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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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Pregnancy mortality in the United States: Top causes of death and timing

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An app to help women and clinicians manage menopausal symptoms

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In North America, women experience menopause (the permanent cessation of menstruation due to loss of ovarian activity) at a median age of 51 years. They may experience symptoms of perimenopause, or the menopause transition, for several years before menstruation ceases. Menopausal symptoms include vasomotor symptoms, such as hot flushes, and vaginal symptoms, such as vaginal dryness and pain during intercourse.1

Women may have questions about treating menopausal symptoms, maintaining their health, and preventing such age-related diseases as osteoporosis and cardiovascular disease. The decision to treat menopausal symptoms is challenging for women as well as their clinicians given that recommendations have changed over the past few years.

A free app with multiple features. The North American Menopause Society (NAMS) has developed a no-cost mobile health application called MenoPro for menopausal symptom management based on the organization’s 2017 recommendations.2 The app has 2 modes: one for clinicians and one for women/patients to support shared decision making.

For clinicians, the app helps identify which patients with menopausal symptoms are candidates for pharmacologic treatment and the options for optimal therapy. The app also can be used to calculate a 10-year cardiovascular disease (heart disease and stroke) risk assessment. In addition, it contains links to a breast cancer risk assessment as well as an osteoporosis/bone fracture risk assessment tool (FRAX model calculator). Finally, MenoPro includes NAMS’s educational materials and information pages on lifestyle modifications to reduce hot flushes, contraindications and cautions to hormone therapy, pros and cons of hormonal versus nonhormonal options, a comparison of oral (pills) and transdermal (patches, gels, sprays) therapies, treatment options for vaginal dryness and pain with sexual activities, and direct links to tables with the various formulations and doses of medications.

The TABLE details the features of the MenoPro app based on a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature used, and important special features).3 I hope that the app described here will assist you in caring for women in the menopausal transition.

References

1. American College of Obstetricians and Gynecologists. Practice bulletin no. 141: Management of menopausal symptoms. Obstet Gynecol. 2014;123:202-216.

2. The 2017 hormone therapy position statement of The North American Menopause Society. Menopause. 2018;25:13621387.

3. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125:1478-1483.
 

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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. She is an  OBG MANAGEMENT Contributing Editor.

The author reports being an advisory board member and 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. She is an  OBG MANAGEMENT Contributing Editor.

The author reports being an advisory board member and 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. She is an  OBG MANAGEMENT Contributing Editor.

The author reports being an advisory board member and receiving royalties from UpToDate, Inc.

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In North America, women experience menopause (the permanent cessation of menstruation due to loss of ovarian activity) at a median age of 51 years. They may experience symptoms of perimenopause, or the menopause transition, for several years before menstruation ceases. Menopausal symptoms include vasomotor symptoms, such as hot flushes, and vaginal symptoms, such as vaginal dryness and pain during intercourse.1

Women may have questions about treating menopausal symptoms, maintaining their health, and preventing such age-related diseases as osteoporosis and cardiovascular disease. The decision to treat menopausal symptoms is challenging for women as well as their clinicians given that recommendations have changed over the past few years.

A free app with multiple features. The North American Menopause Society (NAMS) has developed a no-cost mobile health application called MenoPro for menopausal symptom management based on the organization’s 2017 recommendations.2 The app has 2 modes: one for clinicians and one for women/patients to support shared decision making.

For clinicians, the app helps identify which patients with menopausal symptoms are candidates for pharmacologic treatment and the options for optimal therapy. The app also can be used to calculate a 10-year cardiovascular disease (heart disease and stroke) risk assessment. In addition, it contains links to a breast cancer risk assessment as well as an osteoporosis/bone fracture risk assessment tool (FRAX model calculator). Finally, MenoPro includes NAMS’s educational materials and information pages on lifestyle modifications to reduce hot flushes, contraindications and cautions to hormone therapy, pros and cons of hormonal versus nonhormonal options, a comparison of oral (pills) and transdermal (patches, gels, sprays) therapies, treatment options for vaginal dryness and pain with sexual activities, and direct links to tables with the various formulations and doses of medications.

The TABLE details the features of the MenoPro app based on a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature used, and important special features).3 I hope that the app described here will assist you in caring for women in the menopausal transition.

In North America, women experience menopause (the permanent cessation of menstruation due to loss of ovarian activity) at a median age of 51 years. They may experience symptoms of perimenopause, or the menopause transition, for several years before menstruation ceases. Menopausal symptoms include vasomotor symptoms, such as hot flushes, and vaginal symptoms, such as vaginal dryness and pain during intercourse.1

Women may have questions about treating menopausal symptoms, maintaining their health, and preventing such age-related diseases as osteoporosis and cardiovascular disease. The decision to treat menopausal symptoms is challenging for women as well as their clinicians given that recommendations have changed over the past few years.

A free app with multiple features. The North American Menopause Society (NAMS) has developed a no-cost mobile health application called MenoPro for menopausal symptom management based on the organization’s 2017 recommendations.2 The app has 2 modes: one for clinicians and one for women/patients to support shared decision making.

For clinicians, the app helps identify which patients with menopausal symptoms are candidates for pharmacologic treatment and the options for optimal therapy. The app also can be used to calculate a 10-year cardiovascular disease (heart disease and stroke) risk assessment. In addition, it contains links to a breast cancer risk assessment as well as an osteoporosis/bone fracture risk assessment tool (FRAX model calculator). Finally, MenoPro includes NAMS’s educational materials and information pages on lifestyle modifications to reduce hot flushes, contraindications and cautions to hormone therapy, pros and cons of hormonal versus nonhormonal options, a comparison of oral (pills) and transdermal (patches, gels, sprays) therapies, treatment options for vaginal dryness and pain with sexual activities, and direct links to tables with the various formulations and doses of medications.

The TABLE details the features of the MenoPro app based on a shortened version of the APPLICATIONS scoring system, APPLI (app comprehensiveness, price, platform, literature used, and important special features).3 I hope that the app described here will assist you in caring for women in the menopausal transition.

References

1. American College of Obstetricians and Gynecologists. Practice bulletin no. 141: Management of menopausal symptoms. Obstet Gynecol. 2014;123:202-216.

2. The 2017 hormone therapy position statement of The North American Menopause Society. Menopause. 2018;25:13621387.

3. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125:1478-1483.
 

References

1. American College of Obstetricians and Gynecologists. Practice bulletin no. 141: Management of menopausal symptoms. Obstet Gynecol. 2014;123:202-216.

2. The 2017 hormone therapy position statement of The North American Menopause Society. Menopause. 2018;25:13621387.

3. Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125:1478-1483.
 

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Modern surgical techniques for gastrointestinal endometriosis

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About 10% of all reproductive-aged women and 35% to 50% of women with pelvic pain and infertility are affected by endometriosis.1,2 The disease typically involves the reproductive tract organs, anterior and posterior cul-de-sacs, and uterosacral ligaments. However, disease outside of the reproductive tract occurs frequently and has been found on all organs except the spleen.3

The bowel is the most common site for extragenital endometriosis, affected in an estimated 3.8% to 37% of patients with known endometriosis.4-7 Implants may be superficial, involving the bowel serosa and subserosa (FIGURE 1), or they can manifest as deeply infiltrating lesions involving the muscularis and mucosa (FIGURE 2). The rectosigmoid colon is the most common location for bowel endometriosis, followed by the rectum, ileum, appendix, and cecum4,8 (FIGURES 3, 4, and 5). Case reports also have described endometrial implants on the stomach and transverse colon.9 Although isolated bowel involvement has been recognized, most patients with bowel endometriosis have concurrent disease elsewhere.2,4 

Historically, segmental resection was performed regardless of the anatomical location of the lesion.10 Even today, many surgeons continue to routinely perform segmental bowel resection as a first-line surgical approach.11 Unnecessary segmental resection, however, places patients at risk for short- and long-term postoperative morbidity, including the possibility of permanent ostomy. Modern surgical techniques, such as shaving excision and disc resection, have been performed to successfully treat bowel endometriosis with excellent long-term outcomes and fewer complications when compared with traditional segmental resection.2,12-16

In this article, we focus on the clinical indications and surgical techniques for video-laparoscopic management, but first we describe the pathophysiology, clinical presentation, and diagnosis of bowel endometriosis.

 

Pathophysiology of bowel endometriosis

The pathogenesis of endometriosis remains unknown, as no single mechanism explains all clinical cases of the disease. The most popular proposed theory describes retrograde menstruation through the fallopian tubes.17 Once inside the peritoneal cavity, endometrial cells attach to and invade healthy peritoneum, establishing a blood supply necessary for growth and survival.

In the case of bowel endometriosis, deposition of effluxed endometrial cells may lead to an inflammatory response that increases the risk of adhesion formation, leading to potential cul-de-sac obliteration. Lesions may originate as Allen-Masters peritoneal defects, developing into deeply infiltrative rectovaginal septum lesions. The anatomical shelter theory contributes to lesions within the pelvis, with the rectosigmoid colon blocking the cephalad flow of effluxed menstrual blood from the pelvis, thus leading to a preponderance of lesions in the pelvis and along the rectosigmoid colon.2

Continue to: Clinical presentation and diagnosis...

 

 

Clinical presentation and diagnosis

Women presenting with endometriosis of the bowel are typically of reproductive age and commonly report symptoms of dysmenorrhea, chronic pelvic pain, dyspareunia, and dyschezia. Some women also experience catamenial diarrhea, constipation, hematochezia, and bloating.2 The differential diagnosis of these symptoms is broad and includes irritable bowel disease, ischemic colitis, inflammatory bowel disease, diverticulitis, pelvic inflammatory disease, and malignancy.

Because of its nonspecific symptoms, bowel endometriosis is often misdiagnosed and the disease goes untreated for years.18 Therefore, it is imperative that clinicians maintain a high index of suspicion when evaluating reproductive-aged women with gastrointestinal symptoms and pelvic pain.

Physical examination can be helpful in making the diagnosis of endometriosis. During bimanual examination, findings such as a fixed, tender, or retroverted uterus, uterosacral ligament nodularity, or an enlarged adnexal mass representing an ovarian endometrioma may be appreciated. Rectovaginal exam can identify areas of tenderness and nodularity along the rectovaginal septum. Speculum exam may reveal a laterally displaced cervix or blue powder-burn lesions along the cervix or posterior fornix.19 Rarely, endometriosis is found on the perineum within an episiotomy scar.20

Imaging studies can be used in conjunction with physical examination findings to aid in the diagnosis of endometriosis. Images also guide preoperative planning by characterizing lesions based on their size, location, and depth of invasion. Hudelist and colleagues found transvaginal ultrasound (TVUS) to have an overall sensitivity of 71% to 98% and a specificity of 92% to 100%.21 However, it was noted that the accuracy of the diagnosis was directly related to the experience of the sonographer, and lesions above the sigmoid colon were generally unable to be diagnosed. Other imaging modalities that have been reported to have high sensitivity and specificity for diagnosing bowel endometriosis include rectal water contrast TVUS,22,23 rectal endoscopic sonography,22 magnetic resonance imaging,22 and barium enema.24

 

Medical management

Medical therapy for patients with endometriosis is utilized with the goal of suppressing ovulation, lowering circulating hormone levels, and inducing endometrial atrophy. Medications commonly employed include gonadotropin-releasing hormone agonists and antagonists, anabolic steriods such as danazol, combined oral contraceptive pills, progestins, and aromatase inhibitors.

Continue to: To date, no optimal hormonal regimen...

 

 

To date, no optimal hormonal regimen has been established for the treatment of bowel endometriosis. Vercellini and colleagues demonstrated that progestins with and without low-dose estrogen improved symptoms of dysmenorrhea and dyspareunia.25 Ferrero and colleagues reported that 2.5 mg of norethindrone daily resulted in 53% of women with colorectal endometriosis reporting improved gastrointestinal symptoms.26 However, by 12 months of follow-up, 33% of these patients had elected to undergo surgical management.

Gonadotropin-releasing hormone agonists, such as leuprolide acetate, also can be used to mitigate symptoms of bowel endometriosis or to decrease disease burden at the time of surgery, and they can be used with add-back norethindrone acetate. The use of these medications is limited by adverse effects, such as vasomotor symptoms and decreased bone mineral density when used for longer than 6 months.
2

Medical therapy is commonly used for patients with mild to moderate symptoms and in those who are poor surgical candidates or decline surgical intervention. Medical therapy is especially useful when employed postoperatively to suppress the regrowth of microscopic ectopic endometrial tissue.

Patients must be counseled, however, that even with medical management, they may still require surgery in the future to control their symptoms and/or to preserve organ function.
2

 

Surgical management

Surgical treatment for bowel endometriosis depends on the disease location, the size and depth of the lesion, the presence or absence of stricture, and the surgeon’s level of expertise.2,12,27-30

In our group, we advocate for video-laparoscopy, with or without robotic as sistance. Minimally invasive surgery offers reduced blood loss, shorter recovery time, and fewer postoperative complications compared with laparotomy.2,16,27,31-33 The conversion rate to laparotomy has been reported to be about 3% when performed by an experienced surgeon.12

Darai and colleagues conducted a randomized trial of 52 patients undergoing surgery for colorectal endometriosis via either laparoscopic or open colon resection.33 Blood loss was significantly lower in the laparoscopy group (1.6 vs 2.7 mg/L, P <.05). No difference was noted in long-term outcomes. In a retrospective study of 436 cases, Ruffo and colleagues showed that those who underwent laparoscopic colorectal resection had higher postoperative pregnancy rates compared with those who had laparotomy (57.6% vs 23.1%, P <.035).32

The goal of surgical management of bowel endometriosis is to remove as many of the endometriotic lesions as possible while minimizing short- and long-term complications. Three surgical approaches have been described: shaving excision, disc resection, and segmental resection.2

Some surgeons prefer traditional segmental resection of the bowel regardless of the anatomical site, citing reduced disease recurrence with this approach; however, traditional segmental resection confers increased risk of complications. Increasingly, in an effort to reduce morbidity, more surgeons are advocating for the less aggressive methods of shaving excision and disc resection.

Aggressive resection at the level of the low rectum requires extensive surgical dissection of the retrorectal space, with the potential for inadvertent injury to surrounding neurovascular structures, such as the pelvic splanchnic nerves and superior and inferior hypogastric plexus.29 Injury to these structures can lead to significant complications, including bowel stenosis, fistula formation, constipation, and urinary retention. Complete resection of other areas, such as the small bowel, do not carry the same risks and may have more significant benefit to the patient than less aggressive techniques.

Our group recommends carefully balancing the risks and benefits of aggressive surgical treatment for each individual and treating the patient with the appropriate technique. Regardless of technique, surgical treatment of bowel endometriosis can lead to long-term improvements in pain and infertility.29,30,34,35

Key points
  • The clinical presentation of bowel endometriosis is often nonspecific, with a broad differential diagnosis. Maintain a high index of suspicion when reproductive-aged women present for evaluation of dysmenorrhea, chronic pelvic pain, dyspareunia, bloating, dyschezia, or hematochezia.
  • Symptomatic patients not desiring fertility, poor surgical candidates, and those declining surgical intervention may benefit from medical management. Patients who fail medical therapy, have severe symptoms, or experience infertility are candidates for surgical intervention.
  • Surgical management involves shaving excision, disc resection, and segmental resection. Some surgeons advocate for aggressive segmental resection regardless of the endometriotic lesion's location. Based on our extensive experience, we prefer shaving excision for lesions below the sigmoid to avoid dissection into the retrorectal space and inadvertent injury to nerve tissue controlling bowel and bladder function.
  • Following shaving excision, patients experience low complication rates29,39,40 and favorable long-term outcomes.15,40,56 For lesions above the sigmoid colon, including the small bowel, segmental resection or disc resection for smaller lesions are reasonable surgical approaches.

Continue to: Shaving excision...

 

 

Shaving excision

The most conservative approach to resection of bowel endometriosis is shaving excision; this involves removing endometriotic tissue layer-by-layer until healthy, underlying tissue is encountered.2 With bowel endometriosis, the goal of shaving excision is to remove as much of the diseased tissue as possible while leaving behind the mucosal layer and a portion of the muscularis.2,15,16,36-38 This is the most conservative of the 3 surgical techniques and is associated with the lowest complication rate.2,14,15,36,37

Our group reported on 185 women who underwent shaving excision for bowel endometriosis. At the time of surgery, 80 women had complete obliteration of the cul-de-sac (FIGURE 6). Of the study patients, 174 patients were available for follow-up, with 93% reporting moderate to complete pain relief.15

In a retrospective analysis of 3,298 surgeries for rectovaginal endometriosis in which shaving excision was used on all but 1% of patients, Donnez and colleagues reported a very low complication rate, with 1 case of rectal perforation, 1 case of fecal peritonitis, and 3 cases of ureteral injury.39

Roman and colleagues described the use of shaving excision for rectal endometriosis using plasma energy (n = 54) and laparoscopic scissors (n = 68).40 Only 4% of patients reported experiencing symptom recurrence, and the pregnancy rate was 65.4%, with 59% of those patients spontaneously conceiving. Two cases of rectal fistula were noted.

Disc resection

Laparoscopic disc excision has been described in the literature since the 1980s, and the technique involves the full-thickness removal of the diseased portion of the bowel, followed by closure of the remaining defect.2,12-14,28,29,31,41-45 To be appropriate for this technique, a lesion should involve only a portion of the bowel wall and, preferably, less than one-half of the bowel circumference.2,42 Disc excision results in excellent outcomes with fewer postoperative complications than segmental resection, but with more complications when compared to shaving excision.2,12,13,29,45,46

We reported on a series of 141 women with bowel endometriosis who underwent disc excision.2 At 1-month follow-up, 87% of patients experienced an improvement in their symptoms. No cases required conversion to laparotomy or were complicated by rectovaginal fistula formation, ureteral injury, bowel perforation, or pelvic abscess.2

Continue to: Segmental resection...

 

 

Segmental resection

The most aggressive surgical approach, segmental resection involves complete removal of a diseased portion of bowel, followed by side-to-side or end-to-end reanastomosis of the adjacent segments.2 For this procedure, a multidisciplinary approach is recommended, with involvement of a colorectal surgeon or gynecologic oncologist trained in performing bowel resections. Segmental resection is indicated for lesions that are larger than 3 cm, circumferential, obstructive, or multifocal.

