and squint at it.

Adenomyosis is defined as endometrial glands and stroma embedded within the myometrium. Literature has shown that if you do three sections on a routine hysterectomy specimen the incidence of adenomyosis is 31%; with six sections the incidence is 61%! In other words, it is a very prevalent occurrence.

There is no question that adenomyosis CAN be a source of uterine enlargement, pain, and bleeding. But it is such a prevalent finding that the real question is: What percent of women, especially parous women, will have sonographic evidence of adenomyosis but be totally asymptomatic? Such women represent the denominator while the symptomatic ones represent the numerator. I worry about labeling asymptomatic patients with this entity—when they become perimenopausal and oligo-ovulatory, and may have irregular bleeding—their symptoms can be judged to be FROM adenomyosis and surgical correction is offered.

An important part of successful ultrasound use is being sure that we redefine what is “normal” as we examine patients with this “low power microscope.” So, while transvaginal ultrasound CAN identify glands and stroma within the myometrium, we must be careful not to automatically label this finding as a “disease.”

Reference
1.     Goldstein SR. Endovaginal Ultrasound. 2nd ed. John Wiley & Sons, Inc: Hoboken, NJ; January 1991.

Uterine adenomyosis: Noninvasive diagnosis

Michelle L. Stalnaker, MD
Assistant Professor and Associate Program Director, Obstetrics and Gynecology Residency, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville

Andrew M. Kaunitz, MD
University of Florida Research Foundation Professor and Associate Chairman, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville. Dr. Kaunitz is a member of the OBG Management Board of Editors.

Uterine adenomyosis is a pathologic condition in which endometrial glands and stroma are present in the uterine myometrium. Uterine adenomyosis is common, and may coexist with leiomyomata or endometriosis. When present, it may cause dysmenorrhea and heavy menses. 

Until recently, the best way to establish a diagnosis of uterine adenomyosis was through histologic examination of a hysterectomy specimen. However, transvaginal ultrasound and pelvic magnetic resonance imaging have been shown to be accurate for noninvasive diagnosis.

Signs on imaging include:

  • Globular/bulky uterus
  • Asymmetric thickening of myometrium
  • Loss of clarity of endo-myometrial interface
  • Diffuse heterogenous myometrial echogenicity
  • Myometrial cysts

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References

1. Champaneria R, Abedin P, Daniels J, Balogun M, Khan KS. Ultrasound scan and magnetic resonance imaging for the diagnosis of adenomyosis: systematic review comparing test accuracy. Acta Obstetricia et Gynecologica. 2010;89(11):1374-1384. 

2. Meredith SM, Sanchez-Ramos L, Kaunitz AM. Diagnostic accuracy of transvaginal sonography for the diagnosis of adenomyosis: systematic review and meta-analysis. Am J Obstet Gynecol. 2009;201(1):107.e1-e6.

3. Munro MG. Update: abnormal uterine bleeding. OBG Manag. 2014;26(3):27-32.

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INTRODUCTION

Steven R. Goldstein, MD, CCD, NCMP
Professor, Department of Obstetrics and Gynecology, New York University School of Medicine; Director, Gynecologic Ultrasound; and Co-Director, Bone Densitometry, New York University Medical Center, New York

In this month’s installment of Images in GYN Ultrasound, Drs. Stalnaker and Kaunitz have done an excellent job of describing what adenomyosis will look like on transvaginal ultrasound

In my first book, entitled Endovaginal Ultrasound,1 I coined the phrase “sonomicoscopy.” I maintain that we are seeing things with transvaginal ultrasound that you could not see with your naked eye if you could hold the structure at arms length and squint at it.

Adenomyosis is defined as endometrial glands and stroma embedded within the myometrium. Literature has shown that if you do three sections on a routine hysterectomy specimen the incidence of adenomyosis is 31%; with six sections the incidence is 61%! In other words, it is a very prevalent occurrence.

There is no question that adenomyosis CAN be a source of uterine enlargement, pain, and bleeding. But it is such a prevalent finding that the real question is: What percent of women, especially parous women, will have sonographic evidence of adenomyosis but be totally asymptomatic? Such women represent the denominator while the symptomatic ones represent the numerator. I worry about labeling asymptomatic patients with this entity—when they become perimenopausal and oligo-ovulatory, and may have irregular bleeding—their symptoms can be judged to be FROM adenomyosis and surgical correction is offered.

An important part of successful ultrasound use is being sure that we redefine what is “normal” as we examine patients with this “low power microscope.” So, while transvaginal ultrasound CAN identify glands and stroma within the myometrium, we must be careful not to automatically label this finding as a “disease.”

Reference
1.     Goldstein SR. Endovaginal Ultrasound. 2nd ed. John Wiley & Sons, Inc: Hoboken, NJ; January 1991.

Uterine adenomyosis: Noninvasive diagnosis

Michelle L. Stalnaker, MD
Assistant Professor and Associate Program Director, Obstetrics and Gynecology Residency, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville

Andrew M. Kaunitz, MD
University of Florida Research Foundation Professor and Associate Chairman, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville. Dr. Kaunitz is a member of the OBG Management Board of Editors.

Uterine adenomyosis is a pathologic condition in which endometrial glands and stroma are present in the uterine myometrium. Uterine adenomyosis is common, and may coexist with leiomyomata or endometriosis. When present, it may cause dysmenorrhea and heavy menses. 

Until recently, the best way to establish a diagnosis of uterine adenomyosis was through histologic examination of a hysterectomy specimen. However, transvaginal ultrasound and pelvic magnetic resonance imaging have been shown to be accurate for noninvasive diagnosis.

Signs on imaging include:

  • Globular/bulky uterus
  • Asymmetric thickening of myometrium
  • Loss of clarity of endo-myometrial interface
  • Diffuse heterogenous myometrial echogenicity
  • Myometrial cysts

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

Click to enlarge image

INTRODUCTION

Steven R. Goldstein, MD, CCD, NCMP
Professor, Department of Obstetrics and Gynecology, New York University School of Medicine; Director, Gynecologic Ultrasound; and Co-Director, Bone Densitometry, New York University Medical Center, New York

In this month’s installment of Images in GYN Ultrasound, Drs. Stalnaker and Kaunitz have done an excellent job of describing what adenomyosis will look like on transvaginal ultrasound

In my first book, entitled Endovaginal Ultrasound,1 I coined the phrase “sonomicoscopy.” I maintain that we are seeing things with transvaginal ultrasound that you could not see with your naked eye if you could hold the structure at arms length and squint at it.

Adenomyosis is defined as endometrial glands and stroma embedded within the myometrium. Literature has shown that if you do three sections on a routine hysterectomy specimen the incidence of adenomyosis is 31%; with six sections the incidence is 61%! In other words, it is a very prevalent occurrence.

There is no question that adenomyosis CAN be a source of uterine enlargement, pain, and bleeding. But it is such a prevalent finding that the real question is: What percent of women, especially parous women, will have sonographic evidence of adenomyosis but be totally asymptomatic? Such women represent the denominator while the symptomatic ones represent the numerator. I worry about labeling asymptomatic patients with this entity—when they become perimenopausal and oligo-ovulatory, and may have irregular bleeding—their symptoms can be judged to be FROM adenomyosis and surgical correction is offered.

An important part of successful ultrasound use is being sure that we redefine what is “normal” as we examine patients with this “low power microscope.” So, while transvaginal ultrasound CAN identify glands and stroma within the myometrium, we must be careful not to automatically label this finding as a “disease.”

Reference
1.     Goldstein SR. Endovaginal Ultrasound. 2nd ed. John Wiley & Sons, Inc: Hoboken, NJ; January 1991.

Uterine adenomyosis: Noninvasive diagnosis

Michelle L. Stalnaker, MD
Assistant Professor and Associate Program Director, Obstetrics and Gynecology Residency, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville

Andrew M. Kaunitz, MD
University of Florida Research Foundation Professor and Associate Chairman, Department of Obstetrics and Gynecology at the University of Florida College of Medicine–Jacksonville. Dr. Kaunitz is a member of the OBG Management Board of Editors.

Uterine adenomyosis is a pathologic condition in which endometrial glands and stroma are present in the uterine myometrium. Uterine adenomyosis is common, and may coexist with leiomyomata or endometriosis. When present, it may cause dysmenorrhea and heavy menses. 

Until recently, the best way to establish a diagnosis of uterine adenomyosis was through histologic examination of a hysterectomy specimen. However, transvaginal ultrasound and pelvic magnetic resonance imaging have been shown to be accurate for noninvasive diagnosis.

Signs on imaging include:

  • Globular/bulky uterus
  • Asymmetric thickening of myometrium
  • Loss of clarity of endo-myometrial interface
  • Diffuse heterogenous myometrial echogenicity
  • Myometrial cysts

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References

1. Champaneria R, Abedin P, Daniels J, Balogun M, Khan KS. Ultrasound scan and magnetic resonance imaging for the diagnosis of adenomyosis: systematic review comparing test accuracy. Acta Obstetricia et Gynecologica. 2010;89(11):1374-1384. 

2. Meredith SM, Sanchez-Ramos L, Kaunitz AM. Diagnostic accuracy of transvaginal sonography for the diagnosis of adenomyosis: systematic review and meta-analysis. Am J Obstet Gynecol. 2009;201(1):107.e1-e6.

3. Munro MG. Update: abnormal uterine bleeding. OBG Manag. 2014;26(3):27-32.

References

1. Champaneria R, Abedin P, Daniels J, Balogun M, Khan KS. Ultrasound scan and magnetic resonance imaging for the diagnosis of adenomyosis: systematic review comparing test accuracy. Acta Obstetricia et Gynecologica. 2010;89(11):1374-1384. 

2. Meredith SM, Sanchez-Ramos L, Kaunitz AM. Diagnostic accuracy of transvaginal sonography for the diagnosis of adenomyosis: systematic review and meta-analysis. Am J Obstet Gynecol. 2009;201(1):107.e1-e6.

3. Munro MG. Update: abnormal uterine bleeding. OBG Manag. 2014;26(3):27-32.

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Hypertension and pregnancy and preventing the first cesarean delivery

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Hypertension and pregnancy and preventing the first cesarean delivery

This peer to peer discussion focuses on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines1 and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.2

In this 20-minute audiocast, listen to these experts discuss:

Changing diagnostic tools for preeclampsia
- The 24-hour urinary protein estimation: When is it necessary?
- Use of magnesium sulfate for seizure prophylaxis
Preventing the first cesarean delivery
- Redefining the stages of labor: When is the second-stage too long?
- The lost skill of forceps delivery
- Is cesarean delivery rate the optimal metric for measuring neonatal outcome?

John T. Repke, MD, is University Professor and Chairman of the Department of Obstetrics and Gynecology at Penn State University College of Medicine, and Obstetrician-Gynecologist-in-Chief at the Milton S. Hershey Medical Center in Hershey, Pennsylvania. Dr. Repke is a member of the Board of Editors of OBG Management and is author of the June 2014 Guest Editorial on hypertension and pregnancy.

Errol R. Norwitz, MD, PhD, is the Louis E. Phaneuf Professor and Chairman of the Department of Obstetrics and Gynecology at Tufts Medical Center and Tufts University School of Medicine in Boston, Massachusetts. Dr. Norwitz is a member of the Board of Editors of OBG Management and is author of the June 2014 Update on operative vaginal delivery.

The speakers report no financial relationships relevant to this audiocast.

Click here for a downloadable transcript

TRANSCRIPT

ACOG guidelines on hypertension and pregnancy raise some questions
John T. Repke, MD: So, Errol, I was impressed over the first couple of days of being at the meeting. As you know, we had a postgraduate course, and one of the items that we talked about was the new hypertension and pregnancy document that was released by the Task Force on Hypertension and Pregnancy1 charged by the American College of Obstetricians and Gynecologists. I’ve got to say that while the goal of the document was to provide some standardization and clarification, there still seems to be a lot of confusion in my audience about how to interpret some of the guidelines. Have you found that?

Errol R. Norwitz, MD, PhD: Yes, I have. I found it interesting that it was put out as an executive summary, and not as a practice bulletin, which will probably follow in months. That document, which came out in November 2013, helped to address many of the issues we’ve had over the years of preeclampsia, in terms of its definition and some of the management issues. But, it also raised a number of questions that still need to be resolved.

Dr. Repke: Yes. I think one of the things to keep in mind, and I’ve tabulated all of the recommendations, is that about 60 recommendations came out of that document and only six of the 60 were accompanied by a strong quality of evidence, or rather, a high quality of evidence, and a strong recommendation. And a lot of those things were addressing issues that I think most practitioners already did, in so far as using antenatal steroids for maturation; using magnesium sulfate for patients with preeclampsia with severe features; and using magnesium sulfate as a treatment of eclampsia. But a lot of the other recommendations really were based on either moderate- or low-quality evidence, and had qualified recommendations. And, I think that’s what has led to some of the confusion.

Changing diagnostic tools for preeclampsia
Dr. Repke: What sort of specific things are your practitioners asking you about as far as, “Is this gestational hypertension or is this preeclampsia?” The guidelines say proteinuria is not required anymore. How are you dealing with that?

Should we still do the 24-hour urinary protein estimation?
Dr. Norwitz: The biggest change, in my mind, is the statement that you no longer require significant proteinuria to make the diagnosis of preeclampsia, and, indeed, of severe preeclampsia. So, if you do have significant proteinuria, then that would confirm the diagnosis. But, you can also have preeclampsia in the presence of other endorgan injuries, such as kidney injury and liver injury in the absence of significant proteinuria.

So, one of the questions that comes up is, “Should we actually do the 24-hour urinary protein estimation?”

And, my answer is, “yes.” If you have significant proteinuria, then that would confirm the diagnosis. If you don’t, you can still make the diagnosis in the setting of low platelets, elevated liver enzymes, or abnormal renal function. So, the issue is, and I’d be curious to hear your answer, if you have someone with platelets of, let’s say, 78, a new onset of sustained elevation of blood pressure, would you do the 24-hour urine estimation or just defer it?

 

 

Dr. Repke: We wouldn’t perform the 24-hour urine test under those circumstances. And, we would consider that nuance of hypertension with a severe feature that is now preeclampsia with severe feature, and the management would be based on gestational age. With a platelet count that low, the management would be stabilization and delivery. Although, if stabilized, I think that’s the type of patient that potentially could have delivery delayed until you could get an effective antenatal steroid if she was less that 34 weeks’ gestation.

Dr. Norwitz: So, that’s one issue I think needs to be clarified. If there’s other evidence of endorgan damage, then you can defer the 24-hour urinary protein. That’s another question that comes up. I’m pleased they could resolve the issue of repeated 24-hour urinary estimations. Once you have your 300 mg suggestive of the diagnosis of preeclampsia, there’s no reason to then repeat it looking for elevation and increased leakage of protein into the urine, because it doesn’t correlate with adverse outcome for the mother or fetus. So, that issue was clarified.

Dr. Repke: I think that two questions that came up in our course, and I think they were very legitimate, are, “Do we even need to do urine protein at all?” Because if you look at the guidelines for management, the only difference between preeclampsia management without severe features and gestational hypertension is frequency of antenatal testing until you decide to begin delivery. Now, in the old days, one would say, “Well, another difference would be that the preeclamptic would get magnesium sulfate.” But the current Hypertension in Pregnancy Guidelines1 suggest that preeclampsia without severe features doesn’t necessarily have to be managed with magnesium sulfate. So, I’m still wrestling with whether, other than the fact that it might be for study purposes or for categorization or research, whether proteinuria adds anything to the equation.

And, then the second question is, “How do you resolve the issue of disagreement?” So, the example is protein:creatinine ratio allows for a more rapid diagnosis of significant proteinuria. If that patient doesn’t have to deliver immediately and a 24-hour urine sample is obtained, which do you believe if you have a protein:creatinine ratio greater than 0.3, but now your 24-hour urine is 212 mg/dL? And, I don’t have the answer to that, but that’s another area of confusion.

Dr. Norwitz: And, I think that confusion will persist. I don’t think this document is going to resolve it.

New terminology: Preeclampsia with or without severe features
Dr. Norwitz: I do like the difference in terminology between preeclampsia with severe features and preeclampsia without severe features. I think the old terminology of severe and mild preeclampsia was somewhat confusing. I certainly appreciate that alteration in terminology, although it may take a while for it to catch on. I’m still seeing the term “mild preeclampsia” used quite widely.

Use of magnesium sulfate for seizure prophylaxis
Dr. Norwitz: You did raise the issue of magnesium sulfate for seizure prophylaxis in the setting of severe preeclampsia without severe features. And I was struck by the statement. Not only is it not necessary to give it, but in the Executive Summary, as you suggest, it is not indicated and you recommended against starting it. Is that how you interpret it as the well?

Dr. Repke: Well, I might have interpreted the statement the way I wanted to interpret it. And, as you know, in our institution, because we feel we are a teaching program, people can progress very quickly intrapartum from not having severe features to having severe features, and we don’t want to miss that window of opportunity. Our practice in that regard does not follow the guidelines. We use intrapartum magnesium prophylaxis for all patients with the diagnosis of preeclampsia, and continue it for 24 hours postpartum.

Dr. Norwitz: And I would have to say we decided do the same. So, once a diagnosis of preeclampsia is made, we would give intrapartum, and then postpartum magnesium seizure prophylaxis for 24 hours, regardless of whether there’s evidence of severe features or no severe features.

Dr. Repke: And there again, I think it’s why, for you and I, it will still be important to assess the proteinuria because that diagnostic difference between preeclampsia and gestational hypertension is going to alter management. But if you follow the document word for word, if you’re not going to use magnesium without severe features, I’m not really sure what proteinuria adds. I guess, at the end of the day, you’ve got to be a good doctor. And, you’ve got to be physically assessing your patient on a very regular basis.

 

 

Preventing the first cesarean delivery. Will cesarean rates decline?
Dr. Repke: So, speaking of guidelines, the Society for Maternal Fetal Medicine (SMFM) just came out with a document trying to address this issue of the cesarean-section rate in the United States and are there things that we can be doing to lower the primary C-section rate.2 My feeling is probably disseminated from the recognition that vaginal birth after C-section never got to the levels of acceptance that anybody hoped back when Healthy People 2010 was first written. And, we could eliminate that issue or, at least significantly reduce that issue, if the first C-section never took place.

And, I guess I’d like some of your thoughts about some of the things in that document, some of the things we need to be reconsidering in terms of how we define labor and so on.

Dr. Norwitz: It is true, I think, that there’s been an epidemic of cesarean deliveries in the last decade in the US, but also throughout the world, I think, even in countries that have traditionally had very low cesarean delivery rates, the classic one being Ireland and the UK countries. Their rates are now increasing significantly.

And there are a number of different reasons as to why this may be. I think, certainly the obesity epidemic has contributed to this. You want to deliver patients who have an elevated BMI prior to the postterm period. But, it’s often difficult to monitor these patients, and the cesarean-delivery rate overall is much higher in that population. So, that might be one reason why cesarean-delivery rates overall are going up. But, certainly there are many others.

Dr. Repke: Yes, I think you’re absolutely right: the demographics of change. Childbearing is being delayed. We know that uterine contractility dynamics alter with advanced maternal age. We’ve got a higher incidence of multiple gestations with advanced maternal age. We have more patients that require induction because of supervening medical complications of pregnancy, whether that be Class A2 gestational diabetes, or whether that be pregnancy-induced hypertension.

Redefining the stages of labor
Dr. Repke: I think some of the intriguing data, to me, is a willingness to re-look at how we define the stages of labor. And what are acceptable norms? And, while I have some concerns about how that may be interpreted in the rank and file, I think it’s at least heightened the awareness of my faculty that we just can’t tolerate the C-section at 4 cm, or whether the latent phase of labor should be allowed to go to 6 cm. I don’t think we really have the data for that. But I’d be happy if I could just start to see a reduction in “failure to progress at 4 cm.”

And then the issue of second stage, I think, is also important. What do you think about the guidelines’ recommendation that there may not really be an upper limit of allowability for second-stage labors?

Dr. Norwitz: Well, certainly I think it’s important to think back to the historical context of where the labor curves developed. The original labor curves were actually developed in Zimbabwe (at that time it was Rhodesia) by an obstetrician working in the community called Philpott. And he was trying to determine when it was appropriate to send patients into the tertiary care center. So he designed the labor curve and said if patients failed to progress over a certain number of hours, those are patients that are likely to need an operative delivery, and he would then send them into the tertiary care center.

And, then Dr. Freidman picked up on that idea and developed the Freidman Curve in Boston. But that was an era, again, many years ago when the population demographics were very different, when not many patients received regional anesthesia. I think if you look at the current guidelines, there is a huge discrepancy between women who get epidural anesthesia and those that don’t in terms of the progress of labor, both the first stage and the second stage.

Is it anesthesia?
Dr. Repke: One of the things that, you know, I haven’t looked at this paper in a long time, but you remember at Brigham and Women’s Hospital, probably 20 years ago, we were winding down the Active Management of Labor Study3 that was designed to try to replicate what had gone on at the Dublin Maternity Hospital,4 and if I’m remembering correctly, one of the remarkable things about that is that in Dublin, there were virtually no C-sections in the second stage. And so people assumed that while they were more aggressive with forceps, the operative vaginal delivery rate was no different between Brigham and Women’s Hospital and the Dublin Maternity Hospital. And so there needed to be another explanation.

 

 

And, I know I’m going to incur some of the ire of our anesthesia colleagues, but I really wonder whether there is a contribution of regional anesthesia to some of the labor dystocias that we see, and whether that’s a new demographic that we haven’t really adequately assessed. Even though I recognize some of the anesthesia literature5 seems to suggest very strongly that it has no effect. You know, if you were to plot a graph of regional anesthesia rates and cesarean section rates, they would probably parallel each other.

Dr. Norwitz: I think they do. I think we’ve long known that epidural anesthesia slows down the second stage of labor. These analyses suggest that it also has a significant effect on the first stage. And, I think that needs to be taken into account.

The lost skill of forceps delivery
Dr. Norwitz: I personally think that the skill set, in terms of operative vaginal delivery with forceps and vacuum, has really been lost. And I do feel that’s one of the factors contributing to the increase in cesarean delivery rates. I certainly see that in my practice: that I’m comfortable doing rotational forceps and mid-cavity forceps deliveries, where many of my colleagues have lost that skill, and rely now on the vacuum, which in certain circumstances is a less-than-ideal instrument. So, I believe that’s part of the reason why the cesarean delivery rates have gone up.

Lengthy second stage
Dr. Norwitz: But, certainly, I think, epidural anesthesia has made a difference, and I think we need to be cognizant of the fact that there is no “hard stop” now, in terms of the length of the second stage. If you get to 3 hours, even 4 hours, I would say, and there’s continued descent with pushing and fetal heart-rate tracing is reassuring, it’s reasonable to continue beyond those cutoffs.

Dr. Repke: I agree. I also have a concern about that, and I’m going to use a little bit of a parallel example of, you know, 7 or 8 years ago, there was a big push, and I think it was an appropriate push, to try to avoid elective deliveries prior to 39 weeks.6,7 What ended up happening was that people forgot about the term “elective,” and all they heard was 39 weeks. And what we would see on Board Examinations was, “Why do you have this placenta previa delivering at 39 weeks?”

“Well, that’s our hospital policy. We can’t deliver before 39 weeks.”

And, I think, the complications started to arise, and that’s what led to SMFM and ACOG coming out with guidelines for when it is acceptable to deliver prior to 39 weeks.2,6–8

So, the analogy is: I’m afraid that people are only going to see there is no upper limit for latent phase, there is no upper limit for second stage; that clinical judgment may not get its due in making these decisions. And we’ve all been in situations where, when you are trying to extract the head out of the pelvis, a cesarean section after a 5- or 6-hour second stage has its own set of complications. So my concern is that I hope we will recognize that we have to still use some clinical judgment, what I term the so-called “art of obstetrics,” into managing these patients.

Are you optimistic that we’re going to the lower C-section rate?

Dr. Norwitz: No, I think, it’s going to continue to go up. I think, with the increasing number of multiple pregnancies, obesity, maternal age getting further and further along, I think this is only going to continue to rise. And to be honest, I don’t know the correct cesarean delivery rate, or even if that is the metric that we should be measuring.

What is the right metric to measure neonatal outcome?
Dr. Norwitz: Maybe we should be looking at perinatal outcome. If perinatal outcome is improved, then maybe the cesarean rate is less important. Obviously, the first cesarean does have implications for subsequent pregnancy outcomes, and if we do continue to see this rise in cesarean deliveries, we are going to end up with many more placental accretas and hemorrhages in women in years to come.

So, careful counseling is important. If patients plan to have one or two kids only, maybe a cesarean delivery is very reasonable. If they are planning on having six or seven kids, then maybe you have to have a more careful discussion.

Dr. Repke: Yes, I think, that’s a very good point: the number of cesareans and the potential risks for abnormal placentation. I think societal expectations have changed in terms of what they want. Most mothers are willing to sacrifice maternal risk for presumed benefits to the fetus.

 

 

I think, where we’ve gotten into trouble as a specialty, though, is that we’ve had a hard time proving that neonatal outcome, in fact, has improved—despite an almost tripling of the cesarean section rate since, probably, the early 1970s. Although, anecdotally, what my pediatric and neonatal colleagues will tell me is they don’t get the kind of damaged babies they used to get. So the neonatologists that are closer to my age that have been doing this for a long time, they’re not seeing the really severe meconium aspiration syndromes; they’re not seeing really severe forceps-related injuries, or vacuum-related injuries that they used to see. So, those may be data that we’re going to need to accumulate with a little bit more rigor, and see if that’s true.

