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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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For the management of labor, patience is a virtue

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For the management of labor, patience is a virtue
Start using the ACOG/SMFM labor management guidelines in your practice

During the past 45 years, the cesarean delivery (CD) rate in the United States has increased from 5.5% in 1970 to 33% from 2009 to 2013, followed by a small decrease to 32% in 2014 and 2015.1 Many clinical problems cause clinicians and patients to decide that CD is an optimal birth route, including: abnormal labor progress, abnormal or indeterminate fetal heart rate pattern, breech presentation, multiple gestation, macrosomia, placental and cord abnormalities, preeclampsia, prior uterine surgery, and prior CD.2 Recent secular trends that contribute to the current rate of CD include an adversarial liability environment,3,4 increasing rates of maternal obesity,5 and widespread use of continuous fetal-heart monitoring during labor.6

Wide variation in CD rate has been reported among countries, states, and hospitals. The variation is due, in part, to different perspectives about balancing the harms and benefits of vaginal delivery versus CD. In Europe, in 2010 the CD rates in Sweden and Italy were 17.1% and 38%, respectively.7 In 2010, among the states, Alaska had the lowest rate of CD at 22% and Kentucky had the highest rate at 40%.8 In 2015, the highest rate was 38%, in Mississippi (FIGURE).9 In 2014, among Massachusetts hospitals with more than 2,500 births, the CD rate ranged from a low of 22% to a high of 37%.10

Clinicians, patients, policy experts, and the media are perplexed and troubled by the “high” US CD rate and the major variation in rate among countries, states, and hospitals. Labor management practices likely influence the rate of CD and diverse approaches to labor management likely account for the wide variation in CD rates.

A nationwide effort to standardize and continuously improve labor management might result in a decrease in the CD rate. Building on this opportunity, the American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal-Fetal Medicine (SMFM) have jointly recommended new labor management guidelines that may reduce the primary CD rate.8

The ACOG/SMFM guidelines encourage obstetricians to extend the time for labor progress in both the 1st and 2nd stages prior to recommending a CD.8 These new guidelines emphasize that for a modern obstetrician, patience is a virtue. There are 2 important caveats to this statement: to safely extend the length of time of labor requires both (1) a reassuring fetal heart rate tracing and (2) stable maternal health. If the fetus demonstrates a persistent worrisome Category II or a Category IIIheart-rate tracing, decisive intervention is necessary and permitting an extended labor would not be optimal. Similarly, if the mother has rapidly worsening preeclampsia it may not be wise to extend an induction of labor (IOL) over many days.

There are risks with extending the length of labor. An extended duration of the 1st stage of labor is associated with an increased rate of maternal chorioamnionitis and shoulder dystocia at birth.11 An extended duration of the 2nd stage of labor is associated with an increase in the rate of maternal chorioamnionitis, anal sphincter injury, uterine atony, and neonatal admission to an intensive care unit.12 Clinicians who adopt practices that permit an extended length of labor must weigh the benefits of avoiding a CD against these maternal and fetal complications.

Active phase redefined

Central to the ACOG/SMFM guidelines is a new definition of the active phase of labor. The research of Dr. Emmanuel Friedman indicated that at approximately 4 cm of cervical dilation many women in labor transition from the latent phase, a time of slow change in cervical dilation, to the active phase, a time of more rapid change in cervical dilation.13,14 However, more recent research indicates that the transition between the latent and active phase is difficult to precisely define, but more often occurs at about 6 cm of cervical dilation and not 4 cm of dilation.15 Adopting these new norms means that laboring women will spend much more time in the latent phase, a phase of labor in which patience is a virtue.

The ACOG/SMFM guidelines

Main takeaways from the ACOG/SMFM guidelines are summarized below. Interventions that address common obstetric issues and labor abnormalities are outlined below.

Do not perform CD for a prolonged latent phase of labor, defined as regular contractions of >20 hours duration in nulliparous women and >14 hours duration in multiparous women. Patience with a prolonged latent phase will be rewarded by the majority of women entering the active phase of labor. Alternatively, if appropriate, cervical ripening followed by oxytocin IOL and amniotomy will help the patient with a prolonged latent phase to enter the active phase of labor.16

For women with an unfavorable cervix as assessed by the Bishop score, cervical ripening should be performed prior to IOL. Use of cervical ripening prior to IOL increases the chance of achieving vaginal delivery within 24 hours and may result in a modest decrease in the rate of CD.17,18


Related article:
Should oxytocin and a Foley catheter be used concurrently for cervical ripening in induction of labor?
 

Failed IOL in the latent phase should only be diagnosed following 12 to 18 hours of both ruptured membranes and adequate contractions stimulated with oxytocin. The key ingredients for the successful management of the latent phase of labor are patience, oxytocin, and amniotomy.16

CD for the indication of active phase arrest requires cervical dilation ≥6 cm with ruptured membranes and no change in cervical dilation for ≥4 hours of adequate uterine activity. In the past, most obstetricians defined active phase arrest, a potential indication for CD, as the absence of cervical change for 2 or more hours in the presence of adequate uterine contractions and cervical dilation of at least 4 cm. Given the new definition of active phase arrest, slow but progressive progress in the 1st stage of labor is not an indication for CD.11,19

“A specific absolute maximum length of time spent in the 2nd stage beyond which all women should be offered an operative delivery has not been identified.”8 Diagnosis of arrest of labor in the 2nd stage may be considered after at least 2 hours of pushing in multiparous women and 3 hours of pushing in nulliparous women, especially if no fetal descent is occurring. The guidelines also state “longer durations may be appropriate on an individualized basis (eg, with use of epidural analgesia or with fetal malposition)” as long as fetal descent is observed.

Patience is a virtue, especially in the management of the 2nd stage of labor. Extending the 2nd stage up to 4 hours appears to be reasonably safe if the fetal status is reassuring and the mother is physiologically stable. In a study from San Francisco of 42,268 births with normal newborn outcomes, the 95th percentile for the length of the 2nd stage of labor for nulliparous women was 3.3 hours without an epidural and 5.6 hours with an epidural.20

In a study of 53,285 births, longer duration of pushing was associated with a small increase in the rate of neonatal adverse outcomes. In nulliparous women the rate of adverse neonatal outcomes increased from 1.3% with less than 60 minutes of pushing to 2.4% with greater than 240 minutes of pushing. Remarkably, even after 4 hours of pushing, 78% of nulliparous women who continued to push had a vaginal delivery.21 In this study, among nulliparous women the rate of anal sphincter injury increased from 5% with less than 60 minutes of pushing to 16% with greater than 240 minutes of pushing, and the rate of postpartum hemorrhage increased from 1% with less than 60 minutes of pushing to 3.3% with greater than 240 minutes of pushing.

I am not enthusiastic about patiently watching a labor extend into the 5th hour of the 2nd stage, especially if the fetus is at +2 station or lower. In a nulliparous woman, after 4 hours of managing the 2nd stage of labor, my patience is exhausted and I am inclined to identify a clear plan for delivery, either by enhanced labor coaching, operative vaginal delivery, or CD.

Operative vaginal delivery in the 2nd stage of labor is an acceptable alternative to CD. The rate of operative vaginal delivery in the United States has declined over the past 2 decades (TABLE). In Sweden in 2010 the operative vaginal delivery rate was 7.6% with a CD rate of 17.1%.7 In the United States in 2010 the operative delivery rate was 3.6%, and the CD rate was 33%.1 A renewed focus on operative vaginal delivery with ongoing training and team simulation for the procedure would increase our use of operative delivery and decrease the overall rate of CD.


Related article:
STOP using instruments to assist with delivery of the head at cesarean
 

Encourage the detection of persistent fetal occiput posterior position by physical examination and/or ultrasound and consider manual rotation of the fetal occiput from the posterior to anterior position in the 2nd stage. Persistent occiput posterior is the most common fetal malposition.22 This malposition is associated with an increased rate of CD.23 There are few randomized trials of manual rotation of the fetal occiput from posterior to anterior position in the 2nd stage of labor, and the evidence is insufficient to determine the efficacy of manual rotation.24 Small nonrandomized studies report that manual rotation of the occiput from posterior to anterior position may reduce the CD rate.25–27

For persistent 2nd stage fetal occiput posterior position in a woman with an adequate pelvis, where manual rotation was not successful and the fetus is at +2 station or below, operative vaginal delivery is an option. “Vacuum or forceps?” and “If forceps, to rotate or not to rotate?” those are the clinical questions. Forceps delivery is more likely to be successfulthan vacuum delivery.28 Direct forceps delivery of the occiput posterior fetus is associated with more anal sphincter injuries than forceps delivery after successful rotation, but few clinicians regularly perform rotational forceps.29 In a study of 2,351 women in the 2nd stage of labor with the fetus at +2 station or below, compared with either forceps or vacuum delivery, CD was associated with more maternal infections and fewer perineal lacerations. Neonatal composite morbidity was not significantly different among the 3 routes of operative delivery.30

Amnioinfusion for repetitive variable decelerations of the fetal heart rate may reduce the risk of CD for an indeterminate fetal heart-rate pattern.31

IOL in a well-dated pregnancy at 41 weeks will reduce the risk of CD. In a large clinical trial, 3,407 women at 41 weeks of gestation were randomly assigned to IOL or expectant management. The rate of CD was significantly lower in the women assigned to IOL compared with expectant management (21% vs 25%, respectively; P = .03).32 The rate of neonatal morbidity was similar in the 2 groups.

Women with twin gestations and the first twin in a cephalic presentation may elect vaginal delivery. In a large clinical trial, 1,398 women with a twin gestation and the first twin in a cephalic presentation were randomly assigned to planned vaginal delivery (with cesarean only if necessary) or planned CD.33 The rate of CD was 44% and 91% for the women in the planned-vaginal and planned-cesarean groups, respectively. There was no significant difference in composite fetal or neonatal death or serious morbidity. The authors concluded that, for twin pregnancy with the presenting twin in the cephalic presentation, there were no demonstrated benefits of planned CD.

Develop maternity care systems that encourage the use of trial of labor after cesarean (TOLAC). The ACOG/SMFM guidelines focus on interventions to reduce the rate of primary CD and do not address the role of TOLAC in reducing CD rates. There are little data from clinical trials to assess the benefits and harms from TOLAC versus scheduled repeat CD.34 However, our experience with TOLAC in the 1990s strongly suggests that encouraging TOLAC will decrease the rate of CD. In 1996 the US rate of vaginal birth after cesarean (VBAC) peaked at 28%, and the rate of CD achieved a recent historic nadir of 21%. Growing concerns that TOLAC occasionally results in fetal harm was followed by a decrease in the VBAC rate to 12% in 2015.1 A recent study of obstetric practices in countries with high and low VBAC rates concluded that patient and clinician commitment and comfort with prioritizing TOLAC over scheduled repeat CD greatly influenced the VBAC rate.35


Related article:
Should lower uterine segment thickness measurement be included in the TOLAC decision-making process?

Labor management is an art

During labor obstetricians must balance the unique needs of mother and fetus, which requires great clinical skill and patience. Evolving concepts of normal labor progress necessitate that we change our expectations concerning the acceptable rate of progress in the 1st and 2nd stage of labor. Consistent application of these new labor guidelines may help to reduce the rate of CD.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Martin JA, Hamilton BE, Osterman MJ, Driscoll AK, Matthews TJ. Births: final data for 2015. Natl Vital Stat Rep. 2017;66(1):1–70. https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_01.pdf. Accessed July 5, 2017.
  2. Barber EL, Lundsberg LS, Belanger K, Pettker CM, Funai EF, Illuzzi JL. Indications contributing to the increasing cesarean delivery rate. Obstet Gynecol. 2011;118(1):29–38.
  3. Localio AR, Lawthers AG, Bengtson JM, et al. Relationship between malpractice claims and cesarean delivery. JAMA. 1993;269(3):366–373.
  4. Cheng YW, Snowden JM, Handler SJ, Tager IB, Hubbard AE, Caughey AB. Litigation in obstetrics: does defensive medicine contribute to increases in cesarean delivery? J Matern Fetal Neonatal Med. 2014;27(16):1668–1675.
  5. Graham LE, Brunner Huber LR, Thompson ME, Ersek JL. Does amount of weight gain during pregnancy modify the association between obesity and cesarean section delivery? Birth. 2014;41(1):93–99.
  6. Alfirevic Z, Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane Database Syst Rev. 2013;(5):CD006066.
  7. European Perinatal Health Report. Euro-Peristat website. http://www.europeristat.com/. Published 2012. Accessed July 5, 2017.
  8. American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric care consensus no. 1: safe prevention of the primary cesarean delivery. Obstet Gynecol. 2014;123(3):693–711.
  9. Cesarean delivery rate by state, 2015. Centers for Disease Control and Prevention website. https://www.cdc.gov/nchs/pressroom/sosmap/cesarean_births/cesareans.htm. Updated  January 9, 2017. Accessed July 18, 2017.
  10. Baker CD, Land T; Massachusetts Department of Public Health. Massachusetts Births 2014. Massachusetts Executive Office of Health and Human Services website. http://www.mass.gov/eohhs/gov/departments/dph/programs/admin/dmoa/repi/birth-data.html. Published September 2015. Accessed July 5, 2017.
  11. Henry DE, Cheng YW, Shaffer BL, Kaimal AJ, Bianco K, Caughey AB. Perinatal outcomes in the setting of active phase arrest of labor. Obstet Gynecol. 2008;112(5):1109–1115.
  12. Rouse DJ, Weiner SJ, Bloom SL, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Second-stage labor duration in nulliparous women: relationship to maternal and perinatal outcomes. Am J Obstet Gynecol. 2009;201(4):357.e1–e7.
  13. Friedman EZ. Labour: Clinical evaluation and management. Appleton-Century-Crofts: New York, NY; 1967.
  14. Friedman E. The graphic analysis of labor. Am J Obstet Gynecol. 1954;68(6):1568–1575.
  15. Zhang J, Landy HJ, Branch DW, et al; Consortium on Safe Labor. Contemporary patterns  of spontaneous labor with normal neonatal outcomes. Obstet Gynecol. 2010;116(6):1281–1287.
  16. Wei S, Wo BL, Qi HP, et al. Early amniotomy and early oxytocin for prevention of, or therapy for, delay in first stage spontaneous labour compared with routine care. Cochrane Database Syst Rev. 2013;(8):CD006794.
  17. Thomas J, Fairclough A, Kavanagh J, Kelly AJ. Vaginal prostaglandin (PGE2  and  PGF2a) for induction of labour at term. Cochrane Database Syst Rev. 2014;(6):CD003101.
  18. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane Database Syst Rev. 2009;(4):CD003246.
  19. Rouse DJ, Owen J, Savage KG, Hauth JC. Active phase labor arrest: revisiting the 2-hour minimum. Obstet Gynecol. 2001;98(4):550–554.
  20. Cheng YW, Shaffer BL, Nicholson JM, Caughey AB. Second stage of labor and epidural use: a larger effect than previously suggested. Obstet Gynecol. 2014;123(3):527–535.
  21. Grobman WA, Bailit J, Lai Y, et al; Eunice Kennedy Shriver National Institute of Child  and Human Development (NICHD) Maternal-Fetal Medicine Units (MFMU) Network. Association of the duration of active pushing with obstetric outcomes. Obstet Gynecol. 2016;127(4):667–673.
  22. Barth WH Jr. Persistent occiput posterior. Obstet Gynecol. 2015;125(3):695–709.
  23. Carseldine WJ, Phipps H, Zawada SF, et al. Does occiput posterior position in the second stage of labour increase the operative delivery rate? Aust N Z J Obstet Gynaecol. 2013;53(3):265–270.
  24. Phipps H, de Vries B, Hyett J, Osborn DA. Prophylactic manual rotation for fetal  malposition to reduce operative delivery. Cochrane Database Syst Rev. 2014;(12):CD009298.
  25. Shaffer BL, Cheng YW, Vargas JE, Caughey AB. Manual rotation to reduce caesarean delivery in persistent occiput posterior or transverse position. J Matern Fetal Neonatal Med. 2011;24(1):65–72.
  26. Le Ray C, Serres P, Schmitz T, Cabrol D, Goffinet F. Manual rotation in occiput posterior or transverse positions: risk factors and consequences on the cesarean delivery rate. Obstet Gynecol. 2007;110(4):873–879.
  27. Reichman O, Gdansky E, Latinsky B, Labi S, Samueloff A. Digital rotation from occipito-posterior to occipito-anterior decreases the need for cesarean section. Eur J Obstet Gynecol Repro Biol. 2008;136:25–28.
  28. O’Mahony F, Hofmeyr GJ, Menon V. Choice of instruments for assisted vaginal delivery. Cochrane Database Syst Rev. 2010;(11):CD005455.
  29. Hirsch E, Elue R, Wagner A Jr, et al. Severe perineal laceration during operative vaginal  delivery: the impact of occiput posterior position. J Perinatol. 2014;34(12):898–900.
  30. Bailit JL, Grobman WA, Rice MM, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Evaluation of delivery options for second-stage events. Am J Obstet Gynecol. 2016;214(5):638.e1–e10.
  31. Hofmeyr GJ, Lawrie TA. Amnioinfusion for potential or suspected umbilical cord compression in labour. Cochrane Database Syst Rev. 2012;1:CD000013.
  32. Hannah ME, Hannah WJ, Hellmann J, Hewson S, Milner R, Willan A. Induction of labor as compared with serial antenatal monitoring in post-term pregnancy. A randomized controlled trial. The Canadian Multicenter Post-term Pregnancy Trial Group. N Engl J Med. 1992;326(24): 1587–1592.
  33. Barrett JF, Hannah ME, Hutton EK, et al; Twin Birth Study Collaborative Group. A randomized trial of planned cesarean or vaginal delivery for twin pregnancy. N Engl J Med. 2013;369(14):1295–1305.
  34. Dodd JM, Crowther CA, Huertas E, Guise JM, Horey D. Planned elective repeat cesarean section versus planned vaginal birth for women with a previous caesarean birth. Cochrane Database Syst Rev. 2013;(12):CD004224.
  35. Lundgren I, van Limbeek E, Vehvilainen-Julkunen K, Nilsson C. Clinicians’ views of factors of importance for improving the rate of VBAC (vaginal birth after caesarean section): a qualitative study from countries with high VBAC rates. BMC Pregnancy Childbirth. 2015;15:196.
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Dr. Barbieri reports no financial relationships relevant to this article.