Given the higher complication rate associated with this procedure and the good outcomes associated with less invasive techniques, we avoid segmental resection whenever possible, especially for lesions near the anal verge.2

Complications associated with surgical approach

In 2005, our group reported on a cohort of 178 women who underwent laparoscopic treatment of deeply infiltrative bowel endometriosis with shaving excision (n = 93), disc excision (n = 38), and segmental resection (n = 47).34 The major complication rate was significantly higher for those undergoing segmental resection (12.5%, P <.001); only 7.7% of those who underwent disc resection experienced a major complication; and none were observed in the group treated with shaving excision.

In 2011, De Cicco and colleagues conducted a systematic review of 1,889 patients who underwent segmental bowel resection.35 The major complication rate was 11%, with a leakage rate of 2.7%, fistula rate of 1.8%, major obstruction rate of 2.7%, and hemorrhage rate of 2.5%. Many of these complications, however, occurred in patients who had low rectal resections.

Regardless of surgical approach, the complication rate is related to the surgeon’s ability to preserve the superior and inferior hypogastric plexuses and the sympathetic and parasympathetic nerve bundles (FIGURE 7). Nerve-sparing techniques should be used to decrease the incidence of postoperative bowel, bladder, and sexual function complications.

Our group’s preferences

In our practice, we emphasize that the choice of surgical technique depends on the location, size, and depth of the lesion, as well as the extent of bowel wall circumferential invasion.2

We categorize lesions by their anatomic location: those above the sigmoid colon, on the sigmoid colon, on the rectosigmoid colon, and on the rectum. For lesions above the sigmoid colon, segmental or disc resection is appropriate.2 We recommend segmental resection for multifocal lesions, lesions larger than 3 cm, or for lesions involving more than one-third of the bowel lumen.37,44,45,47 Disc resection is appropriate for lesions smaller than 3 cm even if the bowel lumen is involved.44,45,48 If endometriosis is encountered in any location along the bowel, appendectomy can be performed even without visible disease, due to a high incidence of occult disease of the appendix.49,50

When lesions involve the sigmoid colon, we prefer utilizing shaving excision when possible to limit dissection of the retrorectal space and pelvic sidewall nerves.2 Segmental resection at or below the sigmoid colon has been associated with postoperative surgical site leakage51 and long-term bowel and bladder dysfunction with risk of permanent colostomy.52,53 For lesions smaller than 3 cm or involving less than one-third of the bowel lumen, disc resection can be performed. Segmental resection is required if multifocal disease or obstruction are present, if lesions are larger than 3 cm, or if more than one-third of the bowel lumen is involved.

For lesions along the rectosigmoid colon, we prefer utilizing shaving excision when possible.
2 Disc excision can be performed utilizing a transanal approach, being mindful to minimize dissection of the retroperitoneal space and pelvic sidewall nerves.48 Segmental resection is avoided even with lesions larger than 3 cm, unless prior surgery has failed. Approaches for segmental resection can utilize laparoscopy or the natural orifices of the rectum or vagina.31,51

For lesions on the rectum, we strongly advise shaving excision.2 Evidence fails to show that the benefits of segmental resection outweigh the risks when compared to conservative techniques at the rectum.30,39,54 There is evidence indicating that aggressive surgery 5 to 8 cm from the anal verge is predictive of postoperative complications.55 In our group, we use shaving excision to remove as much disease as possible without compromising the integrity of the bowel wall or surrounding neurovascular structures. We err on the side of caution, leaving some of the disease on the rectum to avoid rectal perforation, and plan for postoperative hormonal suppression in these patients.

For patients desiring fertility, successful pregnancy is often achieved using the shaving technique.41

References
  1. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010;362:2389-2398. 
  2. Nezhat C, Li A, Falik R, et al. Bowel endometriosis: diagnosis and management. Am J Obstet Gynecol. 2018;218:549-562. 
  3. Markham SM, Carpenter SE, Rock JA. Extrapelvic endometriosis. Obstet Gynecol Clin North Am. 1989;16:193-219. 
  4. Veeraswamy A, Lewis M, Mann A, et al. Extragenital endometriosis. Clin Obstet Gynecol. 2010;53:449-466. 
  5. Redwine DB. Ovarian endometriosis: a marker for more extensive pelvic and intestinal disease. Fertil Steril. 1999;72:310-315. 
  6. Weed JC, Ray JE. Endometriosis of the bowel. Obstet Gynecol. 1987;69:727-730. 
  7. Wheeler JM. Epidemiology of endometriosis-associated infertility. J Reprod Med. 1989;34:41-46. 
  8. Redwine DB. Intestinal endometriosis. In: Redwine DB. Surgical Management of Endometriosis. New York, NY: Martin Dunitz; 2004:196. 
  9. Hartmann D, Schilling D, Roth SU, et al. [Endometriosis of the transverse colon--a rare localization]. Dtsch Med Wochenschr. 2002;127:2317-2320. 
  10. Nezhat C, Nezhat F, Nezhat C. Endometriosis: ancient disease, ancient treatments. Fertil Steril. 2012;98(6 suppl):S1-62. 
  11. Macafee CH, Greer HL. Intestinal endometriosis. A report of 29 cases and a survey of the literature. J Obstet Gynaecol Br Emp. 1960;67:539-555. 
  12. Nezhat C, Nezhat F, Ambroze W, et al. Laparoscopic repair of small bowel and colon. A report of 26 cases. Surg Endosc. 1993;7:88-89. 
  13. Nezhat C, Nezhat F, Pennington E, et al. Laparoscopic disk excision and primary repair of the anterior rectal wall for the treatment of full-thickness bowel endometriosis. Surg Endosc. 1994;8:682-685. 
  14. Nezhat C, Nezhat F. Evaluation of safety of videolaseroscopic treatment of bowel endometriosis. Presented at: 44th Annual Meeting of the American Fertility Society; October, 1988; Atlanta, GA. 
  15. Nezhat C, Nezhat F, Pennington E. Laparoscopic treatment of infiltrative rectosigmoid colon and rectovaginal septum endometriosis by the technique of videolaparoscopy and the CO2 laser. Br J Obstet Gynaecol. 1992;99:664-667. 
  16. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45:778-783. 
  17. Sourial S, Tempest N, Hapangama DK. Theories on the pathogenesis of endometriosis. Int J Reprod Med. 2014;2014:179515. 
  18. Skoog SM, Foxx-Orenstein AE, Levy MJ, et al. Intestinal endometriosis: the great masquerader. Curr Gastroenterol Rep. 2004;6:405-409. 
  19. Alabiso G, Alio L, Arena S, et al. How to manage bowel endometriosis: the ETIC approach. J Minim Invasive Gynecol. 2015;22:517-529.  
  20. Heller DS, Lespinasse P, Mirani N. Endometriosis of the perineum: a rare diagnosis usually associated with episiotomy. J Low Genit Tract Dis. 2016;20:e48-e49. 
  21. Hudelist G, English J, Thomas AE, et al. Diagnostic accuracy of transvaginal ultrasound for non-invasive diagnosis of bowel endometriosis: systematic review and meta-analysis. Ultrasound Obstet Gynecol. 2011;37:257-263. 
  22. Nisenblat V, Bossuyt PM, Farquhar C, et al. Imaging modalities for the non-invasive diagnosis of endometriosis. Cochrane Database Syst Rev. 2016;2:CD009591. 
  23. Menada MV, Remorgida V, Abbamonte LH, et al. Transvaginal ultrasonography combined with water-contrast in the rectum in the diagnosis of rectovaginal endometriosis infiltrating the bowel. Fertil Steril. 2008;89:699-700. 
  24. Gordon RL, Evers K, Kressel HY, et al. Double-contrast enema in pelvic endometriosis. AJR Am J Roentgenol. 1982;138:549-552. 
  25. Vercellini P, Pietropaolo G, De Giorgi O, et al. Treatment of symptomatic rectovaginal endometriosis with an estrogen-progestogen combination versus low-dose norethindrone acetate. Fertil Steril. 2005;84:1375-1387. 
  26. Ferrero S, Camerini G, Ragni N, et al. Norethisterone acetate in the treatment of colorectal endometriosis: a pilot study. Hum Reprod. 2010;25:94-100. 
  27. Nezhat C, Hajhosseini B, King LP. Robotic-assisted laparoscopic treatment of bowel, bladder, and ureteral endometriosis. JSLS. 2011;15:387-392. 
  28. Nezhat C, Hajhosseini B, King LP. Laparoscopic management of bowel endometriosis: predictors of severe disease and recurrence. JSLS. 2011;15:431-438. 
  29. Roman H, Milles M, Vassilieff M, et al. Long-term functional outcomes following colorectal resection versus shaving for rectal endometriosis. Am J Obstet Gynecol. 2016;215:762.e1-762.e9. 
  30. Kent A, Shakir F, Rockall T, et al. Laparoscopic surgery for severe rectovaginal endometriosis compromising the bowel: a prospective cohort study. J Minim Invasive Gynecol. 2016;23:526-534. 
  31. Nezhat F, Nezhat C, Pennington E. Laparoscopic proctectomy for infiltrating endometriosis of the rectum. Fertil Steril. 1992;57:1129-1132. 
  32. Ruffo G, Scopelliti F, Scioscia M, et al. Laparoscopic colorectal resection for deep infiltrating endometriosis: analysis of 436 cases. Surg Endosc. 2010;24:63-67. 
  33. Darai E, Dubernard G, Coutant C, et al. Randomized trial of laparoscopically assisted versus open colorectal resection for endometriosis: morbidity, symptoms, quality of life, and fertility. Ann Surg. 2010;251:1018-1023. 
  34. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  35. De Cicco C, Corona R, Schonman R, et al. Bowel resection for deep endometriosis: a systematic review. BJOG. 2011;118:285-291. 
  36. Nezhat C, Nezhat FR. Safe laser endoscopic excision or vaporization of peritoneal endometriosis. Fertil Steril. 1989;52:149-151. 
  37. Donnez J, Squifflet J. Complications, pregnancy and recurrence in a prospective series of 500 patients operated on by the shaving technique for deep rectovaginal endometriotic nodules. Hum Reprod. 2010;25:1949-1958. 
  38. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy and videolaseroscopy. Contrib Gynecol Obstet. 1987;16:303-312. 
  39. Donnez J, Jadoul P, Colette S, et al. Deep rectovaginal endometriotic nodules: perioperative complications from a series of 3,298 patients operated on by the shaving technique. Gynecol Surg. 2013;10:31-40. 
  40. Roman H, Moatassim-Drissa S, Marty N, et al. Rectal shaving for deep endometriosis infiltrating the rectum: a 5-year continuous retrospective series. Fertil Steril. 2016;106:1438-1445.e2. 
  41. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  42. Jerby BL, Kessler H, Falcone T, et al. Laparoscopic management of colorectal endometriosis. Surg Endosc. 1999;13:1125-1128. 
  43. Coronado C, Franklin RR, Lotze EC, et al. Surgical treatment of symptomatic colorectal endometriosis. Fertil Steril. 1990;53:411-416. 
  44. Fanfani F, Fagotti A, Gagliardi ML, et al. Discoid or segmental rectosigmoid resection for deep infiltrating endometriosis: a case-control study. Fertil Steril. 2010;94:444-449. 
  45. Landi S, Pontrelli G, Surico D, et al. Laparoscopic disk resection for bowel endometriosis using a circular stapler and a new endoscopic method to control postoperative bleeding from the stapler line. J Am Coll Surg. 2008;207:205-209. 
  46. Slack A, Child T, Lindsey I, et al. Urological and colorectal complications following surgery for rectovaginal endometriosis. BJOG. 2007;114:1278-1282. 
  47. Ceccaroni M, Clarizia R, Bruni F, et al. Nerve-sparing laparoscopic eradication of deep endometriosis with segmental rectal and parametrial resection: the Negrar method. A single-center, prospective, clinical trial. Surg Endosc. 2012;26:2029-2045. 
  48. Roman H, Abo C, Huet E, et al. Deep shaving and transanal disc excision in large endometriosis of mid and lower rectum: the Rouen technique. Surg Endosc. 2016;30:2626-2627. 
  49. Gustofson RL, Kim N, Liu S, et al. Endometriosis and the appendix: a case series and comprehensive review of the literature. Fertil Steril. 2006;86:298-303. 
  50. Berker B, Lashay N, Davarpanah R, et al. Laparoscopic appendectomy in patients with endometriosis. J Minim Invasive Gynecol. 2005;12:206-209. 
  51. Ret Dávalos ML, De Cicco C, D'Hoore A, et al. Outcome after rectum or sigmoid resection: a review for gynecologists. J Minim Invasive Gynecol. 2007;14:33-38. 
  52. Alves A, Panis Y, Mathieu P, et al; Association Française de Chirurgie (AFC). Mortality and morbidity after surgery of mid and low rectal cancer. Results of a French prospective multicentric study. Gastroenterol Clin Biol. 2005;29:509-514. 
  53. Camilleri-Brennan J, Steele RJ. Objective assessment of morbidity and quality of life after surgery for low rectal cancer. Colorectal Dis. 2002;4:61-66. 
  54. Acien P, Núñez C, Quereda F, et al. Is a bowel resection necessary for deep endometriosis with rectovaginal or colorectal involvement? Int J Womens Health. 2013;5:449-455. 
  55. Abrão MS, Petraglia F, Falcone T, et al. Deep endometriosis infiltrating the recto-sigmoid: critical factors to consider before management. Hum Reprod Update. 2015;21:329-339. 
  56. Donnez J, Nisolle M, Gillerot S, et al. Rectovaginal septum adenomyotic nodules: a series of 500 cases. Br J Obstet Gynaecol. 1997;104:1014-1018.
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Dr. Camran Nezhat is Director of the Camran Nezhat Institute, Palo Alto, California and Founder of Worldwide Endometriosis March (EndoMarch). 

Dr. Burns is Assistant Professor, University of Massachusetts Medical School, Worcester.   

Dr. Wood is Resident, University of Texas. 

Dr. Ceana Nezhat is Director, Nezhat Medical Center, Atlanta, Georgia. 

The authors report no financial relationships relevant to this article. 
 

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Dr. Camran Nezhat is Director of the Camran Nezhat Institute, Palo Alto, California and Founder of Worldwide Endometriosis March (EndoMarch). 

Dr. Burns is Assistant Professor, University of Massachusetts Medical School, Worcester.   

Dr. Wood is Resident, University of Texas. 

Dr. Ceana Nezhat is Director, Nezhat Medical Center, Atlanta, Georgia. 

The authors report no financial relationships relevant to this article. 
 

Author and Disclosure Information

Dr. Camran Nezhat is Director of the Camran Nezhat Institute, Palo Alto, California and Founder of Worldwide Endometriosis March (EndoMarch). 

Dr. Burns is Assistant Professor, University of Massachusetts Medical School, Worcester.   

Dr. Wood is Resident, University of Texas. 

Dr. Ceana Nezhat is Director, Nezhat Medical Center, Atlanta, Georgia. 

The authors report no financial relationships relevant to this article. 
 

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Article PDF

About 10% of all reproductive-aged women and 35% to 50% of women with pelvic pain and infertility are affected by endometriosis.1,2 The disease typically involves the reproductive tract organs, anterior and posterior cul-de-sacs, and uterosacral ligaments. However, disease outside of the reproductive tract occurs frequently and has been found on all organs except the spleen.3

The bowel is the most common site for extragenital endometriosis, affected in an estimated 3.8% to 37% of patients with known endometriosis.4-7 Implants may be superficial, involving the bowel serosa and subserosa (FIGURE 1), or they can manifest as deeply infiltrating lesions involving the muscularis and mucosa (FIGURE 2). The rectosigmoid colon is the most common location for bowel endometriosis, followed by the rectum, ileum, appendix, and cecum4,8 (FIGURES 3, 4, and 5). Case reports also have described endometrial implants on the stomach and transverse colon.9 Although isolated bowel involvement has been recognized, most patients with bowel endometriosis have concurrent disease elsewhere.2,4 

Historically, segmental resection was performed regardless of the anatomical location of the lesion.10 Even today, many surgeons continue to routinely perform segmental bowel resection as a first-line surgical approach.11 Unnecessary segmental resection, however, places patients at risk for short- and long-term postoperative morbidity, including the possibility of permanent ostomy. Modern surgical techniques, such as shaving excision and disc resection, have been performed to successfully treat bowel endometriosis with excellent long-term outcomes and fewer complications when compared with traditional segmental resection.2,12-16

In this article, we focus on the clinical indications and surgical techniques for video-laparoscopic management, but first we describe the pathophysiology, clinical presentation, and diagnosis of bowel endometriosis.

 

Pathophysiology of bowel endometriosis

The pathogenesis of endometriosis remains unknown, as no single mechanism explains all clinical cases of the disease. The most popular proposed theory describes retrograde menstruation through the fallopian tubes.17 Once inside the peritoneal cavity, endometrial cells attach to and invade healthy peritoneum, establishing a blood supply necessary for growth and survival.

In the case of bowel endometriosis, deposition of effluxed endometrial cells may lead to an inflammatory response that increases the risk of adhesion formation, leading to potential cul-de-sac obliteration. Lesions may originate as Allen-Masters peritoneal defects, developing into deeply infiltrative rectovaginal septum lesions. The anatomical shelter theory contributes to lesions within the pelvis, with the rectosigmoid colon blocking the cephalad flow of effluxed menstrual blood from the pelvis, thus leading to a preponderance of lesions in the pelvis and along the rectosigmoid colon.2

Continue to: Clinical presentation and diagnosis...

 

 

Clinical presentation and diagnosis

Women presenting with endometriosis of the bowel are typically of reproductive age and commonly report symptoms of dysmenorrhea, chronic pelvic pain, dyspareunia, and dyschezia. Some women also experience catamenial diarrhea, constipation, hematochezia, and bloating.2 The differential diagnosis of these symptoms is broad and includes irritable bowel disease, ischemic colitis, inflammatory bowel disease, diverticulitis, pelvic inflammatory disease, and malignancy.

Because of its nonspecific symptoms, bowel endometriosis is often misdiagnosed and the disease goes untreated for years.18 Therefore, it is imperative that clinicians maintain a high index of suspicion when evaluating reproductive-aged women with gastrointestinal symptoms and pelvic pain.