But I tend to agree with you. I don’t know what the right cesarean section rate is. I often tell people, I have yet to meet a patient who doesn’t think her cesarean section was indicated. And that’s where I think we hit the crossroads of individual patient-care management. So, we know across all other disciplines in medicine we’re entering the era of personalized medicine, yet we want to make broad public health policy that may not apply to individuals, and run with that. So, that’s also a concern. But, as they say, a story we will follow with interest.

Dr. Norwitz: I think so. I think the other part of that equation is the stillbirth rate, and the fact that there’s a push now to avoid elective inductions before 39 weeks, which I think is very reasonable, with a focus there again on elective inductions.

There’s also a push to induce patients before 42 weeks. And that bar has been pushed back, and in most practices around the country now, deliveries are being affected and recommended at 41 weeks. And clearly, if you take a nulliparous patient with an unfavorable cervix and induce at 41 weeks, you are going to increase the cesarean rate. I would argue that you are also decreasing the chance that there will be a stillbirth. But that data has not been forthcoming.

So this issue is by no means resolved. I think there are going to be many more years of data and studies and consensus opinions before we have a much better sense of what the right cesarean
rate is.

Dr. Repke: Yes, I think that’s a great point. And, one thing that I think people aren’t maybe that familiar with is when this push came, and again, it is an appropriate push to minimize elective deliveries before 39 weeks. When they looked at neonatal outcomes, all they looked at were the group that delivered at 37 weeks, and the group that delivered at 39 weeks. And they didn’t look at what happened with the other ones.9

So, they did look at the stillbirths of fetal distress or the other complications that happened between 37 and 1, and 38 and 6. They just looked at neonates that were born at 37 weeks and compared them to neonates that were born at 39 weeks, and found reduced instances of things like transient tachypnea of the newborn, hyperbilirubinemia, and thermoregulation issues, and those sorts of things. But, never looked at the neonates in that window, so no question 39 is better than 37, but, 37 is better than not making it to 39. So that, as you said, we’ve got a lot more information we’ve got to gather.

Errol, good talking with you.

Dr. Norwitz: Thank you.

References

 

 

  1. American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Obstet Gynecol. 2013;122(5):1122–1131.
  2. Caughey AB, Cahill AG, Guise JM, Rouse DJ; American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric Care Consensus: Safe prevention of the primary cesarean delivery. Am J Obstet Gynecol. 2014;210(3):179–193.
  3. Frigoletto FD, Lieberman E, Lang J, et al. A clinical trial of active management of labor. N Engl J Med. 1995;333(12):745–750.
  4. O’Driscoll K, Meagher D, Boylan P. Active Management of Labor. 3rd ed. London: Mosby- Yearbook; 1993.
  5. Chestnut DH, McGrath JM, Vincent RD, et al. Does early administration of epidural analgesia effect obstetric outcome in nulliparous women who are in spontaneous labor? Anesthesiology. 1994;80(6):1201–1208.
  6. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 560: Medically indicated late-preterm and early-term deliveries. Obstet Gynecol. 2013;121(4):908–910.
  7. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 561: Nonmedically indicated early-term deliveries. Obstet Gynecol. 2013;121(4):911–915.
  8. Spong CY, Mercer BM, D’Alton M, Kilpatrick S, Blackwell S, Saade G. Timing of indicated late-preterm and early-term birth. Obstet Gynecol. 2011;118(2 Pt 1):323–333.
  9. Tita ATN, Landon MB, Spong CY, et al; Eunice Kennedy Shriver NICHD Maternal-Fetal Medicine Units Network. Timing of elective repeat Cesarean Delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
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This peer to peer discussion focuses on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines1 and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.2

In this 20-minute audiocast, listen to these experts discuss:

Changing diagnostic tools for preeclampsia
- The 24-hour urinary protein estimation: When is it necessary?
- Use of magnesium sulfate for seizure prophylaxis
Preventing the first cesarean delivery
- Redefining the stages of labor: When is the second-stage too long?
- The lost skill of forceps delivery
- Is cesarean delivery rate the optimal metric for measuring neonatal outcome?

John T. Repke, MD, is University Professor and Chairman of the Department of Obstetrics and Gynecology at Penn State University College of Medicine, and Obstetrician-Gynecologist-in-Chief at the Milton S. Hershey Medical Center in Hershey, Pennsylvania. Dr. Repke is a member of the Board of Editors of OBG Management and is author of the June 2014 Guest Editorial on hypertension and pregnancy.

Errol R. Norwitz, MD, PhD, is the Louis E. Phaneuf Professor and Chairman of the Department of Obstetrics and Gynecology at Tufts Medical Center and Tufts University School of Medicine in Boston, Massachusetts. Dr. Norwitz is a member of the Board of Editors of OBG Management and is author of the June 2014 Update on operative vaginal delivery.

The speakers report no financial relationships relevant to this audiocast.

Click here for a downloadable transcript

TRANSCRIPT

ACOG guidelines on hypertension and pregnancy raise some questions
John T. Repke, MD: So, Errol, I was impressed over the first couple of days of being at the meeting. As you know, we had a postgraduate course, and one of the items that we talked about was the new hypertension and pregnancy document that was released by the Task Force on Hypertension and Pregnancy1 charged by the American College of Obstetricians and Gynecologists. I’ve got to say that while the goal of the document was to provide some standardization and clarification, there still seems to be a lot of confusion in my audience about how to interpret some of the guidelines. Have you found that?

Errol R. Norwitz, MD, PhD: Yes, I have. I found it interesting that it was put out as an executive summary, and not as a practice bulletin, which will probably follow in months. That document, which came out in November 2013, helped to address many of the issues we’ve had over the years of preeclampsia, in terms of its definition and some of the management issues. But, it also raised a number of questions that still need to be resolved.

Dr. Repke: Yes. I think one of the things to keep in mind, and I’ve tabulated all of the recommendations, is that about 60 recommendations came out of that document and only six of the 60 were accompanied by a strong quality of evidence, or rather, a high quality of evidence, and a strong recommendation. And a lot of those things were addressing issues that I think most practitioners already did, in so far as using antenatal steroids for maturation; using magnesium sulfate for patients with preeclampsia with severe features; and using magnesium sulfate as a treatment of eclampsia. But a lot of the other recommendations really were based on either moderate- or low-quality evidence, and had qualified recommendations. And, I think that’s what has led to some of the confusion.

Changing diagnostic tools for preeclampsia
Dr. Repke: What sort of specific things are your practitioners asking you about as far as, “Is this gestational hypertension or is this preeclampsia?” The guidelines say proteinuria is not required anymore. How are you dealing with that?

Should we still do the 24-hour urinary protein estimation?
Dr. Norwitz: The biggest change, in my mind, is the statement that you no longer require significant proteinuria to make the diagnosis of preeclampsia, and, indeed, of severe preeclampsia. So, if you do have significant proteinuria, then that would confirm the diagnosis. But, you can also have preeclampsia in the presence of other endorgan injuries, such as kidney injury and liver injury in the absence of significant proteinuria.

So, one of the questions that comes up is, “Should we actually do the 24-hour urinary protein estimation?”

And, my answer is, “yes.” If you have significant proteinuria, then that would confirm the diagnosis. If you don’t, you can still make the diagnosis in the setting of low platelets, elevated liver enzymes, or abnormal renal function. So, the issue is, and I’d be curious to hear your answer, if you have someone with platelets of, let’s say, 78, a new onset of sustained elevation of blood pressure, would you do the 24-hour urine estimation or just defer it?

 

 

Dr. Repke: We wouldn’t perform the 24-hour urine test under those circumstances. And, we would consider that nuance of hypertension with a severe feature that is now preeclampsia with severe feature, and the management would be based on gestational age. With a platelet count that low, the management would be stabilization and delivery. Although, if stabilized, I think that’s the type of patient that potentially could have delivery delayed until you could get an effective antenatal steroid if she was less that 34 weeks’ gestation.

Dr. Norwitz: So, that’s one issue I think needs to be clarified. If there’s other evidence of endorgan damage, then you can defer the 24-hour urinary protein. That’s another question that comes up. I’m pleased they could resolve the issue of repeated 24-hour urinary estimations. Once you have your 300 mg suggestive of the diagnosis of preeclampsia, there’s no reason to then repeat it looking for elevation and increased leakage of protein into the urine, because it doesn’t correlate with adverse outcome for the mother or fetus. So, that issue was clarified.

Dr. Repke: I think that two questions that came up in our course, and I think they were very legitimate, are, “Do we even need to do urine protein at all?” Because if you look at the guidelines for management, the only difference between preeclampsia management without severe features and gestational hypertension is frequency of antenatal testing until you decide to begin delivery. Now, in the old days, one would say, “Well, another difference would be that the preeclamptic would get magnesium sulfate.” But the current Hypertension in Pregnancy Guidelines1 suggest that preeclampsia without severe features doesn’t necessarily have to be managed with magnesium sulfate. So, I’m still wrestling with whether, other than the fact that it might be for study purposes or for categorization or research, whether proteinuria adds anything to the equation.

And, then the second question is, “How do you resolve the issue of disagreement?” So, the example is protein:creatinine ratio allows for a more rapid diagnosis of significant proteinuria. If that patient doesn’t have to deliver immediately and a 24-hour urine sample is obtained, which do you believe if you have a protein:creatinine ratio greater than 0.3, but now your 24-hour urine is 212 mg/dL? And, I don’t have the answer to that, but that’s another area of confusion.

Dr. Norwitz: And, I think that confusion will persist. I don’t think this document is going to resolve it.

New terminology: Preeclampsia with or without severe features
Dr. Norwitz: I do like the difference in terminology between preeclampsia with severe features and preeclampsia without severe features. I think the old terminology of severe and mild preeclampsia was somewhat confusing. I certainly appreciate that alteration in terminology, although it may take a while for it to catch on. I’m still seeing the term “mild preeclampsia” used quite widely.

Use of magnesium sulfate for seizure prophylaxis
Dr. Norwitz: You did raise the issue of magnesium sulfate for seizure prophylaxis in the setting of severe preeclampsia without severe features. And I was struck by the statement. Not only is it not necessary to give it, but in the Executive Summary, as you suggest, it is not indicated and you recommended against starting it. Is that how you interpret it as the well?

Dr. Repke: Well, I might have interpreted the statement the way I wanted to interpret it. And, as you know, in our institution, because we feel we are a teaching program, people can progress very quickly intrapartum from not having severe features to having severe features, and we don’t want to miss that window of opportunity. Our practice in that regard does not follow the guidelines. We use intrapartum magnesium prophylaxis for all patients with the diagnosis of preeclampsia, and continue it for 24 hours postpartum.

Dr. Norwitz: And I would have to say we decided do the same. So, once a diagnosis of preeclampsia is made, we would give intrapartum, and then postpartum magnesium seizure prophylaxis for 24 hours, regardless of whether there’s evidence of severe features or no severe features.

Dr. Repke: And there again, I think it’s why, for you and I, it will still be important to assess the proteinuria because that diagnostic difference between preeclampsia and gestational hypertension is going to alter management. But if you follow the document word for word, if you’re not going to use magnesium without severe features, I’m not really sure what proteinuria adds. I guess, at the end of the day, you’ve got to be a good doctor. And, you’ve got to be physically assessing your patient on a very regular basis.

 

 

Preventing the first cesarean delivery. Will cesarean rates decline?
Dr. Repke: So, speaking of guidelines, the Society for Maternal Fetal Medicine (SMFM) just came out with a document trying to address this issue of the cesarean-section rate in the United States and are there things that we can be doing to lower the primary C-section rate.2 My feeling is probably disseminated from the recognition that vaginal birth after C-section never got to the levels of acceptance that anybody hoped back when Healthy People 2010 was first written. And, we could eliminate that issue or, at least significantly reduce that issue, if the first C-section never took place.

And, I guess I’d like some of your thoughts about some of the things in that document, some of the things we need to be reconsidering in terms of how we define labor and so on.

Dr. Norwitz: It is true, I think, that there’s been an epidemic of cesarean deliveries in the last decade in the US, but also throughout the world, I think, even in countries that have traditionally had very low cesarean delivery rates, the classic one being Ireland and the UK countries. Their rates are now increasing significantly.

And there are a number of different reasons as to why this may be. I think, certainly the obesity epidemic has contributed to this. You want to deliver patients who have an elevated BMI prior to the postterm period. But, it’s often difficult to monitor these patients, and the cesarean-delivery rate overall is much higher in that population. So, that might be one reason why cesarean-delivery rates overall are going up. But, certainly there are many others.

Dr. Repke: Yes, I think you’re absolutely right: the demographics of change. Childbearing is being delayed. We know that uterine contractility dynamics alter with advanced maternal age. We’ve got a higher incidence of multiple gestations with advanced maternal age. We have more patients that require induction because of supervening medical complications of pregnancy, whether that be Class A2 gestational diabetes, or whether that be pregnancy-induced hypertension.

Redefining the stages of labor
Dr. Repke: I think some of the intriguing data, to me, is a willingness to re-look at how we define the stages of labor. And what are acceptable norms? And, while I have some concerns about how that may be interpreted in the rank and file, I think it’s at least heightened the awareness of my faculty that we just can’t tolerate the C-section at 4 cm, or whether the latent phase of labor should be allowed to go to 6 cm. I don’t think we really have the data for that. But I’d be happy if I could just start to see a reduction in “failure to progress at 4 cm.”

And then the issue of second stage, I think, is also important. What do you think about the guidelines’ recommendation that there may not really be an upper limit of allowability for second-stage labors?

Dr. Norwitz: Well, certainly I think it’s important to think back to the historical context of where the labor curves developed. The original labor curves were actually developed in Zimbabwe (at that time it was Rhodesia) by an obstetrician working in the community called Philpott. And he was trying to determine when it was appropriate to send patients into the tertiary care center. So he designed the labor curve and said if patients failed to progress over a certain number of hours, those are patients that are likely to need an operative delivery, and he would then send them into the tertiary care center.

And, then Dr. Freidman picked up on that idea and developed the Freidman Curve in Boston. But that was an era, again, many years ago when the population demographics were very different, when not many patients received regional anesthesia. I think if you look at the current guidelines, there is a huge discrepancy between women who get epidural anesthesia and those that don’t in terms of the progress of labor, both the first stage and the second stage.

Is it anesthesia?
Dr. Repke: One of the things that, you know, I haven’t looked at this paper in a long time, but you remember at Brigham and Women’s Hospital, probably 20 years ago, we were winding down the Active Management of Labor Study3 that was designed to try to replicate what had gone on at the Dublin Maternity Hospital,4 and if I’m remembering correctly, one of the remarkable things about that is that in Dublin, there were virtually no C-sections in the second stage. And so people assumed that while they were more aggressive with forceps, the operative vaginal delivery rate was no different between Brigham and Women’s Hospital and the Dublin Maternity Hospital. And so there needed to be another explanation.

 

 

And, I know I’m going to incur some of the ire of our anesthesia colleagues, but I really wonder whether there is a contribution of regional anesthesia to some of the labor dystocias that we see, and whether that’s a new demographic that we haven’t really adequately assessed. Even though I recognize some of the anesthesia literature5 seems to suggest very strongly that it has no effect. You know, if you were to plot a graph of regional anesthesia rates and cesarean section rates, they would probably parallel each other.

Dr. Norwitz: I think they do. I think we’ve long known that epidural anesthesia slows down the second stage of labor. These analyses suggest that it also has a significant effect on the first stage. And, I think that needs to be taken into account.

The lost skill of forceps delivery
Dr. Norwitz: I personally think that the skill set, in terms of operative vaginal delivery with forceps and vacuum, has really been lost. And I do feel that’s one of the factors contributing to the increase in cesarean delivery rates. I certainly see that in my practice: that I’m comfortable doing rotational forceps and mid-cavity forceps deliveries, where many of my colleagues have lost that skill, and rely now on the vacuum, which in certain circumstances is a less-than-ideal instrument. So, I believe that’s part of the reason why the cesarean delivery rates have gone up.

Lengthy second stage
Dr. Norwitz: But, certainly, I think, epidural anesthesia has made a difference, and I think we need to be cognizant of the fact that there is no “hard stop” now, in terms of the length of the second stage. If you get to 3 hours, even 4 hours, I would say, and there’s continued descent with pushing and fetal heart-rate tracing is reassuring, it’s reasonable to continue beyond those cutoffs.

Dr. Repke: I agree. I also have a concern about that, and I’m going to use a little bit of a parallel example of, you know, 7 or 8 years ago, there was a big push, and I think it was an appropriate push, to try to avoid elective deliveries prior to 39 weeks.6,7 What ended up happening was that people forgot about the term “elective,” and all they heard was 39 weeks. And what we would see on Board Examinations was, “Why do you have this placenta previa delivering at 39 weeks?”

“Well, that’s our hospital policy. We can’t deliver before 39 weeks.”

And, I think, the complications started to arise, and that’s what led to SMFM and ACOG coming out with guidelines for when it is acceptable to deliver prior to 39 weeks.2,6–8

So, the analogy is: I’m afraid that people are only going to see there is no upper limit for latent phase, there is no upper limit for second stage; that clinical judgment may not get its due in making these decisions. And we’ve all been in situations where, when you are trying to extract the head out of the pelvis, a cesarean section after a 5- or 6-hour second stage has its own set of complications. So my concern is that I hope we will recognize that we have to still use some clinical judgment, what I term the so-called “art of obstetrics,” into managing these patients.

Are you optimistic that we’re going to the lower C-section rate?

Dr. Norwitz: No, I think, it’s going to continue to go up. I think, with the increasing number of multiple pregnancies, obesity, maternal age getting further and further along, I think this is only going to continue to rise. And to be honest, I don’t know the correct cesarean delivery rate, or even if that is the metric that we should be measuring.

What is the right metric to measure neonatal outcome?
Dr. Norwitz: Maybe we should be looking at perinatal outcome. If perinatal outcome is improved, then maybe the cesarean rate is less important. Obviously, the first cesarean does have implications for subsequent pregnancy outcomes, and if we do continue to see this rise in cesarean deliveries, we are going to end up with many more placental accretas and hemorrhages in women in years to come.

So, careful counseling is important. If patients plan to have one or two kids only, maybe a cesarean delivery is very reasonable. If they are planning on having six or seven kids, then maybe you have to have a more careful discussion.

Dr. Repke: Yes, I think, that’s a very good point: the number of cesareans and the potential risks for abnormal placentation. I think societal expectations have changed in terms of what they want. Most mothers are willing to sacrifice maternal risk for presumed benefits to the fetus.

 

 

I think, where we’ve gotten into trouble as a specialty, though, is that we’ve had a hard time proving that neonatal outcome, in fact, has improved—despite an almost tripling of the cesarean section rate since, probably, the early 1970s. Although, anecdotally, what my pediatric and neonatal colleagues will tell me is they don’t get the kind of damaged babies they used to get. So the neonatologists that are closer to my age that have been doing this for a long time, they’re not seeing the really severe meconium aspiration syndromes; they’re not seeing really severe forceps-related injuries, or vacuum-related injuries that they used to see. So, those may be data that we’re going to need to accumulate with a little bit more rigor, and see if that’s true.

But I tend to agree with you. I don’t know what the right cesarean section rate is. I often tell people, I have yet to meet a patient who doesn’t think her cesarean section was indicated. And that’s where I think we hit the crossroads of individual patient-care management. So, we know across all other disciplines in medicine we’re entering the era of personalized medicine, yet we want to make broad public health policy that may not apply to individuals, and run with that. So, that’s also a concern. But, as they say, a story we will follow with interest.

Dr. Norwitz: I think so. I think the other part of that equation is the stillbirth rate, and the fact that there’s a push now to avoid elective inductions before 39 weeks, which I think is very reasonable, with a focus there again on elective inductions.

There’s also a push to induce patients before 42 weeks. And that bar has been pushed back, and in most practices around the country now, deliveries are being affected and recommended at 41 weeks. And clearly, if you take a nulliparous patient with an unfavorable cervix and induce at 41 weeks, you are going to increase the cesarean rate. I would argue that you are also decreasing the chance that there will be a stillbirth. But that data has not been forthcoming.

So this issue is by no means resolved. I think there are going to be many more years of data and studies and consensus opinions before we have a much better sense of what the right cesarean
rate is.

Dr. Repke: Yes, I think that’s a great point. And, one thing that I think people aren’t maybe that familiar with is when this push came, and again, it is an appropriate push to minimize elective deliveries before 39 weeks. When they looked at neonatal outcomes, all they looked at were the group that delivered at 37 weeks, and the group that delivered at 39 weeks. And they didn’t look at what happened with the other ones.9

So, they did look at the stillbirths of fetal distress or the other complications that happened between 37 and 1, and 38 and 6. They just looked at neonates that were born at 37 weeks and compared them to neonates that were born at 39 weeks, and found reduced instances of things like transient tachypnea of the newborn, hyperbilirubinemia, and thermoregulation issues, and those sorts of things. But, never looked at the neonates in that window, so no question 39 is better than 37, but, 37 is better than not making it to 39. So that, as you said, we’ve got a lot more information we’ve got to gather.

Errol, good talking with you.

Dr. Norwitz: Thank you.

This peer to peer discussion focuses on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines1 and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.2

In this 20-minute audiocast, listen to these experts discuss:

Changing diagnostic tools for preeclampsia
- The 24-hour urinary protein estimation: When is it necessary?
- Use of magnesium sulfate for seizure prophylaxis
Preventing the first cesarean delivery
- Redefining the stages of labor: When is the second-stage too long?
- The lost skill of forceps delivery
- Is cesarean delivery rate the optimal metric for measuring neonatal outcome?

John T. Repke, MD, is University Professor and Chairman of the Department of Obstetrics and Gynecology at Penn State University College of Medicine, and Obstetrician-Gynecologist-in-Chief at the Milton S. Hershey Medical Center in Hershey, Pennsylvania. Dr. Repke is a member of the Board of Editors of OBG Management and is author of the June 2014 Guest Editorial on hypertension and pregnancy.

Errol R. Norwitz, MD, PhD, is the Louis E. Phaneuf Professor and Chairman of the Department of Obstetrics and Gynecology at Tufts Medical Center and Tufts University School of Medicine in Boston, Massachusetts. Dr. Norwitz is a member of the Board of Editors of OBG Management and is author of the June 2014 Update on operative vaginal delivery.

The speakers report no financial relationships relevant to this audiocast.

Click here for a downloadable transcript

TRANSCRIPT

ACOG guidelines on hypertension and pregnancy raise some questions
John T. Repke, MD: So, Errol, I was impressed over the first couple of days of being at the meeting. As you know, we had a postgraduate course, and one of the items that we talked about was the new hypertension and pregnancy document that was released by the Task Force on Hypertension and Pregnancy1 charged by the American College of Obstetricians and Gynecologists. I’ve got to say that while the goal of the document was to provide some standardization and clarification, there still seems to be a lot of confusion in my audience about how to interpret some of the guidelines. Have you found that?

Errol R. Norwitz, MD, PhD: Yes, I have. I found it interesting that it was put out as an executive summary, and not as a practice bulletin, which will probably follow in months. That document, which came out in November 2013, helped to address many of the issues we’ve had over the years of preeclampsia, in terms of its definition and some of the management issues. But, it also raised a number of questions that still need to be resolved.

Dr. Repke: Yes. I think one of the things to keep in mind, and I’ve tabulated all of the recommendations, is that about 60 recommendations came out of that document and only six of the 60 were accompanied by a strong quality of evidence, or rather, a high quality of evidence, and a strong recommendation. And a lot of those things were addressing issues that I think most practitioners already did, in so far as using antenatal steroids for maturation; using magnesium sulfate for patients with preeclampsia with severe features; and using magnesium sulfate as a treatment of eclampsia. But a lot of the other recommendations really were based on either moderate- or low-quality evidence, and had qualified recommendations. And, I think that’s what has led to some of the confusion.

Changing diagnostic tools for preeclampsia
Dr. Repke: What sort of specific things are your practitioners asking you about as far as, “Is this gestational hypertension or is this preeclampsia?” The guidelines say proteinuria is not required anymore. How are you dealing with that?

Should we still do the 24-hour urinary protein estimation?
Dr. Norwitz: The biggest change, in my mind, is the statement that you no longer require significant proteinuria to make the diagnosis of preeclampsia, and, indeed, of severe preeclampsia. So, if you do have significant proteinuria, then that would confirm the diagnosis. But, you can also have preeclampsia in the presence of other endorgan injuries, such as kidney injury and liver injury in the absence of significant proteinuria.

So, one of the questions that comes up is, “Should we actually do the 24-hour urinary protein estimation?”

And, my answer is, “yes.” If you have significant proteinuria, then that would confirm the diagnosis. If you don’t, you can still make the diagnosis in the setting of low platelets, elevated liver enzymes, or abnormal renal function. So, the issue is, and I’d be curious to hear your answer, if you have someone with platelets of, let’s say, 78, a new onset of sustained elevation of blood pressure, would you do the 24-hour urine estimation or just defer it?

 

 

Dr. Repke: We wouldn’t perform the 24-hour urine test under those circumstances. And, we would consider that nuance of hypertension with a severe feature that is now preeclampsia with severe feature, and the management would be based on gestational age. With a platelet count that low, the management would be stabilization and delivery. Although, if stabilized, I think that’s the type of patient that potentially could have delivery delayed until you could get an effective antenatal steroid if she was less that 34 weeks’ gestation.