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Dr. Barbieri reports no financial relationships relevant to this article.

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Dr. Barbieri reports no financial relationships relevant to this article.

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Start using the ACOG/SMFM labor management guidelines in your practice
Start using the ACOG/SMFM labor management guidelines in your practice

During the past 45 years, the cesarean delivery (CD) rate in the United States has increased from 5.5% in 1970 to 33% from 2009 to 2013, followed by a small decrease to 32% in 2014 and 2015.1 Many clinical problems cause clinicians and patients to decide that CD is an optimal birth route, including: abnormal labor progress, abnormal or indeterminate fetal heart rate pattern, breech presentation, multiple gestation, macrosomia, placental and cord abnormalities, preeclampsia, prior uterine surgery, and prior CD.2 Recent secular trends that contribute to the current rate of CD include an adversarial liability environment,3,4 increasing rates of maternal obesity,5 and widespread use of continuous fetal-heart monitoring during labor.6

Wide variation in CD rate has been reported among countries, states, and hospitals. The variation is due, in part, to different perspectives about balancing the harms and benefits of vaginal delivery versus CD. In Europe, in 2010 the CD rates in Sweden and Italy were 17.1% and 38%, respectively.7 In 2010, among the states, Alaska had the lowest rate of CD at 22% and Kentucky had the highest rate at 40%.8 In 2015, the highest rate was 38%, in Mississippi (FIGURE).9 In 2014, among Massachusetts hospitals with more than 2,500 births, the CD rate ranged from a low of 22% to a high of 37%.10

Clinicians, patients, policy experts, and the media are perplexed and troubled by the “high” US CD rate and the major variation in rate among countries, states, and hospitals. Labor management practices likely influence the rate of CD and diverse approaches to labor management likely account for the wide variation in CD rates.

A nationwide effort to standardize and continuously improve labor management might result in a decrease in the CD rate. Building on this opportunity, the American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal-Fetal Medicine (SMFM) have jointly recommended new labor management guidelines that may reduce the primary CD rate.8

The ACOG/SMFM guidelines encourage obstetricians to extend the time for labor progress in both the 1st and 2nd stages prior to recommending a CD.8 These new guidelines emphasize that for a modern obstetrician, patience is a virtue. There are 2 important caveats to this statement: to safely extend the length of time of labor requires both (1) a reassuring fetal heart rate tracing and (2) stable maternal health. If the fetus demonstrates a persistent worrisome Category II or a Category IIIheart-rate tracing, decisive intervention is necessary and permitting an extended labor would not be optimal. Similarly, if the mother has rapidly worsening preeclampsia it may not be wise to extend an induction of labor (IOL) over many days.

There are risks with extending the length of labor. An extended duration of the 1st stage of labor is associated with an increased rate of maternal chorioamnionitis and shoulder dystocia at birth.11 An extended duration of the 2nd stage of labor is associated with an increase in the rate of maternal chorioamnionitis, anal sphincter injury, uterine atony, and neonatal admission to an intensive care unit.12 Clinicians who adopt practices that permit an extended length of labor must weigh the benefits of avoiding a CD against these maternal and fetal complications.

Active phase redefined

Central to the ACOG/SMFM guidelines is a new definition of the active phase of labor. The research of Dr. Emmanuel Friedman indicated that at approximately 4 cm of cervical dilation many women in labor transition from the latent phase, a time of slow change in cervical dilation, to the active phase, a time of more rapid change in cervical dilation.13,14 However, more recent research indicates that the transition between the latent and active phase is difficult to precisely define, but more often occurs at about 6 cm of cervical dilation and not 4 cm of dilation.15 Adopting these new norms means that laboring women will spend much more time in the latent phase, a phase of labor in which patience is a virtue.

The ACOG/SMFM guidelines

Main takeaways from the ACOG/SMFM guidelines are summarized below. Interventions that address common obstetric issues and labor abnormalities are outlined below.

Do not perform CD for a prolonged latent phase of labor, defined as regular contractions of >20 hours duration in nulliparous women and >14 hours duration in multiparous women. Patience with a prolonged latent phase will be rewarded by the majority of women entering the active phase of labor. Alternatively, if appropriate, cervical ripening followed by oxytocin IOL and amniotomy will help the patient with a prolonged latent phase to enter the active phase of labor.16

For women with an unfavorable cervix as assessed by the Bishop score, cervical ripening should be performed prior to IOL. Use of cervical ripening prior to IOL increases the chance of achieving vaginal delivery within 24 hours and may result in a modest decrease in the rate of CD.17,18


Related article:
Should oxytocin and a Foley catheter be used concurrently for cervical ripening in induction of labor?
 

Failed IOL in the latent phase should only be diagnosed following 12 to 18 hours of both ruptured membranes and adequate contractions stimulated with oxytocin. The key ingredients for the successful management of the latent phase of labor are patience, oxytocin, and amniotomy.16

CD for the indication of active phase arrest requires cervical dilation ≥6 cm with ruptured membranes and no change in cervical dilation for ≥4 hours of adequate uterine activity. In the past, most obstetricians defined active phase arrest, a potential indication for CD, as the absence of cervical change for 2 or more hours in the presence of adequate uterine contractions and cervical dilation of at least 4 cm. Given the new definition of active phase arrest, slow but progressive progress in the 1st stage of labor is not an indication for CD.11,19

“A specific absolute maximum length of time spent in the 2nd stage beyond which all women should be offered an operative delivery has not been identified.”8 Diagnosis of arrest of labor in the 2nd stage may be considered after at least 2 hours of pushing in multiparous women and 3 hours of pushing in nulliparous women, especially if no fetal descent is occurring. The guidelines also state “longer durations may be appropriate on an individualized basis (eg, with use of epidural analgesia or with fetal malposition)” as long as fetal descent is observed.

Patience is a virtue, especially in the management of the 2nd stage of labor. Extending the 2nd stage up to 4 hours appears to be reasonably safe if the fetal status is reassuring and the mother is physiologically stable. In a study from San Francisco of 42,268 births with normal newborn outcomes, the 95th percentile for the length of the 2nd stage of labor for nulliparous women was 3.3 hours without an epidural and 5.6 hours with an epidural.20

In a study of 53,285 births, longer duration of pushing was associated with a small increase in the rate of neonatal adverse outcomes. In nulliparous women the rate of adverse neonatal outcomes increased from 1.3% with less than 60 minutes of pushing to 2.4% with greater than 240 minutes of pushing. Remarkably, even after 4 hours of pushing, 78% of nulliparous women who continued to push had a vaginal delivery.21 In this study, among nulliparous women the rate of anal sphincter injury increased from 5% with less than 60 minutes of pushing to 16% with greater than 240 minutes of pushing, and the rate of postpartum hemorrhage increased from 1% with less than 60 minutes of pushing to 3.3% with greater than 240 minutes of pushing.

I am not enthusiastic about patiently watching a labor extend into the 5th hour of the 2nd stage, especially if the fetus is at +2 station or lower. In a nulliparous woman, after 4 hours of managing the 2nd stage of labor, my patience is exhausted and I am inclined to identify a clear plan for delivery, either by enhanced labor coaching, operative vaginal delivery, or CD.

Operative vaginal delivery in the 2nd stage of labor is an acceptable alternative to CD. The rate of operative vaginal delivery in the United States has declined over the past 2 decades (TABLE). In Sweden in 2010 the operative vaginal delivery rate was 7.6% with a CD rate of 17.1%.7 In the United States in 2010 the operative delivery rate was 3.6%, and the CD rate was 33%.1 A renewed focus on operative vaginal delivery with ongoing training and team simulation for the procedure would increase our use of operative delivery and decrease the overall rate of CD.


Related article:
STOP using instruments to assist with delivery of the head at cesarean
 

Encourage the detection of persistent fetal occiput posterior position by physical examination and/or ultrasound and consider manual rotation of the fetal occiput from the posterior to anterior position in the 2nd stage. Persistent occiput posterior is the most common fetal malposition.22 This malposition is associated with an increased rate of CD.23 There are few randomized trials of manual rotation of the fetal occiput from posterior to anterior position in the 2nd stage of labor, and the evidence is insufficient to determine the efficacy of manual rotation.24 Small nonrandomized studies report that manual rotation of the occiput from posterior to anterior position may reduce the CD rate.25–27

For persistent 2nd stage fetal occiput posterior position in a woman with an adequate pelvis, where manual rotation was not successful and the fetus is at +2 station or below, operative vaginal delivery is an option. “Vacuum or forceps?” and “If forceps, to rotate or not to rotate?” those are the clinical questions. Forceps delivery is more likely to be successfulthan vacuum delivery.28 Direct forceps delivery of the occiput posterior fetus is associated with more anal sphincter injuries than forceps delivery after successful rotation, but few clinicians regularly perform rotational forceps.29 In a study of 2,351 women in the 2nd stage of labor with the fetus at +2 station or below, compared with either forceps or vacuum delivery, CD was associated with more maternal infections and fewer perineal lacerations. Neonatal composite morbidity was not significantly different among the 3 routes of operative delivery.30

Amnioinfusion for repetitive variable decelerations of the fetal heart rate may reduce the risk of CD for an indeterminate fetal heart-rate pattern.31

IOL in a well-dated pregnancy at 41 weeks will reduce the risk of CD. In a large clinical trial, 3,407 women at 41 weeks of gestation were randomly assigned to IOL or expectant management. The rate of CD was significantly lower in the women assigned to IOL compared with expectant management (21% vs 25%, respectively; P = .03).32 The rate of neonatal morbidity was similar in the 2 groups.

Women with twin gestations and the first twin in a cephalic presentation may elect vaginal delivery. In a large clinical trial, 1,398 women with a twin gestation and the first twin in a cephalic presentation were randomly assigned to planned vaginal delivery (with cesarean only if necessary) or planned CD.33 The rate of CD was 44% and 91% for the women in the planned-vaginal and planned-cesarean groups, respectively. There was no significant difference in composite fetal or neonatal death or serious morbidity. The authors concluded that, for twin pregnancy with the presenting twin in the cephalic presentation, there were no demonstrated benefits of planned CD.

Develop maternity care systems that encourage the use of trial of labor after cesarean (TOLAC). The ACOG/SMFM guidelines focus on interventions to reduce the rate of primary CD and do not address the role of TOLAC in reducing CD rates. There are little data from clinical trials to assess the benefits and harms from TOLAC versus scheduled repeat CD.34 However, our experience with TOLAC in the 1990s strongly suggests that encouraging TOLAC will decrease the rate of CD. In 1996 the US rate of vaginal birth after cesarean (VBAC) peaked at 28%, and the rate of CD achieved a recent historic nadir of 21%. Growing concerns that TOLAC occasionally results in fetal harm was followed by a decrease in the VBAC rate to 12% in 2015.1 A recent study of obstetric practices in countries with high and low VBAC rates concluded that patient and clinician commitment and comfort with prioritizing TOLAC over scheduled repeat CD greatly influenced the VBAC rate.35


Related article:
Should lower uterine segment thickness measurement be included in the TOLAC decision-making process?

Labor management is an art

During labor obstetricians must balance the unique needs of mother and fetus, which requires great clinical skill and patience. Evolving concepts of normal labor progress necessitate that we change our expectations concerning the acceptable rate of progress in the 1st and 2nd stage of labor. Consistent application of these new labor guidelines may help to reduce the rate of CD.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

During the past 45 years, the cesarean delivery (CD) rate in the United States has increased from 5.5% in 1970 to 33% from 2009 to 2013, followed by a small decrease to 32% in 2014 and 2015.1 Many clinical problems cause clinicians and patients to decide that CD is an optimal birth route, including: abnormal labor progress, abnormal or indeterminate fetal heart rate pattern, breech presentation, multiple gestation, macrosomia, placental and cord abnormalities, preeclampsia, prior uterine surgery, and prior CD.2 Recent secular trends that contribute to the current rate of CD include an adversarial liability environment,3,4 increasing rates of maternal obesity,5 and widespread use of continuous fetal-heart monitoring during labor.6

Wide variation in CD rate has been reported among countries, states, and hospitals. The variation is due, in part, to different perspectives about balancing the harms and benefits of vaginal delivery versus CD. In Europe, in 2010 the CD rates in Sweden and Italy were 17.1% and 38%, respectively.7 In 2010, among the states, Alaska had the lowest rate of CD at 22% and Kentucky had the highest rate at 40%.8 In 2015, the highest rate was 38%, in Mississippi (FIGURE).9 In 2014, among Massachusetts hospitals with more than 2,500 births, the CD rate ranged from a low of 22% to a high of 37%.10

Clinicians, patients, policy experts, and the media are perplexed and troubled by the “high” US CD rate and the major variation in rate among countries, states, and hospitals. Labor management practices likely influence the rate of CD and diverse approaches to labor management likely account for the wide variation in CD rates.

A nationwide effort to standardize and continuously improve labor management might result in a decrease in the CD rate. Building on this opportunity, the American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal-Fetal Medicine (SMFM) have jointly recommended new labor management guidelines that may reduce the primary CD rate.8

The ACOG/SMFM guidelines encourage obstetricians to extend the time for labor progress in both the 1st and 2nd stages prior to recommending a CD.8 These new guidelines emphasize that for a modern obstetrician, patience is a virtue. There are 2 important caveats to this statement: to safely extend the length of time of labor requires both (1) a reassuring fetal heart rate tracing and (2) stable maternal health. If the fetus demonstrates a persistent worrisome Category II or a Category IIIheart-rate tracing, decisive intervention is necessary and permitting an extended labor would not be optimal. Similarly, if the mother has rapidly worsening preeclampsia it may not be wise to extend an induction of labor (IOL) over many days.

There are risks with extending the length of labor. An extended duration of the 1st stage of labor is associated with an increased rate of maternal chorioamnionitis and shoulder dystocia at birth.11 An extended duration of the 2nd stage of labor is associated with an increase in the rate of maternal chorioamnionitis, anal sphincter injury, uterine atony, and neonatal admission to an intensive care unit.12 Clinicians who adopt practices that permit an extended length of labor must weigh the benefits of avoiding a CD against these maternal and fetal complications.