Physical examination can be helpful in making the diagnosis of endometriosis. During bimanual examination, findings such as a fixed, tender, or retroverted uterus, uterosacral ligament nodularity, or an enlarged adnexal mass representing an ovarian endometrioma may be appreciated. Rectovaginal exam can identify areas of tenderness and nodularity along the rectovaginal septum. Speculum exam may reveal a laterally displaced cervix or blue powder-burn lesions along the cervix or posterior fornix.19 Rarely, endometriosis is found on the perineum within an episiotomy scar.20

Imaging studies can be used in conjunction with physical examination findings to aid in the diagnosis of endometriosis. Images also guide preoperative planning by characterizing lesions based on their size, location, and depth of invasion. Hudelist and colleagues found transvaginal ultrasound (TVUS) to have an overall sensitivity of 71% to 98% and a specificity of 92% to 100%.21 However, it was noted that the accuracy of the diagnosis was directly related to the experience of the sonographer, and lesions above the sigmoid colon were generally unable to be diagnosed. Other imaging modalities that have been reported to have high sensitivity and specificity for diagnosing bowel endometriosis include rectal water contrast TVUS,22,23 rectal endoscopic sonography,22 magnetic resonance imaging,22 and barium enema.24

 

Medical management

Medical therapy for patients with endometriosis is utilized with the goal of suppressing ovulation, lowering circulating hormone levels, and inducing endometrial atrophy. Medications commonly employed include gonadotropin-releasing hormone agonists and antagonists, anabolic steriods such as danazol, combined oral contraceptive pills, progestins, and aromatase inhibitors.

Continue to: To date, no optimal hormonal regimen...

 

 

To date, no optimal hormonal regimen has been established for the treatment of bowel endometriosis. Vercellini and colleagues demonstrated that progestins with and without low-dose estrogen improved symptoms of dysmenorrhea and dyspareunia.25 Ferrero and colleagues reported that 2.5 mg of norethindrone daily resulted in 53% of women with colorectal endometriosis reporting improved gastrointestinal symptoms.26 However, by 12 months of follow-up, 33% of these patients had elected to undergo surgical management.

Gonadotropin-releasing hormone agonists, such as leuprolide acetate, also can be used to mitigate symptoms of bowel endometriosis or to decrease disease burden at the time of surgery, and they can be used with add-back norethindrone acetate. The use of these medications is limited by adverse effects, such as vasomotor symptoms and decreased bone mineral density when used for longer than 6 months.
2

Medical therapy is commonly used for patients with mild to moderate symptoms and in those who are poor surgical candidates or decline surgical intervention. Medical therapy is especially useful when employed postoperatively to suppress the regrowth of microscopic ectopic endometrial tissue.

Patients must be counseled, however, that even with medical management, they may still require surgery in the future to control their symptoms and/or to preserve organ function.
2

 

Surgical management

Surgical treatment for bowel endometriosis depends on the disease location, the size and depth of the lesion, the presence or absence of stricture, and the surgeon’s level of expertise.2,12,27-30

In our group, we advocate for video-laparoscopy, with or without robotic as sistance. Minimally invasive surgery offers reduced blood loss, shorter recovery time, and fewer postoperative complications compared with laparotomy.2,16,27,31-33 The conversion rate to laparotomy has been reported to be about 3% when performed by an experienced surgeon.12

Darai and colleagues conducted a randomized trial of 52 patients undergoing surgery for colorectal endometriosis via either laparoscopic or open colon resection.33 Blood loss was significantly lower in the laparoscopy group (1.6 vs 2.7 mg/L, P <.05). No difference was noted in long-term outcomes. In a retrospective study of 436 cases, Ruffo and colleagues showed that those who underwent laparoscopic colorectal resection had higher postoperative pregnancy rates compared with those who had laparotomy (57.6% vs 23.1%, P <.035).32

The goal of surgical management of bowel endometriosis is to remove as many of the endometriotic lesions as possible while minimizing short- and long-term complications. Three surgical approaches have been described: shaving excision, disc resection, and segmental resection.2

Some surgeons prefer traditional segmental resection of the bowel regardless of the anatomical site, citing reduced disease recurrence with this approach; however, traditional segmental resection confers increased risk of complications. Increasingly, in an effort to reduce morbidity, more surgeons are advocating for the less aggressive methods of shaving excision and disc resection.

Aggressive resection at the level of the low rectum requires extensive surgical dissection of the retrorectal space, with the potential for inadvertent injury to surrounding neurovascular structures, such as the pelvic splanchnic nerves and superior and inferior hypogastric plexus.29 Injury to these structures can lead to significant complications, including bowel stenosis, fistula formation, constipation, and urinary retention. Complete resection of other areas, such as the small bowel, do not carry the same risks and may have more significant benefit to the patient than less aggressive techniques.

Our group recommends carefully balancing the risks and benefits of aggressive surgical treatment for each individual and treating the patient with the appropriate technique. Regardless of technique, surgical treatment of bowel endometriosis can lead to long-term improvements in pain and infertility.29,30,34,35

Key points
  • The clinical presentation of bowel endometriosis is often nonspecific, with a broad differential diagnosis. Maintain a high index of suspicion when reproductive-aged women present for evaluation of dysmenorrhea, chronic pelvic pain, dyspareunia, bloating, dyschezia, or hematochezia.
  • Symptomatic patients not desiring fertility, poor surgical candidates, and those declining surgical intervention may benefit from medical management. Patients who fail medical therapy, have severe symptoms, or experience infertility are candidates for surgical intervention.
  • Surgical management involves shaving excision, disc resection, and segmental resection. Some surgeons advocate for aggressive segmental resection regardless of the endometriotic lesion's location. Based on our extensive experience, we prefer shaving excision for lesions below the sigmoid to avoid dissection into the retrorectal space and inadvertent injury to nerve tissue controlling bowel and bladder function.
  • Following shaving excision, patients experience low complication rates29,39,40 and favorable long-term outcomes.15,40,56 For lesions above the sigmoid colon, including the small bowel, segmental resection or disc resection for smaller lesions are reasonable surgical approaches.

Continue to: Shaving excision...

 

 

Shaving excision

The most conservative approach to resection of bowel endometriosis is shaving excision; this involves removing endometriotic tissue layer-by-layer until healthy, underlying tissue is encountered.2 With bowel endometriosis, the goal of shaving excision is to remove as much of the diseased tissue as possible while leaving behind the mucosal layer and a portion of the muscularis.2,15,16,36-38 This is the most conservative of the 3 surgical techniques and is associated with the lowest complication rate.2,14,15,36,37

Our group reported on 185 women who underwent shaving excision for bowel endometriosis. At the time of surgery, 80 women had complete obliteration of the cul-de-sac (FIGURE 6). Of the study patients, 174 patients were available for follow-up, with 93% reporting moderate to complete pain relief.15

In a retrospective analysis of 3,298 surgeries for rectovaginal endometriosis in which shaving excision was used on all but 1% of patients, Donnez and colleagues reported a very low complication rate, with 1 case of rectal perforation, 1 case of fecal peritonitis, and 3 cases of ureteral injury.39

Roman and colleagues described the use of shaving excision for rectal endometriosis using plasma energy (n = 54) and laparoscopic scissors (n = 68).40 Only 4% of patients reported experiencing symptom recurrence, and the pregnancy rate was 65.4%, with 59% of those patients spontaneously conceiving. Two cases of rectal fistula were noted.

Disc resection

Laparoscopic disc excision has been described in the literature since the 1980s, and the technique involves the full-thickness removal of the diseased portion of the bowel, followed by closure of the remaining defect.2,12-14,28,29,31,41-45 To be appropriate for this technique, a lesion should involve only a portion of the bowel wall and, preferably, less than one-half of the bowel circumference.2,42 Disc excision results in excellent outcomes with fewer postoperative complications than segmental resection, but with more complications when compared to shaving excision.2,12,13,29,45,46

We reported on a series of 141 women with bowel endometriosis who underwent disc excision.2 At 1-month follow-up, 87% of patients experienced an improvement in their symptoms. No cases required conversion to laparotomy or were complicated by rectovaginal fistula formation, ureteral injury, bowel perforation, or pelvic abscess.2

Continue to: Segmental resection...

 

 

Segmental resection

The most aggressive surgical approach, segmental resection involves complete removal of a diseased portion of bowel, followed by side-to-side or end-to-end reanastomosis of the adjacent segments.2 For this procedure, a multidisciplinary approach is recommended, with involvement of a colorectal surgeon or gynecologic oncologist trained in performing bowel resections. Segmental resection is indicated for lesions that are larger than 3 cm, circumferential, obstructive, or multifocal.

Given the higher complication rate associated with this procedure and the good outcomes associated with less invasive techniques, we avoid segmental resection whenever possible, especially for lesions near the anal verge.2

Complications associated with surgical approach

In 2005, our group reported on a cohort of 178 women who underwent laparoscopic treatment of deeply infiltrative bowel endometriosis with shaving excision (n = 93), disc excision (n = 38), and segmental resection (n = 47).34 The major complication rate was significantly higher for those undergoing segmental resection (12.5%, P <.001); only 7.7% of those who underwent disc resection experienced a major complication; and none were observed in the group treated with shaving excision.

In 2011, De Cicco and colleagues conducted a systematic review of 1,889 patients who underwent segmental bowel resection.35 The major complication rate was 11%, with a leakage rate of 2.7%, fistula rate of 1.8%, major obstruction rate of 2.7%, and hemorrhage rate of 2.5%. Many of these complications, however, occurred in patients who had low rectal resections.

Regardless of surgical approach, the complication rate is related to the surgeon’s ability to preserve the superior and inferior hypogastric plexuses and the sympathetic and parasympathetic nerve bundles (FIGURE 7). Nerve-sparing techniques should be used to decrease the incidence of postoperative bowel, bladder, and sexual function complications.

Our group’s preferences

In our practice, we emphasize that the choice of surgical technique depends on the location, size, and depth of the lesion, as well as the extent of bowel wall circumferential invasion.2

We categorize lesions by their anatomic location: those above the sigmoid colon, on the sigmoid colon, on the rectosigmoid colon, and on the rectum. For lesions above the sigmoid colon, segmental or disc resection is appropriate.2 We recommend segmental resection for multifocal lesions, lesions larger than 3 cm, or for lesions involving more than one-third of the bowel lumen.37,44,45,47 Disc resection is appropriate for lesions smaller than 3 cm even if the bowel lumen is involved.44,45,48 If endometriosis is encountered in any location along the bowel, appendectomy can be performed even without visible disease, due to a high incidence of occult disease of the appendix.49,50

When lesions involve the sigmoid colon, we prefer utilizing shaving excision when possible to limit dissection of the retrorectal space and pelvic sidewall nerves.2 Segmental resection at or below the sigmoid colon has been associated with postoperative surgical site leakage51 and long-term bowel and bladder dysfunction with risk of permanent colostomy.52,53 For lesions smaller than 3 cm or involving less than one-third of the bowel lumen, disc resection can be performed. Segmental resection is required if multifocal disease or obstruction are present, if lesions are larger than 3 cm, or if more than one-third of the bowel lumen is involved.

For lesions along the rectosigmoid colon, we prefer utilizing shaving excision when possible.
2 Disc excision can be performed utilizing a transanal approach, being mindful to minimize dissection of the retroperitoneal space and pelvic sidewall nerves.48 Segmental resection is avoided even with lesions larger than 3 cm, unless prior surgery has failed. Approaches for segmental resection can utilize laparoscopy or the natural orifices of the rectum or vagina.31,51

For lesions on the rectum, we strongly advise shaving excision.2 Evidence fails to show that the benefits of segmental resection outweigh the risks when compared to conservative techniques at the rectum.30,39,54 There is evidence indicating that aggressive surgery 5 to 8 cm from the anal verge is predictive of postoperative complications.55 In our group, we use shaving excision to remove as much disease as possible without compromising the integrity of the bowel wall or surrounding neurovascular structures. We err on the side of caution, leaving some of the disease on the rectum to avoid rectal perforation, and plan for postoperative hormonal suppression in these patients.

For patients desiring fertility, successful pregnancy is often achieved using the shaving technique.41

About 10% of all reproductive-aged women and 35% to 50% of women with pelvic pain and infertility are affected by endometriosis.1,2 The disease typically involves the reproductive tract organs, anterior and posterior cul-de-sacs, and uterosacral ligaments. However, disease outside of the reproductive tract occurs frequently and has been found on all organs except the spleen.3

The bowel is the most common site for extragenital endometriosis, affected in an estimated 3.8% to 37% of patients with known endometriosis.4-7 Implants may be superficial, involving the bowel serosa and subserosa (FIGURE 1), or they can manifest as deeply infiltrating lesions involving the muscularis and mucosa (FIGURE 2). The rectosigmoid colon is the most common location for bowel endometriosis, followed by the rectum, ileum, appendix, and cecum4,8 (FIGURES 3, 4, and 5). Case reports also have described endometrial implants on the stomach and transverse colon.9 Although isolated bowel involvement has been recognized, most patients with bowel endometriosis have concurrent disease elsewhere.2,4 

Historically, segmental resection was performed regardless of the anatomical location of the lesion.10 Even today, many surgeons continue to routinely perform segmental bowel resection as a first-line surgical approach.11 Unnecessary segmental resection, however, places patients at risk for short- and long-term postoperative morbidity, including the possibility of permanent ostomy. Modern surgical techniques, such as shaving excision and disc resection, have been performed to successfully treat bowel endometriosis with excellent long-term outcomes and fewer complications when compared with traditional segmental resection.2,12-16

In this article, we focus on the clinical indications and surgical techniques for video-laparoscopic management, but first we describe the pathophysiology, clinical presentation, and diagnosis of bowel endometriosis.

 

Pathophysiology of bowel endometriosis

The pathogenesis of endometriosis remains unknown, as no single mechanism explains all clinical cases of the disease. The most popular proposed theory describes retrograde menstruation through the fallopian tubes.17 Once inside the peritoneal cavity, endometrial cells attach to and invade healthy peritoneum, establishing a blood supply necessary for growth and survival.

In the case of bowel endometriosis, deposition of effluxed endometrial cells may lead to an inflammatory response that increases the risk of adhesion formation, leading to potential cul-de-sac obliteration. Lesions may originate as Allen-Masters peritoneal defects, developing into deeply infiltrative rectovaginal septum lesions. The anatomical shelter theory contributes to lesions within the pelvis, with the rectosigmoid colon blocking the cephalad flow of effluxed menstrual blood from the pelvis, thus leading to a preponderance of lesions in the pelvis and along the rectosigmoid colon.2

Continue to: Clinical presentation and diagnosis...

 

 

Clinical presentation and diagnosis

Women presenting with endometriosis of the bowel are typically of reproductive age and commonly report symptoms of dysmenorrhea, chronic pelvic pain, dyspareunia, and dyschezia. Some women also experience catamenial diarrhea, constipation, hematochezia, and bloating.2 The differential diagnosis of these symptoms is broad and includes irritable bowel disease, ischemic colitis, inflammatory bowel disease, diverticulitis, pelvic inflammatory disease, and malignancy.

Because of its nonspecific symptoms, bowel endometriosis is often misdiagnosed and the disease goes untreated for years.18 Therefore, it is imperative that clinicians maintain a high index of suspicion when evaluating reproductive-aged women with gastrointestinal symptoms and pelvic pain.

Physical examination can be helpful in making the diagnosis of endometriosis. During bimanual examination, findings such as a fixed, tender, or retroverted uterus, uterosacral ligament nodularity, or an enlarged adnexal mass representing an ovarian endometrioma may be appreciated. Rectovaginal exam can identify areas of tenderness and nodularity along the rectovaginal septum. Speculum exam may reveal a laterally displaced cervix or blue powder-burn lesions along the cervix or posterior fornix.19 Rarely, endometriosis is found on the perineum within an episiotomy scar.20

Imaging studies can be used in conjunction with physical examination findings to aid in the diagnosis of endometriosis. Images also guide preoperative planning by characterizing lesions based on their size, location, and depth of invasion. Hudelist and colleagues found transvaginal ultrasound (TVUS) to have an overall sensitivity of 71% to 98% and a specificity of 92% to 100%.21 However, it was noted that the accuracy of the diagnosis was directly related to the experience of the sonographer, and lesions above the sigmoid colon were generally unable to be diagnosed. Other imaging modalities that have been reported to have high sensitivity and specificity for diagnosing bowel endometriosis include rectal water contrast TVUS,22,23 rectal endoscopic sonography,22 magnetic resonance imaging,22 and barium enema.24

 

Medical management

Medical therapy for patients with endometriosis is utilized with the goal of suppressing ovulation, lowering circulating hormone levels, and inducing endometrial atrophy. Medications commonly employed include gonadotropin-releasing hormone agonists and antagonists, anabolic steriods such as danazol, combined oral contraceptive pills, progestins, and aromatase inhibitors.

Continue to: To date, no optimal hormonal regimen...

 

 

To date, no optimal hormonal regimen has been established for the treatment of bowel endometriosis. Vercellini and colleagues demonstrated that progestins with and without low-dose estrogen improved symptoms of dysmenorrhea and dyspareunia.25 Ferrero and colleagues reported that 2.5 mg of norethindrone daily resulted in 53% of women with colorectal endometriosis reporting improved gastrointestinal symptoms.26 However, by 12 months of follow-up, 33% of these patients had elected to undergo surgical management.

Gonadotropin-releasing hormone agonists, such as leuprolide acetate, also can be used to mitigate symptoms of bowel endometriosis or to decrease disease burden at the time of surgery, and they can be used with add-back norethindrone acetate. The use of these medications is limited by adverse effects, such as vasomotor symptoms and decreased bone mineral density when used for longer than 6 months.
2

Medical therapy is commonly used for patients with mild to moderate symptoms and in those who are poor surgical candidates or decline surgical intervention. Medical therapy is especially useful when employed postoperatively to suppress the regrowth of microscopic ectopic endometrial tissue.