Dr. Norwitz: So, that’s one issue I think needs to be clarified. If there’s other evidence of endorgan damage, then you can defer the 24-hour urinary protein. That’s another question that comes up. I’m pleased they could resolve the issue of repeated 24-hour urinary estimations. Once you have your 300 mg suggestive of the diagnosis of preeclampsia, there’s no reason to then repeat it looking for elevation and increased leakage of protein into the urine, because it doesn’t correlate with adverse outcome for the mother or fetus. So, that issue was clarified.

Dr. Repke: I think that two questions that came up in our course, and I think they were very legitimate, are, “Do we even need to do urine protein at all?” Because if you look at the guidelines for management, the only difference between preeclampsia management without severe features and gestational hypertension is frequency of antenatal testing until you decide to begin delivery. Now, in the old days, one would say, “Well, another difference would be that the preeclamptic would get magnesium sulfate.” But the current Hypertension in Pregnancy Guidelines1 suggest that preeclampsia without severe features doesn’t necessarily have to be managed with magnesium sulfate. So, I’m still wrestling with whether, other than the fact that it might be for study purposes or for categorization or research, whether proteinuria adds anything to the equation.

And, then the second question is, “How do you resolve the issue of disagreement?” So, the example is protein:creatinine ratio allows for a more rapid diagnosis of significant proteinuria. If that patient doesn’t have to deliver immediately and a 24-hour urine sample is obtained, which do you believe if you have a protein:creatinine ratio greater than 0.3, but now your 24-hour urine is 212 mg/dL? And, I don’t have the answer to that, but that’s another area of confusion.

Dr. Norwitz: And, I think that confusion will persist. I don’t think this document is going to resolve it.

New terminology: Preeclampsia with or without severe features
Dr. Norwitz: I do like the difference in terminology between preeclampsia with severe features and preeclampsia without severe features. I think the old terminology of severe and mild preeclampsia was somewhat confusing. I certainly appreciate that alteration in terminology, although it may take a while for it to catch on. I’m still seeing the term “mild preeclampsia” used quite widely.

Use of magnesium sulfate for seizure prophylaxis
Dr. Norwitz: You did raise the issue of magnesium sulfate for seizure prophylaxis in the setting of severe preeclampsia without severe features. And I was struck by the statement. Not only is it not necessary to give it, but in the Executive Summary, as you suggest, it is not indicated and you recommended against starting it. Is that how you interpret it as the well?

Dr. Repke: Well, I might have interpreted the statement the way I wanted to interpret it. And, as you know, in our institution, because we feel we are a teaching program, people can progress very quickly intrapartum from not having severe features to having severe features, and we don’t want to miss that window of opportunity. Our practice in that regard does not follow the guidelines. We use intrapartum magnesium prophylaxis for all patients with the diagnosis of preeclampsia, and continue it for 24 hours postpartum.

Dr. Norwitz: And I would have to say we decided do the same. So, once a diagnosis of preeclampsia is made, we would give intrapartum, and then postpartum magnesium seizure prophylaxis for 24 hours, regardless of whether there’s evidence of severe features or no severe features.

Dr. Repke: And there again, I think it’s why, for you and I, it will still be important to assess the proteinuria because that diagnostic difference between preeclampsia and gestational hypertension is going to alter management. But if you follow the document word for word, if you’re not going to use magnesium without severe features, I’m not really sure what proteinuria adds. I guess, at the end of the day, you’ve got to be a good doctor. And, you’ve got to be physically assessing your patient on a very regular basis.

 

 

Preventing the first cesarean delivery. Will cesarean rates decline?
Dr. Repke: So, speaking of guidelines, the Society for Maternal Fetal Medicine (SMFM) just came out with a document trying to address this issue of the cesarean-section rate in the United States and are there things that we can be doing to lower the primary C-section rate.2 My feeling is probably disseminated from the recognition that vaginal birth after C-section never got to the levels of acceptance that anybody hoped back when Healthy People 2010 was first written. And, we could eliminate that issue or, at least significantly reduce that issue, if the first C-section never took place.

And, I guess I’d like some of your thoughts about some of the things in that document, some of the things we need to be reconsidering in terms of how we define labor and so on.

Dr. Norwitz: It is true, I think, that there’s been an epidemic of cesarean deliveries in the last decade in the US, but also throughout the world, I think, even in countries that have traditionally had very low cesarean delivery rates, the classic one being Ireland and the UK countries. Their rates are now increasing significantly.

And there are a number of different reasons as to why this may be. I think, certainly the obesity epidemic has contributed to this. You want to deliver patients who have an elevated BMI prior to the postterm period. But, it’s often difficult to monitor these patients, and the cesarean-delivery rate overall is much higher in that population. So, that might be one reason why cesarean-delivery rates overall are going up. But, certainly there are many others.

Dr. Repke: Yes, I think you’re absolutely right: the demographics of change. Childbearing is being delayed. We know that uterine contractility dynamics alter with advanced maternal age. We’ve got a higher incidence of multiple gestations with advanced maternal age. We have more patients that require induction because of supervening medical complications of pregnancy, whether that be Class A2 gestational diabetes, or whether that be pregnancy-induced hypertension.

Redefining the stages of labor
Dr. Repke: I think some of the intriguing data, to me, is a willingness to re-look at how we define the stages of labor. And what are acceptable norms? And, while I have some concerns about how that may be interpreted in the rank and file, I think it’s at least heightened the awareness of my faculty that we just can’t tolerate the C-section at 4 cm, or whether the latent phase of labor should be allowed to go to 6 cm. I don’t think we really have the data for that. But I’d be happy if I could just start to see a reduction in “failure to progress at 4 cm.”

And then the issue of second stage, I think, is also important. What do you think about the guidelines’ recommendation that there may not really be an upper limit of allowability for second-stage labors?

Dr. Norwitz: Well, certainly I think it’s important to think back to the historical context of where the labor curves developed. The original labor curves were actually developed in Zimbabwe (at that time it was Rhodesia) by an obstetrician working in the community called Philpott. And he was trying to determine when it was appropriate to send patients into the tertiary care center. So he designed the labor curve and said if patients failed to progress over a certain number of hours, those are patients that are likely to need an operative delivery, and he would then send them into the tertiary care center.

And, then Dr. Freidman picked up on that idea and developed the Freidman Curve in Boston. But that was an era, again, many years ago when the population demographics were very different, when not many patients received regional anesthesia. I think if you look at the current guidelines, there is a huge discrepancy between women who get epidural anesthesia and those that don’t in terms of the progress of labor, both the first stage and the second stage.

Is it anesthesia?
Dr. Repke: One of the things that, you know, I haven’t looked at this paper in a long time, but you remember at Brigham and Women’s Hospital, probably 20 years ago, we were winding down the Active Management of Labor Study3 that was designed to try to replicate what had gone on at the Dublin Maternity Hospital,4 and if I’m remembering correctly, one of the remarkable things about that is that in Dublin, there were virtually no C-sections in the second stage. And so people assumed that while they were more aggressive with forceps, the operative vaginal delivery rate was no different between Brigham and Women’s Hospital and the Dublin Maternity Hospital. And so there needed to be another explanation.

 

 

And, I know I’m going to incur some of the ire of our anesthesia colleagues, but I really wonder whether there is a contribution of regional anesthesia to some of the labor dystocias that we see, and whether that’s a new demographic that we haven’t really adequately assessed. Even though I recognize some of the anesthesia literature5 seems to suggest very strongly that it has no effect. You know, if you were to plot a graph of regional anesthesia rates and cesarean section rates, they would probably parallel each other.

Dr. Norwitz: I think they do. I think we’ve long known that epidural anesthesia slows down the second stage of labor. These analyses suggest that it also has a significant effect on the first stage. And, I think that needs to be taken into account.

The lost skill of forceps delivery
Dr. Norwitz: I personally think that the skill set, in terms of operative vaginal delivery with forceps and vacuum, has really been lost. And I do feel that’s one of the factors contributing to the increase in cesarean delivery rates. I certainly see that in my practice: that I’m comfortable doing rotational forceps and mid-cavity forceps deliveries, where many of my colleagues have lost that skill, and rely now on the vacuum, which in certain circumstances is a less-than-ideal instrument. So, I believe that’s part of the reason why the cesarean delivery rates have gone up.

Lengthy second stage
Dr. Norwitz: But, certainly, I think, epidural anesthesia has made a difference, and I think we need to be cognizant of the fact that there is no “hard stop” now, in terms of the length of the second stage. If you get to 3 hours, even 4 hours, I would say, and there’s continued descent with pushing and fetal heart-rate tracing is reassuring, it’s reasonable to continue beyond those cutoffs.

Dr. Repke: I agree. I also have a concern about that, and I’m going to use a little bit of a parallel example of, you know, 7 or 8 years ago, there was a big push, and I think it was an appropriate push, to try to avoid elective deliveries prior to 39 weeks.6,7 What ended up happening was that people forgot about the term “elective,” and all they heard was 39 weeks. And what we would see on Board Examinations was, “Why do you have this placenta previa delivering at 39 weeks?”

“Well, that’s our hospital policy. We can’t deliver before 39 weeks.”

And, I think, the complications started to arise, and that’s what led to SMFM and ACOG coming out with guidelines for when it is acceptable to deliver prior to 39 weeks.2,6–8

So, the analogy is: I’m afraid that people are only going to see there is no upper limit for latent phase, there is no upper limit for second stage; that clinical judgment may not get its due in making these decisions. And we’ve all been in situations where, when you are trying to extract the head out of the pelvis, a cesarean section after a 5- or 6-hour second stage has its own set of complications. So my concern is that I hope we will recognize that we have to still use some clinical judgment, what I term the so-called “art of obstetrics,” into managing these patients.

Are you optimistic that we’re going to the lower C-section rate?

Dr. Norwitz: No, I think, it’s going to continue to go up. I think, with the increasing number of multiple pregnancies, obesity, maternal age getting further and further along, I think this is only going to continue to rise. And to be honest, I don’t know the correct cesarean delivery rate, or even if that is the metric that we should be measuring.

What is the right metric to measure neonatal outcome?
Dr. Norwitz: Maybe we should be looking at perinatal outcome. If perinatal outcome is improved, then maybe the cesarean rate is less important. Obviously, the first cesarean does have implications for subsequent pregnancy outcomes, and if we do continue to see this rise in cesarean deliveries, we are going to end up with many more placental accretas and hemorrhages in women in years to come.

So, careful counseling is important. If patients plan to have one or two kids only, maybe a cesarean delivery is very reasonable. If they are planning on having six or seven kids, then maybe you have to have a more careful discussion.

Dr. Repke: Yes, I think, that’s a very good point: the number of cesareans and the potential risks for abnormal placentation. I think societal expectations have changed in terms of what they want. Most mothers are willing to sacrifice maternal risk for presumed benefits to the fetus.

 

 

I think, where we’ve gotten into trouble as a specialty, though, is that we’ve had a hard time proving that neonatal outcome, in fact, has improved—despite an almost tripling of the cesarean section rate since, probably, the early 1970s. Although, anecdotally, what my pediatric and neonatal colleagues will tell me is they don’t get the kind of damaged babies they used to get. So the neonatologists that are closer to my age that have been doing this for a long time, they’re not seeing the really severe meconium aspiration syndromes; they’re not seeing really severe forceps-related injuries, or vacuum-related injuries that they used to see. So, those may be data that we’re going to need to accumulate with a little bit more rigor, and see if that’s true.

But I tend to agree with you. I don’t know what the right cesarean section rate is. I often tell people, I have yet to meet a patient who doesn’t think her cesarean section was indicated. And that’s where I think we hit the crossroads of individual patient-care management. So, we know across all other disciplines in medicine we’re entering the era of personalized medicine, yet we want to make broad public health policy that may not apply to individuals, and run with that. So, that’s also a concern. But, as they say, a story we will follow with interest.

Dr. Norwitz: I think so. I think the other part of that equation is the stillbirth rate, and the fact that there’s a push now to avoid elective inductions before 39 weeks, which I think is very reasonable, with a focus there again on elective inductions.

There’s also a push to induce patients before 42 weeks. And that bar has been pushed back, and in most practices around the country now, deliveries are being affected and recommended at 41 weeks. And clearly, if you take a nulliparous patient with an unfavorable cervix and induce at 41 weeks, you are going to increase the cesarean rate. I would argue that you are also decreasing the chance that there will be a stillbirth. But that data has not been forthcoming.

So this issue is by no means resolved. I think there are going to be many more years of data and studies and consensus opinions before we have a much better sense of what the right cesarean
rate is.

Dr. Repke: Yes, I think that’s a great point. And, one thing that I think people aren’t maybe that familiar with is when this push came, and again, it is an appropriate push to minimize elective deliveries before 39 weeks. When they looked at neonatal outcomes, all they looked at were the group that delivered at 37 weeks, and the group that delivered at 39 weeks. And they didn’t look at what happened with the other ones.9

So, they did look at the stillbirths of fetal distress or the other complications that happened between 37 and 1, and 38 and 6. They just looked at neonates that were born at 37 weeks and compared them to neonates that were born at 39 weeks, and found reduced instances of things like transient tachypnea of the newborn, hyperbilirubinemia, and thermoregulation issues, and those sorts of things. But, never looked at the neonates in that window, so no question 39 is better than 37, but, 37 is better than not making it to 39. So that, as you said, we’ve got a lot more information we’ve got to gather.

Errol, good talking with you.

Dr. Norwitz: Thank you.

References

 

 

  1. American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Obstet Gynecol. 2013;122(5):1122–1131.
  2. Caughey AB, Cahill AG, Guise JM, Rouse DJ; American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric Care Consensus: Safe prevention of the primary cesarean delivery. Am J Obstet Gynecol. 2014;210(3):179–193.
  3. Frigoletto FD, Lieberman E, Lang J, et al. A clinical trial of active management of labor. N Engl J Med. 1995;333(12):745–750.
  4. O’Driscoll K, Meagher D, Boylan P. Active Management of Labor. 3rd ed. London: Mosby- Yearbook; 1993.
  5. Chestnut DH, McGrath JM, Vincent RD, et al. Does early administration of epidural analgesia effect obstetric outcome in nulliparous women who are in spontaneous labor? Anesthesiology. 1994;80(6):1201–1208.
  6. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 560: Medically indicated late-preterm and early-term deliveries. Obstet Gynecol. 2013;121(4):908–910.
  7. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 561: Nonmedically indicated early-term deliveries. Obstet Gynecol. 2013;121(4):911–915.
  8. Spong CY, Mercer BM, D’Alton M, Kilpatrick S, Blackwell S, Saade G. Timing of indicated late-preterm and early-term birth. Obstet Gynecol. 2011;118(2 Pt 1):323–333.
  9. Tita ATN, Landon MB, Spong CY, et al; Eunice Kennedy Shriver NICHD Maternal-Fetal Medicine Units Network. Timing of elective repeat Cesarean Delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
References

 

 

  1. American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Obstet Gynecol. 2013;122(5):1122–1131.
  2. Caughey AB, Cahill AG, Guise JM, Rouse DJ; American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric Care Consensus: Safe prevention of the primary cesarean delivery. Am J Obstet Gynecol. 2014;210(3):179–193.
  3. Frigoletto FD, Lieberman E, Lang J, et al. A clinical trial of active management of labor. N Engl J Med. 1995;333(12):745–750.
  4. O’Driscoll K, Meagher D, Boylan P. Active Management of Labor. 3rd ed. London: Mosby- Yearbook; 1993.
  5. Chestnut DH, McGrath JM, Vincent RD, et al. Does early administration of epidural analgesia effect obstetric outcome in nulliparous women who are in spontaneous labor? Anesthesiology. 1994;80(6):1201–1208.
  6. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 560: Medically indicated late-preterm and early-term deliveries. Obstet Gynecol. 2013;121(4):908–910.
  7. American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 561: Nonmedically indicated early-term deliveries. Obstet Gynecol. 2013;121(4):911–915.
  8. Spong CY, Mercer BM, D’Alton M, Kilpatrick S, Blackwell S, Saade G. Timing of indicated late-preterm and early-term birth. Obstet Gynecol. 2011;118(2 Pt 1):323–333.
  9. Tita ATN, Landon MB, Spong CY, et al; Eunice Kennedy Shriver NICHD Maternal-Fetal Medicine Units Network. Timing of elective repeat Cesarean Delivery at term and neonatal outcomes. N Engl J Med. 2009;360(2):111–120.
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Best Practices in IVF Nursing: Fertility Myths and Misconceptions: Exploring the Common Mistaken Beliefs that Patients May Accept as Truths

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The Importance of Thorough Patient Education by IVF Nurses

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A study conducted in 2013 assessed the knowledge, attitudes, and practices related to fertility and conception among 1000 women of reproductive age in the United States. The results, published in March 2014 in Fertility and Sterility, revealed that 40% of women expressed concern about their ability to conceive, and one-third were unaware of factors that could impact their ability to conceive.

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The Importance of Thorough Patient Education by IVF Nurses

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The Importance of Thorough Patient Education by IVF Nurses

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A study conducted in 2013 assessed the knowledge, attitudes, and practices related to fertility and conception among 1000 women of reproductive age in the United States. The results, published in March 2014 in Fertility and Sterility, revealed that 40% of women expressed concern about their ability to conceive, and one-third were unaware of factors that could impact their ability to conceive.

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Chronic vulvar irritation, itching, and pain. What is the diagnosis?

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Chronic irritation, itching, and pain are only rarely due to infection. These symptoms are more likely to be caused by dermatoses, vaginal abnormalities, and pain syndromes that may be difficult to diagnose. Careful evaluation should include a wet mount and culture to eliminate infection as a cause so that the correct diagnosis can be ascertained and treated.

In Part 2 of this two-part series, we focus on five cases of vulvar dermatologic disruptions:

 

  • atrophic vagina
  • irritant and allergic contact dermatitis
  • complex vulvar aphthosis
  • desquamative inflammatory vaginitis
  • inverse psoriasis.

CASE 1. INTROITAL BURNING AND A FEAR OF BREAST CANCER
A 56-year-old woman visits your office for management of recent-onset introital burning during sexual activity. She reports that her commercial lubricant causes irritation. Topical and oral antifungal therapies have not been beneficial. She has a strong family history of breast cancer.

On examination, she exhibits small, smooth labia minora and experiences pain when a cotton swab is pressed against the vestibule. The vagina is also smooth, with scant secretions. Microscopically, these secretions are almost acellular, with no increase in white blood cells and no clue cells, yeast forms, or lactobacilli. The pH is greater than 6.5, and most epithelial cells are parabasal (FIGURE 1).

You prescribe topical estradiol cream for vaginal use three nights per week, but when the patient returns 1 month later, her condition is unchanged. She explains that she never used the cream after reading the package insert, which reports a risk of breast cancer.

Diagnosis: Atrophic vagina (not atrophic vaginitis, as there is no increase in white blood cells).

Treatment: Re-estrogenization should relieve her symptoms.

Several options for local estrogen replacement are available. Creams include estradiol (Estrace) and conjugated equine estrogen (Premarin), the latter of which is arguably slightly more irritating. These are prescribed at a starting dose of 1 g in the vagina three nights per week. After several weeks, they can be titrated to the lowest frequency that controls symptoms.

The risk of vaginal candidiasis is fairly high during the first 2 or 3 weeks of re-estrogenization, so patients should be warned of this possibility. Also consider prophylactic weekly fluconazole or an azole suppository two or three times a week for the first few weeks. Estradiol tablets (Vagifem) inserted in the vagina are effective, less messy, and more expensive, as is the estradiol ring (Estring), which is inserted and changed quarterly.

It is not unusual for a woman to avoid use of topical estrogen out of fear, or to use insufficient amounts only on the vulva, or to use it for only 1 or 2 weeks.1

Women should be scheduled for a return visit to ensure they have been using the estrogen, their wet mount has normalized, and discomfort has cleared.

Related article: Your menopausal patient's breast biopsy reveals atypical hyperplasia. JoAnn V. Pinkerton, MD (Cases in Menopause; May 2013)

When a woman is reluctant to use local estrogen
We counsel women that small doses of vaginal estrogen used for limited periods of time are unlikely to influence their breast cancer risk and are the most effective treatment for symptoms of atrophy. Usually, this explanation is sufficient to reassure a woman that topical estrogen is safe. Otherwise, use of commercial personal lubricants (silicone-based lubricants are well tolerated) and moisturizers such as Replens and RePhresh can be comforting.

The topical anesthetics lidocaine 2% jelly or lidocaine 5% ointment (which sometimes burns) can minimize pain with sexual activity for those requiring more than lubrication.

Ospemifene (Osphena) is used by some clinicians in this situation, but this medication is labeled as a risk for all of the same contraindications as systemic estrogen, and it is much more expensive than topical estrogen. Ospemifene is an estrogen agonist/antagonist. Although it is the only oral medication indicated for the treatment of menopause-related dyspareunia, the long-term effects on breast cancer risk are unknown. Also, it has an agonist effect on the endometrium and, again, the long-term risk is unknown.

Related article: New treatment option for vulvar and vaginal atrophy. Andrew M. Kaunitz, MD (News for your Practice; May 2013)

Fluconazole use is contraindicated with ospemifene, as is the use of any estrogen products.

 

CASE 2. RECALCITRANT ITCHING, BURNING, AND REDNESS
A 25-year-old woman reports anogenital itching, burning, and redness, which have been present for 3 months. She says she developed a yeast infection after antibiotic therapy for a dental infection; the yeast infection was treated with terconazole. She reports an allergic reaction to the terconazole, with immediate severe burning, redness, and swelling. The clobetasol cream she was given to use twice daily also caused burning, so she discontinued it. Her symptoms improved when she tried cool soaks and applied topical benzocaine gel as a local anesthetic. However,

 

 

2 weeks later, she experienced increasing redness, itching, and burning. Although the benzocaine relieved these symptoms, it required almost continual reapplication for comfort.

A physical examination of the vulva reveals generalized, poorly demarcated redness, edema, and superficial erosions (FIGURE 2).

Diagnosis: Irritant contact dermatitis (as opposed to allergic contact dermatitis) associated with the use of terconazole and clobetasol. This was followed by allergic contact dermatitis in association with benzocaine.

Treatment: Withdrawal of benzocaine, with reinitiation of cool soaks and a switch to clobetasol ointment rather than cream. Nighttime sedation allows the patient to sleep through the itching and gradually allows her skin to heal.

 

Contact dermatitis is a fairly common cause of vulvar irritation, with two main types:

 

  • Irritant contact dermatitis—The most common form, it occurs in any individual exposed to an irritating substance in sufficient quantity or frequency. Irritant contact dermatitis is characterized mostly by sensations of rawness or burning and generally is caused by urine, feces, perspiration, friction, alcohols in topical creams, overwashing, and use of harsh soaps.
  • Allergic contact dermatitis—This form is characterized by itching, although secondary pain and burning from scratching and blistering can occur as well. Common allergens in the genital area include benzocaine, diphenhydramine (Benadryl), neomycin in triple antibiotic ointment (Neosporin), and latex. Allergic contact dermatitis occurs after 1 or 2 weeks of initial exposure or 1 or 2 days after re-exposure.

The diagnosis of an irritant or allergic contact dermatitis can be based on a history of incontinence, application of high-risk substances, or inappropriate washing. Management generally involves ­discontinuation of all panty liners and topical agents except for water, with a topical steroid ointment used twice a day and pure petroleum jelly used as often as necessary for comfort. Nighttime sedation to allow a reprieve from rubbing and scratching may be helpful, and narcotic pain medications may be useful for the first 1 to 2 weeks of treatment.

Women who fail to respond to treatment should be referred for patch testing by a
dermatologist.

Related article: Vulvar pain syndromes: Making the correct diagnosis. Neal M. Lonky, MD, MPH; Libby Edwards, MD; Jennifer Gunter, MD; Hope K. Haefner, MD (Roundtable, part 1 of 3; September 2011)

 

CASE 3. TEENAGER WITH VULVAR PAIN AND SORES
A woman brings her 13-year-old daughter to your office for treatment of sudden-onset vulvar pain and sores. The child developed a sore throat and low-grade fever 3 days earlier, with vulvar pain and vulvar dysuria the next day. The pediatrician diagnosed a herpes simplex virus infection and prescribed oral acyclovir, but the girl’s condition has not improved, and the mother believes her daughter’s claims of sexual abstinence.

The girl is otherwise healthy, aside from a history of trivial oral canker sores without arthritis, headaches, abdominal pain, eye pain, or vision changes.

Physical examination of the vulva reveals soft, painful, well-demarcated ulcers with a white fibrin base (FIGURE 3).

Diagnosis: Complex aphthosis. Further testing is unnecessary.

Treatment: Prednisone 40 mg/day plus hydrocodone in usual doses of 5/325, one or two tablets every 4 to 6 hours, as needed; topical petroleum jelly (especially before urination); and sitz baths. When the patient returns 1 week later, she is much improved.

 

Aphthae are believed to be of hyperimmune origin, often precipitated by a viral syndrome. They are most common in girls aged 9 to 18 years. Vulvar aphthae are triggered by various viral infections, including Epstein-Barr.2 The offending virus is not located in the ulcer proper, however, but is identified serologically.

Aphthae are uncommon and under-recognized on the vulva, and genital aphthae are usually much larger than oral aphthae. Most patients initially are mistakenly evaluated and treated for sexually transmitted disease, but the large, well-demarcated, painful, nonindurated deep nature of the ulcer is pathognomonic for an aphthous ulcer.