Active phase redefined

Central to the ACOG/SMFM guidelines is a new definition of the active phase of labor. The research of Dr. Emmanuel Friedman indicated that at approximately 4 cm of cervical dilation many women in labor transition from the latent phase, a time of slow change in cervical dilation, to the active phase, a time of more rapid change in cervical dilation.13,14 However, more recent research indicates that the transition between the latent and active phase is difficult to precisely define, but more often occurs at about 6 cm of cervical dilation and not 4 cm of dilation.15 Adopting these new norms means that laboring women will spend much more time in the latent phase, a phase of labor in which patience is a virtue.

The ACOG/SMFM guidelines

Main takeaways from the ACOG/SMFM guidelines are summarized below. Interventions that address common obstetric issues and labor abnormalities are outlined below.

Do not perform CD for a prolonged latent phase of labor, defined as regular contractions of >20 hours duration in nulliparous women and >14 hours duration in multiparous women. Patience with a prolonged latent phase will be rewarded by the majority of women entering the active phase of labor. Alternatively, if appropriate, cervical ripening followed by oxytocin IOL and amniotomy will help the patient with a prolonged latent phase to enter the active phase of labor.16

For women with an unfavorable cervix as assessed by the Bishop score, cervical ripening should be performed prior to IOL. Use of cervical ripening prior to IOL increases the chance of achieving vaginal delivery within 24 hours and may result in a modest decrease in the rate of CD.17,18


Related article:
Should oxytocin and a Foley catheter be used concurrently for cervical ripening in induction of labor?
 

Failed IOL in the latent phase should only be diagnosed following 12 to 18 hours of both ruptured membranes and adequate contractions stimulated with oxytocin. The key ingredients for the successful management of the latent phase of labor are patience, oxytocin, and amniotomy.16

CD for the indication of active phase arrest requires cervical dilation ≥6 cm with ruptured membranes and no change in cervical dilation for ≥4 hours of adequate uterine activity. In the past, most obstetricians defined active phase arrest, a potential indication for CD, as the absence of cervical change for 2 or more hours in the presence of adequate uterine contractions and cervical dilation of at least 4 cm. Given the new definition of active phase arrest, slow but progressive progress in the 1st stage of labor is not an indication for CD.11,19

“A specific absolute maximum length of time spent in the 2nd stage beyond which all women should be offered an operative delivery has not been identified.”8 Diagnosis of arrest of labor in the 2nd stage may be considered after at least 2 hours of pushing in multiparous women and 3 hours of pushing in nulliparous women, especially if no fetal descent is occurring. The guidelines also state “longer durations may be appropriate on an individualized basis (eg, with use of epidural analgesia or with fetal malposition)” as long as fetal descent is observed.

Patience is a virtue, especially in the management of the 2nd stage of labor. Extending the 2nd stage up to 4 hours appears to be reasonably safe if the fetal status is reassuring and the mother is physiologically stable. In a study from San Francisco of 42,268 births with normal newborn outcomes, the 95th percentile for the length of the 2nd stage of labor for nulliparous women was 3.3 hours without an epidural and 5.6 hours with an epidural.20

In a study of 53,285 births, longer duration of pushing was associated with a small increase in the rate of neonatal adverse outcomes. In nulliparous women the rate of adverse neonatal outcomes increased from 1.3% with less than 60 minutes of pushing to 2.4% with greater than 240 minutes of pushing. Remarkably, even after 4 hours of pushing, 78% of nulliparous women who continued to push had a vaginal delivery.21 In this study, among nulliparous women the rate of anal sphincter injury increased from 5% with less than 60 minutes of pushing to 16% with greater than 240 minutes of pushing, and the rate of postpartum hemorrhage increased from 1% with less than 60 minutes of pushing to 3.3% with greater than 240 minutes of pushing.

I am not enthusiastic about patiently watching a labor extend into the 5th hour of the 2nd stage, especially if the fetus is at +2 station or lower. In a nulliparous woman, after 4 hours of managing the 2nd stage of labor, my patience is exhausted and I am inclined to identify a clear plan for delivery, either by enhanced labor coaching, operative vaginal delivery, or CD.

Operative vaginal delivery in the 2nd stage of labor is an acceptable alternative to CD. The rate of operative vaginal delivery in the United States has declined over the past 2 decades (TABLE). In Sweden in 2010 the operative vaginal delivery rate was 7.6% with a CD rate of 17.1%.7 In the United States in 2010 the operative delivery rate was 3.6%, and the CD rate was 33%.1 A renewed focus on operative vaginal delivery with ongoing training and team simulation for the procedure would increase our use of operative delivery and decrease the overall rate of CD.


Related article:
STOP using instruments to assist with delivery of the head at cesarean
 

Encourage the detection of persistent fetal occiput posterior position by physical examination and/or ultrasound and consider manual rotation of the fetal occiput from the posterior to anterior position in the 2nd stage. Persistent occiput posterior is the most common fetal malposition.22 This malposition is associated with an increased rate of CD.23 There are few randomized trials of manual rotation of the fetal occiput from posterior to anterior position in the 2nd stage of labor, and the evidence is insufficient to determine the efficacy of manual rotation.24 Small nonrandomized studies report that manual rotation of the occiput from posterior to anterior position may reduce the CD rate.25–27

For persistent 2nd stage fetal occiput posterior position in a woman with an adequate pelvis, where manual rotation was not successful and the fetus is at +2 station or below, operative vaginal delivery is an option. “Vacuum or forceps?” and “If forceps, to rotate or not to rotate?” those are the clinical questions. Forceps delivery is more likely to be successfulthan vacuum delivery.28 Direct forceps delivery of the occiput posterior fetus is associated with more anal sphincter injuries than forceps delivery after successful rotation, but few clinicians regularly perform rotational forceps.29 In a study of 2,351 women in the 2nd stage of labor with the fetus at +2 station or below, compared with either forceps or vacuum delivery, CD was associated with more maternal infections and fewer perineal lacerations. Neonatal composite morbidity was not significantly different among the 3 routes of operative delivery.30

Amnioinfusion for repetitive variable decelerations of the fetal heart rate may reduce the risk of CD for an indeterminate fetal heart-rate pattern.31

IOL in a well-dated pregnancy at 41 weeks will reduce the risk of CD. In a large clinical trial, 3,407 women at 41 weeks of gestation were randomly assigned to IOL or expectant management. The rate of CD was significantly lower in the women assigned to IOL compared with expectant management (21% vs 25%, respectively; P = .03).32 The rate of neonatal morbidity was similar in the 2 groups.

Women with twin gestations and the first twin in a cephalic presentation may elect vaginal delivery. In a large clinical trial, 1,398 women with a twin gestation and the first twin in a cephalic presentation were randomly assigned to planned vaginal delivery (with cesarean only if necessary) or planned CD.33 The rate of CD was 44% and 91% for the women in the planned-vaginal and planned-cesarean groups, respectively. There was no significant difference in composite fetal or neonatal death or serious morbidity. The authors concluded that, for twin pregnancy with the presenting twin in the cephalic presentation, there were no demonstrated benefits of planned CD.

Develop maternity care systems that encourage the use of trial of labor after cesarean (TOLAC). The ACOG/SMFM guidelines focus on interventions to reduce the rate of primary CD and do not address the role of TOLAC in reducing CD rates. There are little data from clinical trials to assess the benefits and harms from TOLAC versus scheduled repeat CD.34 However, our experience with TOLAC in the 1990s strongly suggests that encouraging TOLAC will decrease the rate of CD. In 1996 the US rate of vaginal birth after cesarean (VBAC) peaked at 28%, and the rate of CD achieved a recent historic nadir of 21%. Growing concerns that TOLAC occasionally results in fetal harm was followed by a decrease in the VBAC rate to 12% in 2015.1 A recent study of obstetric practices in countries with high and low VBAC rates concluded that patient and clinician commitment and comfort with prioritizing TOLAC over scheduled repeat CD greatly influenced the VBAC rate.35


Related article:
Should lower uterine segment thickness measurement be included in the TOLAC decision-making process?

Labor management is an art

During labor obstetricians must balance the unique needs of mother and fetus, which requires great clinical skill and patience. Evolving concepts of normal labor progress necessitate that we change our expectations concerning the acceptable rate of progress in the 1st and 2nd stage of labor. Consistent application of these new labor guidelines may help to reduce the rate of CD.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Martin JA, Hamilton BE, Osterman MJ, Driscoll AK, Matthews TJ. Births: final data for 2015. Natl Vital Stat Rep. 2017;66(1):1–70. https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_01.pdf. Accessed July 5, 2017.
  2. Barber EL, Lundsberg LS, Belanger K, Pettker CM, Funai EF, Illuzzi JL. Indications contributing to the increasing cesarean delivery rate. Obstet Gynecol. 2011;118(1):29–38.
  3. Localio AR, Lawthers AG, Bengtson JM, et al. Relationship between malpractice claims and cesarean delivery. JAMA. 1993;269(3):366–373.
  4. Cheng YW, Snowden JM, Handler SJ, Tager IB, Hubbard AE, Caughey AB. Litigation in obstetrics: does defensive medicine contribute to increases in cesarean delivery? J Matern Fetal Neonatal Med. 2014;27(16):1668–1675.
  5. Graham LE, Brunner Huber LR, Thompson ME, Ersek JL. Does amount of weight gain during pregnancy modify the association between obesity and cesarean section delivery? Birth. 2014;41(1):93–99.
  6. Alfirevic Z, Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane Database Syst Rev. 2013;(5):CD006066.
  7. European Perinatal Health Report. Euro-Peristat website. http://www.europeristat.com/. Published 2012. Accessed July 5, 2017.
  8. American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric care consensus no. 1: safe prevention of the primary cesarean delivery. Obstet Gynecol. 2014;123(3):693–711.
  9. Cesarean delivery rate by state, 2015. Centers for Disease Control and Prevention website. https://www.cdc.gov/nchs/pressroom/sosmap/cesarean_births/cesareans.htm. Updated  January 9, 2017. Accessed July 18, 2017.
  10. Baker CD, Land T; Massachusetts Department of Public Health. Massachusetts Births 2014. Massachusetts Executive Office of Health and Human Services website. http://www.mass.gov/eohhs/gov/departments/dph/programs/admin/dmoa/repi/birth-data.html. Published September 2015. Accessed July 5, 2017.
  11. Henry DE, Cheng YW, Shaffer BL, Kaimal AJ, Bianco K, Caughey AB. Perinatal outcomes in the setting of active phase arrest of labor. Obstet Gynecol. 2008;112(5):1109–1115.
  12. Rouse DJ, Weiner SJ, Bloom SL, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Second-stage labor duration in nulliparous women: relationship to maternal and perinatal outcomes. Am J Obstet Gynecol. 2009;201(4):357.e1–e7.
  13. Friedman EZ. Labour: Clinical evaluation and management. Appleton-Century-Crofts: New York, NY; 1967.
  14. Friedman E. The graphic analysis of labor. Am J Obstet Gynecol. 1954;68(6):1568–1575.
  15. Zhang J, Landy HJ, Branch DW, et al; Consortium on Safe Labor. Contemporary patterns  of spontaneous labor with normal neonatal outcomes. Obstet Gynecol. 2010;116(6):1281–1287.
  16. Wei S, Wo BL, Qi HP, et al. Early amniotomy and early oxytocin for prevention of, or therapy for, delay in first stage spontaneous labour compared with routine care. Cochrane Database Syst Rev. 2013;(8):CD006794.
  17. Thomas J, Fairclough A, Kavanagh J, Kelly AJ. Vaginal prostaglandin (PGE2  and  PGF2a) for induction of labour at term. Cochrane Database Syst Rev. 2014;(6):CD003101.
  18. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane Database Syst Rev. 2009;(4):CD003246.
  19. Rouse DJ, Owen J, Savage KG, Hauth JC. Active phase labor arrest: revisiting the 2-hour minimum. Obstet Gynecol. 2001;98(4):550–554.
  20. Cheng YW, Shaffer BL, Nicholson JM, Caughey AB. Second stage of labor and epidural use: a larger effect than previously suggested. Obstet Gynecol. 2014;123(3):527–535.
  21. Grobman WA, Bailit J, Lai Y, et al; Eunice Kennedy Shriver National Institute of Child  and Human Development (NICHD) Maternal-Fetal Medicine Units (MFMU) Network. Association of the duration of active pushing with obstetric outcomes. Obstet Gynecol. 2016;127(4):667–673.
  22. Barth WH Jr. Persistent occiput posterior. Obstet Gynecol. 2015;125(3):695–709.
  23. Carseldine WJ, Phipps H, Zawada SF, et al. Does occiput posterior position in the second stage of labour increase the operative delivery rate? Aust N Z J Obstet Gynaecol. 2013;53(3):265–270.
  24. Phipps H, de Vries B, Hyett J, Osborn DA. Prophylactic manual rotation for fetal  malposition to reduce operative delivery. Cochrane Database Syst Rev. 2014;(12):CD009298.
  25. Shaffer BL, Cheng YW, Vargas JE, Caughey AB. Manual rotation to reduce caesarean delivery in persistent occiput posterior or transverse position. J Matern Fetal Neonatal Med. 2011;24(1):65–72.
  26. Le Ray C, Serres P, Schmitz T, Cabrol D, Goffinet F. Manual rotation in occiput posterior or transverse positions: risk factors and consequences on the cesarean delivery rate. Obstet Gynecol. 2007;110(4):873–879.
  27. Reichman O, Gdansky E, Latinsky B, Labi S, Samueloff A. Digital rotation from occipito-posterior to occipito-anterior decreases the need for cesarean section. Eur J Obstet Gynecol Repro Biol. 2008;136:25–28.
  28. O’Mahony F, Hofmeyr GJ, Menon V. Choice of instruments for assisted vaginal delivery. Cochrane Database Syst Rev. 2010;(11):CD005455.
  29. Hirsch E, Elue R, Wagner A Jr, et al. Severe perineal laceration during operative vaginal  delivery: the impact of occiput posterior position. J Perinatol. 2014;34(12):898–900.
  30. Bailit JL, Grobman WA, Rice MM, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Evaluation of delivery options for second-stage events. Am J Obstet Gynecol. 2016;214(5):638.e1–e10.
  31. Hofmeyr GJ, Lawrie TA. Amnioinfusion for potential or suspected umbilical cord compression in labour. Cochrane Database Syst Rev. 2012;1:CD000013.
  32. Hannah ME, Hannah WJ, Hellmann J, Hewson S, Milner R, Willan A. Induction of labor as compared with serial antenatal monitoring in post-term pregnancy. A randomized controlled trial. The Canadian Multicenter Post-term Pregnancy Trial Group. N Engl J Med. 1992;326(24): 1587–1592.
  33. Barrett JF, Hannah ME, Hutton EK, et al; Twin Birth Study Collaborative Group. A randomized trial of planned cesarean or vaginal delivery for twin pregnancy. N Engl J Med. 2013;369(14):1295–1305.
  34. Dodd JM, Crowther CA, Huertas E, Guise JM, Horey D. Planned elective repeat cesarean section versus planned vaginal birth for women with a previous caesarean birth. Cochrane Database Syst Rev. 2013;(12):CD004224.
  35. Lundgren I, van Limbeek E, Vehvilainen-Julkunen K, Nilsson C. Clinicians’ views of factors of importance for improving the rate of VBAC (vaginal birth after caesarean section): a qualitative study from countries with high VBAC rates. BMC Pregnancy Childbirth. 2015;15:196.
References
  1. Martin JA, Hamilton BE, Osterman MJ, Driscoll AK, Matthews TJ. Births: final data for 2015. Natl Vital Stat Rep. 2017;66(1):1–70. https://www.cdc.gov/nchs/data/nvsr/nvsr66/nvsr66_01.pdf. Accessed July 5, 2017.
  2. Barber EL, Lundsberg LS, Belanger K, Pettker CM, Funai EF, Illuzzi JL. Indications contributing to the increasing cesarean delivery rate. Obstet Gynecol. 2011;118(1):29–38.
  3. Localio AR, Lawthers AG, Bengtson JM, et al. Relationship between malpractice claims and cesarean delivery. JAMA. 1993;269(3):366–373.
  4. Cheng YW, Snowden JM, Handler SJ, Tager IB, Hubbard AE, Caughey AB. Litigation in obstetrics: does defensive medicine contribute to increases in cesarean delivery? J Matern Fetal Neonatal Med. 2014;27(16):1668–1675.
  5. Graham LE, Brunner Huber LR, Thompson ME, Ersek JL. Does amount of weight gain during pregnancy modify the association between obesity and cesarean section delivery? Birth. 2014;41(1):93–99.
  6. Alfirevic Z, Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane Database Syst Rev. 2013;(5):CD006066.
  7. European Perinatal Health Report. Euro-Peristat website. http://www.europeristat.com/. Published 2012. Accessed July 5, 2017.
  8. American College of Obstetricians and Gynecologists; Society for Maternal-Fetal Medicine. Obstetric care consensus no. 1: safe prevention of the primary cesarean delivery. Obstet Gynecol. 2014;123(3):693–711.
  9. Cesarean delivery rate by state, 2015. Centers for Disease Control and Prevention website. https://www.cdc.gov/nchs/pressroom/sosmap/cesarean_births/cesareans.htm. Updated  January 9, 2017. Accessed July 18, 2017.
  10. Baker CD, Land T; Massachusetts Department of Public Health. Massachusetts Births 2014. Massachusetts Executive Office of Health and Human Services website. http://www.mass.gov/eohhs/gov/departments/dph/programs/admin/dmoa/repi/birth-data.html. Published September 2015. Accessed July 5, 2017.
  11. Henry DE, Cheng YW, Shaffer BL, Kaimal AJ, Bianco K, Caughey AB. Perinatal outcomes in the setting of active phase arrest of labor. Obstet Gynecol. 2008;112(5):1109–1115.
  12. Rouse DJ, Weiner SJ, Bloom SL, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Second-stage labor duration in nulliparous women: relationship to maternal and perinatal outcomes. Am J Obstet Gynecol. 2009;201(4):357.e1–e7.
  13. Friedman EZ. Labour: Clinical evaluation and management. Appleton-Century-Crofts: New York, NY; 1967.
  14. Friedman E. The graphic analysis of labor. Am J Obstet Gynecol. 1954;68(6):1568–1575.
  15. Zhang J, Landy HJ, Branch DW, et al; Consortium on Safe Labor. Contemporary patterns  of spontaneous labor with normal neonatal outcomes. Obstet Gynecol. 2010;116(6):1281–1287.
  16. Wei S, Wo BL, Qi HP, et al. Early amniotomy and early oxytocin for prevention of, or therapy for, delay in first stage spontaneous labour compared with routine care. Cochrane Database Syst Rev. 2013;(8):CD006794.
  17. Thomas J, Fairclough A, Kavanagh J, Kelly AJ. Vaginal prostaglandin (PGE2  and  PGF2a) for induction of labour at term. Cochrane Database Syst Rev. 2014;(6):CD003101.
  18. Alfirevic Z, Kelly AJ, Dowswell T. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane Database Syst Rev. 2009;(4):CD003246.
  19. Rouse DJ, Owen J, Savage KG, Hauth JC. Active phase labor arrest: revisiting the 2-hour minimum. Obstet Gynecol. 2001;98(4):550–554.
  20. Cheng YW, Shaffer BL, Nicholson JM, Caughey AB. Second stage of labor and epidural use: a larger effect than previously suggested. Obstet Gynecol. 2014;123(3):527–535.
  21. Grobman WA, Bailit J, Lai Y, et al; Eunice Kennedy Shriver National Institute of Child  and Human Development (NICHD) Maternal-Fetal Medicine Units (MFMU) Network. Association of the duration of active pushing with obstetric outcomes. Obstet Gynecol. 2016;127(4):667–673.
  22. Barth WH Jr. Persistent occiput posterior. Obstet Gynecol. 2015;125(3):695–709.
  23. Carseldine WJ, Phipps H, Zawada SF, et al. Does occiput posterior position in the second stage of labour increase the operative delivery rate? Aust N Z J Obstet Gynaecol. 2013;53(3):265–270.
  24. Phipps H, de Vries B, Hyett J, Osborn DA. Prophylactic manual rotation for fetal  malposition to reduce operative delivery. Cochrane Database Syst Rev. 2014;(12):CD009298.
  25. Shaffer BL, Cheng YW, Vargas JE, Caughey AB. Manual rotation to reduce caesarean delivery in persistent occiput posterior or transverse position. J Matern Fetal Neonatal Med. 2011;24(1):65–72.
  26. Le Ray C, Serres P, Schmitz T, Cabrol D, Goffinet F. Manual rotation in occiput posterior or transverse positions: risk factors and consequences on the cesarean delivery rate. Obstet Gynecol. 2007;110(4):873–879.
  27. Reichman O, Gdansky E, Latinsky B, Labi S, Samueloff A. Digital rotation from occipito-posterior to occipito-anterior decreases the need for cesarean section. Eur J Obstet Gynecol Repro Biol. 2008;136:25–28.
  28. O’Mahony F, Hofmeyr GJ, Menon V. Choice of instruments for assisted vaginal delivery. Cochrane Database Syst Rev. 2010;(11):CD005455.
  29. Hirsch E, Elue R, Wagner A Jr, et al. Severe perineal laceration during operative vaginal  delivery: the impact of occiput posterior position. J Perinatol. 2014;34(12):898–900.
  30. Bailit JL, Grobman WA, Rice MM, et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Evaluation of delivery options for second-stage events. Am J Obstet Gynecol. 2016;214(5):638.e1–e10.
  31. Hofmeyr GJ, Lawrie TA. Amnioinfusion for potential or suspected umbilical cord compression in labour. Cochrane Database Syst Rev. 2012;1:CD000013.
  32. Hannah ME, Hannah WJ, Hellmann J, Hewson S, Milner R, Willan A. Induction of labor as compared with serial antenatal monitoring in post-term pregnancy. A randomized controlled trial. The Canadian Multicenter Post-term Pregnancy Trial Group. N Engl J Med. 1992;326(24): 1587–1592.
  33. Barrett JF, Hannah ME, Hutton EK, et al; Twin Birth Study Collaborative Group. A randomized trial of planned cesarean or vaginal delivery for twin pregnancy. N Engl J Med. 2013;369(14):1295–1305.
  34. Dodd JM, Crowther CA, Huertas E, Guise JM, Horey D. Planned elective repeat cesarean section versus planned vaginal birth for women with a previous caesarean birth. Cochrane Database Syst Rev. 2013;(12):CD004224.
  35. Lundgren I, van Limbeek E, Vehvilainen-Julkunen K, Nilsson C. Clinicians’ views of factors of importance for improving the rate of VBAC (vaginal birth after caesarean section): a qualitative study from countries with high VBAC rates. BMC Pregnancy Childbirth. 2015;15:196.
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Product Update: Hologic Aptima HSV Assay, Cianna SAVI SCOUT, Olympus Hystero-Resectoscope, and Clarius Ultrasound Scanners