Patients must be counseled, however, that even with medical management, they may still require surgery in the future to control their symptoms and/or to preserve organ function.
2

 

Surgical management

Surgical treatment for bowel endometriosis depends on the disease location, the size and depth of the lesion, the presence or absence of stricture, and the surgeon’s level of expertise.2,12,27-30

In our group, we advocate for video-laparoscopy, with or without robotic as sistance. Minimally invasive surgery offers reduced blood loss, shorter recovery time, and fewer postoperative complications compared with laparotomy.2,16,27,31-33 The conversion rate to laparotomy has been reported to be about 3% when performed by an experienced surgeon.12

Darai and colleagues conducted a randomized trial of 52 patients undergoing surgery for colorectal endometriosis via either laparoscopic or open colon resection.33 Blood loss was significantly lower in the laparoscopy group (1.6 vs 2.7 mg/L, P <.05). No difference was noted in long-term outcomes. In a retrospective study of 436 cases, Ruffo and colleagues showed that those who underwent laparoscopic colorectal resection had higher postoperative pregnancy rates compared with those who had laparotomy (57.6% vs 23.1%, P <.035).32

The goal of surgical management of bowel endometriosis is to remove as many of the endometriotic lesions as possible while minimizing short- and long-term complications. Three surgical approaches have been described: shaving excision, disc resection, and segmental resection.2

Some surgeons prefer traditional segmental resection of the bowel regardless of the anatomical site, citing reduced disease recurrence with this approach; however, traditional segmental resection confers increased risk of complications. Increasingly, in an effort to reduce morbidity, more surgeons are advocating for the less aggressive methods of shaving excision and disc resection.

Aggressive resection at the level of the low rectum requires extensive surgical dissection of the retrorectal space, with the potential for inadvertent injury to surrounding neurovascular structures, such as the pelvic splanchnic nerves and superior and inferior hypogastric plexus.29 Injury to these structures can lead to significant complications, including bowel stenosis, fistula formation, constipation, and urinary retention. Complete resection of other areas, such as the small bowel, do not carry the same risks and may have more significant benefit to the patient than less aggressive techniques.

Our group recommends carefully balancing the risks and benefits of aggressive surgical treatment for each individual and treating the patient with the appropriate technique. Regardless of technique, surgical treatment of bowel endometriosis can lead to long-term improvements in pain and infertility.29,30,34,35

Key points
  • The clinical presentation of bowel endometriosis is often nonspecific, with a broad differential diagnosis. Maintain a high index of suspicion when reproductive-aged women present for evaluation of dysmenorrhea, chronic pelvic pain, dyspareunia, bloating, dyschezia, or hematochezia.
  • Symptomatic patients not desiring fertility, poor surgical candidates, and those declining surgical intervention may benefit from medical management. Patients who fail medical therapy, have severe symptoms, or experience infertility are candidates for surgical intervention.
  • Surgical management involves shaving excision, disc resection, and segmental resection. Some surgeons advocate for aggressive segmental resection regardless of the endometriotic lesion's location. Based on our extensive experience, we prefer shaving excision for lesions below the sigmoid to avoid dissection into the retrorectal space and inadvertent injury to nerve tissue controlling bowel and bladder function.
  • Following shaving excision, patients experience low complication rates29,39,40 and favorable long-term outcomes.15,40,56 For lesions above the sigmoid colon, including the small bowel, segmental resection or disc resection for smaller lesions are reasonable surgical approaches.

Continue to: Shaving excision...

 

 

Shaving excision

The most conservative approach to resection of bowel endometriosis is shaving excision; this involves removing endometriotic tissue layer-by-layer until healthy, underlying tissue is encountered.2 With bowel endometriosis, the goal of shaving excision is to remove as much of the diseased tissue as possible while leaving behind the mucosal layer and a portion of the muscularis.2,15,16,36-38 This is the most conservative of the 3 surgical techniques and is associated with the lowest complication rate.2,14,15,36,37

Our group reported on 185 women who underwent shaving excision for bowel endometriosis. At the time of surgery, 80 women had complete obliteration of the cul-de-sac (FIGURE 6). Of the study patients, 174 patients were available for follow-up, with 93% reporting moderate to complete pain relief.15

In a retrospective analysis of 3,298 surgeries for rectovaginal endometriosis in which shaving excision was used on all but 1% of patients, Donnez and colleagues reported a very low complication rate, with 1 case of rectal perforation, 1 case of fecal peritonitis, and 3 cases of ureteral injury.39

Roman and colleagues described the use of shaving excision for rectal endometriosis using plasma energy (n = 54) and laparoscopic scissors (n = 68).40 Only 4% of patients reported experiencing symptom recurrence, and the pregnancy rate was 65.4%, with 59% of those patients spontaneously conceiving. Two cases of rectal fistula were noted.

Disc resection

Laparoscopic disc excision has been described in the literature since the 1980s, and the technique involves the full-thickness removal of the diseased portion of the bowel, followed by closure of the remaining defect.2,12-14,28,29,31,41-45 To be appropriate for this technique, a lesion should involve only a portion of the bowel wall and, preferably, less than one-half of the bowel circumference.2,42 Disc excision results in excellent outcomes with fewer postoperative complications than segmental resection, but with more complications when compared to shaving excision.2,12,13,29,45,46

We reported on a series of 141 women with bowel endometriosis who underwent disc excision.2 At 1-month follow-up, 87% of patients experienced an improvement in their symptoms. No cases required conversion to laparotomy or were complicated by rectovaginal fistula formation, ureteral injury, bowel perforation, or pelvic abscess.2

Continue to: Segmental resection...

 

 

Segmental resection

The most aggressive surgical approach, segmental resection involves complete removal of a diseased portion of bowel, followed by side-to-side or end-to-end reanastomosis of the adjacent segments.2 For this procedure, a multidisciplinary approach is recommended, with involvement of a colorectal surgeon or gynecologic oncologist trained in performing bowel resections. Segmental resection is indicated for lesions that are larger than 3 cm, circumferential, obstructive, or multifocal.

Given the higher complication rate associated with this procedure and the good outcomes associated with less invasive techniques, we avoid segmental resection whenever possible, especially for lesions near the anal verge.2

Complications associated with surgical approach

In 2005, our group reported on a cohort of 178 women who underwent laparoscopic treatment of deeply infiltrative bowel endometriosis with shaving excision (n = 93), disc excision (n = 38), and segmental resection (n = 47).34 The major complication rate was significantly higher for those undergoing segmental resection (12.5%, P <.001); only 7.7% of those who underwent disc resection experienced a major complication; and none were observed in the group treated with shaving excision.

In 2011, De Cicco and colleagues conducted a systematic review of 1,889 patients who underwent segmental bowel resection.35 The major complication rate was 11%, with a leakage rate of 2.7%, fistula rate of 1.8%, major obstruction rate of 2.7%, and hemorrhage rate of 2.5%. Many of these complications, however, occurred in patients who had low rectal resections.

Regardless of surgical approach, the complication rate is related to the surgeon’s ability to preserve the superior and inferior hypogastric plexuses and the sympathetic and parasympathetic nerve bundles (FIGURE 7). Nerve-sparing techniques should be used to decrease the incidence of postoperative bowel, bladder, and sexual function complications.

Our group’s preferences

In our practice, we emphasize that the choice of surgical technique depends on the location, size, and depth of the lesion, as well as the extent of bowel wall circumferential invasion.2

We categorize lesions by their anatomic location: those above the sigmoid colon, on the sigmoid colon, on the rectosigmoid colon, and on the rectum. For lesions above the sigmoid colon, segmental or disc resection is appropriate.2 We recommend segmental resection for multifocal lesions, lesions larger than 3 cm, or for lesions involving more than one-third of the bowel lumen.37,44,45,47 Disc resection is appropriate for lesions smaller than 3 cm even if the bowel lumen is involved.44,45,48 If endometriosis is encountered in any location along the bowel, appendectomy can be performed even without visible disease, due to a high incidence of occult disease of the appendix.49,50

When lesions involve the sigmoid colon, we prefer utilizing shaving excision when possible to limit dissection of the retrorectal space and pelvic sidewall nerves.2 Segmental resection at or below the sigmoid colon has been associated with postoperative surgical site leakage51 and long-term bowel and bladder dysfunction with risk of permanent colostomy.52,53 For lesions smaller than 3 cm or involving less than one-third of the bowel lumen, disc resection can be performed. Segmental resection is required if multifocal disease or obstruction are present, if lesions are larger than 3 cm, or if more than one-third of the bowel lumen is involved.

For lesions along the rectosigmoid colon, we prefer utilizing shaving excision when possible.
2 Disc excision can be performed utilizing a transanal approach, being mindful to minimize dissection of the retroperitoneal space and pelvic sidewall nerves.48 Segmental resection is avoided even with lesions larger than 3 cm, unless prior surgery has failed. Approaches for segmental resection can utilize laparoscopy or the natural orifices of the rectum or vagina.31,51

For lesions on the rectum, we strongly advise shaving excision.2 Evidence fails to show that the benefits of segmental resection outweigh the risks when compared to conservative techniques at the rectum.30,39,54 There is evidence indicating that aggressive surgery 5 to 8 cm from the anal verge is predictive of postoperative complications.55 In our group, we use shaving excision to remove as much disease as possible without compromising the integrity of the bowel wall or surrounding neurovascular structures. We err on the side of caution, leaving some of the disease on the rectum to avoid rectal perforation, and plan for postoperative hormonal suppression in these patients.

For patients desiring fertility, successful pregnancy is often achieved using the shaving technique.41