The presence of oral and genital aphthae does not constitute a diagnosis of Behçet disease, an often-devastating systemic inflammatory condition occurring almost exclusively in men in the Middle and Far East. The diagnosis of Behçet disease requires the identification of objective inflammatory disease of the eyes, joints, gastrointestinal tract, or neurologic system. True Behçet disease is incredibly uncommon in the United States. When it is diagnosed in Western countries, it takes an attenuated form, most often occurring in women who experience multisystem discomfort rather than identifiable inflammatory disease. End-organ damage is uncommon. Evaluation for Behçet disease in women with vulvar aphthae generally is not indicated, although a directed review of systems is reasonable. The rare patient who experiences frequent recurrence and symptoms of systemic disease should be referred to an ophthalmologist and other relevant specialists to evaluate for inflammatory disease.

 

 

The treatment of vulvar aphthae consists of systemic corticosteroids such as prednisone 40 mg/day for smaller individuals and 60 mg/day for larger women, with follow-up to ensure a good response. Often, the prednisone can be discontinued when pain relents rather than continued through complete healing. Reassurance, without discussing Behçet disease, is paramount, as is pain control. The heavy application of petroleum jelly can decrease pain and prevent urine from touching the ulcer.

Some patients experience recurrent ulcers. A second prescription of prednisone can be provided for immediate reinstitution with onset of symptoms. However, frequent recurrences may require ongoing suppressive medication, with dapsone being the usual first choice. Colchicine often is used, and thalidomide and tumor necrosis factor-a blockers (adalimumab, etanercept, and infliximab) also are extremely beneficial.3,4

 

CASE 4. INCREASED NEUTROPHILS AND NO LACTOBACILLI
A 36-year-old woman visits your office reporting introital itching, vulvar dysuria, and superficial dyspareunia that have lasted 6 months. She has tried over-the-counter antifungal therapy, with only slight improvement while using the cream. Her health is normal otherwise, lacking pain syndromes or abnormalities suggestive of pelvic floor dysfunction. She experienced comfortable sexual activity until 6 months ago.

The only abnormalities apparent on physical examination are redness of the vestibule, medial labia minora, and vaginal walls, with edema of the surrounding skin and no oral lesions (FIGURE 4A). Copious vaginal secretions are visible at the introitus. A wet mount shows a marked increase in neutrophils with scattered parabasal cells (FIGURE 4B). There are no clue cells, lactobacilli, or yeast forms. The patient’s pH level is greater than 6.5. Routine and fungal cultures and molecular studies for chlamydia, trichomonas, and gonorrhea are returned as normal.

Diagnosis: Desquamative inflammatory vaginitis.

Treatment: Clindamycin vaginal cream, 1/2 to 1 full applicator nightly, with a weekly oral fluconazole tablet (200 mg is more easily covered by insurance) to prevent secondary candidiasis. You schedule a follow-up visit in 1 month.

 

Desquamative inflammatory vaginitis (DIV) is described as noninfectious inflammatory vaginitis in a setting of normal estrogen and absence of skin disease of the mucous membranes of the vagina. The condition is characterized by an increase in white blood cells and parabasal cells, and absent lactobacilli, with relatively high vaginal pH. DIV is thought to represent an inflammatory dermatosis of the vaginal epithelium.5 Although some clinicians believe that DIV is actually lichen planus, the latter exhibits erosions as well as redness, nearly always affects the mouth and the vulva, and produces remarkable scarring. DIV does not erode, affect any other skin surfaces, or scar.

Other rare skin diseases that produce erosions and scarring also can be ruled out by the presence of erosions, absence of oral disease, and absence of other mucosal involvement. These diseases include cicatricial pemphigoid, pemphigus vulgaris, Stevens-Johnson syndrome, and toxic epidermal necrolysis. Infectious diseases characterized by inflammation are excluded by culture or molecular studies, and atrophic vaginitis and retained foreign bodies (especially retained tampons) can produce a similar picture.

The vulvar itching and irritation that occur with DIV most likely represent an irritant contact dermatitis, with vaginal secretions serving as the irritant.

How to treat DIV
The management of DIV consists of either topical clindamycin cream (theoretically for its anti-inflammatory rather than antimicrobial properties) or intravaginal corticosteroids, especially hydrocortisone acetate.6 Hydrocortisone can be tried at the low commercially available dose of 25-mg rectal suppositories, which should be inserted into the vagina nightly, or it can be compounded at 100 or 200 mg, if needed. If the condition is recalcitrant, combination therapy can be used.

When signs and symptoms abate, the frequency of use can be decreased, or hydrocortisone can be discontinued and restarted again with any recurrence of discomfort. Many clinicians also prescribe weekly fluconazole to prevent intercurrent candidiasis.

Related article: Successful treatment of chronic vaginitis. Robert L. Barbieri, MD (Editorial, July 2013)

 

CASE 5. PLAQUES ON VULVA AND IN SKIN FOLDS
A 43-year-old woman reports a recalcitrant yeast infection of the vulva, with itching and irritation. She is overweight and diabetic, with mild stress incontinence.

Physical examination reveals a fairly well-demarcated plaque of redness of the vulva and labiocrural folds, with satellite red papules and peripheral peeling (FIGURE 5). An examination of other skin surfaces reveals similar plaques in the gluteal cleft, umbilicus, and axillae as well as under the breasts. A fungal preparation of the vagina and skin is negative. You obtain a fungal culture and prescribe topical and oral antifungal therapy and see the patient again 1 week later. Her condition is unchanged.

Diagnosis: You make a presumptive diagnosis of inverse psoriasis and do a confirmatory punch biopsy.

 

 

Treatment: Clobetasol ointment applied to the skin folds, along with continuation of the topical miconazole cream. A week later, the patient’s condition is remarkably improved, and her biopsy shows psoriasiform dermatitis. You reduce the potency of her corticosteroid, switching to desonide cream sparingly applied daily.

 

Psoriasis is a common skin disease of immunologic origin. The skin is classically red and thick, with heavy white scale produced by rapid turnover of epithelium. However, there are several morphologic types of psoriasis, and anogenital psoriasis is most often of the inverse pattern. Inverse psoriasis preferentially affects skin folds and is frequently mistaken for (and often initially superinfected with) candidiasis. Scale is thin and unapparent, and there often is a shiny, glazed appearance to the skin. Tiny satellite lesions often are visible as well. A skin biopsy of inverse psoriasis often is not diagnostic, showing only nonspecific psoriasiform dermatitis; this does not disprove psoriasis.

Psoriasis is a systemic condition and is associated with metabolic syndrome, carrying an increased risk of overweight, hypertension, diabetes, and cardiovascular disease. Management of these conditions is very important in the treatment of the patient overall.

Unlike lichen planus and lichen sclerosus, scarring is rare with psoriasis, and squamous cell carcinoma generally is unassociated.7,8

Anogenital psoriasis is treated with topical corticosteroids and, when needed, topical vitamin D preparations. Generally, inverse psoriasis is controlled with low-potency topical corticosteroids, with management of secondary infection and irritants. Otherwise, ultraviolet light is a time-honored therapy for psoriasis but not practical for skin folds. It also is difficult for many patients to manage with a busy life. Systemic therapy, including methotrexate and oral retinoids are often used, as are newer biologic agents such as etanercept, adalimumab, infliximab, and ustekinumab.

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References

 

 

  1. Kingsberg SA, Krychman ML. Resistance and barriers to local estrogen therapy in women with atrophic vaginitis.
    J Sex Med. 2013;10(6):1567–1574.
  2. Huppert JS, Gerber MA, Deitch HR, et al. Vulvar ulcers in young females: A manifestation of aphthosis. J Pediatr Adolesc Gynecol. 2006;19(3):195–204.
  3. O’Neill ID. Efficacy of tumour necrosis factor-a antagonists in aphthous ulceration: Review of published individual patient data. J Eur Acad Dermatol Venereol. 2012;26(2):231–235.
  4. Sanchez-Cano D, Callejas-Rubio JL, Ruiz-Villaverde R, Ortego-Centeno N. Recalcitrant, recurrent aphthous stomatitis successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2009;23(2):206.
  5. Stockdale CK. Clinical spectrum of desquamative inflammatory vaginitis. Curr Infect Dis Rep. 2010;12(6):479–483.
  6. Sobel JD, Reichman O, Misra D, Yoo W. Prognosis and treatment of desquamative inflammatory vaginitis. Obstet Gynecol. 2011;117(4):850–855.
  7. Albert S, Neill S, Derrick EK, Calonje E. Psoriasis associated with vulvar scarring. Clin Exp Dermatol. 2004;29(4):354–356.
  8. Boffetta P, Gridley G, Lindelöf B. Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol. 2001;117(6):1531–1537.
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Libby Edwards, MD, is Chief of Dermatology at Carolinas Medical Center, Charlotte, North Carolina.

Beth E. Goldbaum, MD, is Clinical Instructor of Obstetrics and Gynecology at Harvard Medical School, Boston, Massachusetts.

The authors report no financial relationships relevant to this article.

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Chronic irritation, itching, and pain are only rarely due to infection. These symptoms are more likely to be caused by dermatoses, vaginal abnormalities, and pain syndromes that may be difficult to diagnose. Careful evaluation should include a wet mount and culture to eliminate infection as a cause so that the correct diagnosis can be ascertained and treated.

In Part 2 of this two-part series, we focus on five cases of vulvar dermatologic disruptions:

 

  • atrophic vagina
  • irritant and allergic contact dermatitis
  • complex vulvar aphthosis
  • desquamative inflammatory vaginitis
  • inverse psoriasis.

CASE 1. INTROITAL BURNING AND A FEAR OF BREAST CANCER
A 56-year-old woman visits your office for management of recent-onset introital burning during sexual activity. She reports that her commercial lubricant causes irritation. Topical and oral antifungal therapies have not been beneficial. She has a strong family history of breast cancer.

On examination, she exhibits small, smooth labia minora and experiences pain when a cotton swab is pressed against the vestibule. The vagina is also smooth, with scant secretions. Microscopically, these secretions are almost acellular, with no increase in white blood cells and no clue cells, yeast forms, or lactobacilli. The pH is greater than 6.5, and most epithelial cells are parabasal (FIGURE 1).

You prescribe topical estradiol cream for vaginal use three nights per week, but when the patient returns 1 month later, her condition is unchanged. She explains that she never used the cream after reading the package insert, which reports a risk of breast cancer.

Diagnosis: Atrophic vagina (not atrophic vaginitis, as there is no increase in white blood cells).

Treatment: Re-estrogenization should relieve her symptoms.

Several options for local estrogen replacement are available. Creams include estradiol (Estrace) and conjugated equine estrogen (Premarin), the latter of which is arguably slightly more irritating. These are prescribed at a starting dose of 1 g in the vagina three nights per week. After several weeks, they can be titrated to the lowest frequency that controls symptoms.

The risk of vaginal candidiasis is fairly high during the first 2 or 3 weeks of re-estrogenization, so patients should be warned of this possibility. Also consider prophylactic weekly fluconazole or an azole suppository two or three times a week for the first few weeks. Estradiol tablets (Vagifem) inserted in the vagina are effective, less messy, and more expensive, as is the estradiol ring (Estring), which is inserted and changed quarterly.

It is not unusual for a woman to avoid use of topical estrogen out of fear, or to use insufficient amounts only on the vulva, or to use it for only 1 or 2 weeks.1

Women should be scheduled for a return visit to ensure they have been using the estrogen, their wet mount has normalized, and discomfort has cleared.

Related article: Your menopausal patient's breast biopsy reveals atypical hyperplasia. JoAnn V. Pinkerton, MD (Cases in Menopause; May 2013)

When a woman is reluctant to use local estrogen
We counsel women that small doses of vaginal estrogen used for limited periods of time are unlikely to influence their breast cancer risk and are the most effective treatment for symptoms of atrophy. Usually, this explanation is sufficient to reassure a woman that topical estrogen is safe. Otherwise, use of commercial personal lubricants (silicone-based lubricants are well tolerated) and moisturizers such as Replens and RePhresh can be comforting.

The topical anesthetics lidocaine 2% jelly or lidocaine 5% ointment (which sometimes burns) can minimize pain with sexual activity for those requiring more than lubrication.

Ospemifene (Osphena) is used by some clinicians in this situation, but this medication is labeled as a risk for all of the same contraindications as systemic estrogen, and it is much more expensive than topical estrogen. Ospemifene is an estrogen agonist/antagonist. Although it is the only oral medication indicated for the treatment of menopause-related dyspareunia, the long-term effects on breast cancer risk are unknown. Also, it has an agonist effect on the endometrium and, again, the long-term risk is unknown.

Related article: New treatment option for vulvar and vaginal atrophy. Andrew M. Kaunitz, MD (News for your Practice; May 2013)

Fluconazole use is contraindicated with ospemifene, as is the use of any estrogen products.

 

CASE 2. RECALCITRANT ITCHING, BURNING, AND REDNESS
A 25-year-old woman reports anogenital itching, burning, and redness, which have been present for 3 months. She says she developed a yeast infection after antibiotic therapy for a dental infection; the yeast infection was treated with terconazole. She reports an allergic reaction to the terconazole, with immediate severe burning, redness, and swelling. The clobetasol cream she was given to use twice daily also caused burning, so she discontinued it. Her symptoms improved when she tried cool soaks and applied topical benzocaine gel as a local anesthetic. However,

 

 

2 weeks later, she experienced increasing redness, itching, and burning. Although the benzocaine relieved these symptoms, it required almost continual reapplication for comfort.

A physical examination of the vulva reveals generalized, poorly demarcated redness, edema, and superficial erosions (FIGURE 2).

Diagnosis: Irritant contact dermatitis (as opposed to allergic contact dermatitis) associated with the use of terconazole and clobetasol. This was followed by allergic contact dermatitis in association with benzocaine.

Treatment: Withdrawal of benzocaine, with reinitiation of cool soaks and a switch to clobetasol ointment rather than cream. Nighttime sedation allows the patient to sleep through the itching and gradually allows her skin to heal.

 

Contact dermatitis is a fairly common cause of vulvar irritation, with two main types:

 

  • Irritant contact dermatitis—The most common form, it occurs in any individual exposed to an irritating substance in sufficient quantity or frequency. Irritant contact dermatitis is characterized mostly by sensations of rawness or burning and generally is caused by urine, feces, perspiration, friction, alcohols in topical creams, overwashing, and use of harsh soaps.
  • Allergic contact dermatitis—This form is characterized by itching, although secondary pain and burning from scratching and blistering can occur as well. Common allergens in the genital area include benzocaine, diphenhydramine (Benadryl), neomycin in triple antibiotic ointment (Neosporin), and latex. Allergic contact dermatitis occurs after 1 or 2 weeks of initial exposure or 1 or 2 days after re-exposure.

The diagnosis of an irritant or allergic contact dermatitis can be based on a history of incontinence, application of high-risk substances, or inappropriate washing. Management generally involves ­discontinuation of all panty liners and topical agents except for water, with a topical steroid ointment used twice a day and pure petroleum jelly used as often as necessary for comfort. Nighttime sedation to allow a reprieve from rubbing and scratching may be helpful, and narcotic pain medications may be useful for the first 1 to 2 weeks of treatment.

Women who fail to respond to treatment should be referred for patch testing by a
dermatologist.

Related article: Vulvar pain syndromes: Making the correct diagnosis. Neal M. Lonky, MD, MPH; Libby Edwards, MD; Jennifer Gunter, MD; Hope K. Haefner, MD (Roundtable, part 1 of 3; September 2011)

 

CASE 3. TEENAGER WITH VULVAR PAIN AND SORES
A woman brings her 13-year-old daughter to your office for treatment of sudden-onset vulvar pain and sores. The child developed a sore throat and low-grade fever 3 days earlier, with vulvar pain and vulvar dysuria the next day. The pediatrician diagnosed a herpes simplex virus infection and prescribed oral acyclovir, but the girl’s condition has not improved, and the mother believes her daughter’s claims of sexual abstinence.

The girl is otherwise healthy, aside from a history of trivial oral canker sores without arthritis, headaches, abdominal pain, eye pain, or vision changes.

Physical examination of the vulva reveals soft, painful, well-demarcated ulcers with a white fibrin base (FIGURE 3).

Diagnosis: Complex aphthosis. Further testing is unnecessary.

Treatment: Prednisone 40 mg/day plus hydrocodone in usual doses of 5/325, one or two tablets every 4 to 6 hours, as needed; topical petroleum jelly (especially before urination); and sitz baths. When the patient returns 1 week later, she is much improved.

 

Aphthae are believed to be of hyperimmune origin, often precipitated by a viral syndrome. They are most common in girls aged 9 to 18 years. Vulvar aphthae are triggered by various viral infections, including Epstein-Barr.2 The offending virus is not located in the ulcer proper, however, but is identified serologically.

Aphthae are uncommon and under-recognized on the vulva, and genital aphthae are usually much larger than oral aphthae. Most patients initially are mistakenly evaluated and treated for sexually transmitted disease, but the large, well-demarcated, painful, nonindurated deep nature of the ulcer is pathognomonic for an aphthous ulcer.

The presence of oral and genital aphthae does not constitute a diagnosis of Behçet disease, an often-devastating systemic inflammatory condition occurring almost exclusively in men in the Middle and Far East. The diagnosis of Behçet disease requires the identification of objective inflammatory disease of the eyes, joints, gastrointestinal tract, or neurologic system. True Behçet disease is incredibly uncommon in the United States. When it is diagnosed in Western countries, it takes an attenuated form, most often occurring in women who experience multisystem discomfort rather than identifiable inflammatory disease. End-organ damage is uncommon. Evaluation for Behçet disease in women with vulvar aphthae generally is not indicated, although a directed review of systems is reasonable. The rare patient who experiences frequent recurrence and symptoms of systemic disease should be referred to an ophthalmologist and other relevant specialists to evaluate for inflammatory disease.

 

 

The treatment of vulvar aphthae consists of systemic corticosteroids such as prednisone 40 mg/day for smaller individuals and 60 mg/day for larger women, with follow-up to ensure a good response. Often, the prednisone can be discontinued when pain relents rather than continued through complete healing. Reassurance, without discussing Behçet disease, is paramount, as is pain control. The heavy application of petroleum jelly can decrease pain and prevent urine from touching the ulcer.

Some patients experience recurrent ulcers. A second prescription of prednisone can be provided for immediate reinstitution with onset of symptoms. However, frequent recurrences may require ongoing suppressive medication, with dapsone being the usual first choice. Colchicine often is used, and thalidomide and tumor necrosis factor-a blockers (adalimumab, etanercept, and infliximab) also are extremely beneficial.3,4

 

CASE 4. INCREASED NEUTROPHILS AND NO LACTOBACILLI
A 36-year-old woman visits your office reporting introital itching, vulvar dysuria, and superficial dyspareunia that have lasted 6 months. She has tried over-the-counter antifungal therapy, with only slight improvement while using the cream. Her health is normal otherwise, lacking pain syndromes or abnormalities suggestive of pelvic floor dysfunction. She experienced comfortable sexual activity until 6 months ago.

The only abnormalities apparent on physical examination are redness of the vestibule, medial labia minora, and vaginal walls, with edema of the surrounding skin and no oral lesions (FIGURE 4A). Copious vaginal secretions are visible at the introitus. A wet mount shows a marked increase in neutrophils with scattered parabasal cells (FIGURE 4B). There are no clue cells, lactobacilli, or yeast forms. The patient’s pH level is greater than 6.5. Routine and fungal cultures and molecular studies for chlamydia, trichomonas, and gonorrhea are returned as normal.

Diagnosis: Desquamative inflammatory vaginitis.

Treatment: Clindamycin vaginal cream, 1/2 to 1 full applicator nightly, with a weekly oral fluconazole tablet (200 mg is more easily covered by insurance) to prevent secondary candidiasis. You schedule a follow-up visit in 1 month.

 

Desquamative inflammatory vaginitis (DIV) is described as noninfectious inflammatory vaginitis in a setting of normal estrogen and absence of skin disease of the mucous membranes of the vagina. The condition is characterized by an increase in white blood cells and parabasal cells, and absent lactobacilli, with relatively high vaginal pH. DIV is thought to represent an inflammatory dermatosis of the vaginal epithelium.5 Although some clinicians believe that DIV is actually lichen planus, the latter exhibits erosions as well as redness, nearly always affects the mouth and the vulva, and produces remarkable scarring. DIV does not erode, affect any other skin surfaces, or scar.

Other rare skin diseases that produce erosions and scarring also can be ruled out by the presence of erosions, absence of oral disease, and absence of other mucosal involvement. These diseases include cicatricial pemphigoid, pemphigus vulgaris, Stevens-Johnson syndrome, and toxic epidermal necrolysis. Infectious diseases characterized by inflammation are excluded by culture or molecular studies, and atrophic vaginitis and retained foreign bodies (especially retained tampons) can produce a similar picture.

The vulvar itching and irritation that occur with DIV most likely represent an irritant contact dermatitis, with vaginal secretions serving as the irritant.

How to treat DIV
The management of DIV consists of either topical clindamycin cream (theoretically for its anti-inflammatory rather than antimicrobial properties) or intravaginal corticosteroids, especially hydrocortisone acetate.6 Hydrocortisone can be tried at the low commercially available dose of 25-mg rectal suppositories, which should be inserted into the vagina nightly, or it can be compounded at 100 or 200 mg, if needed. If the condition is recalcitrant, combination therapy can be used.

When signs and symptoms abate, the frequency of use can be decreased, or hydrocortisone can be discontinued and restarted again with any recurrence of discomfort. Many clinicians also prescribe weekly fluconazole to prevent intercurrent candidiasis.

Related article: Successful treatment of chronic vaginitis. Robert L. Barbieri, MD (Editorial, July 2013)

 

CASE 5. PLAQUES ON VULVA AND IN SKIN FOLDS
A 43-year-old woman reports a recalcitrant yeast infection of the vulva, with itching and irritation. She is overweight and diabetic, with mild stress incontinence.

Physical examination reveals a fairly well-demarcated plaque of redness of the vulva and labiocrural folds, with satellite red papules and peripheral peeling (FIGURE 5). An examination of other skin surfaces reveals similar plaques in the gluteal cleft, umbilicus, and axillae as well as under the breasts. A fungal preparation of the vagina and skin is negative. You obtain a fungal culture and prescribe topical and oral antifungal therapy and see the patient again 1 week later. Her condition is unchanged.

Diagnosis: You make a presumptive diagnosis of inverse psoriasis and do a confirmatory punch biopsy.

 

 

Treatment: Clobetasol ointment applied to the skin folds, along with continuation of the topical miconazole cream. A week later, the patient’s condition is remarkably improved, and her biopsy shows psoriasiform dermatitis. You reduce the potency of her corticosteroid, switching to desonide cream sparingly applied daily.

 

Psoriasis is a common skin disease of immunologic origin. The skin is classically red and thick, with heavy white scale produced by rapid turnover of epithelium. However, there are several morphologic types of psoriasis, and anogenital psoriasis is most often of the inverse pattern. Inverse psoriasis preferentially affects skin folds and is frequently mistaken for (and often initially superinfected with) candidiasis. Scale is thin and unapparent, and there often is a shiny, glazed appearance to the skin. Tiny satellite lesions often are visible as well. A skin biopsy of inverse psoriasis often is not diagnostic, showing only nonspecific psoriasiform dermatitis; this does not disprove psoriasis.

Psoriasis is a systemic condition and is associated with metabolic syndrome, carrying an increased risk of overweight, hypertension, diabetes, and cardiovascular disease. Management of these conditions is very important in the treatment of the patient overall.

Unlike lichen planus and lichen sclerosus, scarring is rare with psoriasis, and squamous cell carcinoma generally is unassociated.7,8

Anogenital psoriasis is treated with topical corticosteroids and, when needed, topical vitamin D preparations. Generally, inverse psoriasis is controlled with low-potency topical corticosteroids, with management of secondary infection and irritants. Otherwise, ultraviolet light is a time-honored therapy for psoriasis but not practical for skin folds. It also is difficult for many patients to manage with a busy life. Systemic therapy, including methotrexate and oral retinoids are often used, as are newer biologic agents such as etanercept, adalimumab, infliximab, and ustekinumab.

WE WANT TO HEAR FROM YOU!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue. Send your letter to: [email protected] Please include the city and state in which you practice. Stay in touch! Your feedback is important to us!

Chronic irritation, itching, and pain are only rarely due to infection. These symptoms are more likely to be caused by dermatoses, vaginal abnormalities, and pain syndromes that may be difficult to diagnose. Careful evaluation should include a wet mount and culture to eliminate infection as a cause so that the correct diagnosis can be ascertained and treated.

In Part 2 of this two-part series, we focus on five cases of vulvar dermatologic disruptions:

 

  • atrophic vagina
  • irritant and allergic contact dermatitis
  • complex vulvar aphthosis
  • desquamative inflammatory vaginitis
  • inverse psoriasis.

CASE 1. INTROITAL BURNING AND A FEAR OF BREAST CANCER
A 56-year-old woman visits your office for management of recent-onset introital burning during sexual activity. She reports that her commercial lubricant causes irritation. Topical and oral antifungal therapies have not been beneficial. She has a strong family history of breast cancer.

On examination, she exhibits small, smooth labia minora and experiences pain when a cotton swab is pressed against the vestibule. The vagina is also smooth, with scant secretions. Microscopically, these secretions are almost acellular, with no increase in white blood cells and no clue cells, yeast forms, or lactobacilli. The pH is greater than 6.5, and most epithelial cells are parabasal (FIGURE 1).

You prescribe topical estradiol cream for vaginal use three nights per week, but when the patient returns 1 month later, her condition is unchanged. She explains that she never used the cream after reading the package insert, which reports a risk of breast cancer.

Diagnosis: Atrophic vagina (not atrophic vaginitis, as there is no increase in white blood cells).