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Product Update: Hologic Aptima HSV Assay, Cianna SAVI SCOUT, Olympus Hystero-Resectoscope, and Clarius Ultrasound Scanners

DIAGNOSE HERPES SIMPLEX VIRUS

Hologic now offers the Aptima Herpes Simplex Virus (HSV) 1 & 2 molecular assay. This nucleic acid amplification test detects and differentiates between HSV-1 and HSV-2 strains in anal and genital lesions. Specimens are collected using the Aptima Multitest Swab Specimen Collection Kit or commercially available viral transport media. The Centers for Disease Control and Prevention (CDC) recommends that all patients with first-episode genital herpes be tested for strain type. According to Hologic, studies show that HSV molecular diagnostics like the Aptima HSV assay are 3 to 5 times more sensitive than live culture samples.

According to the CDC, infections with HSV-2 affect more than 24 million Americans. Patients with HSV-2 strain are at increased risk for contracting and transmitting HIV. Pregnant women infected with HSV-2 are at risk of transmitting the virus to their babies, with increased risk for neurologic complications in the child. 

FOR MORE INFORMATION, VISIT: http://www.hologic.com/search/site/aptima%20hsv

 

PRECISELY TARGET TISSUE DURING LUMPECTOMY OR BIOPSY

Cianna Medical designed the SAVI SCOUT Radar Localization System using radar instead of wires or radiation to help surgeons target tissue during breast lumpectomy or surgical biopsy. According to Cianna Medical, a reflector smaller than a grain of rice is placed into the breast up to 30 days before surgery. During the procedure, the SCOUT guide detects the reflector, allowing surgeons to precisely focus on the affected tissue. SCOUT's detection range is 1 mm to 50 mm. Cianna Medical says that this localization level allows for better surgical planning that may improve cosmetic results as less tissue may need to be removed. 

Cianna Medical reported recent data showing that, when compared with wire localization, the SCOUT reduces breast surgery operating room (OR) delay times by 72.5%, resulted in an average 29- minute reduction in OR waiting time, and significantly improved workflow efficiency.

FOR MORE INFORMATION, VISIT: https://www.ciannamedical.com/savi-scout/

 

PLASMA HYSTEROSCOPIC RESECTION

The 8.5-mm Hystero-Resectoscope and others in the Olympus plasma hysteroscopic resection and vaporization product portfolio have recently received US Food and Drug Administration clearance. Olympus asserts that bipolar electrosurgery featured in the plasma hysteroscopic resection and vaporization system has lower risks of electrolyte imbalance (hyponatremia) compared with monopolar electrosurgery. In addition to improved patient outcomes, Olympus says that its system benefits include cutting precision, better visibility, and cost-savings potential by using a variety of plasma-enabled electrodes in multiple hysteroscopic procedures.

During gynecologic procedures, the Olympus 8.5-mm hystero-resectoscope uses a combination of radio frequency, energy, and saline to create plasma, an electrically conductive gas cloud of vapor and charged particles. Due to its conductivity, plasma allows energy to cross into targeted tissue at lower energy levels than with more traditional approaches. This effect leads to lower operating temperatures and therefore less thermal spread.

FOR MORE INFORMATION, VISIT:  http://olympusmedical.com.sg

 

APP-BASED HANDHELD ULTRASOUND

Clarius Mobile Health is offering Point-and-Shoot Ultrasound Scanners that operate with any iOS or Android smart device using an app. Clarius says its wireless, handheld ultrasound scanners help ObGyns perform quick scans or are used to guide short procedures at bedside without having to rely on the availability of a cart-based ultrasound system. The Clarius C3 Scanner is designed for scanning all parts of the patient's torso, including the heart. The Clarius L7 Linear Array Ultrasound Scanner is ideal for guiding procedures. Both scanners have automated gain and frequency settings.

High-resolution images can be saved, reviewed, and managed on the secure Clarius Cloud. Built with a durable magnesium shell, each device has an IPX7 immersion rating so it can be sterilized. Power is obtained from a rechargeable battery that will last for more than 45 minutes of scanning; 2 batteries come with each Clarius device.

FOR MORE INFORMATION, VISIT: https://www.clarius.me/

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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DIAGNOSE HERPES SIMPLEX VIRUS

Hologic now offers the Aptima Herpes Simplex Virus (HSV) 1 & 2 molecular assay. This nucleic acid amplification test detects and differentiates between HSV-1 and HSV-2 strains in anal and genital lesions. Specimens are collected using the Aptima Multitest Swab Specimen Collection Kit or commercially available viral transport media. The Centers for Disease Control and Prevention (CDC) recommends that all patients with first-episode genital herpes be tested for strain type. According to Hologic, studies show that HSV molecular diagnostics like the Aptima HSV assay are 3 to 5 times more sensitive than live culture samples.

According to the CDC, infections with HSV-2 affect more than 24 million Americans. Patients with HSV-2 strain are at increased risk for contracting and transmitting HIV. Pregnant women infected with HSV-2 are at risk of transmitting the virus to their babies, with increased risk for neurologic complications in the child. 

FOR MORE INFORMATION, VISIT: http://www.hologic.com/search/site/aptima%20hsv

 

PRECISELY TARGET TISSUE DURING LUMPECTOMY OR BIOPSY

Cianna Medical designed the SAVI SCOUT Radar Localization System using radar instead of wires or radiation to help surgeons target tissue during breast lumpectomy or surgical biopsy. According to Cianna Medical, a reflector smaller than a grain of rice is placed into the breast up to 30 days before surgery. During the procedure, the SCOUT guide detects the reflector, allowing surgeons to precisely focus on the affected tissue. SCOUT's detection range is 1 mm to 50 mm. Cianna Medical says that this localization level allows for better surgical planning that may improve cosmetic results as less tissue may need to be removed. 

Cianna Medical reported recent data showing that, when compared with wire localization, the SCOUT reduces breast surgery operating room (OR) delay times by 72.5%, resulted in an average 29- minute reduction in OR waiting time, and significantly improved workflow efficiency.

FOR MORE INFORMATION, VISIT: https://www.ciannamedical.com/savi-scout/

 

PLASMA HYSTEROSCOPIC RESECTION

The 8.5-mm Hystero-Resectoscope and others in the Olympus plasma hysteroscopic resection and vaporization product portfolio have recently received US Food and Drug Administration clearance. Olympus asserts that bipolar electrosurgery featured in the plasma hysteroscopic resection and vaporization system has lower risks of electrolyte imbalance (hyponatremia) compared with monopolar electrosurgery. In addition to improved patient outcomes, Olympus says that its system benefits include cutting precision, better visibility, and cost-savings potential by using a variety of plasma-enabled electrodes in multiple hysteroscopic procedures.

During gynecologic procedures, the Olympus 8.5-mm hystero-resectoscope uses a combination of radio frequency, energy, and saline to create plasma, an electrically conductive gas cloud of vapor and charged particles. Due to its conductivity, plasma allows energy to cross into targeted tissue at lower energy levels than with more traditional approaches. This effect leads to lower operating temperatures and therefore less thermal spread.

FOR MORE INFORMATION, VISIT:  http://olympusmedical.com.sg

 

APP-BASED HANDHELD ULTRASOUND

Clarius Mobile Health is offering Point-and-Shoot Ultrasound Scanners that operate with any iOS or Android smart device using an app. Clarius says its wireless, handheld ultrasound scanners help ObGyns perform quick scans or are used to guide short procedures at bedside without having to rely on the availability of a cart-based ultrasound system. The Clarius C3 Scanner is designed for scanning all parts of the patient's torso, including the heart. The Clarius L7 Linear Array Ultrasound Scanner is ideal for guiding procedures. Both scanners have automated gain and frequency settings.

High-resolution images can be saved, reviewed, and managed on the secure Clarius Cloud. Built with a durable magnesium shell, each device has an IPX7 immersion rating so it can be sterilized. Power is obtained from a rechargeable battery that will last for more than 45 minutes of scanning; 2 batteries come with each Clarius device.

FOR MORE INFORMATION, VISIT: https://www.clarius.me/

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

DIAGNOSE HERPES SIMPLEX VIRUS

Hologic now offers the Aptima Herpes Simplex Virus (HSV) 1 & 2 molecular assay. This nucleic acid amplification test detects and differentiates between HSV-1 and HSV-2 strains in anal and genital lesions. Specimens are collected using the Aptima Multitest Swab Specimen Collection Kit or commercially available viral transport media. The Centers for Disease Control and Prevention (CDC) recommends that all patients with first-episode genital herpes be tested for strain type. According to Hologic, studies show that HSV molecular diagnostics like the Aptima HSV assay are 3 to 5 times more sensitive than live culture samples.

According to the CDC, infections with HSV-2 affect more than 24 million Americans. Patients with HSV-2 strain are at increased risk for contracting and transmitting HIV. Pregnant women infected with HSV-2 are at risk of transmitting the virus to their babies, with increased risk for neurologic complications in the child. 

FOR MORE INFORMATION, VISIT: http://www.hologic.com/search/site/aptima%20hsv

 

PRECISELY TARGET TISSUE DURING LUMPECTOMY OR BIOPSY

Cianna Medical designed the SAVI SCOUT Radar Localization System using radar instead of wires or radiation to help surgeons target tissue during breast lumpectomy or surgical biopsy. According to Cianna Medical, a reflector smaller than a grain of rice is placed into the breast up to 30 days before surgery. During the procedure, the SCOUT guide detects the reflector, allowing surgeons to precisely focus on the affected tissue. SCOUT's detection range is 1 mm to 50 mm. Cianna Medical says that this localization level allows for better surgical planning that may improve cosmetic results as less tissue may need to be removed. 