References
  1. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010;362:2389-2398. 
  2. Nezhat C, Li A, Falik R, et al. Bowel endometriosis: diagnosis and management. Am J Obstet Gynecol. 2018;218:549-562. 
  3. Markham SM, Carpenter SE, Rock JA. Extrapelvic endometriosis. Obstet Gynecol Clin North Am. 1989;16:193-219. 
  4. Veeraswamy A, Lewis M, Mann A, et al. Extragenital endometriosis. Clin Obstet Gynecol. 2010;53:449-466. 
  5. Redwine DB. Ovarian endometriosis: a marker for more extensive pelvic and intestinal disease. Fertil Steril. 1999;72:310-315. 
  6. Weed JC, Ray JE. Endometriosis of the bowel. Obstet Gynecol. 1987;69:727-730. 
  7. Wheeler JM. Epidemiology of endometriosis-associated infertility. J Reprod Med. 1989;34:41-46. 
  8. Redwine DB. Intestinal endometriosis. In: Redwine DB. Surgical Management of Endometriosis. New York, NY: Martin Dunitz; 2004:196. 
  9. Hartmann D, Schilling D, Roth SU, et al. [Endometriosis of the transverse colon--a rare localization]. Dtsch Med Wochenschr. 2002;127:2317-2320. 
  10. Nezhat C, Nezhat F, Nezhat C. Endometriosis: ancient disease, ancient treatments. Fertil Steril. 2012;98(6 suppl):S1-62. 
  11. Macafee CH, Greer HL. Intestinal endometriosis. A report of 29 cases and a survey of the literature. J Obstet Gynaecol Br Emp. 1960;67:539-555. 
  12. Nezhat C, Nezhat F, Ambroze W, et al. Laparoscopic repair of small bowel and colon. A report of 26 cases. Surg Endosc. 1993;7:88-89. 
  13. Nezhat C, Nezhat F, Pennington E, et al. Laparoscopic disk excision and primary repair of the anterior rectal wall for the treatment of full-thickness bowel endometriosis. Surg Endosc. 1994;8:682-685. 
  14. Nezhat C, Nezhat F. Evaluation of safety of videolaseroscopic treatment of bowel endometriosis. Presented at: 44th Annual Meeting of the American Fertility Society; October, 1988; Atlanta, GA. 
  15. Nezhat C, Nezhat F, Pennington E. Laparoscopic treatment of infiltrative rectosigmoid colon and rectovaginal septum endometriosis by the technique of videolaparoscopy and the CO2 laser. Br J Obstet Gynaecol. 1992;99:664-667. 
  16. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45:778-783. 
  17. Sourial S, Tempest N, Hapangama DK. Theories on the pathogenesis of endometriosis. Int J Reprod Med. 2014;2014:179515. 
  18. Skoog SM, Foxx-Orenstein AE, Levy MJ, et al. Intestinal endometriosis: the great masquerader. Curr Gastroenterol Rep. 2004;6:405-409. 
  19. Alabiso G, Alio L, Arena S, et al. How to manage bowel endometriosis: the ETIC approach. J Minim Invasive Gynecol. 2015;22:517-529.  
  20. Heller DS, Lespinasse P, Mirani N. Endometriosis of the perineum: a rare diagnosis usually associated with episiotomy. J Low Genit Tract Dis. 2016;20:e48-e49. 
  21. Hudelist G, English J, Thomas AE, et al. Diagnostic accuracy of transvaginal ultrasound for non-invasive diagnosis of bowel endometriosis: systematic review and meta-analysis. Ultrasound Obstet Gynecol. 2011;37:257-263. 
  22. Nisenblat V, Bossuyt PM, Farquhar C, et al. Imaging modalities for the non-invasive diagnosis of endometriosis. Cochrane Database Syst Rev. 2016;2:CD009591. 
  23. Menada MV, Remorgida V, Abbamonte LH, et al. Transvaginal ultrasonography combined with water-contrast in the rectum in the diagnosis of rectovaginal endometriosis infiltrating the bowel. Fertil Steril. 2008;89:699-700. 
  24. Gordon RL, Evers K, Kressel HY, et al. Double-contrast enema in pelvic endometriosis. AJR Am J Roentgenol. 1982;138:549-552. 
  25. Vercellini P, Pietropaolo G, De Giorgi O, et al. Treatment of symptomatic rectovaginal endometriosis with an estrogen-progestogen combination versus low-dose norethindrone acetate. Fertil Steril. 2005;84:1375-1387. 
  26. Ferrero S, Camerini G, Ragni N, et al. Norethisterone acetate in the treatment of colorectal endometriosis: a pilot study. Hum Reprod. 2010;25:94-100. 
  27. Nezhat C, Hajhosseini B, King LP. Robotic-assisted laparoscopic treatment of bowel, bladder, and ureteral endometriosis. JSLS. 2011;15:387-392. 
  28. Nezhat C, Hajhosseini B, King LP. Laparoscopic management of bowel endometriosis: predictors of severe disease and recurrence. JSLS. 2011;15:431-438. 
  29. Roman H, Milles M, Vassilieff M, et al. Long-term functional outcomes following colorectal resection versus shaving for rectal endometriosis. Am J Obstet Gynecol. 2016;215:762.e1-762.e9. 
  30. Kent A, Shakir F, Rockall T, et al. Laparoscopic surgery for severe rectovaginal endometriosis compromising the bowel: a prospective cohort study. J Minim Invasive Gynecol. 2016;23:526-534. 
  31. Nezhat F, Nezhat C, Pennington E. Laparoscopic proctectomy for infiltrating endometriosis of the rectum. Fertil Steril. 1992;57:1129-1132. 
  32. Ruffo G, Scopelliti F, Scioscia M, et al. Laparoscopic colorectal resection for deep infiltrating endometriosis: analysis of 436 cases. Surg Endosc. 2010;24:63-67. 
  33. Darai E, Dubernard G, Coutant C, et al. Randomized trial of laparoscopically assisted versus open colorectal resection for endometriosis: morbidity, symptoms, quality of life, and fertility. Ann Surg. 2010;251:1018-1023. 
  34. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  35. De Cicco C, Corona R, Schonman R, et al. Bowel resection for deep endometriosis: a systematic review. BJOG. 2011;118:285-291. 
  36. Nezhat C, Nezhat FR. Safe laser endoscopic excision or vaporization of peritoneal endometriosis. Fertil Steril. 1989;52:149-151. 
  37. Donnez J, Squifflet J. Complications, pregnancy and recurrence in a prospective series of 500 patients operated on by the shaving technique for deep rectovaginal endometriotic nodules. Hum Reprod. 2010;25:1949-1958. 
  38. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy and videolaseroscopy. Contrib Gynecol Obstet. 1987;16:303-312. 
  39. Donnez J, Jadoul P, Colette S, et al. Deep rectovaginal endometriotic nodules: perioperative complications from a series of 3,298 patients operated on by the shaving technique. Gynecol Surg. 2013;10:31-40. 
  40. Roman H, Moatassim-Drissa S, Marty N, et al. Rectal shaving for deep endometriosis infiltrating the rectum: a 5-year continuous retrospective series. Fertil Steril. 2016;106:1438-1445.e2. 
  41. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  42. Jerby BL, Kessler H, Falcone T, et al. Laparoscopic management of colorectal endometriosis. Surg Endosc. 1999;13:1125-1128. 
  43. Coronado C, Franklin RR, Lotze EC, et al. Surgical treatment of symptomatic colorectal endometriosis. Fertil Steril. 1990;53:411-416. 
  44. Fanfani F, Fagotti A, Gagliardi ML, et al. Discoid or segmental rectosigmoid resection for deep infiltrating endometriosis: a case-control study. Fertil Steril. 2010;94:444-449. 
  45. Landi S, Pontrelli G, Surico D, et al. Laparoscopic disk resection for bowel endometriosis using a circular stapler and a new endoscopic method to control postoperative bleeding from the stapler line. J Am Coll Surg. 2008;207:205-209. 
  46. Slack A, Child T, Lindsey I, et al. Urological and colorectal complications following surgery for rectovaginal endometriosis. BJOG. 2007;114:1278-1282. 
  47. Ceccaroni M, Clarizia R, Bruni F, et al. Nerve-sparing laparoscopic eradication of deep endometriosis with segmental rectal and parametrial resection: the Negrar method. A single-center, prospective, clinical trial. Surg Endosc. 2012;26:2029-2045. 
  48. Roman H, Abo C, Huet E, et al. Deep shaving and transanal disc excision in large endometriosis of mid and lower rectum: the Rouen technique. Surg Endosc. 2016;30:2626-2627. 
  49. Gustofson RL, Kim N, Liu S, et al. Endometriosis and the appendix: a case series and comprehensive review of the literature. Fertil Steril. 2006;86:298-303. 
  50. Berker B, Lashay N, Davarpanah R, et al. Laparoscopic appendectomy in patients with endometriosis. J Minim Invasive Gynecol. 2005;12:206-209. 
  51. Ret Dávalos ML, De Cicco C, D'Hoore A, et al. Outcome after rectum or sigmoid resection: a review for gynecologists. J Minim Invasive Gynecol. 2007;14:33-38. 
  52. Alves A, Panis Y, Mathieu P, et al; Association Française de Chirurgie (AFC). Mortality and morbidity after surgery of mid and low rectal cancer. Results of a French prospective multicentric study. Gastroenterol Clin Biol. 2005;29:509-514. 
  53. Camilleri-Brennan J, Steele RJ. Objective assessment of morbidity and quality of life after surgery for low rectal cancer. Colorectal Dis. 2002;4:61-66. 
  54. Acien P, Núñez C, Quereda F, et al. Is a bowel resection necessary for deep endometriosis with rectovaginal or colorectal involvement? Int J Womens Health. 2013;5:449-455. 
  55. Abrão MS, Petraglia F, Falcone T, et al. Deep endometriosis infiltrating the recto-sigmoid: critical factors to consider before management. Hum Reprod Update. 2015;21:329-339. 
  56. Donnez J, Nisolle M, Gillerot S, et al. Rectovaginal septum adenomyotic nodules: a series of 500 cases. Br J Obstet Gynaecol. 1997;104:1014-1018.
References
  1. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010;362:2389-2398. 
  2. Nezhat C, Li A, Falik R, et al. Bowel endometriosis: diagnosis and management. Am J Obstet Gynecol. 2018;218:549-562. 
  3. Markham SM, Carpenter SE, Rock JA. Extrapelvic endometriosis. Obstet Gynecol Clin North Am. 1989;16:193-219. 
  4. Veeraswamy A, Lewis M, Mann A, et al. Extragenital endometriosis. Clin Obstet Gynecol. 2010;53:449-466. 
  5. Redwine DB. Ovarian endometriosis: a marker for more extensive pelvic and intestinal disease. Fertil Steril. 1999;72:310-315. 
  6. Weed JC, Ray JE. Endometriosis of the bowel. Obstet Gynecol. 1987;69:727-730. 
  7. Wheeler JM. Epidemiology of endometriosis-associated infertility. J Reprod Med. 1989;34:41-46. 
  8. Redwine DB. Intestinal endometriosis. In: Redwine DB. Surgical Management of Endometriosis. New York, NY: Martin Dunitz; 2004:196. 
  9. Hartmann D, Schilling D, Roth SU, et al. [Endometriosis of the transverse colon--a rare localization]. Dtsch Med Wochenschr. 2002;127:2317-2320. 
  10. Nezhat C, Nezhat F, Nezhat C. Endometriosis: ancient disease, ancient treatments. Fertil Steril. 2012;98(6 suppl):S1-62. 
  11. Macafee CH, Greer HL. Intestinal endometriosis. A report of 29 cases and a survey of the literature. J Obstet Gynaecol Br Emp. 1960;67:539-555. 
  12. Nezhat C, Nezhat F, Ambroze W, et al. Laparoscopic repair of small bowel and colon. A report of 26 cases. Surg Endosc. 1993;7:88-89. 
  13. Nezhat C, Nezhat F, Pennington E, et al. Laparoscopic disk excision and primary repair of the anterior rectal wall for the treatment of full-thickness bowel endometriosis. Surg Endosc. 1994;8:682-685. 
  14. Nezhat C, Nezhat F. Evaluation of safety of videolaseroscopic treatment of bowel endometriosis. Presented at: 44th Annual Meeting of the American Fertility Society; October, 1988; Atlanta, GA. 
  15. Nezhat C, Nezhat F, Pennington E. Laparoscopic treatment of infiltrative rectosigmoid colon and rectovaginal septum endometriosis by the technique of videolaparoscopy and the CO2 laser. Br J Obstet Gynaecol. 1992;99:664-667. 
  16. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45:778-783. 
  17. Sourial S, Tempest N, Hapangama DK. Theories on the pathogenesis of endometriosis. Int J Reprod Med. 2014;2014:179515. 
  18. Skoog SM, Foxx-Orenstein AE, Levy MJ, et al. Intestinal endometriosis: the great masquerader. Curr Gastroenterol Rep. 2004;6:405-409. 
  19. Alabiso G, Alio L, Arena S, et al. How to manage bowel endometriosis: the ETIC approach. J Minim Invasive Gynecol. 2015;22:517-529.  
  20. Heller DS, Lespinasse P, Mirani N. Endometriosis of the perineum: a rare diagnosis usually associated with episiotomy. J Low Genit Tract Dis. 2016;20:e48-e49. 
  21. Hudelist G, English J, Thomas AE, et al. Diagnostic accuracy of transvaginal ultrasound for non-invasive diagnosis of bowel endometriosis: systematic review and meta-analysis. Ultrasound Obstet Gynecol. 2011;37:257-263. 
  22. Nisenblat V, Bossuyt PM, Farquhar C, et al. Imaging modalities for the non-invasive diagnosis of endometriosis. Cochrane Database Syst Rev. 2016;2:CD009591. 
  23. Menada MV, Remorgida V, Abbamonte LH, et al. Transvaginal ultrasonography combined with water-contrast in the rectum in the diagnosis of rectovaginal endometriosis infiltrating the bowel. Fertil Steril. 2008;89:699-700. 
  24. Gordon RL, Evers K, Kressel HY, et al. Double-contrast enema in pelvic endometriosis. AJR Am J Roentgenol. 1982;138:549-552. 
  25. Vercellini P, Pietropaolo G, De Giorgi O, et al. Treatment of symptomatic rectovaginal endometriosis with an estrogen-progestogen combination versus low-dose norethindrone acetate. Fertil Steril. 2005;84:1375-1387. 
  26. Ferrero S, Camerini G, Ragni N, et al. Norethisterone acetate in the treatment of colorectal endometriosis: a pilot study. Hum Reprod. 2010;25:94-100. 
  27. Nezhat C, Hajhosseini B, King LP. Robotic-assisted laparoscopic treatment of bowel, bladder, and ureteral endometriosis. JSLS. 2011;15:387-392. 
  28. Nezhat C, Hajhosseini B, King LP. Laparoscopic management of bowel endometriosis: predictors of severe disease and recurrence. JSLS. 2011;15:431-438. 
  29. Roman H, Milles M, Vassilieff M, et al. Long-term functional outcomes following colorectal resection versus shaving for rectal endometriosis. Am J Obstet Gynecol. 2016;215:762.e1-762.e9. 
  30. Kent A, Shakir F, Rockall T, et al. Laparoscopic surgery for severe rectovaginal endometriosis compromising the bowel: a prospective cohort study. J Minim Invasive Gynecol. 2016;23:526-534. 
  31. Nezhat F, Nezhat C, Pennington E. Laparoscopic proctectomy for infiltrating endometriosis of the rectum. Fertil Steril. 1992;57:1129-1132. 
  32. Ruffo G, Scopelliti F, Scioscia M, et al. Laparoscopic colorectal resection for deep infiltrating endometriosis: analysis of 436 cases. Surg Endosc. 2010;24:63-67. 
  33. Darai E, Dubernard G, Coutant C, et al. Randomized trial of laparoscopically assisted versus open colorectal resection for endometriosis: morbidity, symptoms, quality of life, and fertility. Ann Surg. 2010;251:1018-1023. 
  34. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  35. De Cicco C, Corona R, Schonman R, et al. Bowel resection for deep endometriosis: a systematic review. BJOG. 2011;118:285-291. 
  36. Nezhat C, Nezhat FR. Safe laser endoscopic excision or vaporization of peritoneal endometriosis. Fertil Steril. 1989;52:149-151. 
  37. Donnez J, Squifflet J. Complications, pregnancy and recurrence in a prospective series of 500 patients operated on by the shaving technique for deep rectovaginal endometriotic nodules. Hum Reprod. 2010;25:1949-1958. 
  38. Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy and videolaseroscopy. Contrib Gynecol Obstet. 1987;16:303-312. 
  39. Donnez J, Jadoul P, Colette S, et al. Deep rectovaginal endometriotic nodules: perioperative complications from a series of 3,298 patients operated on by the shaving technique. Gynecol Surg. 2013;10:31-40. 
  40. Roman H, Moatassim-Drissa S, Marty N, et al. Rectal shaving for deep endometriosis infiltrating the rectum: a 5-year continuous retrospective series. Fertil Steril. 2016;106:1438-1445.e2. 
  41. Mohr C, Nezhat FR, Nezhat CH, et al. Fertility considerations in laparoscopic treatment of infiltrative bowel endometriosis. JSLS. 2005;9:16-24. 
  42. Jerby BL, Kessler H, Falcone T, et al. Laparoscopic management of colorectal endometriosis. Surg Endosc. 1999;13:1125-1128. 
  43. Coronado C, Franklin RR, Lotze EC, et al. Surgical treatment of symptomatic colorectal endometriosis. Fertil Steril. 1990;53:411-416. 
  44. Fanfani F, Fagotti A, Gagliardi ML, et al. Discoid or segmental rectosigmoid resection for deep infiltrating endometriosis: a case-control study. Fertil Steril. 2010;94:444-449. 
  45. Landi S, Pontrelli G, Surico D, et al. Laparoscopic disk resection for bowel endometriosis using a circular stapler and a new endoscopic method to control postoperative bleeding from the stapler line. J Am Coll Surg. 2008;207:205-209. 
  46. Slack A, Child T, Lindsey I, et al. Urological and colorectal complications following surgery for rectovaginal endometriosis. BJOG. 2007;114:1278-1282. 
  47. Ceccaroni M, Clarizia R, Bruni F, et al. Nerve-sparing laparoscopic eradication of deep endometriosis with segmental rectal and parametrial resection: the Negrar method. A single-center, prospective, clinical trial. Surg Endosc. 2012;26:2029-2045. 
  48. Roman H, Abo C, Huet E, et al. Deep shaving and transanal disc excision in large endometriosis of mid and lower rectum: the Rouen technique. Surg Endosc. 2016;30:2626-2627. 
  49. Gustofson RL, Kim N, Liu S, et al. Endometriosis and the appendix: a case series and comprehensive review of the literature. Fertil Steril. 2006;86:298-303. 
  50. Berker B, Lashay N, Davarpanah R, et al. Laparoscopic appendectomy in patients with endometriosis. J Minim Invasive Gynecol. 2005;12:206-209. 
  51. Ret Dávalos ML, De Cicco C, D'Hoore A, et al. Outcome after rectum or sigmoid resection: a review for gynecologists. J Minim Invasive Gynecol. 2007;14:33-38. 
  52. Alves A, Panis Y, Mathieu P, et al; Association Française de Chirurgie (AFC). Mortality and morbidity after surgery of mid and low rectal cancer. Results of a French prospective multicentric study. Gastroenterol Clin Biol. 2005;29:509-514. 
  53. Camilleri-Brennan J, Steele RJ. Objective assessment of morbidity and quality of life after surgery for low rectal cancer. Colorectal Dis. 2002;4:61-66. 
  54. Acien P, Núñez C, Quereda F, et al. Is a bowel resection necessary for deep endometriosis with rectovaginal or colorectal involvement? Int J Womens Health. 2013;5:449-455. 
  55. Abrão MS, Petraglia F, Falcone T, et al. Deep endometriosis infiltrating the recto-sigmoid: critical factors to consider before management. Hum Reprod Update. 2015;21:329-339. 
  56. Donnez J, Nisolle M, Gillerot S, et al. Rectovaginal septum adenomyotic nodules: a series of 500 cases. Br J Obstet Gynaecol. 1997;104:1014-1018.
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2019 Update on menopause

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Thu, 12/15/2022 - 17:43

Among peri- and postmenopausal women, abnormal bleeding, breast cancer, and mood disorders represent prevalent conditions. In this Update, we discuss data from a review that provides quantitative information on the likelihood of finding endometrial cancer among women with postmenopausal bleeding (PMB). We also summarize 2 recent consensus recommendations: One addresses the clinically important but controversial issue of the treatment of genitourinary syndrome of menopause (GSM) in breast cancer survivors, and the other provides guidance on the management of depression in perimenopausal women.

Endometrial cancer is associated with a high prevalence of PMB 

Clarke MA, Long BJ, Del Mar Morillo A, et al. Association of endometrial cancer risk with postmenopausal bleeding in women: a systematic review and meta-analysis. JAMA Intern Med. 2018;178:1210-1222. 

Endometrial cancer is the most common gynecologic malignancy and the fourth most common cancer among US women. In recent years, the incidence of and mortality from endometrial cancer have increased.1 Despite the high prevalence of endometrial cancer, population-based screening currently is not recommended. 

PMB affects up to 10% of women and can be caused by endometrial atrophy, endometrial polyps, uterine leiomyoma, and malignancy. While it is well known that PMB is a common presenting symptom of endometrial cancer, we do not have good data to guide counseling patients with PMB on the likelihood that endometrial cancer is present. Similarly, estimates are lacking regarding what proportion of women with endometrial cancer will present with PMB. 

To address these 2 issues, Clarke and colleagues conducted a comprehensive systematic review and meta-analysis of the prevalence of PMB among women with endometrial cancer (sensitivity) and the risk of endometrial cancer among women with PMB (positive predictive value). The authors included 129 studies--with 34,432 women with PMB and 6,358 with endometrial cancer--in their report.

Cancer prevalence varied with HT use, geographic location 

The study findings demonstrated that the prevalence of PMB in women with endometrial cancer was 90% (95% confidence interval [CI], 84%-94%), and there was no significant difference in the occurrence of PMB by cancer stage. The risk of endometrial cancer in women with PMB ranged from 0% to 48%, yielding an overall pooled estimate of 9% (95% CI, 8%-11%). As an editorialist pointed out, the risk of endometrial cancer in women with PMB is similar to that of colorectal cancer in individuals with rectal bleeding (8%) and breast cancer in women with a palpable mass (10%), supporting current guidance that recommends evaluation of women with PMB.2 Evaluating 100 women with PMB to diagnose 9 endometrial cancers does not seem excessive. 

Interestingly, among women with PMB, the prevalence of endometrial cancer was significantly higher among women not using hormone therapy (HT) than among users of HT (12% and 7%, respectively). In 7 studies restricted to women with PMB and polyps (n = 2,801), the pooled risk of endometrial cancer was 3% (95% CI, 3%-4%). In an analysis stratified by geographic region, a striking difference was noted in the risk of endometrial cancer among women with PMB in North America (5%), Northern Europe (7%), and in Western Europe (13%). This finding may be explained by regional differences in the approach to evaluating PMB, cultural perceptions of PMB that can affect thresholds to present for care, and differences in risk factors between these populations. 

The study had several limitations, including an inability to evaluate the number of years since menopause and the effects of body mass index. Additionally, the study did not address endometrial hyperplasia or endometrial intraepithelial neoplasia. 

 
WHAT THIS EVIDENCE MEANS FOR PRACTICE

PMB accounts for two-thirds of all gynecologic visits among perimenopausal and postmenopausal women.3 This study revealed a 9% risk of endometrial cancer in patients experiencing PMB, which supports current practice guidelines to further evaluate and rule out endometrial cancer among all women presenting with PMB4; it also provides reassurance that targeting this high-risk group of women for early detection and prevention strategies will capture most cases of endometrial cancers. However, the relatively low positive predictive value of PMB emphasizes the need for additional triage tests with high specificity to improve management of PMB and minimize unnecessary biopsies in low-risk women.

 

Treating GSM in breast cancer survivors: New guidance targets QoL and sexuality 

Faubion SS, Larkin LC, Stuenkel CA, et al. Management of genitourinary syndrome of menopause in women with or at high risk for breast cancer: consensus recommendations from The North American Menopause Society and The International Society for the Study of Women's Sexual Health. Menopause. 2018;25:596-608. 

More than 3 million breast cancer survivors reside in the United States. Accordingly, ObGyns see survivors on a frequent basis. For several reasons, genitourinary syndrome of menopause (also known as vulvovaginal atrophy) is particularly prevalent in women who have been treated for breast cancer. Chemotherapy, for example, often induces ovarian failure. For some premenopausal women, bilateral salpingo-oophorectomy may be performed or gonadotropin-releasing hormone agonists may be prescribed as part of breast cancer treatment. In postmenopausal survivors with hormone receptor-positive tumors, adjuvant aromatase inhibitor (AI) therapy may be used for up to 10 years. Treatment with AIs is associated with GSM symptoms.5 Although vaginal estrogen is an effective treatment for GSM, package labeling for all estrogens, including vaginal estrogens, lists a personal history of breast cancer as a contraindication. 

Given that there is little evidence addressing the safety of vaginal estrogen, other hormonal therapies, and nonprescription treatments for GSM in breast cancer survivors, many survivors with bothersome GSM symptoms are not appropriately treated.

 

Continue to: Expert panel creates evidence-based guidance...

 

 

Expert panel creates evidence-based guidance 

Against this backdrop, The North American Menopause Society and the International Society for the Study of Women's Sexual Health convened a group comprised of menopause specialists (ObGyns, internists, and nurse practitioners), specialists in sexuality, medical oncologists specializing in breast cancer, and a psychologist to create evidence-based interdisciplinary consensus guidelines for enhancing quality of life and sexuality for breast cancer survivors with GSM. 

Measures to help enhance quality of life and sexuality 

The group's key recommendations for clinicians include: 

  • Sexual function and quality of life (QoL) should be assessed in all women with or at high risk for breast cancer. 
  • Management of GSM should be individualized based on shared decision-making involving the patient and her oncologist. 
  • Initial treatment options include: 

—over-the-counter vaginal moisturizers used several times weekly on a regular basis 
—lubricants used with intercourse  
—vaginal dilator therapy  
—pelvic floor physical therapy. 
 

  • Low-dose vaginal estrogen therapy may be appropriate for select women who have been treated for breast cancer: 

—With use of vaginal estrogen, serum estradiol levels remain in the postmenopausal range. 
—Based on limited data, use of vaginal estrogen is associated with a minimal risk for recurrence of breast cancer. 
—Because their use is associated with the lowest serum estradiol levels, vaginal tablets, rings, or inserts may be preferable to creams.  
—Decisions regarding use of vaginal estrogen in breast cancer survivors should involve the woman's oncologist. Appropriate candidates for off-label use of vaginal estrogen may be survivors:

–who are at relatively low risk for recurrence 
–with hormone receptor-negative disease
–using tamoxifen rather than an AI 
–who are particularly concerned about quality of life.

—Given that AIs prevent recurrence by lowering estrogen levels, oncologists may be reluctant to consider use of vaginal estrogen in survivors using adjuvant agents. 
—With respect to use of vaginal estrogen, oncologists may be more comfortable with use in patients taking tamoxifen. 

  • Neither intravaginal dehydroepiandrosterone (DHEA; prasterone) nor the oral selective estrogen receptor modulator ospemifene has been studied in breast cancer survivors. 

In women with metastatic disease, QoL, comfort, and sexual intimacy are key considerations when weighing potential therapies; optimal choices will vary with probability of long-term survival. 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although more data addressing the safety of vaginal estrogen as well as prasterone and ospemifene in breast cancer survivors clearly are needed, these guidelines should help clinicians who care for breast cancer survivors with GSM.