Treatment: Re-estrogenization should relieve her symptoms.

Several options for local estrogen replacement are available. Creams include estradiol (Estrace) and conjugated equine estrogen (Premarin), the latter of which is arguably slightly more irritating. These are prescribed at a starting dose of 1 g in the vagina three nights per week. After several weeks, they can be titrated to the lowest frequency that controls symptoms.

The risk of vaginal candidiasis is fairly high during the first 2 or 3 weeks of re-estrogenization, so patients should be warned of this possibility. Also consider prophylactic weekly fluconazole or an azole suppository two or three times a week for the first few weeks. Estradiol tablets (Vagifem) inserted in the vagina are effective, less messy, and more expensive, as is the estradiol ring (Estring), which is inserted and changed quarterly.

It is not unusual for a woman to avoid use of topical estrogen out of fear, or to use insufficient amounts only on the vulva, or to use it for only 1 or 2 weeks.1

Women should be scheduled for a return visit to ensure they have been using the estrogen, their wet mount has normalized, and discomfort has cleared.

Related article: Your menopausal patient's breast biopsy reveals atypical hyperplasia. JoAnn V. Pinkerton, MD (Cases in Menopause; May 2013)

When a woman is reluctant to use local estrogen
We counsel women that small doses of vaginal estrogen used for limited periods of time are unlikely to influence their breast cancer risk and are the most effective treatment for symptoms of atrophy. Usually, this explanation is sufficient to reassure a woman that topical estrogen is safe. Otherwise, use of commercial personal lubricants (silicone-based lubricants are well tolerated) and moisturizers such as Replens and RePhresh can be comforting.

The topical anesthetics lidocaine 2% jelly or lidocaine 5% ointment (which sometimes burns) can minimize pain with sexual activity for those requiring more than lubrication.

Ospemifene (Osphena) is used by some clinicians in this situation, but this medication is labeled as a risk for all of the same contraindications as systemic estrogen, and it is much more expensive than topical estrogen. Ospemifene is an estrogen agonist/antagonist. Although it is the only oral medication indicated for the treatment of menopause-related dyspareunia, the long-term effects on breast cancer risk are unknown. Also, it has an agonist effect on the endometrium and, again, the long-term risk is unknown.

Related article: New treatment option for vulvar and vaginal atrophy. Andrew M. Kaunitz, MD (News for your Practice; May 2013)

Fluconazole use is contraindicated with ospemifene, as is the use of any estrogen products.

 

CASE 2. RECALCITRANT ITCHING, BURNING, AND REDNESS
A 25-year-old woman reports anogenital itching, burning, and redness, which have been present for 3 months. She says she developed a yeast infection after antibiotic therapy for a dental infection; the yeast infection was treated with terconazole. She reports an allergic reaction to the terconazole, with immediate severe burning, redness, and swelling. The clobetasol cream she was given to use twice daily also caused burning, so she discontinued it. Her symptoms improved when she tried cool soaks and applied topical benzocaine gel as a local anesthetic. However,

 

 

2 weeks later, she experienced increasing redness, itching, and burning. Although the benzocaine relieved these symptoms, it required almost continual reapplication for comfort.

A physical examination of the vulva reveals generalized, poorly demarcated redness, edema, and superficial erosions (FIGURE 2).

Diagnosis: Irritant contact dermatitis (as opposed to allergic contact dermatitis) associated with the use of terconazole and clobetasol. This was followed by allergic contact dermatitis in association with benzocaine.

Treatment: Withdrawal of benzocaine, with reinitiation of cool soaks and a switch to clobetasol ointment rather than cream. Nighttime sedation allows the patient to sleep through the itching and gradually allows her skin to heal.

 

Contact dermatitis is a fairly common cause of vulvar irritation, with two main types:

 

  • Irritant contact dermatitis—The most common form, it occurs in any individual exposed to an irritating substance in sufficient quantity or frequency. Irritant contact dermatitis is characterized mostly by sensations of rawness or burning and generally is caused by urine, feces, perspiration, friction, alcohols in topical creams, overwashing, and use of harsh soaps.
  • Allergic contact dermatitis—This form is characterized by itching, although secondary pain and burning from scratching and blistering can occur as well. Common allergens in the genital area include benzocaine, diphenhydramine (Benadryl), neomycin in triple antibiotic ointment (Neosporin), and latex. Allergic contact dermatitis occurs after 1 or 2 weeks of initial exposure or 1 or 2 days after re-exposure.

The diagnosis of an irritant or allergic contact dermatitis can be based on a history of incontinence, application of high-risk substances, or inappropriate washing. Management generally involves ­discontinuation of all panty liners and topical agents except for water, with a topical steroid ointment used twice a day and pure petroleum jelly used as often as necessary for comfort. Nighttime sedation to allow a reprieve from rubbing and scratching may be helpful, and narcotic pain medications may be useful for the first 1 to 2 weeks of treatment.

Women who fail to respond to treatment should be referred for patch testing by a
dermatologist.

Related article: Vulvar pain syndromes: Making the correct diagnosis. Neal M. Lonky, MD, MPH; Libby Edwards, MD; Jennifer Gunter, MD; Hope K. Haefner, MD (Roundtable, part 1 of 3; September 2011)

 

CASE 3. TEENAGER WITH VULVAR PAIN AND SORES
A woman brings her 13-year-old daughter to your office for treatment of sudden-onset vulvar pain and sores. The child developed a sore throat and low-grade fever 3 days earlier, with vulvar pain and vulvar dysuria the next day. The pediatrician diagnosed a herpes simplex virus infection and prescribed oral acyclovir, but the girl’s condition has not improved, and the mother believes her daughter’s claims of sexual abstinence.

The girl is otherwise healthy, aside from a history of trivial oral canker sores without arthritis, headaches, abdominal pain, eye pain, or vision changes.

Physical examination of the vulva reveals soft, painful, well-demarcated ulcers with a white fibrin base (FIGURE 3).

Diagnosis: Complex aphthosis. Further testing is unnecessary.

Treatment: Prednisone 40 mg/day plus hydrocodone in usual doses of 5/325, one or two tablets every 4 to 6 hours, as needed; topical petroleum jelly (especially before urination); and sitz baths. When the patient returns 1 week later, she is much improved.

 

Aphthae are believed to be of hyperimmune origin, often precipitated by a viral syndrome. They are most common in girls aged 9 to 18 years. Vulvar aphthae are triggered by various viral infections, including Epstein-Barr.2 The offending virus is not located in the ulcer proper, however, but is identified serologically.

Aphthae are uncommon and under-recognized on the vulva, and genital aphthae are usually much larger than oral aphthae. Most patients initially are mistakenly evaluated and treated for sexually transmitted disease, but the large, well-demarcated, painful, nonindurated deep nature of the ulcer is pathognomonic for an aphthous ulcer.

The presence of oral and genital aphthae does not constitute a diagnosis of Behçet disease, an often-devastating systemic inflammatory condition occurring almost exclusively in men in the Middle and Far East. The diagnosis of Behçet disease requires the identification of objective inflammatory disease of the eyes, joints, gastrointestinal tract, or neurologic system. True Behçet disease is incredibly uncommon in the United States. When it is diagnosed in Western countries, it takes an attenuated form, most often occurring in women who experience multisystem discomfort rather than identifiable inflammatory disease. End-organ damage is uncommon. Evaluation for Behçet disease in women with vulvar aphthae generally is not indicated, although a directed review of systems is reasonable. The rare patient who experiences frequent recurrence and symptoms of systemic disease should be referred to an ophthalmologist and other relevant specialists to evaluate for inflammatory disease.

 

 

The treatment of vulvar aphthae consists of systemic corticosteroids such as prednisone 40 mg/day for smaller individuals and 60 mg/day for larger women, with follow-up to ensure a good response. Often, the prednisone can be discontinued when pain relents rather than continued through complete healing. Reassurance, without discussing Behçet disease, is paramount, as is pain control. The heavy application of petroleum jelly can decrease pain and prevent urine from touching the ulcer.

Some patients experience recurrent ulcers. A second prescription of prednisone can be provided for immediate reinstitution with onset of symptoms. However, frequent recurrences may require ongoing suppressive medication, with dapsone being the usual first choice. Colchicine often is used, and thalidomide and tumor necrosis factor-a blockers (adalimumab, etanercept, and infliximab) also are extremely beneficial.3,4

 

CASE 4. INCREASED NEUTROPHILS AND NO LACTOBACILLI
A 36-year-old woman visits your office reporting introital itching, vulvar dysuria, and superficial dyspareunia that have lasted 6 months. She has tried over-the-counter antifungal therapy, with only slight improvement while using the cream. Her health is normal otherwise, lacking pain syndromes or abnormalities suggestive of pelvic floor dysfunction. She experienced comfortable sexual activity until 6 months ago.

The only abnormalities apparent on physical examination are redness of the vestibule, medial labia minora, and vaginal walls, with edema of the surrounding skin and no oral lesions (FIGURE 4A). Copious vaginal secretions are visible at the introitus. A wet mount shows a marked increase in neutrophils with scattered parabasal cells (FIGURE 4B). There are no clue cells, lactobacilli, or yeast forms. The patient’s pH level is greater than 6.5. Routine and fungal cultures and molecular studies for chlamydia, trichomonas, and gonorrhea are returned as normal.

Diagnosis: Desquamative inflammatory vaginitis.

Treatment: Clindamycin vaginal cream, 1/2 to 1 full applicator nightly, with a weekly oral fluconazole tablet (200 mg is more easily covered by insurance) to prevent secondary candidiasis. You schedule a follow-up visit in 1 month.

 

Desquamative inflammatory vaginitis (DIV) is described as noninfectious inflammatory vaginitis in a setting of normal estrogen and absence of skin disease of the mucous membranes of the vagina. The condition is characterized by an increase in white blood cells and parabasal cells, and absent lactobacilli, with relatively high vaginal pH. DIV is thought to represent an inflammatory dermatosis of the vaginal epithelium.5 Although some clinicians believe that DIV is actually lichen planus, the latter exhibits erosions as well as redness, nearly always affects the mouth and the vulva, and produces remarkable scarring. DIV does not erode, affect any other skin surfaces, or scar.

Other rare skin diseases that produce erosions and scarring also can be ruled out by the presence of erosions, absence of oral disease, and absence of other mucosal involvement. These diseases include cicatricial pemphigoid, pemphigus vulgaris, Stevens-Johnson syndrome, and toxic epidermal necrolysis. Infectious diseases characterized by inflammation are excluded by culture or molecular studies, and atrophic vaginitis and retained foreign bodies (especially retained tampons) can produce a similar picture.

The vulvar itching and irritation that occur with DIV most likely represent an irritant contact dermatitis, with vaginal secretions serving as the irritant.

How to treat DIV
The management of DIV consists of either topical clindamycin cream (theoretically for its anti-inflammatory rather than antimicrobial properties) or intravaginal corticosteroids, especially hydrocortisone acetate.6 Hydrocortisone can be tried at the low commercially available dose of 25-mg rectal suppositories, which should be inserted into the vagina nightly, or it can be compounded at 100 or 200 mg, if needed. If the condition is recalcitrant, combination therapy can be used.

When signs and symptoms abate, the frequency of use can be decreased, or hydrocortisone can be discontinued and restarted again with any recurrence of discomfort. Many clinicians also prescribe weekly fluconazole to prevent intercurrent candidiasis.

Related article: Successful treatment of chronic vaginitis. Robert L. Barbieri, MD (Editorial, July 2013)

 

CASE 5. PLAQUES ON VULVA AND IN SKIN FOLDS
A 43-year-old woman reports a recalcitrant yeast infection of the vulva, with itching and irritation. She is overweight and diabetic, with mild stress incontinence.

Physical examination reveals a fairly well-demarcated plaque of redness of the vulva and labiocrural folds, with satellite red papules and peripheral peeling (FIGURE 5). An examination of other skin surfaces reveals similar plaques in the gluteal cleft, umbilicus, and axillae as well as under the breasts. A fungal preparation of the vagina and skin is negative. You obtain a fungal culture and prescribe topical and oral antifungal therapy and see the patient again 1 week later. Her condition is unchanged.

Diagnosis: You make a presumptive diagnosis of inverse psoriasis and do a confirmatory punch biopsy.

 

 

Treatment: Clobetasol ointment applied to the skin folds, along with continuation of the topical miconazole cream. A week later, the patient’s condition is remarkably improved, and her biopsy shows psoriasiform dermatitis. You reduce the potency of her corticosteroid, switching to desonide cream sparingly applied daily.

 

Psoriasis is a common skin disease of immunologic origin. The skin is classically red and thick, with heavy white scale produced by rapid turnover of epithelium. However, there are several morphologic types of psoriasis, and anogenital psoriasis is most often of the inverse pattern. Inverse psoriasis preferentially affects skin folds and is frequently mistaken for (and often initially superinfected with) candidiasis. Scale is thin and unapparent, and there often is a shiny, glazed appearance to the skin. Tiny satellite lesions often are visible as well. A skin biopsy of inverse psoriasis often is not diagnostic, showing only nonspecific psoriasiform dermatitis; this does not disprove psoriasis.

Psoriasis is a systemic condition and is associated with metabolic syndrome, carrying an increased risk of overweight, hypertension, diabetes, and cardiovascular disease. Management of these conditions is very important in the treatment of the patient overall.

Unlike lichen planus and lichen sclerosus, scarring is rare with psoriasis, and squamous cell carcinoma generally is unassociated.7,8

Anogenital psoriasis is treated with topical corticosteroids and, when needed, topical vitamin D preparations. Generally, inverse psoriasis is controlled with low-potency topical corticosteroids, with management of secondary infection and irritants. Otherwise, ultraviolet light is a time-honored therapy for psoriasis but not practical for skin folds. It also is difficult for many patients to manage with a busy life. Systemic therapy, including methotrexate and oral retinoids are often used, as are newer biologic agents such as etanercept, adalimumab, infliximab, and ustekinumab.

WE WANT TO HEAR FROM YOU!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue. Send your letter to: [email protected] Please include the city and state in which you practice. Stay in touch! Your feedback is important to us!

References

 

 

  1. Kingsberg SA, Krychman ML. Resistance and barriers to local estrogen therapy in women with atrophic vaginitis.
    J Sex Med. 2013;10(6):1567–1574.
  2. Huppert JS, Gerber MA, Deitch HR, et al. Vulvar ulcers in young females: A manifestation of aphthosis. J Pediatr Adolesc Gynecol. 2006;19(3):195–204.
  3. O’Neill ID. Efficacy of tumour necrosis factor-a antagonists in aphthous ulceration: Review of published individual patient data. J Eur Acad Dermatol Venereol. 2012;26(2):231–235.
  4. Sanchez-Cano D, Callejas-Rubio JL, Ruiz-Villaverde R, Ortego-Centeno N. Recalcitrant, recurrent aphthous stomatitis successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2009;23(2):206.
  5. Stockdale CK. Clinical spectrum of desquamative inflammatory vaginitis. Curr Infect Dis Rep. 2010;12(6):479–483.
  6. Sobel JD, Reichman O, Misra D, Yoo W. Prognosis and treatment of desquamative inflammatory vaginitis. Obstet Gynecol. 2011;117(4):850–855.
  7. Albert S, Neill S, Derrick EK, Calonje E. Psoriasis associated with vulvar scarring. Clin Exp Dermatol. 2004;29(4):354–356.
  8. Boffetta P, Gridley G, Lindelöf B. Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol. 2001;117(6):1531–1537.
References

 

 

  1. Kingsberg SA, Krychman ML. Resistance and barriers to local estrogen therapy in women with atrophic vaginitis.
    J Sex Med. 2013;10(6):1567–1574.
  2. Huppert JS, Gerber MA, Deitch HR, et al. Vulvar ulcers in young females: A manifestation of aphthosis. J Pediatr Adolesc Gynecol. 2006;19(3):195–204.
  3. O’Neill ID. Efficacy of tumour necrosis factor-a antagonists in aphthous ulceration: Review of published individual patient data. J Eur Acad Dermatol Venereol. 2012;26(2):231–235.
  4. Sanchez-Cano D, Callejas-Rubio JL, Ruiz-Villaverde R, Ortego-Centeno N. Recalcitrant, recurrent aphthous stomatitis successfully treated with adalimumab. J Eur Acad Dermatol Venereol. 2009;23(2):206.
  5. Stockdale CK. Clinical spectrum of desquamative inflammatory vaginitis. Curr Infect Dis Rep. 2010;12(6):479–483.
  6. Sobel JD, Reichman O, Misra D, Yoo W. Prognosis and treatment of desquamative inflammatory vaginitis. Obstet Gynecol. 2011;117(4):850–855.
  7. Albert S, Neill S, Derrick EK, Calonje E. Psoriasis associated with vulvar scarring. Clin Exp Dermatol. 2004;29(4):354–356.
  8. Boffetta P, Gridley G, Lindelöf B. Cancer risk in a population-based cohort of patients hospitalized for psoriasis in Sweden. J Invest Dermatol. 2001;117(6):1531–1537.
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Few ObGyn clinicians have faced a patient with a cesarean-scar pregnancy (CSP). Those few were confronted with a management dilemma. Continue the gestation, which would expose the mother to an elevated risk of heavy bleeding? Or terminate the pregnancy? And if termination is the patient’s choice, what is the most effective method?

The literature contains more than 750 reports of CSP, ranging from a single sporadic case to a series of one to two dozen cases. It is impossible to make sense of the numerous treatments used in the past, which were “tested” on extremely small numbers of patients (sometimes as few as one). In this article, we formulate a management plan for the diagnosis and treatment of CSP based on an in-depth review of the published literature and our personal experience in treating more than four dozen patients with CSP.

We’re all familiar with the “epidemic” of cesarean deliveries in this country, including late consequences of cesarean such as placenta previa and morbidly adherent placenta. One of the long-term consequences of cesarean delivery—the first-trimester CSP—is less well known and documented.

Our in-depth review of 751 CSP cases found no less than 30 published therapeutic approaches.1 No consensus exists as to management guidelines. We have formulated this clinical guide, based on the literature and our experience managing CSP, for clinicians who encounter this dangerous form of pregnancy.2

DIAGNOSIS REQUIRES TRANSVAGINAL SONOGRAPHY
Transvaginal sonography (TVS) is thought to be the best and first-line diagnostic tool, with magnetic resonance imaging (MRI) reserved for cases in which there is a diagnostic problem.

In making a diagnosis, consider two main differential diagnoses:

 

  • Cervical pregnancy—This type of gestation is more likely to occur in women with no history of cesarean delivery
  • Spontaneous miscarriage in progress—In a number of cases, the miscarriage happened to be caught on imaging as it passed the area where the CSP usually resides. Because there is no live embryo or fetus in spontaneous miscarriage, a heartbeat cannot be documented.

Components of diagnosis by TVS
Accurate identification of CSP depends on the following sonographic criteria:

 

  • empty uterine cavity and cervical canal (FIGURE 1A)
  • close proximity of the gestational sac and the placenta to the anterior uterine surface within the scar or niche of the previous cesarean delivery (FIGURES 1B, 2A, and 2B)
  • color flow signals between the posterior bladder wall and the gestation within the placenta (FIGURES 1B, 2B, and 3B)
  • abundant blood flow around the gestational sac, at times morphing into an arteriovenous malformation with a high peak systolic velocity blood flow demonstrable on pulsed Doppler.

Our analysis of 751 cases of CSP found that almost a third—30%—were misdiagnosed, contributing to a large number of treatment complications. Most of these complications could have been avoided if diagnosis had been early and correct. The earlier the diagnosis, the better the outcome seemed to be. This was true even when treatment modalities with slightly higher complication rates were used in very early gestation.

Related articles:
• Is the hCG discriminatory zone a reliable indicator of intrauterine or ectopic pregnancy? Andrew M. Kaunitz, MD (Examining the Evidence; February 2012)
Can a single progesterone test distinguish viable and nonviable pregnancies accurately in women with pain or bleeding? Linda R. Chambliss, MD, MPH (Examining the Evidence; March 2013)

THOROUGH COUNSELING OF THE PATIENT IS PARAMOUNT
Once a diagnosis of CSP has been established, the patient should be counseled about her options. The presence of a live CSP requires immediate and decisive action to prevent further growth of the embryo or fetus. Literature from the past decade, particularly from the past several years, makes evidence-based counseling possible.

In general, treatment should be individualized, based on the patient’s age, number of previous cesarean deliveries, number of children, and the expertise of the clinicians managing her care. Options include:

 

  • termination of the pregnancy
  • continuation of the pregnancy with the possibility of delivering a live offspring, provided the patient understands that a morbidly adherent placenta may occur, often necessitating emergency hysterectomy.3,4

MANAGEMENT APPROACHES
Most treatment regimens and combinations thereof can be classified as one of the following:

 

  • Surgical—requiring general anesthesia and either laparotomy with excision or hysterectomy, or laparoscopic or hysteroscopic excision followed by dilation and curettage (D&C).
  • Minimally invasive—involving local injection of methotrexate or potassium chloride or systemic intervention, involving a major procedure such as uterine artery embolization in combination with a less complicated one: intramuscular injection of methotrexate in a single or a multidose regimen.

A variety of simultaneous as well as sequential combination treatments also were used. More recently, an ingenious adjunct to treatment is gaining attention: insertion and inflation of a Foley balloon catheter to prevent or tamponade bleeding.

 

 

A large number of treatments described in the literature—and their different combinations—have been reported as relatively small case series. Gynecologic surgeons generally perform D&C, laparoscopy, and hysteroscopy or laparotomy as the first-line approach. Obstetricians, radiologists, and in vitro fertilization specialists usually prefer systemic, parenteral administration of methotrexate or ultrasound-guided local methotrexate (or potassium chloride) as an injection into the gestational sac. On occasion, the help of an interventional radiologist was requested to embolize the area of the CSP through the uterine arteries.

POTENTIAL COMPLICATIONS
In our analysis of 751 cases of CSP, we used a rigorous definition of complication, which included an immediate or delayed need for a secondary treatment for blood loss exceeding 200 mL or requiring blood transfusion. If general anesthesia or major surgery was required, we classified that need as a complication.

Utilizing these criteria, we observed an overall complication rate of 44.1% (331 of 751 cases).1

Complications occurred most often when the following treatment modalities were used alone:

 

  • single systemic dose of methotrexate
  • D&C
  • uterine artery embolization.

Of the 751 cases reviewed, 21.8% resulted in major surgery or interventional radiology procedures (primary or emergency). The total planned primary (nonemergency) interventions performed were 66 (8.7%), which included 3 hysterectomies, 14 laparotomies, and 49 uterine artery embolizations or ligations. There were 98 (13.0%) emergency interventions, which included 36 hysterectomies, 40 laparotomies, and 22 uterine artery embolizations or ligations.1

Related article: Eight tools for improving obstetric patient safety and unit performance. Henry M. Lerner, MD (Professional Liability; March 2014)

NINE TREATMENTS AND THEIR COMPLICATIONS
1. Systemic, single-dose methotrexate
The usual protocols were 1 mg/kg of body weight or 50 mg/m2 of body surface area. This treatment was associated with a complication rate of 64.6%, mostly because it required a second treatment when the fetal heart beat did not cease after several days.1

We speculate that the high failure rate with this treatment may be caused by its slow action and questionable ability to stop cardiac activity and placental expansion. The expected result can take days, and all the while the gestational sac, the embryo or fetus, and its vascularity are growing. Secondary treatment has to address a larger gestation with more abundant vascularization.

2. Systemic, multidose, sequential methotrexate
In this regimen, the amounts of methotrexate injected are similar to the dose for the single-dose regimen. Two to three intramuscular injections (1 mg/kg of body weight or 50 mg/mm2 of surface area) are given at an interval of 2 or 3 days over the course of a week. Be aware of the cumulative adverse effects of this drug on the liver and bone marrow—and the fact that even multidose treatment can fail.1

We found it impossible to assess the complication rate associated with this approach because it was often used in conjunction with another “first-line” treatment or after it. However, it is clear that methotrexate can be combined with other, mostly nonsurgical treatments.

3. Suction aspiration or D&C, alone or in combination
This option requires general anesthesia. The 305 cases involving this treatment had a mean complication rate of about 62% (range, 29%–86%).1 This approach caused the greatest number of bleeding complications, necessitating a third-line treatment that almost always was surgical.

At delivery or the time of spontaneous abortion, the multilayered myometrial grid in the uterine body is able to contain bleeding vessels after placental separation. However, in CSP, the exposed vessels in the cervical scar tissue bleed because there is no muscle grid to contract and contain the profuse bleeding.

If you choose D&C or aspiration, have blood products available and a Foley balloon catheter handy! In several reports, a Foley balloon catheter was used as backup after significant bleeding occurred following curettage.5,6

In one of the series involving 45 cases treated by methotrexate followed by suction curettage, mean blood loss was significant at 707 mL (standard deviation, 642 mL; range, 100–2,000 mL), and treatment failed in three patients despite insertion of a Foley balloon catheter.

4. Uterine artery embolization, alone or in combination
This treatment requires general anesthesia. The complication rate was 47% among the 64 cases described in the literature.1 Uterine artery embolization appeared to work better when it was combined with other noninvasive treatments. It probably is not the best first-line treatment because the delay between treatment and effect allows the gestation to grow and vascularity to increase. And if uterine artery embolization fails, the clinician must contend with a larger gestation.