Cianna Medical reported recent data showing that, when compared with wire localization, the SCOUT reduces breast surgery operating room (OR) delay times by 72.5%, resulted in an average 29- minute reduction in OR waiting time, and significantly improved workflow efficiency.

FOR MORE INFORMATION, VISIT: https://www.ciannamedical.com/savi-scout/

 

PLASMA HYSTEROSCOPIC RESECTION

The 8.5-mm Hystero-Resectoscope and others in the Olympus plasma hysteroscopic resection and vaporization product portfolio have recently received US Food and Drug Administration clearance. Olympus asserts that bipolar electrosurgery featured in the plasma hysteroscopic resection and vaporization system has lower risks of electrolyte imbalance (hyponatremia) compared with monopolar electrosurgery. In addition to improved patient outcomes, Olympus says that its system benefits include cutting precision, better visibility, and cost-savings potential by using a variety of plasma-enabled electrodes in multiple hysteroscopic procedures.

During gynecologic procedures, the Olympus 8.5-mm hystero-resectoscope uses a combination of radio frequency, energy, and saline to create plasma, an electrically conductive gas cloud of vapor and charged particles. Due to its conductivity, plasma allows energy to cross into targeted tissue at lower energy levels than with more traditional approaches. This effect leads to lower operating temperatures and therefore less thermal spread.

FOR MORE INFORMATION, VISIT:  http://olympusmedical.com.sg

 

APP-BASED HANDHELD ULTRASOUND

Clarius Mobile Health is offering Point-and-Shoot Ultrasound Scanners that operate with any iOS or Android smart device using an app. Clarius says its wireless, handheld ultrasound scanners help ObGyns perform quick scans or are used to guide short procedures at bedside without having to rely on the availability of a cart-based ultrasound system. The Clarius C3 Scanner is designed for scanning all parts of the patient's torso, including the heart. The Clarius L7 Linear Array Ultrasound Scanner is ideal for guiding procedures. Both scanners have automated gain and frequency settings.

High-resolution images can be saved, reviewed, and managed on the secure Clarius Cloud. Built with a durable magnesium shell, each device has an IPX7 immersion rating so it can be sterilized. Power is obtained from a rechargeable battery that will last for more than 45 minutes of scanning; 2 batteries come with each Clarius device.

FOR MORE INFORMATION, VISIT: https://www.clarius.me/

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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Product Update: Hologic Aptima HSV Assay, Cianna SAVI SCOUT, Olympus Hystero-Resectoscope, and Clarius Ultrasound Scanners
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Eye spy: Name that IUD

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Eye spy: Name that IUD
Can you identify the specific intrauterine device found on ultrasound?

A) Mirena or Liletta (52 mg LNG-IUD) CORRECT
Mirena (Bayer) and Liletta (Allergan) are progestin-releasing intrauterine devices (IUDs) of similar size and shape. On ultrasonography, both the arms and the distal tip are echogenic. The progestin-containing plastic sleeve surrounding the stem in the middle demonstrates a laminated acoustic shadowing with distinctive parallel lines.1–4

(A) Transvaginal pelvic ultrasound demonstrates a well-positioned (fundally positioned) Mirena or Liletta levonorgestrel (LNG) IUD. Note the laminated appearance of the stem (short arrow). (B) Illustration of Mirena IUD with the plastic sleeve surrounding the stem (long arrow) corresponds to the laminated appearance on ultrasound.

 

B) Small-framed LNG-IUDs: Skyla (13.5 mg) or Kyleena (19.5 mg) INCORRECT
Skyla (Bayer) and Kyleena (Bayer) are small-framed LNG-IUDs. The ultrasound appearance of Skyla (LNG 13.5 mg) is similar to that of Mirena but has a markedly echogenic silver ring superiorly just below the crossbar, best seen with 2D (sagittal) views but also imaged with 3D ultrasound.1,2,5

The Kyleena device (LNG 19.5 mg) uses the same smaller T-shaped frame and metal ring, but the plastic sleeve is longer to accommodate the greater quantity of progestin.6

(A) Transvaginal ultrasound and (B) 3D surface-rendered ultrasound of the uterus demonstrate the echogenic ring (short arrow) below the crossbar. (C) Illustration of Skyla shows the silver ring (long arrow).

 

C) Paragard (intrauterine copper contraceptive) INCORRECT
Paragard (Teva Women’s Health) is a nonhormonal IUD containing copper wire wrapped around its stem and solid copper bands on each crossbar. On ultrasonography, the stem is uniformly and markedly echogenic due to the copper wire.1,2,7

(A) Transvaginal ultrasound of the uterus demonstrates a uniformly and markedly echogenic stem seen in its entirety (short arrow). (B) 3D surface-rendered ultrasound of the uterus shows the solid copper bands on the crossbars (arrowhead). (C) Illustration of the Paragard IUD with the copper wire in the stem (long arrow) and solid copper bands on the crossbars (arrow heads).

References
  1. Stalnaker ML, Kaunitz AM. How to identify and localize IUDs on ultrasound. OBG Manag. 2014;26(8):38,40–41,44.
  2. Boortz HE, Margolis DJ, Ragavendra N, Patel MK, Kadell BM. Migration of intrauterine devices: Radiologic findings and implications for patient care. Radiographics. 2012;32(2):335–352.
  3. Mirena [package insert]. Whippany, NJ: Bayer; 2000.
  4. Liletta [package insert]. Parsippany, NJ: Allergan; 2015.
  5. Skyla [package insert]. Whippany, NJ: Bayer; 2000.
  6. Kyleena [package insert]. Whippany, NJ: Bayer; 2000.
  7. Paragard [package insert]. North Wales, PA: Teva Women’s Health, Inc; 2014.
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Dr. Kanmaniraja is Assistant Professor and Chief, Division of Abdominal Imaging, Department of Radiology, University of Florida College of Medicine–Jacksonville.

Dr. Kaunitz is University of Florida Research Foundation Professor and Associate Chairman, Department of Obstetrics and Gynecology, University of Florida College of Medicine–Jacksonville. He is Medical Director and Director of Menopause and Gynecologic Ultrasound Services at UF Women’s Health Specialists–Emerson. He also serves on the OBG Management Board of Editors.

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Can you identify the specific intrauterine device found on ultrasound?
Can you identify the specific intrauterine device found on ultrasound?

A) Mirena or Liletta (52 mg LNG-IUD) CORRECT
Mirena (Bayer) and Liletta (Allergan) are progestin-releasing intrauterine devices (IUDs) of similar size and shape. On ultrasonography, both the arms and the distal tip are echogenic. The progestin-containing plastic sleeve surrounding the stem in the middle demonstrates a laminated acoustic shadowing with distinctive parallel lines.1–4

(A) Transvaginal pelvic ultrasound demonstrates a well-positioned (fundally positioned) Mirena or Liletta levonorgestrel (LNG) IUD. Note the laminated appearance of the stem (short arrow). (B) Illustration of Mirena IUD with the plastic sleeve surrounding the stem (long arrow) corresponds to the laminated appearance on ultrasound.

 

B) Small-framed LNG-IUDs: Skyla (13.5 mg) or Kyleena (19.5 mg) INCORRECT
Skyla (Bayer) and Kyleena (Bayer) are small-framed LNG-IUDs. The ultrasound appearance of Skyla (LNG 13.5 mg) is similar to that of Mirena but has a markedly echogenic silver ring superiorly just below the crossbar, best seen with 2D (sagittal) views but also imaged with 3D ultrasound.1,2,5

The Kyleena device (LNG 19.5 mg) uses the same smaller T-shaped frame and metal ring, but the plastic sleeve is longer to accommodate the greater quantity of progestin.6

(A) Transvaginal ultrasound and (B) 3D surface-rendered ultrasound of the uterus demonstrate the echogenic ring (short arrow) below the crossbar. (C) Illustration of Skyla shows the silver ring (long arrow).

 

C) Paragard (intrauterine copper contraceptive) INCORRECT
Paragard (Teva Women’s Health) is a nonhormonal IUD containing copper wire wrapped around its stem and solid copper bands on each crossbar. On ultrasonography, the stem is uniformly and markedly echogenic due to the copper wire.1,2,7

(A) Transvaginal ultrasound of the uterus demonstrates a uniformly and markedly echogenic stem seen in its entirety (short arrow). (B) 3D surface-rendered ultrasound of the uterus shows the solid copper bands on the crossbars (arrowhead). (C) Illustration of the Paragard IUD with the copper wire in the stem (long arrow) and solid copper bands on the crossbars (arrow heads).

A) Mirena or Liletta (52 mg LNG-IUD) CORRECT
Mirena (Bayer) and Liletta (Allergan) are progestin-releasing intrauterine devices (IUDs) of similar size and shape. On ultrasonography, both the arms and the distal tip are echogenic. The progestin-containing plastic sleeve surrounding the stem in the middle demonstrates a laminated acoustic shadowing with distinctive parallel lines.1–4

(A) Transvaginal pelvic ultrasound demonstrates a well-positioned (fundally positioned) Mirena or Liletta levonorgestrel (LNG) IUD. Note the laminated appearance of the stem (short arrow). (B) Illustration of Mirena IUD with the plastic sleeve surrounding the stem (long arrow) corresponds to the laminated appearance on ultrasound.

 

B) Small-framed LNG-IUDs: Skyla (13.5 mg) or Kyleena (19.5 mg) INCORRECT
Skyla (Bayer) and Kyleena (Bayer) are small-framed LNG-IUDs. The ultrasound appearance of Skyla (LNG 13.5 mg) is similar to that of Mirena but has a markedly echogenic silver ring superiorly just below the crossbar, best seen with 2D (sagittal) views but also imaged with 3D ultrasound.1,2,5

The Kyleena device (LNG 19.5 mg) uses the same smaller T-shaped frame and metal ring, but the plastic sleeve is longer to accommodate the greater quantity of progestin.6

(A) Transvaginal ultrasound and (B) 3D surface-rendered ultrasound of the uterus demonstrate the echogenic ring (short arrow) below the crossbar. (C) Illustration of Skyla shows the silver ring (long arrow).

 

C) Paragard (intrauterine copper contraceptive) INCORRECT
Paragard (Teva Women’s Health) is a nonhormonal IUD containing copper wire wrapped around its stem and solid copper bands on each crossbar. On ultrasonography, the stem is uniformly and markedly echogenic due to the copper wire.1,2,7

(A) Transvaginal ultrasound of the uterus demonstrates a uniformly and markedly echogenic stem seen in its entirety (short arrow). (B) 3D surface-rendered ultrasound of the uterus shows the solid copper bands on the crossbars (arrowhead). (C) Illustration of the Paragard IUD with the copper wire in the stem (long arrow) and solid copper bands on the crossbars (arrow heads).

References
  1. Stalnaker ML, Kaunitz AM. How to identify and localize IUDs on ultrasound. OBG Manag. 2014;26(8):38,40–41,44.
  2. Boortz HE, Margolis DJ, Ragavendra N, Patel MK, Kadell BM. Migration of intrauterine devices: Radiologic findings and implications for patient care. Radiographics. 2012;32(2):335–352.
  3. Mirena [package insert]. Whippany, NJ: Bayer; 2000.
  4. Liletta [package insert]. Parsippany, NJ: Allergan; 2015.
  5. Skyla [package insert]. Whippany, NJ: Bayer; 2000.
  6. Kyleena [package insert]. Whippany, NJ: Bayer; 2000.
  7. Paragard [package insert]. North Wales, PA: Teva Women’s Health, Inc; 2014.
References
  1. Stalnaker ML, Kaunitz AM. How to identify and localize IUDs on ultrasound. OBG Manag. 2014;26(8):38,40–41,44.
  2. Boortz HE, Margolis DJ, Ragavendra N, Patel MK, Kadell BM. Migration of intrauterine devices: Radiologic findings and implications for patient care. Radiographics. 2012;32(2):335–352.
  3. Mirena [package insert]. Whippany, NJ: Bayer; 2000.
  4. Liletta [package insert]. Parsippany, NJ: Allergan; 2015.
  5. Skyla [package insert]. Whippany, NJ: Bayer; 2000.
  6. Kyleena [package insert]. Whippany, NJ: Bayer; 2000.
  7. Paragard [package insert]. North Wales, PA: Teva Women’s Health, Inc; 2014.
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A 25-year-old woman using an IUD presented to her ObGyn’s office for follow-up care of a 4- to 5-cm left simple ovarian cyst. A pelvic ultrasound was performed. The ovarian cyst had resolved and a fundally-positioned IUD was imaged.

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Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition

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Endometriomas are called chocolate cysts due to the dark brown color of the fluid they contain. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis with spilled endometriotic contents.
Endometriosis, a disorder in which tissue resembling endometrium develops outside the uterine cavity, is a common cause of pelvic pain and infertility, affecting 6% to 10% of women.1 Although endometriosis occurs in almost all organs and anatomic locations, it most often affects the pelvic organs.2 An ovarian endometrioma, an ovarian cystic mass generally consisting of endometrial glands and stroma, is seen in 17% to 44% of women with endometriosis.3 Endometriomas are sometimes called chocolate cysts for the dark brown, thick, and tarry concentrated hemosiderin-laden fluid they contain, but histology shows that not all chocolate cysts have endometriosis within their walls.4 Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition.

Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis

Etiology

Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8

Read about the classification of endometriomas

 

 

Disease classification

Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3

Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4

Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).

Related article:
Imaging the endometrioma and mature cystic teratoma

Presentation and diagnosis

Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12

Read about the surgical management of endometriomas

 

 

Surgical management

Clinical indications

Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.

 

Don't miss the video that accompanies this article!

To watch the authors perform laparoscopic excision of type I and type II endometriomas, click here


 

 

Approach

Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8

With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8

Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1

Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.

The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.

Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
 

Key takeaways
  • Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
  • Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
  • Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
  • The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.  
  • We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue. 

Conclusion

Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
  2. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
  3. Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
  4. Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
  5. Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
  6. Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
  7. Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
  8. Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
  9. Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
  10. Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
  11. Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
  12. Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
  13. Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
  14. Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
  15. Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
  16. Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
  17. Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
  18. Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
  19. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
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Author and Disclosure Information

Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.

Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.

At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.

Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.

Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia. 

Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.

Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.

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Author and Disclosure Information

Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.

Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.

At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.

Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.

Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia. 

Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.

Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.

Author and Disclosure Information

Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.

Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.

At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.

Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.

Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia. 

Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.

Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.

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Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition
Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition

Illustration: Kimberly Martens for OBG Management
Endometriomas are called chocolate cysts due to the dark brown color of the fluid they contain. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis with spilled endometriotic contents.
Endometriosis, a disorder in which tissue resembling endometrium develops outside the uterine cavity, is a common cause of pelvic pain and infertility, affecting 6% to 10% of women.1 Although endometriosis occurs in almost all organs and anatomic locations, it most often affects the pelvic organs.2 An ovarian endometrioma, an ovarian cystic mass generally consisting of endometrial glands and stroma, is seen in 17% to 44% of women with endometriosis.3 Endometriomas are sometimes called chocolate cysts for the dark brown, thick, and tarry concentrated hemosiderin-laden fluid they contain, but histology shows that not all chocolate cysts have endometriosis within their walls.4 Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition.

Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis

Etiology

Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8

Read about the classification of endometriomas

 

 

Disease classification

Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3

Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4

Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).

Related article:
Imaging the endometrioma and mature cystic teratoma

Presentation and diagnosis

Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12

Read about the surgical management of endometriomas

 

 

Surgical management

Clinical indications

Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.

 

Don't miss the video that accompanies this article!

To watch the authors perform laparoscopic excision of type I and type II endometriomas, click here


 

 

Approach

Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8

With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8

Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1

Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.

The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.

Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
 

Key takeaways
  • Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
  • Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
  • Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
  • The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.  
  • We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue. 