Framework provided for managing depressive disorders in perimenopausal women 

Maki PM, Kornstein SG, Joffe H, et al; Board of Trustees for The North American Menopause Society (NAMS) and the Women and Mood Disorders Task Force of the National Network of Depression Centers. Guidelines for the evaluation and treatment of perimenopausal depression: summary and recommendations. Menopause. 2018;25:1069-1085. 

Although perimenopausal women are more susceptible to the development of depressive symptoms and major depressive episodes (MDE), there is a lack of consensus regarding how to evaluate and treat depression in women during the menopausal transition and postmenopausal period. 

Recently, an expert panel comprised of representatives from The North American Menopause Society and the National Network of Depression Centers Women and Mood Disorders Task Group developed clinical guidelines addressing epidemiology, clinical presentation, therapeutic effects of antidepressants, effects of HT, and efficacy of other therapies. Here we provide a summary of the expert panel's findings and guidelines. 

 

Continue to: Certain factors are associated with higher risk for depression...

 

 

Certain factors are associated with higher risk for depression 

The perimenopause represents a time of increased risk for depressive symptoms and major depressive disorder (MDD), even in women with no prior history of depression. Several characteristics and health factors are associated with the increased risk during the menopause transition. These include a prior history of MDD, current antidepressant use, anxiety, premenstrual depressive symptoms, African American race, high body mass index, younger age, social isolation, upsetting life events, and menopausal sleep disturbances.  

Although data are inconclusive on whether surgical menopause increases or decreases the risk for developing depression compared with women who transition through menopause naturally, recent studies show an elevated risk of depression in women following hysterectomy with and without oophorectomy.6,7 

Menopausal and depressive symptoms can overlap 

Midlife depression presents with classic depressive symptoms that commonly occur in combination with menopausal symptoms, including vasomotor symptoms, sleep and sexual disturbances, and weight and energy changes. These menopausal symptoms can complicate, co-occur, and overlap with the clinical presentation of depression. 

Conversely, depression may affect an individual's judgment of the degree of bother from menopausal somatic symptoms, thereby further magnifying the effect of symptoms on quality of life. The interrelationship between depressive symptoms and menopausal symptoms may pose a challenge when attempting to parse out contributing etiologies, relative contributions of each etiology, and the potential additive effects. 

Diagnosis and treatment options 

Diagnosis involves identifying the menopausal stage, assessing for co-existing psychiatric and menopause symptoms, appreciating the psychosocial factors common in midlife, and considering the differential diagnosis. Validated screening instruments can be helpful. Although a menopause-specific mood disorder scale does not yet exist, several general validated screening measures, such as the Patient Health Questionnaire-9, or PHQ-9, can be used for categorical determination of mood disorder diagnoses during the menopause transition. 

Antidepressants, cognitive-behavioral therapy, and other psychotherapies are considered first-line treatments for perimenopausal major depressive episodes. Only desvenlafaxine has been studied in large randomized placebo-controlled trials and has proven efficacious for the treatment of MDD in perimenopausal and postmenopausal women. 

A number of small open-label studies of other selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and mirtazapine to treat MDD in perimenopausal and postmenopausal women have demonstrated a positive effect on mood, and several SSRIs and SNRIs also have the added benefit of improving menopause-related symptoms. 

In women with a history of MDD, a prior adequate response to a particular antidepressant should guide treatment selection when MDD recurs during the midlife years. 

Although estrogen is not approved by the US Food and Drug Administration specifically for the treatment of mood disturbances, some evidence suggests that unopposed estrogen therapy has efficacy similar to that of antidepressant medications in treating depressive disorders in perimenopausal women,8-11 but it is ineffective in treating depressive disorders in postmenopausal women. Estrogen therapy also may augment the clinical response to antidepressants in midlife and older women.12,13 The data on combined HT (estrogen plus progestogen) or for different progestogens in treating depressive disorders in perimenopausal women are lacking and inconclusive.  

 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
The findings from this expert review panel demonstrate that women in the perimenopausal transition are at increased risk for depressive symptoms, major depressive episodes, and major depressive disorder. The interrelationship between symptoms of depression and menopause can complicate, co-occur, overlap, and magnify one another. Clinicians treating perimenopausal women with depression that is unresponsive to conventional antidepressant therapy should consider concurrent use of estrogen-based hormone therapy or referring the patient to a clinician comfortable doing so.

References
  1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67:7-30. 
  2. Matteson KA, Robison K, Jacoby VL. Opportunities for early detection of endometrial cancer in women with postmenopausal bleeding. JAMA Intern Med. 2018;178:1222-1223.  
  3. van Hanegem N, Breijer MC, Khan KS, et al. Diagnostic evaluation of the endometrium in postmenopausal bleeding: an evidence-based approach. Maturitas. 2011;68:155-164.  
  4. American College of Obstetricians and Gynecologists. ACOG Committee Opinion no. 734 summary. The role of transvaginal ultrasonography in evaluating the endometrium of women with postmenopausal bleeding. Obstet Gynecol. 2018; 131:945-946. 
  5. Baumgart J, Nilsson K, Evers AS, et al. Sexual dysfunction in women on adjuvant endocrine therapy after breast cancer. Menopause. 2013;20:162-168. 
  6. Chou PH, Lin CH, Cheng C, et al. Risk of depressive disorders in women undergoing hysterectomy: a population-based follow-up study. J Psychiatr Res. 2015;68:186-191. 
  7. Wilson L, Pandeya N, Byles J, et al. Hysterectomy and incidence of depressive symptoms in midlife women: the Australian Longitudinal Study on Women's Health. Epidemiol Psychiatr Sci. 2018;27:381-392. 
  8. Schmidt PJ, Nieman L, Danaceau MA, et al. Estrogen replacement in perimenopause-related depression: a preliminary report. Am J Obstet Gynecol. 2000;183:414-420. 
  9. Rasgon NL, Altshuler LL, Fairbanks L. Estrogen-replacement therapy for depression. Am J Psychiatry. 2001;158:1738. 
  10. Soares CN, Almeida OP, Joffe H, et al. Efficacy of estradiol for the treatment of major depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry. 2001;58:529-534. 
  11. Cohen LS, Soares CN, Poitras JR, et al. Short-term use of estradiol for depression in perimenopausal and postmenopausal women: a preliminary report. Am J Psychiatry. 2003;160:1519-1522. 
  12. Schneider LS, Small GW, Hamilton SH, et al. Estrogen replacement and response to fluoxetine in a multicenter geriatric depression trial. Fluoxetine Collaborative Study Group. Am J Geriatr Psychiatry. 1997;5:97-106. 
  13. Schneider LS, Small GW, Clary CM. Estrogen replacement therapy and antidepressant response to sertraline in older depressed women. Am J Geriatr Psychiatry. 2001;9:393-399. 
     
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Andrew M. Kaunitz, MD, NCMP 

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

Deanna C. McCullough, MD  

Dr. McCullough is Assistant Professor, Department of Obstetrics and Gynecology, University of Florida College of Medicine-Jacksonville. 

Dr. Kaunitz reports receiving grant or research support from Allergan and Mithra and that he is a consultant to AMAG, Merck, and Pfizer. Dr. McCullough reports no financial relationships relevant to this article. 
 

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Andrew M. Kaunitz, MD, NCMP 

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

Deanna C. McCullough, MD  

Dr. McCullough is Assistant Professor, Department of Obstetrics and Gynecology, University of Florida College of Medicine-Jacksonville. 

Dr. Kaunitz reports receiving grant or research support from Allergan and Mithra and that he is a consultant to AMAG, Merck, and Pfizer. Dr. McCullough reports no financial relationships relevant to this article. 
 

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Andrew M. Kaunitz, MD, NCMP 

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

Deanna C. McCullough, MD  

Dr. McCullough is Assistant Professor, Department of Obstetrics and Gynecology, University of Florida College of Medicine-Jacksonville. 

Dr. Kaunitz reports receiving grant or research support from Allergan and Mithra and that he is a consultant to AMAG, Merck, and Pfizer. Dr. McCullough reports no financial relationships relevant to this article. 
 

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Among peri- and postmenopausal women, abnormal bleeding, breast cancer, and mood disorders represent prevalent conditions. In this Update, we discuss data from a review that provides quantitative information on the likelihood of finding endometrial cancer among women with postmenopausal bleeding (PMB). We also summarize 2 recent consensus recommendations: One addresses the clinically important but controversial issue of the treatment of genitourinary syndrome of menopause (GSM) in breast cancer survivors, and the other provides guidance on the management of depression in perimenopausal women.

Endometrial cancer is associated with a high prevalence of PMB 

Clarke MA, Long BJ, Del Mar Morillo A, et al. Association of endometrial cancer risk with postmenopausal bleeding in women: a systematic review and meta-analysis. JAMA Intern Med. 2018;178:1210-1222. 

Endometrial cancer is the most common gynecologic malignancy and the fourth most common cancer among US women. In recent years, the incidence of and mortality from endometrial cancer have increased.1 Despite the high prevalence of endometrial cancer, population-based screening currently is not recommended. 

PMB affects up to 10% of women and can be caused by endometrial atrophy, endometrial polyps, uterine leiomyoma, and malignancy. While it is well known that PMB is a common presenting symptom of endometrial cancer, we do not have good data to guide counseling patients with PMB on the likelihood that endometrial cancer is present. Similarly, estimates are lacking regarding what proportion of women with endometrial cancer will present with PMB. 

To address these 2 issues, Clarke and colleagues conducted a comprehensive systematic review and meta-analysis of the prevalence of PMB among women with endometrial cancer (sensitivity) and the risk of endometrial cancer among women with PMB (positive predictive value). The authors included 129 studies--with 34,432 women with PMB and 6,358 with endometrial cancer--in their report.

Cancer prevalence varied with HT use, geographic location 

The study findings demonstrated that the prevalence of PMB in women with endometrial cancer was 90% (95% confidence interval [CI], 84%-94%), and there was no significant difference in the occurrence of PMB by cancer stage. The risk of endometrial cancer in women with PMB ranged from 0% to 48%, yielding an overall pooled estimate of 9% (95% CI, 8%-11%). As an editorialist pointed out, the risk of endometrial cancer in women with PMB is similar to that of colorectal cancer in individuals with rectal bleeding (8%) and breast cancer in women with a palpable mass (10%), supporting current guidance that recommends evaluation of women with PMB.2 Evaluating 100 women with PMB to diagnose 9 endometrial cancers does not seem excessive. 

Interestingly, among women with PMB, the prevalence of endometrial cancer was significantly higher among women not using hormone therapy (HT) than among users of HT (12% and 7%, respectively). In 7 studies restricted to women with PMB and polyps (n = 2,801), the pooled risk of endometrial cancer was 3% (95% CI, 3%-4%). In an analysis stratified by geographic region, a striking difference was noted in the risk of endometrial cancer among women with PMB in North America (5%), Northern Europe (7%), and in Western Europe (13%). This finding may be explained by regional differences in the approach to evaluating PMB, cultural perceptions of PMB that can affect thresholds to present for care, and differences in risk factors between these populations. 

The study had several limitations, including an inability to evaluate the number of years since menopause and the effects of body mass index. Additionally, the study did not address endometrial hyperplasia or endometrial intraepithelial neoplasia. 

 
WHAT THIS EVIDENCE MEANS FOR PRACTICE

PMB accounts for two-thirds of all gynecologic visits among perimenopausal and postmenopausal women.3 This study revealed a 9% risk of endometrial cancer in patients experiencing PMB, which supports current practice guidelines to further evaluate and rule out endometrial cancer among all women presenting with PMB4; it also provides reassurance that targeting this high-risk group of women for early detection and prevention strategies will capture most cases of endometrial cancers. However, the relatively low positive predictive value of PMB emphasizes the need for additional triage tests with high specificity to improve management of PMB and minimize unnecessary biopsies in low-risk women.

 

Treating GSM in breast cancer survivors: New guidance targets QoL and sexuality 

Faubion SS, Larkin LC, Stuenkel CA, et al. Management of genitourinary syndrome of menopause in women with or at high risk for breast cancer: consensus recommendations from The North American Menopause Society and The International Society for the Study of Women's Sexual Health. Menopause. 2018;25:596-608. 

More than 3 million breast cancer survivors reside in the United States. Accordingly, ObGyns see survivors on a frequent basis. For several reasons, genitourinary syndrome of menopause (also known as vulvovaginal atrophy) is particularly prevalent in women who have been treated for breast cancer. Chemotherapy, for example, often induces ovarian failure. For some premenopausal women, bilateral salpingo-oophorectomy may be performed or gonadotropin-releasing hormone agonists may be prescribed as part of breast cancer treatment. In postmenopausal survivors with hormone receptor-positive tumors, adjuvant aromatase inhibitor (AI) therapy may be used for up to 10 years. Treatment with AIs is associated with GSM symptoms.5 Although vaginal estrogen is an effective treatment for GSM, package labeling for all estrogens, including vaginal estrogens, lists a personal history of breast cancer as a contraindication. 

Given that there is little evidence addressing the safety of vaginal estrogen, other hormonal therapies, and nonprescription treatments for GSM in breast cancer survivors, many survivors with bothersome GSM symptoms are not appropriately treated.

 

Continue to: Expert panel creates evidence-based guidance...

 

 

Expert panel creates evidence-based guidance 

Against this backdrop, The North American Menopause Society and the International Society for the Study of Women's Sexual Health convened a group comprised of menopause specialists (ObGyns, internists, and nurse practitioners), specialists in sexuality, medical oncologists specializing in breast cancer, and a psychologist to create evidence-based interdisciplinary consensus guidelines for enhancing quality of life and sexuality for breast cancer survivors with GSM. 

Measures to help enhance quality of life and sexuality 

The group's key recommendations for clinicians include: 

  • Sexual function and quality of life (QoL) should be assessed in all women with or at high risk for breast cancer. 
  • Management of GSM should be individualized based on shared decision-making involving the patient and her oncologist. 
  • Initial treatment options include: 

—over-the-counter vaginal moisturizers used several times weekly on a regular basis 
—lubricants used with intercourse  
—vaginal dilator therapy  
—pelvic floor physical therapy. 
 

  • Low-dose vaginal estrogen therapy may be appropriate for select women who have been treated for breast cancer: 

—With use of vaginal estrogen, serum estradiol levels remain in the postmenopausal range. 
—Based on limited data, use of vaginal estrogen is associated with a minimal risk for recurrence of breast cancer. 
—Because their use is associated with the lowest serum estradiol levels, vaginal tablets, rings, or inserts may be preferable to creams.  
—Decisions regarding use of vaginal estrogen in breast cancer survivors should involve the woman's oncologist. Appropriate candidates for off-label use of vaginal estrogen may be survivors:

–who are at relatively low risk for recurrence 
–with hormone receptor-negative disease
–using tamoxifen rather than an AI 
–who are particularly concerned about quality of life.

—Given that AIs prevent recurrence by lowering estrogen levels, oncologists may be reluctant to consider use of vaginal estrogen in survivors using adjuvant agents. 
—With respect to use of vaginal estrogen, oncologists may be more comfortable with use in patients taking tamoxifen. 

  • Neither intravaginal dehydroepiandrosterone (DHEA; prasterone) nor the oral selective estrogen receptor modulator ospemifene has been studied in breast cancer survivors. 

In women with metastatic disease, QoL, comfort, and sexual intimacy are key considerations when weighing potential therapies; optimal choices will vary with probability of long-term survival. 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although more data addressing the safety of vaginal estrogen as well as prasterone and ospemifene in breast cancer survivors clearly are needed, these guidelines should help clinicians who care for breast cancer survivors with GSM.

Framework provided for managing depressive disorders in perimenopausal women 

Maki PM, Kornstein SG, Joffe H, et al; Board of Trustees for The North American Menopause Society (NAMS) and the Women and Mood Disorders Task Force of the National Network of Depression Centers. Guidelines for the evaluation and treatment of perimenopausal depression: summary and recommendations. Menopause. 2018;25:1069-1085. 

Although perimenopausal women are more susceptible to the development of depressive symptoms and major depressive episodes (MDE), there is a lack of consensus regarding how to evaluate and treat depression in women during the menopausal transition and postmenopausal period. 

Recently, an expert panel comprised of representatives from The North American Menopause Society and the National Network of Depression Centers Women and Mood Disorders Task Group developed clinical guidelines addressing epidemiology, clinical presentation, therapeutic effects of antidepressants, effects of HT, and efficacy of other therapies. Here we provide a summary of the expert panel's findings and guidelines. 

 

Continue to: Certain factors are associated with higher risk for depression...

 

 

Certain factors are associated with higher risk for depression 

The perimenopause represents a time of increased risk for depressive symptoms and major depressive disorder (MDD), even in women with no prior history of depression. Several characteristics and health factors are associated with the increased risk during the menopause transition. These include a prior history of MDD, current antidepressant use, anxiety, premenstrual depressive symptoms, African American race, high body mass index, younger age, social isolation, upsetting life events, and menopausal sleep disturbances.  

Although data are inconclusive on whether surgical menopause increases or decreases the risk for developing depression compared with women who transition through menopause naturally, recent studies show an elevated risk of depression in women following hysterectomy with and without oophorectomy.6,7 

Menopausal and depressive symptoms can overlap 

Midlife depression presents with classic depressive symptoms that commonly occur in combination with menopausal symptoms, including vasomotor symptoms, sleep and sexual disturbances, and weight and energy changes. These menopausal symptoms can complicate, co-occur, and overlap with the clinical presentation of depression. 

Conversely, depression may affect an individual's judgment of the degree of bother from menopausal somatic symptoms, thereby further magnifying the effect of symptoms on quality of life. The interrelationship between depressive symptoms and menopausal symptoms may pose a challenge when attempting to parse out contributing etiologies, relative contributions of each etiology, and the potential additive effects. 

Diagnosis and treatment options 

Diagnosis involves identifying the menopausal stage, assessing for co-existing psychiatric and menopause symptoms, appreciating the psychosocial factors common in midlife, and considering the differential diagnosis. Validated screening instruments can be helpful. Although a menopause-specific mood disorder scale does not yet exist, several general validated screening measures, such as the Patient Health Questionnaire-9, or PHQ-9, can be used for categorical determination of mood disorder diagnoses during the menopause transition. 