5. Excision by laparotomy, alone or in combination with hysteroscopy
General anesthesia is required. Of the 18 cases described in the literature, only five complications were reported—and only when used in an emergency situation.1

 

 

6. Laparoscopic excision
Again, general anesthesia is required. Fifteen of the 49 cases (30.6%) described in the literature involved complications, but only one of five cases (20%) experienced complications if hysteroscopy and laparoscopy were combined. Small numbers may not allow meaningful evaluation of the latter approach.1

7. Operative hysteroscopy, alone or in combination
General anesthesia is required. The overall complication rate for 108 cases was 13.8%. However, if hysteroscopy was combined with transabdominal ultrasound guidance (as it was in nine cases), no complications were noted. If hysteroscopy was combined with mifepristone, the complication rate was 17%.1 It appears that, when it is performed by an experienced clinician with ultrasound guidance, hysteroscopy may be a reasonable operative solution to CSP.

8. Intragestational-sac injection of methotrexate or potassium chloride, with ultrasound guidance
No anesthesia is required. This approach (FIGURE 4) had the fewest and least-involved complications. Of 83 cases, only 9 (10.8%) involved complications.

Cases performed with transabdominal sonography guidance had a slighter higher complication rate (15%) than those using TVS guidance.1

Because local injections are performed without general anesthesia and provide a final treatment by stopping heart activity, they appear to be the most effective intervention and may be especially useful when future fertility is desired.

9. Use of a Foley balloon catheter
Inserting a Foley balloon catheter and inflating it at the site of the CSP is an ­ingenious, relatively new approach.1,2,5–7 The catheters come with balloons of different capacity (FIGURE 5A). They can be used alone (usually in gestations of 5–7 weeks) in the hope of stopping the evolution of the pregnancy by placing pressure on a small gestational sac. Even so, this approach is almost always used in a planned fashion in conjunction with another treatment or as backup if bleeding occurs.

Our impression of the value of the balloon catheters is positive. We suggest the French-12 size 10-mL silicone balloon catheter (prices range from $2 to $20), although we used a French-14 catheter with a 30-mL balloon successfully in a case of an 8-week CSP.

Insert the catheter using real-time transabdominal sonographic guidance when the patient has a comfortably full bladder. One also can switch to TVS guidance to allow for more precise placement and assess the pressure, avoiding overinflation of the balloon (FIGURE 5B).

There is no information in the literature about how long such a catheter should be kept in place. In our experience, 24 to 48 hours is the preferred duration, with the outer end of the catheter fastened to the patient’s thigh. We also provide antibiotic coverage and reevaluate the effect in 2 days or as needed. General anesthesia is not required.

KEY TAKEAWAYS
Is there any single and effective treatment protocol? Probably not. Our management approach is presented as an algorithm (FIGURE 6).

We also offer the following guidelines:

 

  • Do not confuse CSP with ectopic pregnancy. Such nomenclature has caused some referring physicians to simply use methotrexate protocols developed on “garden variety” tubal ectopic pregnancies, which not only failed but yielded disastrous results.
  • Early diagnosis matters. TVS is the most effective and preferred diagnostic tool. Delay in the diagnosis delays treatment, increasing the possibility of complications.
  • Cervical pregnancy is rare. In a patient who has had a cesarean delivery, a low chorionic sac is almost always a CSP.
  • A key first step: Determine whether heart activity is present, and avoid methotrexate if no heart activity is observed.
  • Counsel the patient. If heart activity is documented, provide evidence-based counseling about the patient’s options.
  • Act fast. If continuation of the pregnancy is not desired, provide a reliable treatment that stops the embryonic or fetal heart beat without delay. Early treatment minimizes complications.
  • Avoid single treatments unlikely to be effective, including D&C, suction curettage, single-dose intramuscular methotrexate, and uterine artery embolization applied alone.
  • Keep a catheter at hand. Foley balloon tamponade to prevent or treat bleeding is a useful adjunct to have within easy reach.
  • Consider combination treatments, as they may provide the best results.
  • Fully inform the patient of the risks of pregnancy continuation. If a patient elects to continue the pregnancy, schedule an additional counseling session in which a more detailed overview of the anticipated clinical road is thoroughly explained.

WE WANT TO HEAR FROM YOU!
Share your thoughts on this article. Send your letter to the Editor to: [email protected] Please include the city and state in which you practice. 

References

 

 

  1. Timor-Tritsch IE, Monteagudo A. Unforeseen consequences of the increasing rate of cesarean deliveries: early placenta accreta and cesarean scar pregnancy. A review. [published correction appears in Am J Obstet Gynecol. 2014;210(4):371–374.] Am J Obstet Gynecol. 2012;207(1):14–29.
  2. Timor-Tritsch IE, Monteagudo A, Santos R, Tsymbal T, Pineda G, Arslan AA. The diagnosis, treatment, and follow-up of cesarean scar pregnancy. Am J Obstet Gynecol. 2012;207(1):44.e1–e13.
  3. Ballas J, Pretorius D, Hull AD, Resnik R, Ramos GA. Identifying sonographic markers for placenta accreta in the first trimester. J Ultrasound Med. 2012;31(11):1835–1841.
  4. Timor-Tritsch IE, Monteagudo A, Cali P, et al. Cesarean scar pregnancy and early placenta accreta share a common histology. Ultrasound Obstet Gynecol. 2014;43(4):383–395.
  5. Yu XL, Zhang N, Zuo WL. Cesarean scar pregnancy: An analysis of 100 cases [in Chinese]. Zhonghua Yi Xue Za Zhi. 2011;91(45):3186–3189.
  6. Jiang T, Liu G, Huang L, Ma H, Zhang S. Methotrexate therapy followed by suction curettage followed by Foley tamponade for cesarean scar pregnancy. Eur J Obstet Gynecol Reprod Biol. 2011;156(2):209–211.
  7. Hamilton BE, Martin JA, Ventura SJ. Births: Preliminary data for 2012. Natl Vital Stat Rep. 2013;62(3):1–20.
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Ilan E. Timor-Tritsch, MD, is Professor and Director of ObGyn Imaging at New York University Medical Center in New York, New York.

Ana Monteagudo, MD;  is Professor of Obstetrics and Gynecology and Director of Maternal Fetal Medicine at New York University School of Medicine in New York, New York.

Steven R. Goldstein, MD, is Professor of Obstetrics and Gynecology at New York University School of Medicine and Director of Gynecologic Ultrasound and Co-Director of Bone Densitometry at New York University Medical Center in New York, New York. He serves on the OBG Management Board of Editors.

Drs. Timor-Tritsch and Monteagudo report no financial relationships relevant to this article. Dr. Goldstein reports that he is a consultant for Cook Ob/Gyn and Philips Ultrasound.

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Ilan E. Timor-Tritsch, MD, is Professor and Director of ObGyn Imaging at New York University Medical Center in New York, New York.

Ana Monteagudo, MD;  is Professor of Obstetrics and Gynecology and Director of Maternal Fetal Medicine at New York University School of Medicine in New York, New York.

Steven R. Goldstein, MD, is Professor of Obstetrics and Gynecology at New York University School of Medicine and Director of Gynecologic Ultrasound and Co-Director of Bone Densitometry at New York University Medical Center in New York, New York. He serves on the OBG Management Board of Editors.

Drs. Timor-Tritsch and Monteagudo report no financial relationships relevant to this article. Dr. Goldstein reports that he is a consultant for Cook Ob/Gyn and Philips Ultrasound.

Author and Disclosure Information

 

Ilan E. Timor-Tritsch, MD, is Professor and Director of ObGyn Imaging at New York University Medical Center in New York, New York.

Ana Monteagudo, MD;  is Professor of Obstetrics and Gynecology and Director of Maternal Fetal Medicine at New York University School of Medicine in New York, New York.

Steven R. Goldstein, MD, is Professor of Obstetrics and Gynecology at New York University School of Medicine and Director of Gynecologic Ultrasound and Co-Director of Bone Densitometry at New York University Medical Center in New York, New York. He serves on the OBG Management Board of Editors.

Drs. Timor-Tritsch and Monteagudo report no financial relationships relevant to this article. Dr. Goldstein reports that he is a consultant for Cook Ob/Gyn and Philips Ultrasound.

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Related Articles

Few ObGyn clinicians have faced a patient with a cesarean-scar pregnancy (CSP). Those few were confronted with a management dilemma. Continue the gestation, which would expose the mother to an elevated risk of heavy bleeding? Or terminate the pregnancy? And if termination is the patient’s choice, what is the most effective method?

The literature contains more than 750 reports of CSP, ranging from a single sporadic case to a series of one to two dozen cases. It is impossible to make sense of the numerous treatments used in the past, which were “tested” on extremely small numbers of patients (sometimes as few as one). In this article, we formulate a management plan for the diagnosis and treatment of CSP based on an in-depth review of the published literature and our personal experience in treating more than four dozen patients with CSP.

We’re all familiar with the “epidemic” of cesarean deliveries in this country, including late consequences of cesarean such as placenta previa and morbidly adherent placenta. One of the long-term consequences of cesarean delivery—the first-trimester CSP—is less well known and documented.

Our in-depth review of 751 CSP cases found no less than 30 published therapeutic approaches.1 No consensus exists as to management guidelines. We have formulated this clinical guide, based on the literature and our experience managing CSP, for clinicians who encounter this dangerous form of pregnancy.2

DIAGNOSIS REQUIRES TRANSVAGINAL SONOGRAPHY
Transvaginal sonography (TVS) is thought to be the best and first-line diagnostic tool, with magnetic resonance imaging (MRI) reserved for cases in which there is a diagnostic problem.

In making a diagnosis, consider two main differential diagnoses:

 

  • Cervical pregnancy—This type of gestation is more likely to occur in women with no history of cesarean delivery
  • Spontaneous miscarriage in progress—In a number of cases, the miscarriage happened to be caught on imaging as it passed the area where the CSP usually resides. Because there is no live embryo or fetus in spontaneous miscarriage, a heartbeat cannot be documented.

Components of diagnosis by TVS
Accurate identification of CSP depends on the following sonographic criteria:

 

  • empty uterine cavity and cervical canal (FIGURE 1A)
  • close proximity of the gestational sac and the placenta to the anterior uterine surface within the scar or niche of the previous cesarean delivery (FIGURES 1B, 2A, and 2B)
  • color flow signals between the posterior bladder wall and the gestation within the placenta (FIGURES 1B, 2B, and 3B)
  • abundant blood flow around the gestational sac, at times morphing into an arteriovenous malformation with a high peak systolic velocity blood flow demonstrable on pulsed Doppler.

Our analysis of 751 cases of CSP found that almost a third—30%—were misdiagnosed, contributing to a large number of treatment complications. Most of these complications could have been avoided if diagnosis had been early and correct. The earlier the diagnosis, the better the outcome seemed to be. This was true even when treatment modalities with slightly higher complication rates were used in very early gestation.

Related articles:
• Is the hCG discriminatory zone a reliable indicator of intrauterine or ectopic pregnancy? Andrew M. Kaunitz, MD (Examining the Evidence; February 2012)
Can a single progesterone test distinguish viable and nonviable pregnancies accurately in women with pain or bleeding? Linda R. Chambliss, MD, MPH (Examining the Evidence; March 2013)

THOROUGH COUNSELING OF THE PATIENT IS PARAMOUNT
Once a diagnosis of CSP has been established, the patient should be counseled about her options. The presence of a live CSP requires immediate and decisive action to prevent further growth of the embryo or fetus. Literature from the past decade, particularly from the past several years, makes evidence-based counseling possible.

In general, treatment should be individualized, based on the patient’s age, number of previous cesarean deliveries, number of children, and the expertise of the clinicians managing her care. Options include:

 

  • termination of the pregnancy
  • continuation of the pregnancy with the possibility of delivering a live offspring, provided the patient understands that a morbidly adherent placenta may occur, often necessitating emergency hysterectomy.3,4

MANAGEMENT APPROACHES
Most treatment regimens and combinations thereof can be classified as one of the following:

 

  • Surgical—requiring general anesthesia and either laparotomy with excision or hysterectomy, or laparoscopic or hysteroscopic excision followed by dilation and curettage (D&C).
  • Minimally invasive—involving local injection of methotrexate or potassium chloride or systemic intervention, involving a major procedure such as uterine artery embolization in combination with a less complicated one: intramuscular injection of methotrexate in a single or a multidose regimen.

A variety of simultaneous as well as sequential combination treatments also were used. More recently, an ingenious adjunct to treatment is gaining attention: insertion and inflation of a Foley balloon catheter to prevent or tamponade bleeding.

 

 

A large number of treatments described in the literature—and their different combinations—have been reported as relatively small case series. Gynecologic surgeons generally perform D&C, laparoscopy, and hysteroscopy or laparotomy as the first-line approach. Obstetricians, radiologists, and in vitro fertilization specialists usually prefer systemic, parenteral administration of methotrexate or ultrasound-guided local methotrexate (or potassium chloride) as an injection into the gestational sac. On occasion, the help of an interventional radiologist was requested to embolize the area of the CSP through the uterine arteries.

POTENTIAL COMPLICATIONS
In our analysis of 751 cases of CSP, we used a rigorous definition of complication, which included an immediate or delayed need for a secondary treatment for blood loss exceeding 200 mL or requiring blood transfusion. If general anesthesia or major surgery was required, we classified that need as a complication.

Utilizing these criteria, we observed an overall complication rate of 44.1% (331 of 751 cases).1

Complications occurred most often when the following treatment modalities were used alone:

 

  • single systemic dose of methotrexate
  • D&C
  • uterine artery embolization.

Of the 751 cases reviewed, 21.8% resulted in major surgery or interventional radiology procedures (primary or emergency). The total planned primary (nonemergency) interventions performed were 66 (8.7%), which included 3 hysterectomies, 14 laparotomies, and 49 uterine artery embolizations or ligations. There were 98 (13.0%) emergency interventions, which included 36 hysterectomies, 40 laparotomies, and 22 uterine artery embolizations or ligations.1

Related article: Eight tools for improving obstetric patient safety and unit performance. Henry M. Lerner, MD (Professional Liability; March 2014)

NINE TREATMENTS AND THEIR COMPLICATIONS
1. Systemic, single-dose methotrexate
The usual protocols were 1 mg/kg of body weight or 50 mg/m2 of body surface area. This treatment was associated with a complication rate of 64.6%, mostly because it required a second treatment when the fetal heart beat did not cease after several days.1

We speculate that the high failure rate with this treatment may be caused by its slow action and questionable ability to stop cardiac activity and placental expansion. The expected result can take days, and all the while the gestational sac, the embryo or fetus, and its vascularity are growing. Secondary treatment has to address a larger gestation with more abundant vascularization.

2. Systemic, multidose, sequential methotrexate
In this regimen, the amounts of methotrexate injected are similar to the dose for the single-dose regimen. Two to three intramuscular injections (1 mg/kg of body weight or 50 mg/mm2 of surface area) are given at an interval of 2 or 3 days over the course of a week. Be aware of the cumulative adverse effects of this drug on the liver and bone marrow—and the fact that even multidose treatment can fail.1

We found it impossible to assess the complication rate associated with this approach because it was often used in conjunction with another “first-line” treatment or after it. However, it is clear that methotrexate can be combined with other, mostly nonsurgical treatments.

3. Suction aspiration or D&C, alone or in combination
This option requires general anesthesia. The 305 cases involving this treatment had a mean complication rate of about 62% (range, 29%–86%).1 This approach caused the greatest number of bleeding complications, necessitating a third-line treatment that almost always was surgical.

At delivery or the time of spontaneous abortion, the multilayered myometrial grid in the uterine body is able to contain bleeding vessels after placental separation. However, in CSP, the exposed vessels in the cervical scar tissue bleed because there is no muscle grid to contract and contain the profuse bleeding.

If you choose D&C or aspiration, have blood products available and a Foley balloon catheter handy! In several reports, a Foley balloon catheter was used as backup after significant bleeding occurred following curettage.5,6

In one of the series involving 45 cases treated by methotrexate followed by suction curettage, mean blood loss was significant at 707 mL (standard deviation, 642 mL; range, 100–2,000 mL), and treatment failed in three patients despite insertion of a Foley balloon catheter.

4. Uterine artery embolization, alone or in combination
This treatment requires general anesthesia. The complication rate was 47% among the 64 cases described in the literature.1 Uterine artery embolization appeared to work better when it was combined with other noninvasive treatments. It probably is not the best first-line treatment because the delay between treatment and effect allows the gestation to grow and vascularity to increase. And if uterine artery embolization fails, the clinician must contend with a larger gestation.

5. Excision by laparotomy, alone or in combination with hysteroscopy
General anesthesia is required. Of the 18 cases described in the literature, only five complications were reported—and only when used in an emergency situation.1

 

 

6. Laparoscopic excision
Again, general anesthesia is required. Fifteen of the 49 cases (30.6%) described in the literature involved complications, but only one of five cases (20%) experienced complications if hysteroscopy and laparoscopy were combined. Small numbers may not allow meaningful evaluation of the latter approach.1

7. Operative hysteroscopy, alone or in combination
General anesthesia is required. The overall complication rate for 108 cases was 13.8%. However, if hysteroscopy was combined with transabdominal ultrasound guidance (as it was in nine cases), no complications were noted. If hysteroscopy was combined with mifepristone, the complication rate was 17%.1 It appears that, when it is performed by an experienced clinician with ultrasound guidance, hysteroscopy may be a reasonable operative solution to CSP.

8. Intragestational-sac injection of methotrexate or potassium chloride, with ultrasound guidance
No anesthesia is required. This approach (FIGURE 4) had the fewest and least-involved complications. Of 83 cases, only 9 (10.8%) involved complications.

Cases performed with transabdominal sonography guidance had a slighter higher complication rate (15%) than those using TVS guidance.1

Because local injections are performed without general anesthesia and provide a final treatment by stopping heart activity, they appear to be the most effective intervention and may be especially useful when future fertility is desired.

9. Use of a Foley balloon catheter
Inserting a Foley balloon catheter and inflating it at the site of the CSP is an ­ingenious, relatively new approach.1,2,5–7 The catheters come with balloons of different capacity (FIGURE 5A). They can be used alone (usually in gestations of 5–7 weeks) in the hope of stopping the evolution of the pregnancy by placing pressure on a small gestational sac. Even so, this approach is almost always used in a planned fashion in conjunction with another treatment or as backup if bleeding occurs.

Our impression of the value of the balloon catheters is positive. We suggest the French-12 size 10-mL silicone balloon catheter (prices range from $2 to $20), although we used a French-14 catheter with a 30-mL balloon successfully in a case of an 8-week CSP.

Insert the catheter using real-time transabdominal sonographic guidance when the patient has a comfortably full bladder. One also can switch to TVS guidance to allow for more precise placement and assess the pressure, avoiding overinflation of the balloon (FIGURE 5B).

There is no information in the literature about how long such a catheter should be kept in place. In our experience, 24 to 48 hours is the preferred duration, with the outer end of the catheter fastened to the patient’s thigh. We also provide antibiotic coverage and reevaluate the effect in 2 days or as needed. General anesthesia is not required.

KEY TAKEAWAYS
Is there any single and effective treatment protocol? Probably not. Our management approach is presented as an algorithm (FIGURE 6).

We also offer the following guidelines:

 

  • Do not confuse CSP with ectopic pregnancy. Such nomenclature has caused some referring physicians to simply use methotrexate protocols developed on “garden variety” tubal ectopic pregnancies, which not only failed but yielded disastrous results.
  • Early diagnosis matters. TVS is the most effective and preferred diagnostic tool. Delay in the diagnosis delays treatment, increasing the possibility of complications.
  • Cervical pregnancy is rare. In a patient who has had a cesarean delivery, a low chorionic sac is almost always a CSP.
  • A key first step: Determine whether heart activity is present, and avoid methotrexate if no heart activity is observed.
  • Counsel the patient. If heart activity is documented, provide evidence-based counseling about the patient’s options.
  • Act fast. If continuation of the pregnancy is not desired, provide a reliable treatment that stops the embryonic or fetal heart beat without delay. Early treatment minimizes complications.
  • Avoid single treatments unlikely to be effective, including D&C, suction curettage, single-dose intramuscular methotrexate, and uterine artery embolization applied alone.
  • Keep a catheter at hand. Foley balloon tamponade to prevent or treat bleeding is a useful adjunct to have within easy reach.
  • Consider combination treatments, as they may provide the best results.
  • Fully inform the patient of the risks of pregnancy continuation. If a patient elects to continue the pregnancy, schedule an additional counseling session in which a more detailed overview of the anticipated clinical road is thoroughly explained.

WE WANT TO HEAR FROM YOU!
Share your thoughts on this article. Send your letter to the Editor to: [email protected] Please include the city and state in which you practice. 

Few ObGyn clinicians have faced a patient with a cesarean-scar pregnancy (CSP). Those few were confronted with a management dilemma. Continue the gestation, which would expose the mother to an elevated risk of heavy bleeding? Or terminate the pregnancy? And if termination is the patient’s choice, what is the most effective method?

The literature contains more than 750 reports of CSP, ranging from a single sporadic case to a series of one to two dozen cases. It is impossible to make sense of the numerous treatments used in the past, which were “tested” on extremely small numbers of patients (sometimes as few as one). In this article, we formulate a management plan for the diagnosis and treatment of CSP based on an in-depth review of the published literature and our personal experience in treating more than four dozen patients with CSP.

We’re all familiar with the “epidemic” of cesarean deliveries in this country, including late consequences of cesarean such as placenta previa and morbidly adherent placenta. One of the long-term consequences of cesarean delivery—the first-trimester CSP—is less well known and documented.

Our in-depth review of 751 CSP cases found no less than 30 published therapeutic approaches.1 No consensus exists as to management guidelines. We have formulated this clinical guide, based on the literature and our experience managing CSP, for clinicians who encounter this dangerous form of pregnancy.2

DIAGNOSIS REQUIRES TRANSVAGINAL SONOGRAPHY
Transvaginal sonography (TVS) is thought to be the best and first-line diagnostic tool, with magnetic resonance imaging (MRI) reserved for cases in which there is a diagnostic problem.

In making a diagnosis, consider two main differential diagnoses:

 

  • Cervical pregnancy—This type of gestation is more likely to occur in women with no history of cesarean delivery
  • Spontaneous miscarriage in progress—In a number of cases, the miscarriage happened to be caught on imaging as it passed the area where the CSP usually resides. Because there is no live embryo or fetus in spontaneous miscarriage, a heartbeat cannot be documented.

Components of diagnosis by TVS
Accurate identification of CSP depends on the following sonographic criteria:

 

  • empty uterine cavity and cervical canal (FIGURE 1A)
  • close proximity of the gestational sac and the placenta to the anterior uterine surface within the scar or niche of the previous cesarean delivery (FIGURES 1B, 2A, and 2B)
  • color flow signals between the posterior bladder wall and the gestation within the placenta (FIGURES 1B, 2B, and 3B)
  • abundant blood flow around the gestational sac, at times morphing into an arteriovenous malformation with a high peak systolic velocity blood flow demonstrable on pulsed Doppler.

Our analysis of 751 cases of CSP found that almost a third—30%—were misdiagnosed, contributing to a large number of treatment complications. Most of these complications could have been avoided if diagnosis had been early and correct. The earlier the diagnosis, the better the outcome seemed to be. This was true even when treatment modalities with slightly higher complication rates were used in very early gestation.

Related articles:
• Is the hCG discriminatory zone a reliable indicator of intrauterine or ectopic pregnancy? Andrew M. Kaunitz, MD (Examining the Evidence; February 2012)
Can a single progesterone test distinguish viable and nonviable pregnancies accurately in women with pain or bleeding? Linda R. Chambliss, MD, MPH (Examining the Evidence; March 2013)

THOROUGH COUNSELING OF THE PATIENT IS PARAMOUNT
Once a diagnosis of CSP has been established, the patient should be counseled about her options. The presence of a live CSP requires immediate and decisive action to prevent further growth of the embryo or fetus. Literature from the past decade, particularly from the past several years, makes evidence-based counseling possible.

In general, treatment should be individualized, based on the patient’s age, number of previous cesarean deliveries, number of children, and the expertise of the clinicians managing her care. Options include:

 

  • termination of the pregnancy
  • continuation of the pregnancy with the possibility of delivering a live offspring, provided the patient understands that a morbidly adherent placenta may occur, often necessitating emergency hysterectomy.3,4

MANAGEMENT APPROACHES
Most treatment regimens and combinations thereof can be classified as one of the following:

 

  • Surgical—requiring general anesthesia and either laparotomy with excision or hysterectomy, or laparoscopic or hysteroscopic excision followed by dilation and curettage (D&C).
  • Minimally invasive—involving local injection of methotrexate or potassium chloride or systemic intervention, involving a major procedure such as uterine artery embolization in combination with a less complicated one: intramuscular injection of methotrexate in a single or a multidose regimen.

A variety of simultaneous as well as sequential combination treatments also were used. More recently, an ingenious adjunct to treatment is gaining attention: insertion and inflation of a Foley balloon catheter to prevent or tamponade bleeding.

 

 

A large number of treatments described in the literature—and their different combinations—have been reported as relatively small case series. Gynecologic surgeons generally perform D&C, laparoscopy, and hysteroscopy or laparotomy as the first-line approach. Obstetricians, radiologists, and in vitro fertilization specialists usually prefer systemic, parenteral administration of methotrexate or ultrasound-guided local methotrexate (or potassium chloride) as an injection into the gestational sac. On occasion, the help of an interventional radiologist was requested to embolize the area of the CSP through the uterine arteries.

POTENTIAL COMPLICATIONS
In our analysis of 751 cases of CSP, we used a rigorous definition of complication, which included an immediate or delayed need for a secondary treatment for blood loss exceeding 200 mL or requiring blood transfusion. If general anesthesia or major surgery was required, we classified that need as a complication.