Conclusion

Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Illustration: Kimberly Martens for OBG Management
Endometriomas are called chocolate cysts due to the dark brown color of the fluid they contain. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis with spilled endometriotic contents.
Endometriosis, a disorder in which tissue resembling endometrium develops outside the uterine cavity, is a common cause of pelvic pain and infertility, affecting 6% to 10% of women.1 Although endometriosis occurs in almost all organs and anatomic locations, it most often affects the pelvic organs.2 An ovarian endometrioma, an ovarian cystic mass generally consisting of endometrial glands and stroma, is seen in 17% to 44% of women with endometriosis.3 Endometriomas are sometimes called chocolate cysts for the dark brown, thick, and tarry concentrated hemosiderin-laden fluid they contain, but histology shows that not all chocolate cysts have endometriosis within their walls.4 Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition.

Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis

Etiology

Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8

Read about the classification of endometriomas

 

 

Disease classification

Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3

Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4

Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).

Related article:
Imaging the endometrioma and mature cystic teratoma

Presentation and diagnosis

Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12

Read about the surgical management of endometriomas

 

 

Surgical management

Clinical indications

Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.

 

Don't miss the video that accompanies this article!

To watch the authors perform laparoscopic excision of type I and type II endometriomas, click here


 

 

Approach

Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8

With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8

Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1

Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.

The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.

Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
 

Key takeaways
  • Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
  • Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
  • Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
  • The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.  
  • We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue. 

Conclusion

Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
  2. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
  3. Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
  4. Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
  5. Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
  6. Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
  7. Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
  8. Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
  9. Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
  10. Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
  11. Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
  12. Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
  13. Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
  14. Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
  15. Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
  16. Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
  17. Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
  18. Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
  19. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
References
  1. Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
  2. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
  3. Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
  4. Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
  5. Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
  6. Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
  7. Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
  8. Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
  9. Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
  10. Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
  11. Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
  12. Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
  13. Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
  14. Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
  15. Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
  16. Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
  17. Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
  18. Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
  19. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
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Effective treatment of recurrent bacterial vaginosis

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The 3 treatment options presented herein may help to suppress the rate of bacterial vaginosis recurrence and improve patients' symptoms as well as quality of life

Bacterial vaginosis (BV) is caused by a complex change in vaginal bacterial flora, with a reduction in lactobacilli (which help maintain an acidic environment) and an increase in anaerobic gram-negative organisms including Gardnerella vaginalis species and Bacteroides, Prevotella, and Mobiluncus genera. Infection with G vaginalis is thought to trigger a cascade of changes in vaginal flora that leads to BV.1

Photo: CDC/ M. Rein
Photomicrograph revealing clue cells (epithelial cells that have had bacteria adhere to their surface). Clue cell presence on a saline wet mount is a sign of bacterial vaginosis.

BV is present in 30% to 50% of sexually active women, and of these women 50% to 75% have an abnormal vaginal discharge, which is gray, thin, and homogeneous and may have a fishy odor.2 In addition to causing an abnormal vaginal discharge, BV is a cause of postpartum fever, posthysterectomy vaginal cuff cellulitis, and postabortion infection, and it increases the risk of acquiring HIV, herpes simplex type 2, gonorrhea, chlamydia, and trichomoniasis infection.3

When using microscopy and the Amsel criteria, the diagnosis of BV is made when at least 3 of the following 4 criteria are present:  

  1. homogeneous, thin, gray discharge  
  2. vaginal pH >4.5  
  3. positive whiff-amine test when applying a drop of 10% KOH to a sample of the vaginal discharge  
  4. clue cells detected with microscopy on a saline wet mount.  

If microscopy is not available, the Affirm VPIII test (BD Diagnostic Systems, Franklin Lakes, New Jersey) for DNA sequences of G vaginalis has high sensitivity and specificity.4 The OSOM BVBlue test (Sekisui Diagnostics, Lexington, Massachusetts), a Clinical Laboratory Improvement Amendments-waived point of service test, measures vaginal sialidase, which is produced by Gardnerella and other pathogens associated with BV.5 BV may be detected in routine cervical cytology testing and, if the patient is symptomatic, treatment is recommended.

Initial treatment of BV. The Centers for Disease Control and Prevention (CDC) has recommended 3 treatment regimens for BV and 4 alternative treatment options (TABLE).6 In addition to antimicrobial treatment, the CDC recommends that women with BV use condoms with sexual intercourse. The CDC also advises that clinicians should con-sider testing women with BV for HIV and other sexually transmitted infections.

Related article:
Successful treatment of chronic vaginitis

Treatment of recurrent BV

A major problem with BV is that, although initial treatment is successful in about 80% of cases, up to 50% of women will have a recurrence of BV within 12 months of initial treatment.2 Preliminary studies suggest that for women with 3 or more episodes of BV, the regimens below may be effective.  

Regimen 1
Following the completion of a CDC-recommended treatment regimen (see TABLE), prescribe metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 6 months.7

In a prospective randomized trial examining this regimen, following initial treatment with a 10-day metronidazole vaginal gel regimen 112 women were randomly assigned to chronic suppressive therapy with metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 16 weeks or a placebo. During the treatment period, recurrent BV was diagnosed in 26% of the women taking metronidazole gel and 59% of the women taking placebo.7 This regimen may be complicated by secondary vaginal candidiasis, which may be treated with a vaginal or oral antifungal agent. 

Regimen 2
Initiate a 21-day course of vaginal boric acid capsules 600 mg once daily at bedtime and simultaneously prescribe a standard CDC treatment regimen (see TABLE). At the completion of the vaginal boric acid treatment initiate metronidazole vaginal gel 0.75% twice weekly for 6 months.8

NOTE: Boric acid can cause death if consumed orally.9 Boric acid capsules should be stored securely to ensure that they are not accidentally taken orally. Boric acid poisoning may present with vomiting, fever, skin rash, neutropenia, thrombocytopenia, metabolic acidosis, and renal failure.10 Boric acid should not be used by pregnant women because it is a teratogen.11

The bacterial organisms responsible for BV reside in a self-produced matrix, referred to as a biofilm, that protect the organisms from antimicrobial agents.12 Boric acid may prevent the formation of a biofilm and increase the effectiveness of anti-microbial treatment.

Regimen 3
Following the completion of a standard treatment regimen (see TABLE), prescribe oral metronidazole 2 g and fluconazole 150 mg administered once every month.13

In a randomized clinical trial, 310 female sex workers were randomly assigned to monthly treatment with oral metronidazole 2 g plus fluconazole 150 mg or placebo for up to 12 months.13 In the treatment and placebo groups episodes of BV were 199 and 326 per 100 person-years, respectively (hazard ratio, 0.55; 95% confidence interval, 0.49-0.63; P<.001). In Canada, a vaginal ovule containing both a high dose of metronidazole (500 mg) and nystatin (10,000 IU) is available and could be used intermittently to prevent recurrence.14

Treatment of partners

The CDC does not recommend treatment of the partners of women with BV because there are no definitive data to support such a recommendation. However, the 6 published clinical trials testing the utility of treating sex partners of women with BV have significant methodologic flaws, including underpowered studies and suboptimal antibiotic treatment regimens.15 Hence, whether partners should be treated remains an open question. Many experts believe that, in most cases, BV is a sexually transmitted disease.16,17 For women who have sex with women, the rate of BV concordance among partners is high. If one woman has diagnosed BV and symptoms are present in her partner, treatment of the partner is reasonable. For women with BV who have sex with men, sexual intercourse influences disease activity, and consistent use of condoms may reduce the rate of recurrence.18 Male circumcision may reduce the risk of BV in female partners.19

Related article:
Bacterial vaginosis: Meet patients' needs with effective diagnosis and treatment

Over-the-counter treatments

In women with BV it is thought that the vaginal administration of lactic acid can help restore the normal acidic pH of the vagina, encourage the growth of lactobacilli, and suppress the growth of the bacteria that cause BV.20 Many products containing lactic acid in a formulation for vaginal use are available (among them Luvena and Gynofit gel).

Lactobacilli play an important role in maintaining vaginal health. Lactobacillus rhamnosus and Lactobacillus reuteri are available for purchase as supplements for oral administration. It is thought that oral administration of lactobacilli can help improve the vaginal microbiome. In one clinical trial, 125 women with BV were randomly assigned to receive the combination of 1 week of metronidazole plus oral Lactobacillus twice daily for 30 days or metronidazole plus placebo.21 Resolution of symptoms was reported as 88% and 40% in the metronidazole-lactobacilli and metronidazole-placebo groups, respectively.21 By contrast, one systematic review of probiotic treatment of BV concluded that there is insufficient evidence to recommend for or against probiotic treatment of BV.22 Patients with recurrent BV commonly report that they believe a probiotic was helpful in resolving their symptoms.

On the horizon

In one trial, a single 2-g oral dose of secnidazole was as effective as a 7-day course of oral metronidazole 500 mg twice daily.23 In a small dose-finding study, a single dose of either secnidazole 1 g or 2 g was equally effective in treating BV.24 An effective single-dose treatment of BV would likely improve patient adherence with therapy. Symbiomix is preparing for FDA review of this medication (secnidazole, Solosec) for use in the United States.

BV is a prevalent problem and often adversely impacts a woman's quality of life and love relationships. BV recurrence is very common. Many women report that their BV was resistant to intermittet treatment and recurred, repetitively  over many years. The 3 treatment options presented in this editorial may help to suppress the recurrence rate and improve symptoms.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Schwebke JR, Muzny CA, Josey WE. Role of Gardnerella vaginalis in the pathogenesis of bacterial vaginosis: a conceptual model. J Infect Dis. 2014;210(3):338-343.   
  2. Bradshaw CS, Morton AN, Hocking J, et al. High recurrence rates of bacterial vaginosis over the course of 12 months after oral metronidazole therapy and factors associated with recurrence. J Infect Dis. 2006;193(11):1478-1486.   
  3. Murphy K, Mitchell CM. The interplay of host immunity, environment and the risk of bacterial vaginosis and associated reproductive health outcomes. J Infect Dis. 2016;214(suppl 1):S29-S35.
  4. Mulhem E, Boyanton BL Jr, Robinson-Dunn B, Ebert C, Dzebo R. Performance of the Affirm VP-III using residual vaginal discharge collected from the speculum to characterize vaginitis in symptomatic women. J Low Genit Tract Dis. 2014;18(4):344-346.  
  5. Bradshaw CS, Morton AN, Garland SM, Horvath LB, Kuzevska I, Fairley CK. Evaluation of a point-of-care test, BVBLue, and clinical and laboratory criteria for diagnosis of bacterial vaginosis. J Clin Microbiol. 2005;43(3):1304-1308.
  6. 2015 Sexually transmitted disease treatment guidelines: Bacterial vaginosis. Centers for Disease Control and Prevention website. https://www.cdc.gov/std/tg2015/bv.htm. Updated June 4,2015. Accessed June 9, 2017.
  7. Sobel JD, Ferris D, Schwebke J, et al. Suppressive antibacterial therapy with 0.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Am J Obstet Gynecol. 2006;194(5):1283-1289.  
  8. Reichman O, Akins R, Sobel JD. Boric acid addition to suppressive antimicrobial therapy for recurrent bacterial vaginosis. Sex Transm Dis. 2009;36(11):732-734.   
  9. Wong LC, Heimbach MD, Truscott DR, Duncan BD. Boric acid poisoning: report of 11 cases. Can Med Assoc J. 1964;90:1018-1023.
  10. Teshima D, Morishita K, Ueda Y, et al. Clinical management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric acid poisoning. J Pharmacobiodyn. 1992;15(6):287-294.
  11. Di Renzo F, Cappelletti G, Broccia ML, Giavini E, Menegola E. Boric acid inhibits embryonic histone deacetylases: a suggested mechanism to explain boric acid-related teratogenicity. Toxicol Appl Pharmacol. 2007;220(2):178-185.
  12. Muzny CA, Schwebke JR. Biofilms: an underappreciated mechanism of treatment failure and recurrence in vaginal infections. Clin Infect Dis. 2015;61(4):601-606.   
  13. McClelland RS, Richardson BA, Hassan WM, et al. Improvement of vaginal health for Kenyan women at risk for acquisition of human immunodeficiency virus type 1: results of a randomized trial. J Infect Dis. 2008;197(10):1361-1368.  
  14. Sanchez S, Garcia PJ, Thomas KK, Catlin M, Holmes KK. Intravaginal metronidazole gel versus metronidazole plus nystatin ovules for bacterial vaginosis: a randomized controlled trial. Am J Obstet Gynecol. 2004;191(6):1898-1906.
  15. Mehta SD. Systematic review of randomized trials of treatment of male sexual partners for improved bacteria vaginosis outcomes in women. Sex Transm Dis. 2012;39(10):822-830.
  16. Muzny CA, Schwebke JR. Pathogenesis of bacterial vaginosis: discussion of current hypotheses. J Infect Dis. 2016;214(suppl 1):S1-S5.  
  17. Vodstrcil LA, Walker SM, Hocking JS, et al. Incident bacterial vaginosis (BV) in women who have sex with women is associated with behaviors that suggest sexual transmission of BV. Clin Infect Dis. 2015;60(7):1042-1053.
  18. Bradshaw CS, Vodstrcil LA, Hocking JS, et al. Recurrence of bacterial vaginosis is significantly associated with posttreatment sexual activities and hormonal contraceptive use. Clin Infect Dis. 2013;56(6):777-786.   
  19. Gray RH, Kigozi G, Serwadda D, et al. The effects of male circumcision on female partners' genital tract symptoms and vaginal infections in a randomized trial in Rakai, Uganda. Am J Obstet Gynecol. 2009;200(1):42.e1-e7.
  20. O'Hanlon DE, Moench TR, Cone RA. In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide. BMC Infect Dis. 2011;11:200.
  21. Anukam K, Osazuwa E, Ahonkhai I, et al. Augmentation of antimicrobial metronidazole therapy of bacterial vaginosis with oral probiotic Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14: randomized, double-blind, placebo controlled trial. Microbes Infect. 2006;8(6):1450-1454.
  22. Senok AC, Verstraelen H, Temmerman M, Botta GA. Probiotics for the treatment of bacterial vaginosis. Cochrane Database Syst Rev. 2009;(4):CD006289.
  23. Bohbot JM, Vicaut E, Fagnen D, Brauman M. Treatment of bacterial vaginosis: a multicenter, double-blind, double-dummy, randomised phase III study comparing secnidazole and metronidazole. Infect Dis Obstet Gynecol. 2010;2010. doi:10.1155/2010/705692.
  24. Núñez JT, Gómez G. Low-dose secnidazole in the treatment of bacterial vaginosis. Int J Gynaecol Obstet. 2005;88(3):281-285.
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The 3 treatment options presented herein may help to suppress the rate of bacterial vaginosis recurrence and improve patients' symptoms as well as quality of life
The 3 treatment options presented herein may help to suppress the rate of bacterial vaginosis recurrence and improve patients' symptoms as well as quality of life

Bacterial vaginosis (BV) is caused by a complex change in vaginal bacterial flora, with a reduction in lactobacilli (which help maintain an acidic environment) and an increase in anaerobic gram-negative organisms including Gardnerella vaginalis species and Bacteroides, Prevotella, and Mobiluncus genera. Infection with G vaginalis is thought to trigger a cascade of changes in vaginal flora that leads to BV.1

Photo: CDC/ M. Rein
Photomicrograph revealing clue cells (epithelial cells that have had bacteria adhere to their surface). Clue cell presence on a saline wet mount is a sign of bacterial vaginosis.

BV is present in 30% to 50% of sexually active women, and of these women 50% to 75% have an abnormal vaginal discharge, which is gray, thin, and homogeneous and may have a fishy odor.2 In addition to causing an abnormal vaginal discharge, BV is a cause of postpartum fever, posthysterectomy vaginal cuff cellulitis, and postabortion infection, and it increases the risk of acquiring HIV, herpes simplex type 2, gonorrhea, chlamydia, and trichomoniasis infection.3

When using microscopy and the Amsel criteria, the diagnosis of BV is made when at least 3 of the following 4 criteria are present:  

  1. homogeneous, thin, gray discharge  
  2. vaginal pH >4.5  
  3. positive whiff-amine test when applying a drop of 10% KOH to a sample of the vaginal discharge  
  4. clue cells detected with microscopy on a saline wet mount.  