Antidepressants, cognitive-behavioral therapy, and other psychotherapies are considered first-line treatments for perimenopausal major depressive episodes. Only desvenlafaxine has been studied in large randomized placebo-controlled trials and has proven efficacious for the treatment of MDD in perimenopausal and postmenopausal women. 

A number of small open-label studies of other selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and mirtazapine to treat MDD in perimenopausal and postmenopausal women have demonstrated a positive effect on mood, and several SSRIs and SNRIs also have the added benefit of improving menopause-related symptoms. 

In women with a history of MDD, a prior adequate response to a particular antidepressant should guide treatment selection when MDD recurs during the midlife years. 

Although estrogen is not approved by the US Food and Drug Administration specifically for the treatment of mood disturbances, some evidence suggests that unopposed estrogen therapy has efficacy similar to that of antidepressant medications in treating depressive disorders in perimenopausal women,8-11 but it is ineffective in treating depressive disorders in postmenopausal women. Estrogen therapy also may augment the clinical response to antidepressants in midlife and older women.12,13 The data on combined HT (estrogen plus progestogen) or for different progestogens in treating depressive disorders in perimenopausal women are lacking and inconclusive.  

 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
The findings from this expert review panel demonstrate that women in the perimenopausal transition are at increased risk for depressive symptoms, major depressive episodes, and major depressive disorder. The interrelationship between symptoms of depression and menopause can complicate, co-occur, overlap, and magnify one another. Clinicians treating perimenopausal women with depression that is unresponsive to conventional antidepressant therapy should consider concurrent use of estrogen-based hormone therapy or referring the patient to a clinician comfortable doing so.

Among peri- and postmenopausal women, abnormal bleeding, breast cancer, and mood disorders represent prevalent conditions. In this Update, we discuss data from a review that provides quantitative information on the likelihood of finding endometrial cancer among women with postmenopausal bleeding (PMB). We also summarize 2 recent consensus recommendations: One addresses the clinically important but controversial issue of the treatment of genitourinary syndrome of menopause (GSM) in breast cancer survivors, and the other provides guidance on the management of depression in perimenopausal women.

Endometrial cancer is associated with a high prevalence of PMB 

Clarke MA, Long BJ, Del Mar Morillo A, et al. Association of endometrial cancer risk with postmenopausal bleeding in women: a systematic review and meta-analysis. JAMA Intern Med. 2018;178:1210-1222. 

Endometrial cancer is the most common gynecologic malignancy and the fourth most common cancer among US women. In recent years, the incidence of and mortality from endometrial cancer have increased.1 Despite the high prevalence of endometrial cancer, population-based screening currently is not recommended. 

PMB affects up to 10% of women and can be caused by endometrial atrophy, endometrial polyps, uterine leiomyoma, and malignancy. While it is well known that PMB is a common presenting symptom of endometrial cancer, we do not have good data to guide counseling patients with PMB on the likelihood that endometrial cancer is present. Similarly, estimates are lacking regarding what proportion of women with endometrial cancer will present with PMB. 

To address these 2 issues, Clarke and colleagues conducted a comprehensive systematic review and meta-analysis of the prevalence of PMB among women with endometrial cancer (sensitivity) and the risk of endometrial cancer among women with PMB (positive predictive value). The authors included 129 studies--with 34,432 women with PMB and 6,358 with endometrial cancer--in their report.

Cancer prevalence varied with HT use, geographic location 

The study findings demonstrated that the prevalence of PMB in women with endometrial cancer was 90% (95% confidence interval [CI], 84%-94%), and there was no significant difference in the occurrence of PMB by cancer stage. The risk of endometrial cancer in women with PMB ranged from 0% to 48%, yielding an overall pooled estimate of 9% (95% CI, 8%-11%). As an editorialist pointed out, the risk of endometrial cancer in women with PMB is similar to that of colorectal cancer in individuals with rectal bleeding (8%) and breast cancer in women with a palpable mass (10%), supporting current guidance that recommends evaluation of women with PMB.2 Evaluating 100 women with PMB to diagnose 9 endometrial cancers does not seem excessive. 

Interestingly, among women with PMB, the prevalence of endometrial cancer was significantly higher among women not using hormone therapy (HT) than among users of HT (12% and 7%, respectively). In 7 studies restricted to women with PMB and polyps (n = 2,801), the pooled risk of endometrial cancer was 3% (95% CI, 3%-4%). In an analysis stratified by geographic region, a striking difference was noted in the risk of endometrial cancer among women with PMB in North America (5%), Northern Europe (7%), and in Western Europe (13%). This finding may be explained by regional differences in the approach to evaluating PMB, cultural perceptions of PMB that can affect thresholds to present for care, and differences in risk factors between these populations. 

The study had several limitations, including an inability to evaluate the number of years since menopause and the effects of body mass index. Additionally, the study did not address endometrial hyperplasia or endometrial intraepithelial neoplasia. 

 
WHAT THIS EVIDENCE MEANS FOR PRACTICE

PMB accounts for two-thirds of all gynecologic visits among perimenopausal and postmenopausal women.3 This study revealed a 9% risk of endometrial cancer in patients experiencing PMB, which supports current practice guidelines to further evaluate and rule out endometrial cancer among all women presenting with PMB4; it also provides reassurance that targeting this high-risk group of women for early detection and prevention strategies will capture most cases of endometrial cancers. However, the relatively low positive predictive value of PMB emphasizes the need for additional triage tests with high specificity to improve management of PMB and minimize unnecessary biopsies in low-risk women.

 

Treating GSM in breast cancer survivors: New guidance targets QoL and sexuality 

Faubion SS, Larkin LC, Stuenkel CA, et al. Management of genitourinary syndrome of menopause in women with or at high risk for breast cancer: consensus recommendations from The North American Menopause Society and The International Society for the Study of Women's Sexual Health. Menopause. 2018;25:596-608. 

More than 3 million breast cancer survivors reside in the United States. Accordingly, ObGyns see survivors on a frequent basis. For several reasons, genitourinary syndrome of menopause (also known as vulvovaginal atrophy) is particularly prevalent in women who have been treated for breast cancer. Chemotherapy, for example, often induces ovarian failure. For some premenopausal women, bilateral salpingo-oophorectomy may be performed or gonadotropin-releasing hormone agonists may be prescribed as part of breast cancer treatment. In postmenopausal survivors with hormone receptor-positive tumors, adjuvant aromatase inhibitor (AI) therapy may be used for up to 10 years. Treatment with AIs is associated with GSM symptoms.5 Although vaginal estrogen is an effective treatment for GSM, package labeling for all estrogens, including vaginal estrogens, lists a personal history of breast cancer as a contraindication. 

Given that there is little evidence addressing the safety of vaginal estrogen, other hormonal therapies, and nonprescription treatments for GSM in breast cancer survivors, many survivors with bothersome GSM symptoms are not appropriately treated.

 

Continue to: Expert panel creates evidence-based guidance...

 

 

Expert panel creates evidence-based guidance 

Against this backdrop, The North American Menopause Society and the International Society for the Study of Women's Sexual Health convened a group comprised of menopause specialists (ObGyns, internists, and nurse practitioners), specialists in sexuality, medical oncologists specializing in breast cancer, and a psychologist to create evidence-based interdisciplinary consensus guidelines for enhancing quality of life and sexuality for breast cancer survivors with GSM. 

Measures to help enhance quality of life and sexuality 

The group's key recommendations for clinicians include: 

  • Sexual function and quality of life (QoL) should be assessed in all women with or at high risk for breast cancer. 
  • Management of GSM should be individualized based on shared decision-making involving the patient and her oncologist. 
  • Initial treatment options include: 

—over-the-counter vaginal moisturizers used several times weekly on a regular basis 
—lubricants used with intercourse  
—vaginal dilator therapy  
—pelvic floor physical therapy. 
 

  • Low-dose vaginal estrogen therapy may be appropriate for select women who have been treated for breast cancer: 

—With use of vaginal estrogen, serum estradiol levels remain in the postmenopausal range. 
—Based on limited data, use of vaginal estrogen is associated with a minimal risk for recurrence of breast cancer. 
—Because their use is associated with the lowest serum estradiol levels, vaginal tablets, rings, or inserts may be preferable to creams.  
—Decisions regarding use of vaginal estrogen in breast cancer survivors should involve the woman's oncologist. Appropriate candidates for off-label use of vaginal estrogen may be survivors:

–who are at relatively low risk for recurrence 
–with hormone receptor-negative disease
–using tamoxifen rather than an AI 
–who are particularly concerned about quality of life.

—Given that AIs prevent recurrence by lowering estrogen levels, oncologists may be reluctant to consider use of vaginal estrogen in survivors using adjuvant agents. 
—With respect to use of vaginal estrogen, oncologists may be more comfortable with use in patients taking tamoxifen. 

  • Neither intravaginal dehydroepiandrosterone (DHEA; prasterone) nor the oral selective estrogen receptor modulator ospemifene has been studied in breast cancer survivors. 

In women with metastatic disease, QoL, comfort, and sexual intimacy are key considerations when weighing potential therapies; optimal choices will vary with probability of long-term survival. 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
Although more data addressing the safety of vaginal estrogen as well as prasterone and ospemifene in breast cancer survivors clearly are needed, these guidelines should help clinicians who care for breast cancer survivors with GSM.

Framework provided for managing depressive disorders in perimenopausal women 

Maki PM, Kornstein SG, Joffe H, et al; Board of Trustees for The North American Menopause Society (NAMS) and the Women and Mood Disorders Task Force of the National Network of Depression Centers. Guidelines for the evaluation and treatment of perimenopausal depression: summary and recommendations. Menopause. 2018;25:1069-1085. 

Although perimenopausal women are more susceptible to the development of depressive symptoms and major depressive episodes (MDE), there is a lack of consensus regarding how to evaluate and treat depression in women during the menopausal transition and postmenopausal period. 

Recently, an expert panel comprised of representatives from The North American Menopause Society and the National Network of Depression Centers Women and Mood Disorders Task Group developed clinical guidelines addressing epidemiology, clinical presentation, therapeutic effects of antidepressants, effects of HT, and efficacy of other therapies. Here we provide a summary of the expert panel's findings and guidelines. 

 

Continue to: Certain factors are associated with higher risk for depression...

 

 

Certain factors are associated with higher risk for depression 

The perimenopause represents a time of increased risk for depressive symptoms and major depressive disorder (MDD), even in women with no prior history of depression. Several characteristics and health factors are associated with the increased risk during the menopause transition. These include a prior history of MDD, current antidepressant use, anxiety, premenstrual depressive symptoms, African American race, high body mass index, younger age, social isolation, upsetting life events, and menopausal sleep disturbances.  

Although data are inconclusive on whether surgical menopause increases or decreases the risk for developing depression compared with women who transition through menopause naturally, recent studies show an elevated risk of depression in women following hysterectomy with and without oophorectomy.6,7 

Menopausal and depressive symptoms can overlap 

Midlife depression presents with classic depressive symptoms that commonly occur in combination with menopausal symptoms, including vasomotor symptoms, sleep and sexual disturbances, and weight and energy changes. These menopausal symptoms can complicate, co-occur, and overlap with the clinical presentation of depression. 

Conversely, depression may affect an individual's judgment of the degree of bother from menopausal somatic symptoms, thereby further magnifying the effect of symptoms on quality of life. The interrelationship between depressive symptoms and menopausal symptoms may pose a challenge when attempting to parse out contributing etiologies, relative contributions of each etiology, and the potential additive effects. 

Diagnosis and treatment options 

Diagnosis involves identifying the menopausal stage, assessing for co-existing psychiatric and menopause symptoms, appreciating the psychosocial factors common in midlife, and considering the differential diagnosis. Validated screening instruments can be helpful. Although a menopause-specific mood disorder scale does not yet exist, several general validated screening measures, such as the Patient Health Questionnaire-9, or PHQ-9, can be used for categorical determination of mood disorder diagnoses during the menopause transition. 

Antidepressants, cognitive-behavioral therapy, and other psychotherapies are considered first-line treatments for perimenopausal major depressive episodes. Only desvenlafaxine has been studied in large randomized placebo-controlled trials and has proven efficacious for the treatment of MDD in perimenopausal and postmenopausal women. 

A number of small open-label studies of other selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and mirtazapine to treat MDD in perimenopausal and postmenopausal women have demonstrated a positive effect on mood, and several SSRIs and SNRIs also have the added benefit of improving menopause-related symptoms. 

In women with a history of MDD, a prior adequate response to a particular antidepressant should guide treatment selection when MDD recurs during the midlife years. 

Although estrogen is not approved by the US Food and Drug Administration specifically for the treatment of mood disturbances, some evidence suggests that unopposed estrogen therapy has efficacy similar to that of antidepressant medications in treating depressive disorders in perimenopausal women,8-11 but it is ineffective in treating depressive disorders in postmenopausal women. Estrogen therapy also may augment the clinical response to antidepressants in midlife and older women.12,13 The data on combined HT (estrogen plus progestogen) or for different progestogens in treating depressive disorders in perimenopausal women are lacking and inconclusive.  

 

WHAT THIS EVIDENCE MEANS FOR PRACTICE
The findings from this expert review panel demonstrate that women in the perimenopausal transition are at increased risk for depressive symptoms, major depressive episodes, and major depressive disorder. The interrelationship between symptoms of depression and menopause can complicate, co-occur, overlap, and magnify one another. Clinicians treating perimenopausal women with depression that is unresponsive to conventional antidepressant therapy should consider concurrent use of estrogen-based hormone therapy or referring the patient to a clinician comfortable doing so.

References
  1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67:7-30. 
  2. Matteson KA, Robison K, Jacoby VL. Opportunities for early detection of endometrial cancer in women with postmenopausal bleeding. JAMA Intern Med. 2018;178:1222-1223.  
  3. van Hanegem N, Breijer MC, Khan KS, et al. Diagnostic evaluation of the endometrium in postmenopausal bleeding: an evidence-based approach. Maturitas. 2011;68:155-164.  
  4. American College of Obstetricians and Gynecologists. ACOG Committee Opinion no. 734 summary. The role of transvaginal ultrasonography in evaluating the endometrium of women with postmenopausal bleeding. Obstet Gynecol. 2018; 131:945-946. 
  5. Baumgart J, Nilsson K, Evers AS, et al. Sexual dysfunction in women on adjuvant endocrine therapy after breast cancer. Menopause. 2013;20:162-168. 
  6. Chou PH, Lin CH, Cheng C, et al. Risk of depressive disorders in women undergoing hysterectomy: a population-based follow-up study. J Psychiatr Res. 2015;68:186-191. 
  7. Wilson L, Pandeya N, Byles J, et al. Hysterectomy and incidence of depressive symptoms in midlife women: the Australian Longitudinal Study on Women's Health. Epidemiol Psychiatr Sci. 2018;27:381-392. 
  8. Schmidt PJ, Nieman L, Danaceau MA, et al. Estrogen replacement in perimenopause-related depression: a preliminary report. Am J Obstet Gynecol. 2000;183:414-420. 
  9. Rasgon NL, Altshuler LL, Fairbanks L. Estrogen-replacement therapy for depression. Am J Psychiatry. 2001;158:1738. 
  10. Soares CN, Almeida OP, Joffe H, et al. Efficacy of estradiol for the treatment of major depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry. 2001;58:529-534. 
  11. Cohen LS, Soares CN, Poitras JR, et al. Short-term use of estradiol for depression in perimenopausal and postmenopausal women: a preliminary report. Am J Psychiatry. 2003;160:1519-1522. 
  12. Schneider LS, Small GW, Hamilton SH, et al. Estrogen replacement and response to fluoxetine in a multicenter geriatric depression trial. Fluoxetine Collaborative Study Group. Am J Geriatr Psychiatry. 1997;5:97-106. 
  13. Schneider LS, Small GW, Clary CM. Estrogen replacement therapy and antidepressant response to sertraline in older depressed women. Am J Geriatr Psychiatry. 2001;9:393-399. 
     
References
  1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017. CA Cancer J Clin. 2017;67:7-30. 
  2. Matteson KA, Robison K, Jacoby VL. Opportunities for early detection of endometrial cancer in women with postmenopausal bleeding. JAMA Intern Med. 2018;178:1222-1223.  
  3. van Hanegem N, Breijer MC, Khan KS, et al. Diagnostic evaluation of the endometrium in postmenopausal bleeding: an evidence-based approach. Maturitas. 2011;68:155-164.  
  4. American College of Obstetricians and Gynecologists. ACOG Committee Opinion no. 734 summary. The role of transvaginal ultrasonography in evaluating the endometrium of women with postmenopausal bleeding. Obstet Gynecol. 2018; 131:945-946. 
  5. Baumgart J, Nilsson K, Evers AS, et al. Sexual dysfunction in women on adjuvant endocrine therapy after breast cancer. Menopause. 2013;20:162-168. 
  6. Chou PH, Lin CH, Cheng C, et al. Risk of depressive disorders in women undergoing hysterectomy: a population-based follow-up study. J Psychiatr Res. 2015;68:186-191. 
  7. Wilson L, Pandeya N, Byles J, et al. Hysterectomy and incidence of depressive symptoms in midlife women: the Australian Longitudinal Study on Women's Health. Epidemiol Psychiatr Sci. 2018;27:381-392. 
  8. Schmidt PJ, Nieman L, Danaceau MA, et al. Estrogen replacement in perimenopause-related depression: a preliminary report. Am J Obstet Gynecol. 2000;183:414-420. 
  9. Rasgon NL, Altshuler LL, Fairbanks L. Estrogen-replacement therapy for depression. Am J Psychiatry. 2001;158:1738. 
  10. Soares CN, Almeida OP, Joffe H, et al. Efficacy of estradiol for the treatment of major depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry. 2001;58:529-534. 
  11. Cohen LS, Soares CN, Poitras JR, et al. Short-term use of estradiol for depression in perimenopausal and postmenopausal women: a preliminary report. Am J Psychiatry. 2003;160:1519-1522. 
  12. Schneider LS, Small GW, Hamilton SH, et al. Estrogen replacement and response to fluoxetine in a multicenter geriatric depression trial. Fluoxetine Collaborative Study Group. Am J Geriatr Psychiatry. 1997;5:97-106. 
  13. Schneider LS, Small GW, Clary CM. Estrogen replacement therapy and antidepressant response to sertraline in older depressed women. Am J Geriatr Psychiatry. 2001;9:393-399. 
     