Utilizing these criteria, we observed an overall complication rate of 44.1% (331 of 751 cases).1

Complications occurred most often when the following treatment modalities were used alone:

 

  • single systemic dose of methotrexate
  • D&C
  • uterine artery embolization.

Of the 751 cases reviewed, 21.8% resulted in major surgery or interventional radiology procedures (primary or emergency). The total planned primary (nonemergency) interventions performed were 66 (8.7%), which included 3 hysterectomies, 14 laparotomies, and 49 uterine artery embolizations or ligations. There were 98 (13.0%) emergency interventions, which included 36 hysterectomies, 40 laparotomies, and 22 uterine artery embolizations or ligations.1

Related article: Eight tools for improving obstetric patient safety and unit performance. Henry M. Lerner, MD (Professional Liability; March 2014)

NINE TREATMENTS AND THEIR COMPLICATIONS
1. Systemic, single-dose methotrexate
The usual protocols were 1 mg/kg of body weight or 50 mg/m2 of body surface area. This treatment was associated with a complication rate of 64.6%, mostly because it required a second treatment when the fetal heart beat did not cease after several days.1

We speculate that the high failure rate with this treatment may be caused by its slow action and questionable ability to stop cardiac activity and placental expansion. The expected result can take days, and all the while the gestational sac, the embryo or fetus, and its vascularity are growing. Secondary treatment has to address a larger gestation with more abundant vascularization.

2. Systemic, multidose, sequential methotrexate
In this regimen, the amounts of methotrexate injected are similar to the dose for the single-dose regimen. Two to three intramuscular injections (1 mg/kg of body weight or 50 mg/mm2 of surface area) are given at an interval of 2 or 3 days over the course of a week. Be aware of the cumulative adverse effects of this drug on the liver and bone marrow—and the fact that even multidose treatment can fail.1

We found it impossible to assess the complication rate associated with this approach because it was often used in conjunction with another “first-line” treatment or after it. However, it is clear that methotrexate can be combined with other, mostly nonsurgical treatments.

3. Suction aspiration or D&C, alone or in combination
This option requires general anesthesia. The 305 cases involving this treatment had a mean complication rate of about 62% (range, 29%–86%).1 This approach caused the greatest number of bleeding complications, necessitating a third-line treatment that almost always was surgical.

At delivery or the time of spontaneous abortion, the multilayered myometrial grid in the uterine body is able to contain bleeding vessels after placental separation. However, in CSP, the exposed vessels in the cervical scar tissue bleed because there is no muscle grid to contract and contain the profuse bleeding.

If you choose D&C or aspiration, have blood products available and a Foley balloon catheter handy! In several reports, a Foley balloon catheter was used as backup after significant bleeding occurred following curettage.5,6

In one of the series involving 45 cases treated by methotrexate followed by suction curettage, mean blood loss was significant at 707 mL (standard deviation, 642 mL; range, 100–2,000 mL), and treatment failed in three patients despite insertion of a Foley balloon catheter.

4. Uterine artery embolization, alone or in combination
This treatment requires general anesthesia. The complication rate was 47% among the 64 cases described in the literature.1 Uterine artery embolization appeared to work better when it was combined with other noninvasive treatments. It probably is not the best first-line treatment because the delay between treatment and effect allows the gestation to grow and vascularity to increase. And if uterine artery embolization fails, the clinician must contend with a larger gestation.

5. Excision by laparotomy, alone or in combination with hysteroscopy
General anesthesia is required. Of the 18 cases described in the literature, only five complications were reported—and only when used in an emergency situation.1

 

 

6. Laparoscopic excision
Again, general anesthesia is required. Fifteen of the 49 cases (30.6%) described in the literature involved complications, but only one of five cases (20%) experienced complications if hysteroscopy and laparoscopy were combined. Small numbers may not allow meaningful evaluation of the latter approach.1

7. Operative hysteroscopy, alone or in combination
General anesthesia is required. The overall complication rate for 108 cases was 13.8%. However, if hysteroscopy was combined with transabdominal ultrasound guidance (as it was in nine cases), no complications were noted. If hysteroscopy was combined with mifepristone, the complication rate was 17%.1 It appears that, when it is performed by an experienced clinician with ultrasound guidance, hysteroscopy may be a reasonable operative solution to CSP.

8. Intragestational-sac injection of methotrexate or potassium chloride, with ultrasound guidance
No anesthesia is required. This approach (FIGURE 4) had the fewest and least-involved complications. Of 83 cases, only 9 (10.8%) involved complications.

Cases performed with transabdominal sonography guidance had a slighter higher complication rate (15%) than those using TVS guidance.1

Because local injections are performed without general anesthesia and provide a final treatment by stopping heart activity, they appear to be the most effective intervention and may be especially useful when future fertility is desired.

9. Use of a Foley balloon catheter
Inserting a Foley balloon catheter and inflating it at the site of the CSP is an ­ingenious, relatively new approach.1,2,5–7 The catheters come with balloons of different capacity (FIGURE 5A). They can be used alone (usually in gestations of 5–7 weeks) in the hope of stopping the evolution of the pregnancy by placing pressure on a small gestational sac. Even so, this approach is almost always used in a planned fashion in conjunction with another treatment or as backup if bleeding occurs.

Our impression of the value of the balloon catheters is positive. We suggest the French-12 size 10-mL silicone balloon catheter (prices range from $2 to $20), although we used a French-14 catheter with a 30-mL balloon successfully in a case of an 8-week CSP.

Insert the catheter using real-time transabdominal sonographic guidance when the patient has a comfortably full bladder. One also can switch to TVS guidance to allow for more precise placement and assess the pressure, avoiding overinflation of the balloon (FIGURE 5B).

There is no information in the literature about how long such a catheter should be kept in place. In our experience, 24 to 48 hours is the preferred duration, with the outer end of the catheter fastened to the patient’s thigh. We also provide antibiotic coverage and reevaluate the effect in 2 days or as needed. General anesthesia is not required.

KEY TAKEAWAYS
Is there any single and effective treatment protocol? Probably not. Our management approach is presented as an algorithm (FIGURE 6).

We also offer the following guidelines:

 

  • Do not confuse CSP with ectopic pregnancy. Such nomenclature has caused some referring physicians to simply use methotrexate protocols developed on “garden variety” tubal ectopic pregnancies, which not only failed but yielded disastrous results.
  • Early diagnosis matters. TVS is the most effective and preferred diagnostic tool. Delay in the diagnosis delays treatment, increasing the possibility of complications.
  • Cervical pregnancy is rare. In a patient who has had a cesarean delivery, a low chorionic sac is almost always a CSP.
  • A key first step: Determine whether heart activity is present, and avoid methotrexate if no heart activity is observed.
  • Counsel the patient. If heart activity is documented, provide evidence-based counseling about the patient’s options.
  • Act fast. If continuation of the pregnancy is not desired, provide a reliable treatment that stops the embryonic or fetal heart beat without delay. Early treatment minimizes complications.
  • Avoid single treatments unlikely to be effective, including D&C, suction curettage, single-dose intramuscular methotrexate, and uterine artery embolization applied alone.
  • Keep a catheter at hand. Foley balloon tamponade to prevent or treat bleeding is a useful adjunct to have within easy reach.
  • Consider combination treatments, as they may provide the best results.
  • Fully inform the patient of the risks of pregnancy continuation. If a patient elects to continue the pregnancy, schedule an additional counseling session in which a more detailed overview of the anticipated clinical road is thoroughly explained.

WE WANT TO HEAR FROM YOU!
Share your thoughts on this article. Send your letter to the Editor to: [email protected] Please include the city and state in which you practice. 

References

 

 

  1. Timor-Tritsch IE, Monteagudo A. Unforeseen consequences of the increasing rate of cesarean deliveries: early placenta accreta and cesarean scar pregnancy. A review. [published correction appears in Am J Obstet Gynecol. 2014;210(4):371–374.] Am J Obstet Gynecol. 2012;207(1):14–29.
  2. Timor-Tritsch IE, Monteagudo A, Santos R, Tsymbal T, Pineda G, Arslan AA. The diagnosis, treatment, and follow-up of cesarean scar pregnancy. Am J Obstet Gynecol. 2012;207(1):44.e1–e13.
  3. Ballas J, Pretorius D, Hull AD, Resnik R, Ramos GA. Identifying sonographic markers for placenta accreta in the first trimester. J Ultrasound Med. 2012;31(11):1835–1841.
  4. Timor-Tritsch IE, Monteagudo A, Cali P, et al. Cesarean scar pregnancy and early placenta accreta share a common histology. Ultrasound Obstet Gynecol. 2014;43(4):383–395.
  5. Yu XL, Zhang N, Zuo WL. Cesarean scar pregnancy: An analysis of 100 cases [in Chinese]. Zhonghua Yi Xue Za Zhi. 2011;91(45):3186–3189.
  6. Jiang T, Liu G, Huang L, Ma H, Zhang S. Methotrexate therapy followed by suction curettage followed by Foley tamponade for cesarean scar pregnancy. Eur J Obstet Gynecol Reprod Biol. 2011;156(2):209–211.
  7. Hamilton BE, Martin JA, Ventura SJ. Births: Preliminary data for 2012. Natl Vital Stat Rep. 2013;62(3):1–20.
References

 

 

  1. Timor-Tritsch IE, Monteagudo A. Unforeseen consequences of the increasing rate of cesarean deliveries: early placenta accreta and cesarean scar pregnancy. A review. [published correction appears in Am J Obstet Gynecol. 2014;210(4):371–374.] Am J Obstet Gynecol. 2012;207(1):14–29.
  2. Timor-Tritsch IE, Monteagudo A, Santos R, Tsymbal T, Pineda G, Arslan AA. The diagnosis, treatment, and follow-up of cesarean scar pregnancy. Am J Obstet Gynecol. 2012;207(1):44.e1–e13.
  3. Ballas J, Pretorius D, Hull AD, Resnik R, Ramos GA. Identifying sonographic markers for placenta accreta in the first trimester. J Ultrasound Med. 2012;31(11):1835–1841.
  4. Timor-Tritsch IE, Monteagudo A, Cali P, et al. Cesarean scar pregnancy and early placenta accreta share a common histology. Ultrasound Obstet Gynecol. 2014;43(4):383–395.
  5. Yu XL, Zhang N, Zuo WL. Cesarean scar pregnancy: An analysis of 100 cases [in Chinese]. Zhonghua Yi Xue Za Zhi. 2011;91(45):3186–3189.
  6. Jiang T, Liu G, Huang L, Ma H, Zhang S. Methotrexate therapy followed by suction curettage followed by Foley tamponade for cesarean scar pregnancy. Eur J Obstet Gynecol Reprod Biol. 2011;156(2):209–211.
  7. Hamilton BE, Martin JA, Ventura SJ. Births: Preliminary data for 2012. Natl Vital Stat Rep. 2013;62(3):1–20.
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2014 Update on operative vaginal delivery

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2014 Update on operative vaginal delivery

The past year has seen the publication of four studies with relevance for clinicians:

 

  • a retrospective cohort study that examined the maternal risks of operative vaginal delivery using forceps, vacuum extraction (FIGURE 1), or a combination of forceps and vacuum
  • a prospective cohort study that investigated the efficacy and safety of three different techniques for midcavity rotational delivery in the setting of transverse arrest, namely manual rotation, vacuum rotation, and rotational forceps
  • another retrospective cohort study that compared maternal morbidity among operative vaginal deliveries performed by midwives and physician providers in the United Kingdom
  • a description of a new technique for instrumental vaginal delivery that is low-cost, simple, and easy to perform.

FIGURE 1. In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery when nonreassuring fetal
testing is noted during the second stage of labor.

OBSTETRIC PRACTICE CHANGERS 2014
Hypertension and pregnancy and preventing the first cesarean delivery

A peer-to-peer audiocast
John T. Repke, MD, author of the June Guest Editorial titled "Low-dose aspirin and preeclampsia prevention: Ready for prime time, but as a 're-run' or as a 'new series'?" recently sat down with Errol R. Norwitz, MD, PhD, fellow OBG Management Board of Editors Member and author of this month’s "Update on Operative Vaginal Delivery." Their discussion focused on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.
From their conversation:
Dr. Repke: About 60 recommendations came out of ACOG’s Hypertension in Pregnancy document; only six had high-quality supporting evidence, and I think most practitioners already did them. Many really were based on either moderate- or low-quality evidence, with qualified recommendations. I think this has led to confusion.
Dr. Norwitz, how do you answer when a clinician asks you, “Is this gestational hypertension or is this preeclampsia?” 

Click here to access the audiocast with full transcript.

 

DO NOT SWITCH INSTRUMENTS

Fong A, Wu E, Pan D, Chung HJ, Ogunyemi DA. Temporal trends and morbidities of vacuum, forceps, and combined use of both [published online ahead of print April 9, 2014]. J Matern Fetal Neonatal Med. doi:10.3109/14767058.2014.904282.

In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery in the setting of nonreassuring fetal testing (“fetal distress”) in the second stage of labor. It takes just a few minutes to perform and can avert a frantic dash to the operating room for an emergent cesarean delivery. What to do then in a situation where the vacuum extractor keeps popping off, the vertex is at +3/+5 station, and the fetal heart rate has been at 80 bpm for 8 minutes? It is extremely tempting to discard the ventouse and grab the forceps. But would that be the right decision?

Related article: Is the rate of progress the same for induced and spontaneous labors? William F. Rayburn, MD, MBA (Examining the Evidence; November 2012)

Details of the study
Earlier studies suggested that the combination of vacuum and forceps is associated with an increased risk of fetal injury. Whether this is also true of injury to the mother was not known. To address this issue, Fong and colleagues performed a retrospective cohort study of all successful operative vaginal deliveries identified using ICD-9 procedure codes in the California Health Discharge Dataset from 2001 through 2007. Maternal outcomes were compared between the 202,439 fetuses delivered by vacuum extraction (reference group), 13,555 fetuses delivered by forceps, and 710 fetuses delivered using a combination of the two methods.

Using multivariate analysis modeling, Fong and colleagues demonstrated that, when compared with the vacuum alone, the combined use of vacuum and forceps was associated with significantly higher odds of:

 

  • third- and fourth-degree perineal lacerations (adjusted odds ratio [aOR], 2.86; 95% confidence interval [CI], 2.43–3.36)
  • postpartum hemorrhage (aOR, 1.81; 95% CI, 1.33–2.46)
  • operative delivery failure (aOR, 2.81; 95% CI, 2.27–3.48).

Related articles:
• Develop and use a checklist for 3rd- and 4th-degree perineal lacerations. Robert L. Barbieri, MD (Editorial; August 2013)
Postpartum hemorrhage: 11 critical questions, answered by an expert. Q&A with Haywood L. Brown, MD (January 2011)

Fortunately, combined vacuum/forceps deliveries are uncommon, comprising only 0.33% of operative deliveries in this cohort.

Despite the large dataset used, the study was underpowered to examine the effect of combined vacuum/forceps on the incidence of rare events, such as pelvic hematoma, cervical laceration, thromboembolism, and maternal death.

What this EVIDENCE means for practice
The message is clear: Avoid combined vacuum/forceps deliveries. Choose your initial instrument with care because a failed operative vaginal delivery means a cesarean. You don’t get to choose again. The American College of Obstetricians and Gynecologists also recommends against using multiple instruments “unless there is a compelling and justifiable reason.”1

 

 

LEARN TO PERFORM MIDCAVITY ROTATIONAL DELIVERIES

Bahl R, Van de Venne M, Macleod M, Strachan B, Murphy DJ. Maternal and neonatal morbidity in relation to the instrument used for midcavity rotational operative vaginal delivery: A prospective cohort study. BJOG. 2013;120(12):1526–1532.

Cesarean delivery during the second stage of labor used to be an uncommon event. It was said that if labor progressed adequately to achieve full cervical dilatation, a vaginal delivery should be achieved. Over the past few decades, however, the rate of cesarean delivery at full cervical dilatation has increased substantially, thereby contributing to the well-documented cesarean epidemic.

The most common indication for cesarean delivery during the second stage of labor is arrest of descent due to malposition of the fetal head, typically a transverse arrest. A number of alternatives to cesarean are available, all of which involve assisted rotation of the fetal head. Historical case series reporting increased neonatal morbidity have led to a reduction in the use of rotational forceps to facilitate this rotation. Attempted manual rotation and “rotational vacuum extraction” are now preferred, particularly by less experienced providers. Which of these three approaches is most effective is unknown.

Related article: You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; July 2011)

Details of the study
A prospective cohort study was carried out at two university hospitals in Scotland and England to compare maternal and neonatal morbidity associated with alternative techniques for midcavity rotational delivery. The choice of instrument was left to the provider.

Of the 381 nulliparous women who had an attempted midcavity rotational operative vaginal delivery, 163 (42.8%) underwent manual rotation followed by nonrotational forceps delivery, 73 (19.1%) had a rotational vacuum delivery, and 145 (38.1%) delivered with the assistance of rotational (Kielland) forceps.

Regardless of the instrument used, successful rotation and vaginal delivery were achieved in more than 90% of cases, with a cesarean rate of 4.2%, 6.8%, and 9.6% for manual rotation, vacuum, and rotational forceps, respectively (aOR, 0.39; 95% CI, 0.14–1.06). There were no significant differences in maternal complications (postpartum hemorrhage, third- and fourth-degree perineal lacerations) and neonatal morbidity (low cord pH, neonatal trauma, and neonatal intensive care unit admission) between the three instruments.

What this EVIDENCE means for practice
Midcavity rotational delivery can be achieved with a high degree of success and few adverse events in women who develop transverse arrest in the second stage of labor. Maternal and perinatal outcomes are comparable with rotational forceps, vacuum extraction, and manual rotation. With appropriate training, midcavity rotational delivery can be practiced safely, including the use of Kielland forceps.

 

SHOULD MIDWIVES PERFORM OPERATIVE VAGINAL DELIVERIES?

Black M, Mitchell E, Danielian P. Instrumental vaginal deliveries; are midwives safer practitioners? A retrospective cohort study. Acta Obstet Gynecol Scand. 2013;92(12):1383–1387.

In the United States, instrumental vaginal deliveries are performed only by physicians. In the United Kingdom, the opportunity to perform such deliveries has recently become available to midwives as well. Because midwives have less experience in performing surgical procedures, the question has arisen as to whether their complication rate is higher than that of physicians. Alternatively, because midwives typically are more patient than physicians and more reluctant to resort to obstetric interventions, it is possible that their complication rate may be lower.

Details of the study
To address this issue, Black and colleagues performed a retrospective cohort study of consecutive women who had a successful nonrotational instrumental vaginal delivery of a liveborn singleton infant outside of the operating room between June 2005 and June 2010 at Aberdeen Maternity Hospital in the United Kingdom.

Of the 2,540 women included in the final analysis, 330 (13%) were delivered by midwives and the remaining 2,210 (87%) by physicians—1,049 (41%) by junior doctors and 1,161 (46%) by more senior doctors. All midwives had undergone formal training at the University of Bradford. There were no differences between groups in demographic characteristics (maternal age, gestational age, parity, body mass index, or birth weight) or in the indications for instrumental delivery.

Major findings were that midwives were significantly less likely than junior and senior physicians to use forceps as the instrument of choice for delivery (OR, 0.6; 95% CI, 0.4–0.7). Mean blood loss was significantly lower in the midwife group (57 mL), although it is unlikely that this finding was clinically significant. There were no differences in severe perineal injury (third- or fourth-degree perineal lacerations), arterial cord pH, or postpartum hemorrhage.

A secondary analysis comparing the outcome of operative vaginal deliveries by trained midwives with the outcome by junior physicians alone produced almost identical results.

 

 

Strengths of the study include the fact that it was conducted at a single center and had a large sample number. Weaknesses include its retrospective design and the fact that one major outcome (namely, failed operative vaginal delivery leading to cesarean) was not examined. This study was not designed or powered to examine neonatal outcomes.

What this EVIDENCE means for practice
These data demonstrate that midwives can perform operative vaginal deliveries using either forceps or vacuum with a rate of maternal morbidity equivalent to those performed by physicians.

Are these findings truly revolutionary? Although midwives do not perform cesarean deliveries, they do perform and repair episiotomies when indicated. Restricting instrumental vaginal deliveries to physicians alone may be motivated more by tradition and logistics than concerns over patient safety. Indeed, the ability of a midwife working in a remote area to perform an instrumental vaginal delivery in an emergency situation may be highly beneficial to perinatal outcome, although it should be stressed that such an approach ought to be limited to practitioners who have undergone rigorous formal training.

Other benefits of midwives performing operative vaginal deliveries may include increased autonomy for the midwifery providers, improvements in physician-midwife interactions, and enhanced continuity of care for women.

 

IN THE PIPELINE: THE ODÓN DEVICE FOR OPERATIVE VAGINAL DELIVERY

World Health Organization Odón Device Research Group. Feasibility and safety study of a new device (Odón device) for assisted vaginal deliveries: Study protocol. Reprod Health. 2013;10:33.

Childbirth remains a risky venture. According to the World Health Organization (WHO), approximately 2.6 million babies are stillborn and 260,000 women die in childbirth each year, with developing countries disproportionately affected. Many of these adverse events result from complications at the time of delivery. Instrumental vaginal delivery is used to shorten the second stage of labor and improve perinatal and maternal outcomes.

Operative vaginal delivery likely does reduce the rate of stillbirth and early neonatal death and lower the cesarean delivery rate, but the instruments themselves do occasionally cause maternal and fetal injury, including cephalohematoma, retinal hemorrhage, facial nerve palsy, and skull fractures. Although numerous modifications to the design of forceps and the vacuum extractor have been made over the years, no new technology has been introduced for centuries.

In 2005, Mr. Jorge Odón, a car mechanic from Argentina with no formal training in medicine or obstetrics (aside from being the father of five), came up with an idea for a novel technique to assist in delivery. He was inspired by a simple trick he used to entertain his friends. It involved removing a loose cork from the inside of an empty bottle using a plastic bag. It occurred to him one day that this same scientific principle could be used to expedite delivery of the fetal head from the birth canal, and so he built the first prototype. The device has since been named in his honor.

Description of the Odón device
The Odón device consists of a tube containing a polyethylene bag. The tube is inserted into the birth canal and the bag is deployed and inflated to create a plastic sleeve that hugs the baby’s head. The applicator tube is then discarded and traction is applied to the plastic bag to move the head (and the entire fetus) down the birth canal (FIGURE 2).

To watch a brief video from the WHO about the Odón device, click here.

The advantages of the Odón device are that it is:

 

  • low-cost
  • simple to use
  • compact, easy to transport and store
  • designed to minimize trauma to the mother and fetus.

Current stage of development
The Odón device already has been piloted in the United States and South America. The WHO plans to introduce it into the obstetric armamentarium in a three-phase clinical trial outlined in the Odón Device Research Project report. The first phase is under way and involves testing the device under normal delivery conditions in tertiary hospitals in Argentina and South Africa. The next two phases will 1) assess its efficacy in women with a prolonged second stage of labor but no “fetal distress” and 2) compare its performance head-to-head against the vacuum extractor and forceps.

What this EVIDENCE means for practice
Enthusiasm for the Odón device is fueled by its simplicity and the likelihood that midlevel providers working in remote obstetric units can be trained in its use, thereby increasing access to an important modality of emergency obstetric care. This is particularly important in centers that lack immediate access to cesarean delivery capabilities. Whether the device can be used in developing countries to more effectively manage the second stage of labor and thereby reduce infectious morbidity and pelvic floor injuries has yet to be confirmed but is a testable hypothesis.

 

 

WE WANT TO HEAR FROM YOU! Share your thoughts on this article. Send your Letter to the Editor to: [email protected] 

References

Reference

 

  1. American College of Obstetricians and Gynecologists. ACOG practice bulletin #17: Operative vaginal delivery. Washington, DC: ACOG; 2000.
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The author reports no financial relationships relevant to this article.

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The author reports no financial relationships relevant to this article.

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Errol R. Norwitz, MD, PhD, is Louis E. Phaneuf Professor of Obstetrics and Gynecology, Tufts University School of Medicine, and Chairman of the Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts. Dr. Norwitz serves on the OBG Management Board of Editors.

The author reports no financial relationships relevant to this article.

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Related Articles

The past year has seen the publication of four studies with relevance for clinicians:

 

  • a retrospective cohort study that examined the maternal risks of operative vaginal delivery using forceps, vacuum extraction (FIGURE 1), or a combination of forceps and vacuum
  • a prospective cohort study that investigated the efficacy and safety of three different techniques for midcavity rotational delivery in the setting of transverse arrest, namely manual rotation, vacuum rotation, and rotational forceps
  • another retrospective cohort study that compared maternal morbidity among operative vaginal deliveries performed by midwives and physician providers in the United Kingdom
  • a description of a new technique for instrumental vaginal delivery that is low-cost, simple, and easy to perform.

FIGURE 1. In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery when nonreassuring fetal
testing is noted during the second stage of labor.

OBSTETRIC PRACTICE CHANGERS 2014
Hypertension and pregnancy and preventing the first cesarean delivery

A peer-to-peer audiocast
John T. Repke, MD, author of the June Guest Editorial titled "Low-dose aspirin and preeclampsia prevention: Ready for prime time, but as a 're-run' or as a 'new series'?" recently sat down with Errol R. Norwitz, MD, PhD, fellow OBG Management Board of Editors Member and author of this month’s "Update on Operative Vaginal Delivery." Their discussion focused on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.
From their conversation:
Dr. Repke: About 60 recommendations came out of ACOG’s Hypertension in Pregnancy document; only six had high-quality supporting evidence, and I think most practitioners already did them. Many really were based on either moderate- or low-quality evidence, with qualified recommendations. I think this has led to confusion.
Dr. Norwitz, how do you answer when a clinician asks you, “Is this gestational hypertension or is this preeclampsia?” 