If microscopy is not available, the Affirm VPIII test (BD Diagnostic Systems, Franklin Lakes, New Jersey) for DNA sequences of G vaginalis has high sensitivity and specificity.4 The OSOM BVBlue test (Sekisui Diagnostics, Lexington, Massachusetts), a Clinical Laboratory Improvement Amendments-waived point of service test, measures vaginal sialidase, which is produced by Gardnerella and other pathogens associated with BV.5 BV may be detected in routine cervical cytology testing and, if the patient is symptomatic, treatment is recommended.

Initial treatment of BV. The Centers for Disease Control and Prevention (CDC) has recommended 3 treatment regimens for BV and 4 alternative treatment options (TABLE).6 In addition to antimicrobial treatment, the CDC recommends that women with BV use condoms with sexual intercourse. The CDC also advises that clinicians should con-sider testing women with BV for HIV and other sexually transmitted infections.

Related article:
Successful treatment of chronic vaginitis

Treatment of recurrent BV

A major problem with BV is that, although initial treatment is successful in about 80% of cases, up to 50% of women will have a recurrence of BV within 12 months of initial treatment.2 Preliminary studies suggest that for women with 3 or more episodes of BV, the regimens below may be effective.  

Regimen 1
Following the completion of a CDC-recommended treatment regimen (see TABLE), prescribe metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 6 months.7

In a prospective randomized trial examining this regimen, following initial treatment with a 10-day metronidazole vaginal gel regimen 112 women were randomly assigned to chronic suppressive therapy with metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 16 weeks or a placebo. During the treatment period, recurrent BV was diagnosed in 26% of the women taking metronidazole gel and 59% of the women taking placebo.7 This regimen may be complicated by secondary vaginal candidiasis, which may be treated with a vaginal or oral antifungal agent. 

Regimen 2
Initiate a 21-day course of vaginal boric acid capsules 600 mg once daily at bedtime and simultaneously prescribe a standard CDC treatment regimen (see TABLE). At the completion of the vaginal boric acid treatment initiate metronidazole vaginal gel 0.75% twice weekly for 6 months.8

NOTE: Boric acid can cause death if consumed orally.9 Boric acid capsules should be stored securely to ensure that they are not accidentally taken orally. Boric acid poisoning may present with vomiting, fever, skin rash, neutropenia, thrombocytopenia, metabolic acidosis, and renal failure.10 Boric acid should not be used by pregnant women because it is a teratogen.11

The bacterial organisms responsible for BV reside in a self-produced matrix, referred to as a biofilm, that protect the organisms from antimicrobial agents.12 Boric acid may prevent the formation of a biofilm and increase the effectiveness of anti-microbial treatment.

Regimen 3
Following the completion of a standard treatment regimen (see TABLE), prescribe oral metronidazole 2 g and fluconazole 150 mg administered once every month.13

In a randomized clinical trial, 310 female sex workers were randomly assigned to monthly treatment with oral metronidazole 2 g plus fluconazole 150 mg or placebo for up to 12 months.13 In the treatment and placebo groups episodes of BV were 199 and 326 per 100 person-years, respectively (hazard ratio, 0.55; 95% confidence interval, 0.49-0.63; P<.001). In Canada, a vaginal ovule containing both a high dose of metronidazole (500 mg) and nystatin (10,000 IU) is available and could be used intermittently to prevent recurrence.14

Treatment of partners

The CDC does not recommend treatment of the partners of women with BV because there are no definitive data to support such a recommendation. However, the 6 published clinical trials testing the utility of treating sex partners of women with BV have significant methodologic flaws, including underpowered studies and suboptimal antibiotic treatment regimens.15 Hence, whether partners should be treated remains an open question. Many experts believe that, in most cases, BV is a sexually transmitted disease.16,17 For women who have sex with women, the rate of BV concordance among partners is high. If one woman has diagnosed BV and symptoms are present in her partner, treatment of the partner is reasonable. For women with BV who have sex with men, sexual intercourse influences disease activity, and consistent use of condoms may reduce the rate of recurrence.18 Male circumcision may reduce the risk of BV in female partners.19

Related article:
Bacterial vaginosis: Meet patients' needs with effective diagnosis and treatment

Over-the-counter treatments

In women with BV it is thought that the vaginal administration of lactic acid can help restore the normal acidic pH of the vagina, encourage the growth of lactobacilli, and suppress the growth of the bacteria that cause BV.20 Many products containing lactic acid in a formulation for vaginal use are available (among them Luvena and Gynofit gel).

Lactobacilli play an important role in maintaining vaginal health. Lactobacillus rhamnosus and Lactobacillus reuteri are available for purchase as supplements for oral administration. It is thought that oral administration of lactobacilli can help improve the vaginal microbiome. In one clinical trial, 125 women with BV were randomly assigned to receive the combination of 1 week of metronidazole plus oral Lactobacillus twice daily for 30 days or metronidazole plus placebo.21 Resolution of symptoms was reported as 88% and 40% in the metronidazole-lactobacilli and metronidazole-placebo groups, respectively.21 By contrast, one systematic review of probiotic treatment of BV concluded that there is insufficient evidence to recommend for or against probiotic treatment of BV.22 Patients with recurrent BV commonly report that they believe a probiotic was helpful in resolving their symptoms.

On the horizon

In one trial, a single 2-g oral dose of secnidazole was as effective as a 7-day course of oral metronidazole 500 mg twice daily.23 In a small dose-finding study, a single dose of either secnidazole 1 g or 2 g was equally effective in treating BV.24 An effective single-dose treatment of BV would likely improve patient adherence with therapy. Symbiomix is preparing for FDA review of this medication (secnidazole, Solosec) for use in the United States.

BV is a prevalent problem and often adversely impacts a woman's quality of life and love relationships. BV recurrence is very common. Many women report that their BV was resistant to intermittet treatment and recurred, repetitively  over many years. The 3 treatment options presented in this editorial may help to suppress the recurrence rate and improve symptoms.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Bacterial vaginosis (BV) is caused by a complex change in vaginal bacterial flora, with a reduction in lactobacilli (which help maintain an acidic environment) and an increase in anaerobic gram-negative organisms including Gardnerella vaginalis species and Bacteroides, Prevotella, and Mobiluncus genera. Infection with G vaginalis is thought to trigger a cascade of changes in vaginal flora that leads to BV.1

Photo: CDC/ M. Rein
Photomicrograph revealing clue cells (epithelial cells that have had bacteria adhere to their surface). Clue cell presence on a saline wet mount is a sign of bacterial vaginosis.

BV is present in 30% to 50% of sexually active women, and of these women 50% to 75% have an abnormal vaginal discharge, which is gray, thin, and homogeneous and may have a fishy odor.2 In addition to causing an abnormal vaginal discharge, BV is a cause of postpartum fever, posthysterectomy vaginal cuff cellulitis, and postabortion infection, and it increases the risk of acquiring HIV, herpes simplex type 2, gonorrhea, chlamydia, and trichomoniasis infection.3

When using microscopy and the Amsel criteria, the diagnosis of BV is made when at least 3 of the following 4 criteria are present:  

  1. homogeneous, thin, gray discharge  
  2. vaginal pH >4.5  
  3. positive whiff-amine test when applying a drop of 10% KOH to a sample of the vaginal discharge  
  4. clue cells detected with microscopy on a saline wet mount.  

If microscopy is not available, the Affirm VPIII test (BD Diagnostic Systems, Franklin Lakes, New Jersey) for DNA sequences of G vaginalis has high sensitivity and specificity.4 The OSOM BVBlue test (Sekisui Diagnostics, Lexington, Massachusetts), a Clinical Laboratory Improvement Amendments-waived point of service test, measures vaginal sialidase, which is produced by Gardnerella and other pathogens associated with BV.5 BV may be detected in routine cervical cytology testing and, if the patient is symptomatic, treatment is recommended.

Initial treatment of BV. The Centers for Disease Control and Prevention (CDC) has recommended 3 treatment regimens for BV and 4 alternative treatment options (TABLE).6 In addition to antimicrobial treatment, the CDC recommends that women with BV use condoms with sexual intercourse. The CDC also advises that clinicians should con-sider testing women with BV for HIV and other sexually transmitted infections.

Related article:
Successful treatment of chronic vaginitis

Treatment of recurrent BV

A major problem with BV is that, although initial treatment is successful in about 80% of cases, up to 50% of women will have a recurrence of BV within 12 months of initial treatment.2 Preliminary studies suggest that for women with 3 or more episodes of BV, the regimens below may be effective.  

Regimen 1
Following the completion of a CDC-recommended treatment regimen (see TABLE), prescribe metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 6 months.7

In a prospective randomized trial examining this regimen, following initial treatment with a 10-day metronidazole vaginal gel regimen 112 women were randomly assigned to chronic suppressive therapy with metronidazole vaginal gel 0.75%, one full applicator, twice weekly for 16 weeks or a placebo. During the treatment period, recurrent BV was diagnosed in 26% of the women taking metronidazole gel and 59% of the women taking placebo.7 This regimen may be complicated by secondary vaginal candidiasis, which may be treated with a vaginal or oral antifungal agent. 

Regimen 2
Initiate a 21-day course of vaginal boric acid capsules 600 mg once daily at bedtime and simultaneously prescribe a standard CDC treatment regimen (see TABLE). At the completion of the vaginal boric acid treatment initiate metronidazole vaginal gel 0.75% twice weekly for 6 months.8

NOTE: Boric acid can cause death if consumed orally.9 Boric acid capsules should be stored securely to ensure that they are not accidentally taken orally. Boric acid poisoning may present with vomiting, fever, skin rash, neutropenia, thrombocytopenia, metabolic acidosis, and renal failure.10 Boric acid should not be used by pregnant women because it is a teratogen.11

The bacterial organisms responsible for BV reside in a self-produced matrix, referred to as a biofilm, that protect the organisms from antimicrobial agents.12 Boric acid may prevent the formation of a biofilm and increase the effectiveness of anti-microbial treatment.

Regimen 3
Following the completion of a standard treatment regimen (see TABLE), prescribe oral metronidazole 2 g and fluconazole 150 mg administered once every month.13

In a randomized clinical trial, 310 female sex workers were randomly assigned to monthly treatment with oral metronidazole 2 g plus fluconazole 150 mg or placebo for up to 12 months.13 In the treatment and placebo groups episodes of BV were 199 and 326 per 100 person-years, respectively (hazard ratio, 0.55; 95% confidence interval, 0.49-0.63; P<.001). In Canada, a vaginal ovule containing both a high dose of metronidazole (500 mg) and nystatin (10,000 IU) is available and could be used intermittently to prevent recurrence.14

Treatment of partners

The CDC does not recommend treatment of the partners of women with BV because there are no definitive data to support such a recommendation. However, the 6 published clinical trials testing the utility of treating sex partners of women with BV have significant methodologic flaws, including underpowered studies and suboptimal antibiotic treatment regimens.15 Hence, whether partners should be treated remains an open question. Many experts believe that, in most cases, BV is a sexually transmitted disease.16,17 For women who have sex with women, the rate of BV concordance among partners is high. If one woman has diagnosed BV and symptoms are present in her partner, treatment of the partner is reasonable. For women with BV who have sex with men, sexual intercourse influences disease activity, and consistent use of condoms may reduce the rate of recurrence.18 Male circumcision may reduce the risk of BV in female partners.19

Related article:
Bacterial vaginosis: Meet patients' needs with effective diagnosis and treatment

Over-the-counter treatments

In women with BV it is thought that the vaginal administration of lactic acid can help restore the normal acidic pH of the vagina, encourage the growth of lactobacilli, and suppress the growth of the bacteria that cause BV.20 Many products containing lactic acid in a formulation for vaginal use are available (among them Luvena and Gynofit gel).

Lactobacilli play an important role in maintaining vaginal health. Lactobacillus rhamnosus and Lactobacillus reuteri are available for purchase as supplements for oral administration. It is thought that oral administration of lactobacilli can help improve the vaginal microbiome. In one clinical trial, 125 women with BV were randomly assigned to receive the combination of 1 week of metronidazole plus oral Lactobacillus twice daily for 30 days or metronidazole plus placebo.21 Resolution of symptoms was reported as 88% and 40% in the metronidazole-lactobacilli and metronidazole-placebo groups, respectively.21 By contrast, one systematic review of probiotic treatment of BV concluded that there is insufficient evidence to recommend for or against probiotic treatment of BV.22 Patients with recurrent BV commonly report that they believe a probiotic was helpful in resolving their symptoms.

On the horizon

In one trial, a single 2-g oral dose of secnidazole was as effective as a 7-day course of oral metronidazole 500 mg twice daily.23 In a small dose-finding study, a single dose of either secnidazole 1 g or 2 g was equally effective in treating BV.24 An effective single-dose treatment of BV would likely improve patient adherence with therapy. Symbiomix is preparing for FDA review of this medication (secnidazole, Solosec) for use in the United States.

BV is a prevalent problem and often adversely impacts a woman's quality of life and love relationships. BV recurrence is very common. Many women report that their BV was resistant to intermittet treatment and recurred, repetitively  over many years. The 3 treatment options presented in this editorial may help to suppress the recurrence rate and improve symptoms.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Schwebke JR, Muzny CA, Josey WE. Role of Gardnerella vaginalis in the pathogenesis of bacterial vaginosis: a conceptual model. J Infect Dis. 2014;210(3):338-343.   
  2. Bradshaw CS, Morton AN, Hocking J, et al. High recurrence rates of bacterial vaginosis over the course of 12 months after oral metronidazole therapy and factors associated with recurrence. J Infect Dis. 2006;193(11):1478-1486.   
  3. Murphy K, Mitchell CM. The interplay of host immunity, environment and the risk of bacterial vaginosis and associated reproductive health outcomes. J Infect Dis. 2016;214(suppl 1):S29-S35.
  4. Mulhem E, Boyanton BL Jr, Robinson-Dunn B, Ebert C, Dzebo R. Performance of the Affirm VP-III using residual vaginal discharge collected from the speculum to characterize vaginitis in symptomatic women. J Low Genit Tract Dis. 2014;18(4):344-346.  
  5. Bradshaw CS, Morton AN, Garland SM, Horvath LB, Kuzevska I, Fairley CK. Evaluation of a point-of-care test, BVBLue, and clinical and laboratory criteria for diagnosis of bacterial vaginosis. J Clin Microbiol. 2005;43(3):1304-1308.
  6. 2015 Sexually transmitted disease treatment guidelines: Bacterial vaginosis. Centers for Disease Control and Prevention website. https://www.cdc.gov/std/tg2015/bv.htm. Updated June 4,2015. Accessed June 9, 2017.
  7. Sobel JD, Ferris D, Schwebke J, et al. Suppressive antibacterial therapy with 0.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Am J Obstet Gynecol. 2006;194(5):1283-1289.  
  8. Reichman O, Akins R, Sobel JD. Boric acid addition to suppressive antimicrobial therapy for recurrent bacterial vaginosis. Sex Transm Dis. 2009;36(11):732-734.   
  9. Wong LC, Heimbach MD, Truscott DR, Duncan BD. Boric acid poisoning: report of 11 cases. Can Med Assoc J. 1964;90:1018-1023.
  10. Teshima D, Morishita K, Ueda Y, et al. Clinical management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric acid poisoning. J Pharmacobiodyn. 1992;15(6):287-294.
  11. Di Renzo F, Cappelletti G, Broccia ML, Giavini E, Menegola E. Boric acid inhibits embryonic histone deacetylases: a suggested mechanism to explain boric acid-related teratogenicity. Toxicol Appl Pharmacol. 2007;220(2):178-185.
  12. Muzny CA, Schwebke JR. Biofilms: an underappreciated mechanism of treatment failure and recurrence in vaginal infections. Clin Infect Dis. 2015;61(4):601-606.   
  13. McClelland RS, Richardson BA, Hassan WM, et al. Improvement of vaginal health for Kenyan women at risk for acquisition of human immunodeficiency virus type 1: results of a randomized trial. J Infect Dis. 2008;197(10):1361-1368.  
  14. Sanchez S, Garcia PJ, Thomas KK, Catlin M, Holmes KK. Intravaginal metronidazole gel versus metronidazole plus nystatin ovules for bacterial vaginosis: a randomized controlled trial. Am J Obstet Gynecol. 2004;191(6):1898-1906.
  15. Mehta SD. Systematic review of randomized trials of treatment of male sexual partners for improved bacteria vaginosis outcomes in women. Sex Transm Dis. 2012;39(10):822-830.
  16. Muzny CA, Schwebke JR. Pathogenesis of bacterial vaginosis: discussion of current hypotheses. J Infect Dis. 2016;214(suppl 1):S1-S5.  
  17. Vodstrcil LA, Walker SM, Hocking JS, et al. Incident bacterial vaginosis (BV) in women who have sex with women is associated with behaviors that suggest sexual transmission of BV. Clin Infect Dis. 2015;60(7):1042-1053.
  18. Bradshaw CS, Vodstrcil LA, Hocking JS, et al. Recurrence of bacterial vaginosis is significantly associated with posttreatment sexual activities and hormonal contraceptive use. Clin Infect Dis. 2013;56(6):777-786.   
  19. Gray RH, Kigozi G, Serwadda D, et al. The effects of male circumcision on female partners' genital tract symptoms and vaginal infections in a randomized trial in Rakai, Uganda. Am J Obstet Gynecol. 2009;200(1):42.e1-e7.
  20. O'Hanlon DE, Moench TR, Cone RA. In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide. BMC Infect Dis. 2011;11:200.
  21. Anukam K, Osazuwa E, Ahonkhai I, et al. Augmentation of antimicrobial metronidazole therapy of bacterial vaginosis with oral probiotic Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14: randomized, double-blind, placebo controlled trial. Microbes Infect. 2006;8(6):1450-1454.
  22. Senok AC, Verstraelen H, Temmerman M, Botta GA. Probiotics for the treatment of bacterial vaginosis. Cochrane Database Syst Rev. 2009;(4):CD006289.
  23. Bohbot JM, Vicaut E, Fagnen D, Brauman M. Treatment of bacterial vaginosis: a multicenter, double-blind, double-dummy, randomised phase III study comparing secnidazole and metronidazole. Infect Dis Obstet Gynecol. 2010;2010. doi:10.1155/2010/705692.
  24. Núñez JT, Gómez G. Low-dose secnidazole in the treatment of bacterial vaginosis. Int J Gynaecol Obstet. 2005;88(3):281-285.
References
  1. Schwebke JR, Muzny CA, Josey WE. Role of Gardnerella vaginalis in the pathogenesis of bacterial vaginosis: a conceptual model. J Infect Dis. 2014;210(3):338-343.   
  2. Bradshaw CS, Morton AN, Hocking J, et al. High recurrence rates of bacterial vaginosis over the course of 12 months after oral metronidazole therapy and factors associated with recurrence. J Infect Dis. 2006;193(11):1478-1486.   
  3. Murphy K, Mitchell CM. The interplay of host immunity, environment and the risk of bacterial vaginosis and associated reproductive health outcomes. J Infect Dis. 2016;214(suppl 1):S29-S35.
  4. Mulhem E, Boyanton BL Jr, Robinson-Dunn B, Ebert C, Dzebo R. Performance of the Affirm VP-III using residual vaginal discharge collected from the speculum to characterize vaginitis in symptomatic women. J Low Genit Tract Dis. 2014;18(4):344-346.  
  5. Bradshaw CS, Morton AN, Garland SM, Horvath LB, Kuzevska I, Fairley CK. Evaluation of a point-of-care test, BVBLue, and clinical and laboratory criteria for diagnosis of bacterial vaginosis. J Clin Microbiol. 2005;43(3):1304-1308.
  6. 2015 Sexually transmitted disease treatment guidelines: Bacterial vaginosis. Centers for Disease Control and Prevention website. https://www.cdc.gov/std/tg2015/bv.htm. Updated June 4,2015. Accessed June 9, 2017.
  7. Sobel JD, Ferris D, Schwebke J, et al. Suppressive antibacterial therapy with 0.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Am J Obstet Gynecol. 2006;194(5):1283-1289.  
  8. Reichman O, Akins R, Sobel JD. Boric acid addition to suppressive antimicrobial therapy for recurrent bacterial vaginosis. Sex Transm Dis. 2009;36(11):732-734.   
  9. Wong LC, Heimbach MD, Truscott DR, Duncan BD. Boric acid poisoning: report of 11 cases. Can Med Assoc J. 1964;90:1018-1023.
  10. Teshima D, Morishita K, Ueda Y, et al. Clinical management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric acid poisoning. J Pharmacobiodyn. 1992;15(6):287-294.
  11. Di Renzo F, Cappelletti G, Broccia ML, Giavini E, Menegola E. Boric acid inhibits embryonic histone deacetylases: a suggested mechanism to explain boric acid-related teratogenicity. Toxicol Appl Pharmacol. 2007;220(2):178-185.
  12. Muzny CA, Schwebke JR. Biofilms: an underappreciated mechanism of treatment failure and recurrence in vaginal infections. Clin Infect Dis. 2015;61(4):601-606.   
  13. McClelland RS, Richardson BA, Hassan WM, et al. Improvement of vaginal health for Kenyan women at risk for acquisition of human immunodeficiency virus type 1: results of a randomized trial. J Infect Dis. 2008;197(10):1361-1368.  
  14. Sanchez S, Garcia PJ, Thomas KK, Catlin M, Holmes KK. Intravaginal metronidazole gel versus metronidazole plus nystatin ovules for bacterial vaginosis: a randomized controlled trial. Am J Obstet Gynecol. 2004;191(6):1898-1906.
  15. Mehta SD. Systematic review of randomized trials of treatment of male sexual partners for improved bacteria vaginosis outcomes in women. Sex Transm Dis. 2012;39(10):822-830.
  16. Muzny CA, Schwebke JR. Pathogenesis of bacterial vaginosis: discussion of current hypotheses. J Infect Dis. 2016;214(suppl 1):S1-S5.  
  17. Vodstrcil LA, Walker SM, Hocking JS, et al. Incident bacterial vaginosis (BV) in women who have sex with women is associated with behaviors that suggest sexual transmission of BV. Clin Infect Dis. 2015;60(7):1042-1053.
  18. Bradshaw CS, Vodstrcil LA, Hocking JS, et al. Recurrence of bacterial vaginosis is significantly associated with posttreatment sexual activities and hormonal contraceptive use. Clin Infect Dis. 2013;56(6):777-786.   
  19. Gray RH, Kigozi G, Serwadda D, et al. The effects of male circumcision on female partners' genital tract symptoms and vaginal infections in a randomized trial in Rakai, Uganda. Am J Obstet Gynecol. 2009;200(1):42.e1-e7.
  20. O'Hanlon DE, Moench TR, Cone RA. In vaginal fluid, bacteria associated with bacterial vaginosis can be suppressed with lactic acid but not hydrogen peroxide. BMC Infect Dis. 2011;11:200.
  21. Anukam K, Osazuwa E, Ahonkhai I, et al. Augmentation of antimicrobial metronidazole therapy of bacterial vaginosis with oral probiotic Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14: randomized, double-blind, placebo controlled trial. Microbes Infect. 2006;8(6):1450-1454.
  22. Senok AC, Verstraelen H, Temmerman M, Botta GA. Probiotics for the treatment of bacterial vaginosis. Cochrane Database Syst Rev. 2009;(4):CD006289.
  23. Bohbot JM, Vicaut E, Fagnen D, Brauman M. Treatment of bacterial vaginosis: a multicenter, double-blind, double-dummy, randomised phase III study comparing secnidazole and metronidazole. Infect Dis Obstet Gynecol. 2010;2010. doi:10.1155/2010/705692.
  24. Núñez JT, Gómez G. Low-dose secnidazole in the treatment of bacterial vaginosis. Int J Gynaecol Obstet. 2005;88(3):281-285.
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Top free menstrual cycle tracking apps for your patients

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Top free menstrual cycle tracking apps for your patients
Clue, Glow, and Pink Pad Period Tracker Pro are popular because of their accuracy and special features

App overload is a challenge for both providers and patients. As of September 2015, the number of health apps in the US Apple iTunes and Google Play stores exceeded 165,000, with approximately 7% focused on women's health and pregnancy.1 Clinicians express interest in promoting the use of health apps with their patients and seek guidance about making app recommendations.2 In my prior articles in this "App review" series, I have recommended due date calculator and drug reference apps.

One area in which an app may enhance your patient care is in menstrual cycle tracking. Patients may be more honest with their phones than with their health care professionals, and the results are more accurate than paper questionnaires and calendars.3 Of note, menstrual cycle tracking apps are the fourth most popular health app among adults and likely even more popular if limited to adult women.4

Dr. Paula Castano and her team systematically identified and evaluated free menstrual cycle tracking apps.5 The accuracy of each app was determined by menstrual cycle predictions based on average cycle lengths of at least 3 previous cycles, ovulation predicted at 13 to 15 days prior to the start of the next cycle, and qualification that the application contained no misinformation.5

The top 3 recommended menstrual cycle tracking apps from Dr. Castano and colleagues' study are listed in the TABLE alphabetically and are detailed with a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature use, and important special features).6 I hope this column will allow you to feel more comfortable recommending these "vetted" apps to your patients.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. IMS Institute for Healthcare Informatics. Patient adoption of mHealth. Parsippany (NJ): IMS Institute for Healthcare Informatics; 2015. http://www.imshealth.com/files/web/IMSH%20Institute/Reports/Patient%20Adoption%20of%20mHealth/IIHI_Patient_Adoption_of_mHealth.pdf. Published September 2015. Accessed June 6, 2017.
  2. Terry K. Prescribing mobile apps: What to consider. Med Econ. 2015;92(12):35-38, 40.
  3. Wortham J. We're more honest with our phones than our doctors. NY Times Magazine. https://www.nytimes.com/2016/03/27/magazine/were-more-honest-with-our-phones-than-with-our-doctors.html?_r=0. Published March 23, 2016. Accessed June 6. 2017.
  4. Fox S, Duggan M. Pew Research Center. Mobile Health 2012. http://www.pewinternet.org/files/old-media//Files/Reports/2012/PIP_MobileHealth2012_FINAL.pdf. Published November 8, 2012. Accessed June 6, 2017.
  5. Moglia M, Nguyen H, Chyjek K, Chen KT, Castano PM. Evaluation of smartphone menstrual cycle tracking applications using an adapted APPLICATIONS scoring system. Obstet Gynecol. 2016;127(6):1153-1160.
  6. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
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Dr. Chen is Professor of Obstetrics, Gynecology, and Reproductive Science and Medical Education, Vice-Chair of Ob-Gyn Education for the Mount Sinai Health System, Icahn School of Medicine, Mount Sinai, New York, New York.

The author reports receiving royalties from UpToDate, Inc.

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Dr. Chen is Professor of Obstetrics, Gynecology, and Reproductive Science and Medical Education, Vice-Chair of Ob-Gyn Education for the Mount Sinai Health System, Icahn School of Medicine, Mount Sinai, New York, New York.

The author reports receiving royalties from UpToDate, Inc.

Author and Disclosure Information

Dr. Chen is Professor of Obstetrics, Gynecology, and Reproductive Science and Medical Education, Vice-Chair of Ob-Gyn Education for the Mount Sinai Health System, Icahn School of Medicine, Mount Sinai, New York, New York.

The author reports receiving royalties from UpToDate, Inc.

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Related Articles
Clue, Glow, and Pink Pad Period Tracker Pro are popular because of their accuracy and special features
Clue, Glow, and Pink Pad Period Tracker Pro are popular because of their accuracy and special features

App overload is a challenge for both providers and patients. As of September 2015, the number of health apps in the US Apple iTunes and Google Play stores exceeded 165,000, with approximately 7% focused on women's health and pregnancy.1 Clinicians express interest in promoting the use of health apps with their patients and seek guidance about making app recommendations.2 In my prior articles in this "App review" series, I have recommended due date calculator and drug reference apps.

One area in which an app may enhance your patient care is in menstrual cycle tracking. Patients may be more honest with their phones than with their health care professionals, and the results are more accurate than paper questionnaires and calendars.3 Of note, menstrual cycle tracking apps are the fourth most popular health app among adults and likely even more popular if limited to adult women.4

Dr. Paula Castano and her team systematically identified and evaluated free menstrual cycle tracking apps.5 The accuracy of each app was determined by menstrual cycle predictions based on average cycle lengths of at least 3 previous cycles, ovulation predicted at 13 to 15 days prior to the start of the next cycle, and qualification that the application contained no misinformation.5

The top 3 recommended menstrual cycle tracking apps from Dr. Castano and colleagues' study are listed in the TABLE alphabetically and are detailed with a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature use, and important special features).6 I hope this column will allow you to feel more comfortable recommending these "vetted" apps to your patients.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

App overload is a challenge for both providers and patients. As of September 2015, the number of health apps in the US Apple iTunes and Google Play stores exceeded 165,000, with approximately 7% focused on women's health and pregnancy.1 Clinicians express interest in promoting the use of health apps with their patients and seek guidance about making app recommendations.2 In my prior articles in this "App review" series, I have recommended due date calculator and drug reference apps.

One area in which an app may enhance your patient care is in menstrual cycle tracking. Patients may be more honest with their phones than with their health care professionals, and the results are more accurate than paper questionnaires and calendars.3 Of note, menstrual cycle tracking apps are the fourth most popular health app among adults and likely even more popular if limited to adult women.4

Dr. Paula Castano and her team systematically identified and evaluated free menstrual cycle tracking apps.5 The accuracy of each app was determined by menstrual cycle predictions based on average cycle lengths of at least 3 previous cycles, ovulation predicted at 13 to 15 days prior to the start of the next cycle, and qualification that the application contained no misinformation.5

The top 3 recommended menstrual cycle tracking apps from Dr. Castano and colleagues' study are listed in the TABLE alphabetically and are detailed with a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature use, and important special features).6 I hope this column will allow you to feel more comfortable recommending these "vetted" apps to your patients.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. IMS Institute for Healthcare Informatics. Patient adoption of mHealth. Parsippany (NJ): IMS Institute for Healthcare Informatics; 2015. http://www.imshealth.com/files/web/IMSH%20Institute/Reports/Patient%20Adoption%20of%20mHealth/IIHI_Patient_Adoption_of_mHealth.pdf. Published September 2015. Accessed June 6, 2017.
  2. Terry K. Prescribing mobile apps: What to consider. Med Econ. 2015;92(12):35-38, 40.
  3. Wortham J. We're more honest with our phones than our doctors. NY Times Magazine. https://www.nytimes.com/2016/03/27/magazine/were-more-honest-with-our-phones-than-with-our-doctors.html?_r=0. Published March 23, 2016. Accessed June 6. 2017.
  4. Fox S, Duggan M. Pew Research Center. Mobile Health 2012. http://www.pewinternet.org/files/old-media//Files/Reports/2012/PIP_MobileHealth2012_FINAL.pdf. Published November 8, 2012. Accessed June 6, 2017.
  5. Moglia M, Nguyen H, Chyjek K, Chen KT, Castano PM. Evaluation of smartphone menstrual cycle tracking applications using an adapted APPLICATIONS scoring system. Obstet Gynecol. 2016;127(6):1153-1160.
  6. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
References
  1. IMS Institute for Healthcare Informatics. Patient adoption of mHealth. Parsippany (NJ): IMS Institute for Healthcare Informatics; 2015. http://www.imshealth.com/files/web/IMSH%20Institute/Reports/Patient%20Adoption%20of%20mHealth/IIHI_Patient_Adoption_of_mHealth.pdf. Published September 2015. Accessed June 6, 2017.
  2. Terry K. Prescribing mobile apps: What to consider. Med Econ. 2015;92(12):35-38, 40.
  3. Wortham J. We're more honest with our phones than our doctors. NY Times Magazine. https://www.nytimes.com/2016/03/27/magazine/were-more-honest-with-our-phones-than-with-our-doctors.html?_r=0. Published March 23, 2016. Accessed June 6. 2017.
  4. Fox S, Duggan M. Pew Research Center. Mobile Health 2012. http://www.pewinternet.org/files/old-media//Files/Reports/2012/PIP_MobileHealth2012_FINAL.pdf. Published November 8, 2012. Accessed June 6, 2017.
  5. Moglia M, Nguyen H, Chyjek K, Chen KT, Castano PM. Evaluation of smartphone menstrual cycle tracking applications using an adapted APPLICATIONS scoring system. Obstet Gynecol. 2016;127(6):1153-1160.
  6. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
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