Click here to access the audiocast with full transcript.

 

DO NOT SWITCH INSTRUMENTS

Fong A, Wu E, Pan D, Chung HJ, Ogunyemi DA. Temporal trends and morbidities of vacuum, forceps, and combined use of both [published online ahead of print April 9, 2014]. J Matern Fetal Neonatal Med. doi:10.3109/14767058.2014.904282.

In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery in the setting of nonreassuring fetal testing (“fetal distress”) in the second stage of labor. It takes just a few minutes to perform and can avert a frantic dash to the operating room for an emergent cesarean delivery. What to do then in a situation where the vacuum extractor keeps popping off, the vertex is at +3/+5 station, and the fetal heart rate has been at 80 bpm for 8 minutes? It is extremely tempting to discard the ventouse and grab the forceps. But would that be the right decision?

Related article: Is the rate of progress the same for induced and spontaneous labors? William F. Rayburn, MD, MBA (Examining the Evidence; November 2012)

Details of the study
Earlier studies suggested that the combination of vacuum and forceps is associated with an increased risk of fetal injury. Whether this is also true of injury to the mother was not known. To address this issue, Fong and colleagues performed a retrospective cohort study of all successful operative vaginal deliveries identified using ICD-9 procedure codes in the California Health Discharge Dataset from 2001 through 2007. Maternal outcomes were compared between the 202,439 fetuses delivered by vacuum extraction (reference group), 13,555 fetuses delivered by forceps, and 710 fetuses delivered using a combination of the two methods.

Using multivariate analysis modeling, Fong and colleagues demonstrated that, when compared with the vacuum alone, the combined use of vacuum and forceps was associated with significantly higher odds of:

 

  • third- and fourth-degree perineal lacerations (adjusted odds ratio [aOR], 2.86; 95% confidence interval [CI], 2.43–3.36)
  • postpartum hemorrhage (aOR, 1.81; 95% CI, 1.33–2.46)
  • operative delivery failure (aOR, 2.81; 95% CI, 2.27–3.48).

Related articles:
• Develop and use a checklist for 3rd- and 4th-degree perineal lacerations. Robert L. Barbieri, MD (Editorial; August 2013)
Postpartum hemorrhage: 11 critical questions, answered by an expert. Q&A with Haywood L. Brown, MD (January 2011)

Fortunately, combined vacuum/forceps deliveries are uncommon, comprising only 0.33% of operative deliveries in this cohort.

Despite the large dataset used, the study was underpowered to examine the effect of combined vacuum/forceps on the incidence of rare events, such as pelvic hematoma, cervical laceration, thromboembolism, and maternal death.

What this EVIDENCE means for practice
The message is clear: Avoid combined vacuum/forceps deliveries. Choose your initial instrument with care because a failed operative vaginal delivery means a cesarean. You don’t get to choose again. The American College of Obstetricians and Gynecologists also recommends against using multiple instruments “unless there is a compelling and justifiable reason.”1

 

 

LEARN TO PERFORM MIDCAVITY ROTATIONAL DELIVERIES

Bahl R, Van de Venne M, Macleod M, Strachan B, Murphy DJ. Maternal and neonatal morbidity in relation to the instrument used for midcavity rotational operative vaginal delivery: A prospective cohort study. BJOG. 2013;120(12):1526–1532.

Cesarean delivery during the second stage of labor used to be an uncommon event. It was said that if labor progressed adequately to achieve full cervical dilatation, a vaginal delivery should be achieved. Over the past few decades, however, the rate of cesarean delivery at full cervical dilatation has increased substantially, thereby contributing to the well-documented cesarean epidemic.

The most common indication for cesarean delivery during the second stage of labor is arrest of descent due to malposition of the fetal head, typically a transverse arrest. A number of alternatives to cesarean are available, all of which involve assisted rotation of the fetal head. Historical case series reporting increased neonatal morbidity have led to a reduction in the use of rotational forceps to facilitate this rotation. Attempted manual rotation and “rotational vacuum extraction” are now preferred, particularly by less experienced providers. Which of these three approaches is most effective is unknown.

Related article: You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; July 2011)

Details of the study
A prospective cohort study was carried out at two university hospitals in Scotland and England to compare maternal and neonatal morbidity associated with alternative techniques for midcavity rotational delivery. The choice of instrument was left to the provider.

Of the 381 nulliparous women who had an attempted midcavity rotational operative vaginal delivery, 163 (42.8%) underwent manual rotation followed by nonrotational forceps delivery, 73 (19.1%) had a rotational vacuum delivery, and 145 (38.1%) delivered with the assistance of rotational (Kielland) forceps.

Regardless of the instrument used, successful rotation and vaginal delivery were achieved in more than 90% of cases, with a cesarean rate of 4.2%, 6.8%, and 9.6% for manual rotation, vacuum, and rotational forceps, respectively (aOR, 0.39; 95% CI, 0.14–1.06). There were no significant differences in maternal complications (postpartum hemorrhage, third- and fourth-degree perineal lacerations) and neonatal morbidity (low cord pH, neonatal trauma, and neonatal intensive care unit admission) between the three instruments.

What this EVIDENCE means for practice
Midcavity rotational delivery can be achieved with a high degree of success and few adverse events in women who develop transverse arrest in the second stage of labor. Maternal and perinatal outcomes are comparable with rotational forceps, vacuum extraction, and manual rotation. With appropriate training, midcavity rotational delivery can be practiced safely, including the use of Kielland forceps.

 

SHOULD MIDWIVES PERFORM OPERATIVE VAGINAL DELIVERIES?

Black M, Mitchell E, Danielian P. Instrumental vaginal deliveries; are midwives safer practitioners? A retrospective cohort study. Acta Obstet Gynecol Scand. 2013;92(12):1383–1387.

In the United States, instrumental vaginal deliveries are performed only by physicians. In the United Kingdom, the opportunity to perform such deliveries has recently become available to midwives as well. Because midwives have less experience in performing surgical procedures, the question has arisen as to whether their complication rate is higher than that of physicians. Alternatively, because midwives typically are more patient than physicians and more reluctant to resort to obstetric interventions, it is possible that their complication rate may be lower.

Details of the study
To address this issue, Black and colleagues performed a retrospective cohort study of consecutive women who had a successful nonrotational instrumental vaginal delivery of a liveborn singleton infant outside of the operating room between June 2005 and June 2010 at Aberdeen Maternity Hospital in the United Kingdom.

Of the 2,540 women included in the final analysis, 330 (13%) were delivered by midwives and the remaining 2,210 (87%) by physicians—1,049 (41%) by junior doctors and 1,161 (46%) by more senior doctors. All midwives had undergone formal training at the University of Bradford. There were no differences between groups in demographic characteristics (maternal age, gestational age, parity, body mass index, or birth weight) or in the indications for instrumental delivery.

Major findings were that midwives were significantly less likely than junior and senior physicians to use forceps as the instrument of choice for delivery (OR, 0.6; 95% CI, 0.4–0.7). Mean blood loss was significantly lower in the midwife group (57 mL), although it is unlikely that this finding was clinically significant. There were no differences in severe perineal injury (third- or fourth-degree perineal lacerations), arterial cord pH, or postpartum hemorrhage.

A secondary analysis comparing the outcome of operative vaginal deliveries by trained midwives with the outcome by junior physicians alone produced almost identical results.

 

 

Strengths of the study include the fact that it was conducted at a single center and had a large sample number. Weaknesses include its retrospective design and the fact that one major outcome (namely, failed operative vaginal delivery leading to cesarean) was not examined. This study was not designed or powered to examine neonatal outcomes.

What this EVIDENCE means for practice
These data demonstrate that midwives can perform operative vaginal deliveries using either forceps or vacuum with a rate of maternal morbidity equivalent to those performed by physicians.

Are these findings truly revolutionary? Although midwives do not perform cesarean deliveries, they do perform and repair episiotomies when indicated. Restricting instrumental vaginal deliveries to physicians alone may be motivated more by tradition and logistics than concerns over patient safety. Indeed, the ability of a midwife working in a remote area to perform an instrumental vaginal delivery in an emergency situation may be highly beneficial to perinatal outcome, although it should be stressed that such an approach ought to be limited to practitioners who have undergone rigorous formal training.

Other benefits of midwives performing operative vaginal deliveries may include increased autonomy for the midwifery providers, improvements in physician-midwife interactions, and enhanced continuity of care for women.

 

IN THE PIPELINE: THE ODÓN DEVICE FOR OPERATIVE VAGINAL DELIVERY

World Health Organization Odón Device Research Group. Feasibility and safety study of a new device (Odón device) for assisted vaginal deliveries: Study protocol. Reprod Health. 2013;10:33.

Childbirth remains a risky venture. According to the World Health Organization (WHO), approximately 2.6 million babies are stillborn and 260,000 women die in childbirth each year, with developing countries disproportionately affected. Many of these adverse events result from complications at the time of delivery. Instrumental vaginal delivery is used to shorten the second stage of labor and improve perinatal and maternal outcomes.

Operative vaginal delivery likely does reduce the rate of stillbirth and early neonatal death and lower the cesarean delivery rate, but the instruments themselves do occasionally cause maternal and fetal injury, including cephalohematoma, retinal hemorrhage, facial nerve palsy, and skull fractures. Although numerous modifications to the design of forceps and the vacuum extractor have been made over the years, no new technology has been introduced for centuries.

In 2005, Mr. Jorge Odón, a car mechanic from Argentina with no formal training in medicine or obstetrics (aside from being the father of five), came up with an idea for a novel technique to assist in delivery. He was inspired by a simple trick he used to entertain his friends. It involved removing a loose cork from the inside of an empty bottle using a plastic bag. It occurred to him one day that this same scientific principle could be used to expedite delivery of the fetal head from the birth canal, and so he built the first prototype. The device has since been named in his honor.

Description of the Odón device
The Odón device consists of a tube containing a polyethylene bag. The tube is inserted into the birth canal and the bag is deployed and inflated to create a plastic sleeve that hugs the baby’s head. The applicator tube is then discarded and traction is applied to the plastic bag to move the head (and the entire fetus) down the birth canal (FIGURE 2).

To watch a brief video from the WHO about the Odón device, click here.

The advantages of the Odón device are that it is:

 

  • low-cost
  • simple to use
  • compact, easy to transport and store
  • designed to minimize trauma to the mother and fetus.

Current stage of development
The Odón device already has been piloted in the United States and South America. The WHO plans to introduce it into the obstetric armamentarium in a three-phase clinical trial outlined in the Odón Device Research Project report. The first phase is under way and involves testing the device under normal delivery conditions in tertiary hospitals in Argentina and South Africa. The next two phases will 1) assess its efficacy in women with a prolonged second stage of labor but no “fetal distress” and 2) compare its performance head-to-head against the vacuum extractor and forceps.

What this EVIDENCE means for practice
Enthusiasm for the Odón device is fueled by its simplicity and the likelihood that midlevel providers working in remote obstetric units can be trained in its use, thereby increasing access to an important modality of emergency obstetric care. This is particularly important in centers that lack immediate access to cesarean delivery capabilities. Whether the device can be used in developing countries to more effectively manage the second stage of labor and thereby reduce infectious morbidity and pelvic floor injuries has yet to be confirmed but is a testable hypothesis.

 

 

WE WANT TO HEAR FROM YOU! Share your thoughts on this article. Send your Letter to the Editor to: [email protected] 

The past year has seen the publication of four studies with relevance for clinicians:

 

  • a retrospective cohort study that examined the maternal risks of operative vaginal delivery using forceps, vacuum extraction (FIGURE 1), or a combination of forceps and vacuum
  • a prospective cohort study that investigated the efficacy and safety of three different techniques for midcavity rotational delivery in the setting of transverse arrest, namely manual rotation, vacuum rotation, and rotational forceps
  • another retrospective cohort study that compared maternal morbidity among operative vaginal deliveries performed by midwives and physician providers in the United Kingdom
  • a description of a new technique for instrumental vaginal delivery that is low-cost, simple, and easy to perform.

FIGURE 1. In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery when nonreassuring fetal
testing is noted during the second stage of labor.

OBSTETRIC PRACTICE CHANGERS 2014
Hypertension and pregnancy and preventing the first cesarean delivery

A peer-to-peer audiocast
John T. Repke, MD, author of the June Guest Editorial titled "Low-dose aspirin and preeclampsia prevention: Ready for prime time, but as a 're-run' or as a 'new series'?" recently sat down with Errol R. Norwitz, MD, PhD, fellow OBG Management Board of Editors Member and author of this month’s "Update on Operative Vaginal Delivery." Their discussion focused on individual takeaways from ACOG’s Hypertension in Pregnancy guidelines and the recent joint ACOG−Society of Maternal-Fetal Medicine report on emerging clinical and scientific advances in safe prevention of the primary cesarean delivery.
From their conversation:
Dr. Repke: About 60 recommendations came out of ACOG’s Hypertension in Pregnancy document; only six had high-quality supporting evidence, and I think most practitioners already did them. Many really were based on either moderate- or low-quality evidence, with qualified recommendations. I think this has led to confusion.
Dr. Norwitz, how do you answer when a clinician asks you, “Is this gestational hypertension or is this preeclampsia?” 

Click here to access the audiocast with full transcript.

 

DO NOT SWITCH INSTRUMENTS

Fong A, Wu E, Pan D, Chung HJ, Ogunyemi DA. Temporal trends and morbidities of vacuum, forceps, and combined use of both [published online ahead of print April 9, 2014]. J Matern Fetal Neonatal Med. doi:10.3109/14767058.2014.904282.

In trained hands, operative vaginal delivery can be an extremely effective intervention to expedite delivery in the setting of nonreassuring fetal testing (“fetal distress”) in the second stage of labor. It takes just a few minutes to perform and can avert a frantic dash to the operating room for an emergent cesarean delivery. What to do then in a situation where the vacuum extractor keeps popping off, the vertex is at +3/+5 station, and the fetal heart rate has been at 80 bpm for 8 minutes? It is extremely tempting to discard the ventouse and grab the forceps. But would that be the right decision?

Related article: Is the rate of progress the same for induced and spontaneous labors? William F. Rayburn, MD, MBA (Examining the Evidence; November 2012)

Details of the study
Earlier studies suggested that the combination of vacuum and forceps is associated with an increased risk of fetal injury. Whether this is also true of injury to the mother was not known. To address this issue, Fong and colleagues performed a retrospective cohort study of all successful operative vaginal deliveries identified using ICD-9 procedure codes in the California Health Discharge Dataset from 2001 through 2007. Maternal outcomes were compared between the 202,439 fetuses delivered by vacuum extraction (reference group), 13,555 fetuses delivered by forceps, and 710 fetuses delivered using a combination of the two methods.

Using multivariate analysis modeling, Fong and colleagues demonstrated that, when compared with the vacuum alone, the combined use of vacuum and forceps was associated with significantly higher odds of:

 

  • third- and fourth-degree perineal lacerations (adjusted odds ratio [aOR], 2.86; 95% confidence interval [CI], 2.43–3.36)
  • postpartum hemorrhage (aOR, 1.81; 95% CI, 1.33–2.46)
  • operative delivery failure (aOR, 2.81; 95% CI, 2.27–3.48).

Related articles:
• Develop and use a checklist for 3rd- and 4th-degree perineal lacerations. Robert L. Barbieri, MD (Editorial; August 2013)
Postpartum hemorrhage: 11 critical questions, answered by an expert. Q&A with Haywood L. Brown, MD (January 2011)

Fortunately, combined vacuum/forceps deliveries are uncommon, comprising only 0.33% of operative deliveries in this cohort.

Despite the large dataset used, the study was underpowered to examine the effect of combined vacuum/forceps on the incidence of rare events, such as pelvic hematoma, cervical laceration, thromboembolism, and maternal death.

What this EVIDENCE means for practice
The message is clear: Avoid combined vacuum/forceps deliveries. Choose your initial instrument with care because a failed operative vaginal delivery means a cesarean. You don’t get to choose again. The American College of Obstetricians and Gynecologists also recommends against using multiple instruments “unless there is a compelling and justifiable reason.”1

 

 

LEARN TO PERFORM MIDCAVITY ROTATIONAL DELIVERIES

Bahl R, Van de Venne M, Macleod M, Strachan B, Murphy DJ. Maternal and neonatal morbidity in relation to the instrument used for midcavity rotational operative vaginal delivery: A prospective cohort study. BJOG. 2013;120(12):1526–1532.

Cesarean delivery during the second stage of labor used to be an uncommon event. It was said that if labor progressed adequately to achieve full cervical dilatation, a vaginal delivery should be achieved. Over the past few decades, however, the rate of cesarean delivery at full cervical dilatation has increased substantially, thereby contributing to the well-documented cesarean epidemic.

The most common indication for cesarean delivery during the second stage of labor is arrest of descent due to malposition of the fetal head, typically a transverse arrest. A number of alternatives to cesarean are available, all of which involve assisted rotation of the fetal head. Historical case series reporting increased neonatal morbidity have led to a reduction in the use of rotational forceps to facilitate this rotation. Attempted manual rotation and “rotational vacuum extraction” are now preferred, particularly by less experienced providers. Which of these three approaches is most effective is unknown.

Related article: You are the second responder to a shoulder dystocia emergency. What do you do first? Robert L. Barbieri, MD (Editorial; July 2011)

Details of the study
A prospective cohort study was carried out at two university hospitals in Scotland and England to compare maternal and neonatal morbidity associated with alternative techniques for midcavity rotational delivery. The choice of instrument was left to the provider.

Of the 381 nulliparous women who had an attempted midcavity rotational operative vaginal delivery, 163 (42.8%) underwent manual rotation followed by nonrotational forceps delivery, 73 (19.1%) had a rotational vacuum delivery, and 145 (38.1%) delivered with the assistance of rotational (Kielland) forceps.

Regardless of the instrument used, successful rotation and vaginal delivery were achieved in more than 90% of cases, with a cesarean rate of 4.2%, 6.8%, and 9.6% for manual rotation, vacuum, and rotational forceps, respectively (aOR, 0.39; 95% CI, 0.14–1.06). There were no significant differences in maternal complications (postpartum hemorrhage, third- and fourth-degree perineal lacerations) and neonatal morbidity (low cord pH, neonatal trauma, and neonatal intensive care unit admission) between the three instruments.

What this EVIDENCE means for practice
Midcavity rotational delivery can be achieved with a high degree of success and few adverse events in women who develop transverse arrest in the second stage of labor. Maternal and perinatal outcomes are comparable with rotational forceps, vacuum extraction, and manual rotation. With appropriate training, midcavity rotational delivery can be practiced safely, including the use of Kielland forceps.

 

SHOULD MIDWIVES PERFORM OPERATIVE VAGINAL DELIVERIES?

Black M, Mitchell E, Danielian P. Instrumental vaginal deliveries; are midwives safer practitioners? A retrospective cohort study. Acta Obstet Gynecol Scand. 2013;92(12):1383–1387.

In the United States, instrumental vaginal deliveries are performed only by physicians. In the United Kingdom, the opportunity to perform such deliveries has recently become available to midwives as well. Because midwives have less experience in performing surgical procedures, the question has arisen as to whether their complication rate is higher than that of physicians. Alternatively, because midwives typically are more patient than physicians and more reluctant to resort to obstetric interventions, it is possible that their complication rate may be lower.

Details of the study
To address this issue, Black and colleagues performed a retrospective cohort study of consecutive women who had a successful nonrotational instrumental vaginal delivery of a liveborn singleton infant outside of the operating room between June 2005 and June 2010 at Aberdeen Maternity Hospital in the United Kingdom.

Of the 2,540 women included in the final analysis, 330 (13%) were delivered by midwives and the remaining 2,210 (87%) by physicians—1,049 (41%) by junior doctors and 1,161 (46%) by more senior doctors. All midwives had undergone formal training at the University of Bradford. There were no differences between groups in demographic characteristics (maternal age, gestational age, parity, body mass index, or birth weight) or in the indications for instrumental delivery.

Major findings were that midwives were significantly less likely than junior and senior physicians to use forceps as the instrument of choice for delivery (OR, 0.6; 95% CI, 0.4–0.7). Mean blood loss was significantly lower in the midwife group (57 mL), although it is unlikely that this finding was clinically significant. There were no differences in severe perineal injury (third- or fourth-degree perineal lacerations), arterial cord pH, or postpartum hemorrhage.

A secondary analysis comparing the outcome of operative vaginal deliveries by trained midwives with the outcome by junior physicians alone produced almost identical results.

 

 

Strengths of the study include the fact that it was conducted at a single center and had a large sample number. Weaknesses include its retrospective design and the fact that one major outcome (namely, failed operative vaginal delivery leading to cesarean) was not examined. This study was not designed or powered to examine neonatal outcomes.

What this EVIDENCE means for practice
These data demonstrate that midwives can perform operative vaginal deliveries using either forceps or vacuum with a rate of maternal morbidity equivalent to those performed by physicians.

Are these findings truly revolutionary? Although midwives do not perform cesarean deliveries, they do perform and repair episiotomies when indicated. Restricting instrumental vaginal deliveries to physicians alone may be motivated more by tradition and logistics than concerns over patient safety. Indeed, the ability of a midwife working in a remote area to perform an instrumental vaginal delivery in an emergency situation may be highly beneficial to perinatal outcome, although it should be stressed that such an approach ought to be limited to practitioners who have undergone rigorous formal training.

Other benefits of midwives performing operative vaginal deliveries may include increased autonomy for the midwifery providers, improvements in physician-midwife interactions, and enhanced continuity of care for women.

 

IN THE PIPELINE: THE ODÓN DEVICE FOR OPERATIVE VAGINAL DELIVERY

World Health Organization Odón Device Research Group. Feasibility and safety study of a new device (Odón device) for assisted vaginal deliveries: Study protocol. Reprod Health. 2013;10:33.

Childbirth remains a risky venture. According to the World Health Organization (WHO), approximately 2.6 million babies are stillborn and 260,000 women die in childbirth each year, with developing countries disproportionately affected. Many of these adverse events result from complications at the time of delivery. Instrumental vaginal delivery is used to shorten the second stage of labor and improve perinatal and maternal outcomes.

Operative vaginal delivery likely does reduce the rate of stillbirth and early neonatal death and lower the cesarean delivery rate, but the instruments themselves do occasionally cause maternal and fetal injury, including cephalohematoma, retinal hemorrhage, facial nerve palsy, and skull fractures. Although numerous modifications to the design of forceps and the vacuum extractor have been made over the years, no new technology has been introduced for centuries.

In 2005, Mr. Jorge Odón, a car mechanic from Argentina with no formal training in medicine or obstetrics (aside from being the father of five), came up with an idea for a novel technique to assist in delivery. He was inspired by a simple trick he used to entertain his friends. It involved removing a loose cork from the inside of an empty bottle using a plastic bag. It occurred to him one day that this same scientific principle could be used to expedite delivery of the fetal head from the birth canal, and so he built the first prototype. The device has since been named in his honor.

Description of the Odón device
The Odón device consists of a tube containing a polyethylene bag. The tube is inserted into the birth canal and the bag is deployed and inflated to create a plastic sleeve that hugs the baby’s head. The applicator tube is then discarded and traction is applied to the plastic bag to move the head (and the entire fetus) down the birth canal (FIGURE 2).

To watch a brief video from the WHO about the Odón device, click here.

The advantages of the Odón device are that it is:

 

  • low-cost
  • simple to use
  • compact, easy to transport and store
  • designed to minimize trauma to the mother and fetus.

Current stage of development
The Odón device already has been piloted in the United States and South America. The WHO plans to introduce it into the obstetric armamentarium in a three-phase clinical trial outlined in the Odón Device Research Project report. The first phase is under way and involves testing the device under normal delivery conditions in tertiary hospitals in Argentina and South Africa. The next two phases will 1) assess its efficacy in women with a prolonged second stage of labor but no “fetal distress” and 2) compare its performance head-to-head against the vacuum extractor and forceps.

What this EVIDENCE means for practice
Enthusiasm for the Odón device is fueled by its simplicity and the likelihood that midlevel providers working in remote obstetric units can be trained in its use, thereby increasing access to an important modality of emergency obstetric care. This is particularly important in centers that lack immediate access to cesarean delivery capabilities. Whether the device can be used in developing countries to more effectively manage the second stage of labor and thereby reduce infectious morbidity and pelvic floor injuries has yet to be confirmed but is a testable hypothesis.

 

 

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References

Reference

 

  1. American College of Obstetricians and Gynecologists. ACOG practice bulletin #17: Operative vaginal delivery. Washington, DC: ACOG; 2000.
References

Reference

 

  1. American College of Obstetricians and Gynecologists. ACOG practice bulletin #17: Operative vaginal delivery. Washington, DC: ACOG; 2000.
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OBG Management - 26(6)
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Errol R. Norwitz,operative vaginal delivery,forceps,vacuum extraction,midcavity rotational delivery,transverse arrest,manual rotation,vacuum rotation,rotational forceps,maternal morbidity,midwives,physician providers,instrumental vaginal delivery,Odon device,emergent cesarean delivery,perineal lacerations,postpartum hemorrhage,operative delivery failure,second stage of labor,WHO,World Health Organization,childbirth,stillborn,Jorge Odon,polyethylene bag,Odón Device Research Project,American College of Obstetricians and Gynecologists,ACOG
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