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What’s in store for ObGyn reimbursement in the EHR age and beyond

Article Type
Changed
Thu, 06/06/2019 - 15:39

In an effort to reduce burden on physicians and qualified health care professionals, the Centers for Medicare and Medicaid Services ( CMS) has made changes to Evaluation and Management (E/M) documentation requirements and payment policies. Get ready for fairly extensive changes planned for CY 2021. Here we outline already-implemented and future changes and describe the commitment of the American College of Obstetricians and Gynecologists (ACOG) to ObGyn payment in its collaborations with CMS and the American Medical Association (AMA).

E/M services: CMS reduced documentation

Effective January 2019, the CMS made changes to the documentation requirements for E/M services to provide some common-sense relief for physicians facing excessive documentation requirements in their practices. Most physicians agree that modern medical practice, with the use of electronic health records (EHRs), is different now than in the mid-1990s, when the current E/M structures were developed and implemented. Streamlining documentation requirements reduces paperwork burden and some of the time-consuming duplicative work involved in medical practice today.

For instance, when relevant information is already contained in the medical record, it is not necessary to re-document a full medical history. Physicians will now be able to focus their documentation on the interval since the previous visit. Physicians should still review prior data, update as necessary, and indicate in the medical record that they have done so.

Also, for E/M office and outpatient visits for both new and established patients, physicians are no longer required to re-document information that has already been entered in the patient’s record by practice staff or by the patient. If the patient’s chief complaint and history already has been entered by ancillary staff or the beneficiary, the physician should simply indicate in the medical record that the information has been reviewed and verified.

For E/M visits furnished by teaching physicians, CMS has removed the requirement for
potentially duplicative notations that may have been made previously in the medical records by residents or other members of the medical team.

Finally, CMS eliminated the requirement to document the medical necessity of a home visit in lieu of an office visit.

Continue to: Outpatient coding changes for 2021...

 

 

Outpatient coding changes for 2021

Outpatient coding for E/M will continue in its current form for the remainder of 2019 and 2020. However, in 2021, expect substantial changes to take effect. If the CMS rule is instituted, payment for E/M office and outpatient visits will be drastically “simplified.” The current CMS plan for 2021 is to collapse payment for existing E/M Levels 2 through 4 to one payment level for new patients and one payment level for established patients, with optional add-on codes. Level 5 visits will continue at a separate payment level and with continuation of current documentation requirements.

In addition to collapsing the payment in E/M Levels 2, 3, and 4, CMS also will allow flexibility in how those E/M office and outpatient visits are documented. Specifically, documentation may be based on any of the following:

  • current framework (1995 or 1997 guidelines)
  • medical decision making (MDM)
  • time.

When using MDM or the current 1995/1997 framework to document an office visit, Medicare will only require documentation to support a Level 2 E/M outpatient visit code for history, exam, and/or MDM. When time is used as the basis for coding the visit, physicians will document the medical necessity of the visit and that the billing practitioner personally spent the required amount of time face-to-face with the beneficiary.

CMS also has finalized the creation of new add-on codes that describe the additional resources inherent in visits for primary care and particular kinds of nonprocedural specialized medical care (and will not be restricted by physician specialty). These codes would only be reportable with E/M office and outpatient level 2 through 4 visits, and their use generally would not impose new documentation requirements. It is not clear which types of visits would support the use of these add-on codes at this time.

Finally, a new “extended visit” add-on code will be available for use only with E/M Level 2 through 4 visits to account for the additional resources required when spending extended time with a patient.

CMS believes these policies will allow physicians, and all who bill E/M codes, greater flexibility to exercise clinical judgment in their documentation, so that they can focus on what is clinically relevant and medically necessary for the beneficiary.

ACOG’s voice in the process

ACOG strongly opposed several proposals that CMS made during the rule-making process that the agency decided not to finalize. These aspects of the proposal would have:

1. reduced payment by 50% for the least expensive procedure or visit when an E/M office or outpatient visit is furnished on the same day as a procedure by the same physician. These are separately identifiable E/M visits that normally would be reported with a modifier 25.
2. established separate coding and payment for podiatric E/M visits, or
3. standardized the allocation of practice expense relative value units (RVUs) for the codes that describe these services.

CMS has stated that they intend to engage in further discussions with the public and stakeholders to potentially further refine the policies for CY 2021.

Continue to: AMA-CPT and RUC initiative...

 

 

AMA-CPT and RUC initiative

Although the AMA, ACOG, and physicians in general applauded the CMS initiative to reduce the administrative and documentation burden on providers, there was concern about the unintended consequences of the payment changes that are currently scheduled to take effect in 2021. To address these concerns, the AMA convened a work group of physician experts who are knowledgeable in the Current Procedural Terminology (CPT) code development and valuation processes. The charge to the E/M work group is to collaborate across the provider, payer, and coding communities to establish or revise the coding structure and guidelines for outpatient E/M services. The members formed a multispecialty work group representing primary care and surgical specialties and have experience in developing, defining, and valuing codes.

Dr. Barbara Levy, ACOG’s Vice President of Health Policy, co-chaired this expert panel with geriatrician Dr. Peter Hollmann to develop comprehensive consensus-led changes to revise and modernize E/M codes. The work group followed 4 guiding principles to inform their E/M work:

  1. to decrease the administrative burden of documentation and coding
  2. to decrease the need for audits
  3. to decrease unnecessary and redundant documentation in the medical record that is not needed for patient care
  4. to ensure that payment for E/M services is resource based. There is no direct goal for payment redistribution among specialties.

A primary concern expressed by physicians about the CMS proposal was that the collapse of payment for E/M visit across levels 2–4 might lead to a lack of appropriate care for more complex patients since the CMS rule does not provide payment based on the resources required to perform the work of the visit. No one believes that the work needed to care for someone with a sore throat or pink eye is equivalent to the work involved in diagnosing and managing depression, for example.

Beginning in August 2018, the work group met regularly to build consensus. The work group worked at an accelerated pace to develop and value codes that better fit the current medical workflows and meet patient needs.

The work group submitted a code change proposal for E/M codes to the CPT Editorial Panel for consideration during the February 2019 meeting. The next step was the code valuation process through the AMA/Specialty Society RVS Update Committee (RUC) process.

CMS has stated that the 2-year delay to 2021 in implementation of their original proposed changes is to allow time for the E/M code change proposals to move through the development and valuation process and subsequent review by the agency. To date, commercial payers and coders have been supportive of the AMA E/M work group proposals. Dr. Levy, Dr. Hollmann, and AMA staff are meeting with CMS and Department of Health and Human Services staff to provide clarity as they review the CPT proposals. ACOG supports the changes, which would simplify documentation for outpatient E/M codes while retaining differential payments. CMS is closely following the progress of the code changes through the CPT process and RUC code valuation process. We await further rulemaking by CMS in defining and valuing this important code set.

Summary of CPT Editorial Panel actions for office or other outpatient services, February 2019 (Effective Date January 1, 2021)
  • CPT code 99201 to be deleted
  • Revision of codes 99202-99215 as follows:
  • removing history and examination as key components

(A) for selecting the level of service but requiring a medically appropriate history and or examination be performed in order to report codes 99202-99215

(B) making the basis for code selection on either the level of medical decision making (MDM) performed or the total time spent performing the service on the day of the encounter

(C) changing the definition of the time element associated with codes 99202-99215 from typical face-to-face time to total time spent on the day of the encounter and changing the amount of time associated with each code.

  • Revision of the MDM elements associated with codes 99202-99215 as follows:

(i) revising "Number of Diagnoses or Management Options" to "Number and Complexity of Problems Addressed";

(ii) revising "Amount and/or Complexity of Data to be Reviewed" to "Amount and/or Complexity of Data to be Reviewed and Analyzed"; and

(iii) revising "Risk of Complications and/or Morbidity or Mortality" to "Risk of Complications and/or Morbidity or Mortality of Patient Management."

  • Revision of the E/M guidelines by:

(A) restructuring the guidelines into three sections: "Guidelines Common to All E/M Services," "Guidelines for Hospital Observation, Hospital Inpatient, Consultations, Emergency Department, Nursing Facility, Domiciliary, Rest Home or Custodial Care and Home E/M Services," and "Guidelines for Office or Other Outpatient E/M Services" to distinguish the new reporting guidelines for the Office or Other Outpatient Services codes 99202-99215

(B) adding new guidelines that are applicable only to Office or Other Outpatient codes (99202-99215); adding a Summary of Guideline Differences table of the differences between the sets of guidelines

(C) revised existing E/M guidelines to ensure there is no conflicting information between the different sets of guidelines

(D) adding definitions of terms associated with the elements of MDM applicable to codes 99202-99215

(E) adding an MDM table that is applicable to codes 99202-99215

(F) defining total time associated with codes 99202-99215

(G) adding guidelines for reporting time when more than one individual performs distinct parts of an E/M service; revision of the MDM table in the Amount and/or Complexity of Data to be Reviewed and Analyzed column:

(1) inserted a dash (-) after the asterisk in the asterisk definition, "* - Each unique test, order, or document may be summed if multiple," to clarify this is the meaning of the asterisk and not an asterisked item itself

(2) for limited amount of data to be reviewed and analyzed (codes 99203/99213), the parenthetical regarding the number of categories for which requirements must be met was revised to state, "¬categories of tests and documents, or independent historian(s)" rather than "categories within tests, documents, or independent historian(s)"

(3) removing the word "or" after each of the bulleted items for limited, moderate (codes 99202/99214), and high (99205/99215) amount and/or complexity of data to be reviewed and analyzed.

Continue to: ACOG is at the helm, with a watchful eye...

 

 

ACOG is at the helm, with a watchful eye

This is a challenging undertaking because E/M codes are used across specialties for office visits and outpatient care. The potential for unintended consequences for all services that include E/M, such as the global obstetrical services or 90-day global surgical services, is substantial. ACOG is intimately involved in this undertaking, watching the developments carefully to ensure that the interests of ObGyns and their patients are protected.

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Ms. Tyler is Director of Coding, American College of Obstetricians and Gynecologists (ACOG), Washington, DC.

Dr. Levy is Vice President for Health Policy at ACOG.

The authors report no financial relationships relevant to this article.

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Ms. Tyler is Director of Coding, American College of Obstetricians and Gynecologists (ACOG), Washington, DC.

Dr. Levy is Vice President for Health Policy at ACOG.

The authors report no financial relationships relevant to this article.

Author and Disclosure Information

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Dr. Levy is Vice President for Health Policy at ACOG.

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In an effort to reduce burden on physicians and qualified health care professionals, the Centers for Medicare and Medicaid Services ( CMS) has made changes to Evaluation and Management (E/M) documentation requirements and payment policies. Get ready for fairly extensive changes planned for CY 2021. Here we outline already-implemented and future changes and describe the commitment of the American College of Obstetricians and Gynecologists (ACOG) to ObGyn payment in its collaborations with CMS and the American Medical Association (AMA).

E/M services: CMS reduced documentation

Effective January 2019, the CMS made changes to the documentation requirements for E/M services to provide some common-sense relief for physicians facing excessive documentation requirements in their practices. Most physicians agree that modern medical practice, with the use of electronic health records (EHRs), is different now than in the mid-1990s, when the current E/M structures were developed and implemented. Streamlining documentation requirements reduces paperwork burden and some of the time-consuming duplicative work involved in medical practice today.

For instance, when relevant information is already contained in the medical record, it is not necessary to re-document a full medical history. Physicians will now be able to focus their documentation on the interval since the previous visit. Physicians should still review prior data, update as necessary, and indicate in the medical record that they have done so.

Also, for E/M office and outpatient visits for both new and established patients, physicians are no longer required to re-document information that has already been entered in the patient’s record by practice staff or by the patient. If the patient’s chief complaint and history already has been entered by ancillary staff or the beneficiary, the physician should simply indicate in the medical record that the information has been reviewed and verified.

For E/M visits furnished by teaching physicians, CMS has removed the requirement for
potentially duplicative notations that may have been made previously in the medical records by residents or other members of the medical team.

Finally, CMS eliminated the requirement to document the medical necessity of a home visit in lieu of an office visit.

Continue to: Outpatient coding changes for 2021...

 

 

Outpatient coding changes for 2021

Outpatient coding for E/M will continue in its current form for the remainder of 2019 and 2020. However, in 2021, expect substantial changes to take effect. If the CMS rule is instituted, payment for E/M office and outpatient visits will be drastically “simplified.” The current CMS plan for 2021 is to collapse payment for existing E/M Levels 2 through 4 to one payment level for new patients and one payment level for established patients, with optional add-on codes. Level 5 visits will continue at a separate payment level and with continuation of current documentation requirements.

In addition to collapsing the payment in E/M Levels 2, 3, and 4, CMS also will allow flexibility in how those E/M office and outpatient visits are documented. Specifically, documentation may be based on any of the following:

  • current framework (1995 or 1997 guidelines)
  • medical decision making (MDM)
  • time.

When using MDM or the current 1995/1997 framework to document an office visit, Medicare will only require documentation to support a Level 2 E/M outpatient visit code for history, exam, and/or MDM. When time is used as the basis for coding the visit, physicians will document the medical necessity of the visit and that the billing practitioner personally spent the required amount of time face-to-face with the beneficiary.

CMS also has finalized the creation of new add-on codes that describe the additional resources inherent in visits for primary care and particular kinds of nonprocedural specialized medical care (and will not be restricted by physician specialty). These codes would only be reportable with E/M office and outpatient level 2 through 4 visits, and their use generally would not impose new documentation requirements. It is not clear which types of visits would support the use of these add-on codes at this time.

Finally, a new “extended visit” add-on code will be available for use only with E/M Level 2 through 4 visits to account for the additional resources required when spending extended time with a patient.

CMS believes these policies will allow physicians, and all who bill E/M codes, greater flexibility to exercise clinical judgment in their documentation, so that they can focus on what is clinically relevant and medically necessary for the beneficiary.

ACOG’s voice in the process

ACOG strongly opposed several proposals that CMS made during the rule-making process that the agency decided not to finalize. These aspects of the proposal would have:

1. reduced payment by 50% for the least expensive procedure or visit when an E/M office or outpatient visit is furnished on the same day as a procedure by the same physician. These are separately identifiable E/M visits that normally would be reported with a modifier 25.
2. established separate coding and payment for podiatric E/M visits, or
3. standardized the allocation of practice expense relative value units (RVUs) for the codes that describe these services.

CMS has stated that they intend to engage in further discussions with the public and stakeholders to potentially further refine the policies for CY 2021.

Continue to: AMA-CPT and RUC initiative...

 

 

AMA-CPT and RUC initiative

Although the AMA, ACOG, and physicians in general applauded the CMS initiative to reduce the administrative and documentation burden on providers, there was concern about the unintended consequences of the payment changes that are currently scheduled to take effect in 2021. To address these concerns, the AMA convened a work group of physician experts who are knowledgeable in the Current Procedural Terminology (CPT) code development and valuation processes. The charge to the E/M work group is to collaborate across the provider, payer, and coding communities to establish or revise the coding structure and guidelines for outpatient E/M services. The members formed a multispecialty work group representing primary care and surgical specialties and have experience in developing, defining, and valuing codes.

Dr. Barbara Levy, ACOG’s Vice President of Health Policy, co-chaired this expert panel with geriatrician Dr. Peter Hollmann to develop comprehensive consensus-led changes to revise and modernize E/M codes. The work group followed 4 guiding principles to inform their E/M work:

  1. to decrease the administrative burden of documentation and coding
  2. to decrease the need for audits
  3. to decrease unnecessary and redundant documentation in the medical record that is not needed for patient care
  4. to ensure that payment for E/M services is resource based. There is no direct goal for payment redistribution among specialties.

A primary concern expressed by physicians about the CMS proposal was that the collapse of payment for E/M visit across levels 2–4 might lead to a lack of appropriate care for more complex patients since the CMS rule does not provide payment based on the resources required to perform the work of the visit. No one believes that the work needed to care for someone with a sore throat or pink eye is equivalent to the work involved in diagnosing and managing depression, for example.

Beginning in August 2018, the work group met regularly to build consensus. The work group worked at an accelerated pace to develop and value codes that better fit the current medical workflows and meet patient needs.

The work group submitted a code change proposal for E/M codes to the CPT Editorial Panel for consideration during the February 2019 meeting. The next step was the code valuation process through the AMA/Specialty Society RVS Update Committee (RUC) process.

CMS has stated that the 2-year delay to 2021 in implementation of their original proposed changes is to allow time for the E/M code change proposals to move through the development and valuation process and subsequent review by the agency. To date, commercial payers and coders have been supportive of the AMA E/M work group proposals. Dr. Levy, Dr. Hollmann, and AMA staff are meeting with CMS and Department of Health and Human Services staff to provide clarity as they review the CPT proposals. ACOG supports the changes, which would simplify documentation for outpatient E/M codes while retaining differential payments. CMS is closely following the progress of the code changes through the CPT process and RUC code valuation process. We await further rulemaking by CMS in defining and valuing this important code set.

Summary of CPT Editorial Panel actions for office or other outpatient services, February 2019 (Effective Date January 1, 2021)
  • CPT code 99201 to be deleted
  • Revision of codes 99202-99215 as follows:
  • removing history and examination as key components

(A) for selecting the level of service but requiring a medically appropriate history and or examination be performed in order to report codes 99202-99215

(B) making the basis for code selection on either the level of medical decision making (MDM) performed or the total time spent performing the service on the day of the encounter

(C) changing the definition of the time element associated with codes 99202-99215 from typical face-to-face time to total time spent on the day of the encounter and changing the amount of time associated with each code.

  • Revision of the MDM elements associated with codes 99202-99215 as follows:

(i) revising "Number of Diagnoses or Management Options" to "Number and Complexity of Problems Addressed";

(ii) revising "Amount and/or Complexity of Data to be Reviewed" to "Amount and/or Complexity of Data to be Reviewed and Analyzed"; and

(iii) revising "Risk of Complications and/or Morbidity or Mortality" to "Risk of Complications and/or Morbidity or Mortality of Patient Management."

  • Revision of the E/M guidelines by:

(A) restructuring the guidelines into three sections: "Guidelines Common to All E/M Services," "Guidelines for Hospital Observation, Hospital Inpatient, Consultations, Emergency Department, Nursing Facility, Domiciliary, Rest Home or Custodial Care and Home E/M Services," and "Guidelines for Office or Other Outpatient E/M Services" to distinguish the new reporting guidelines for the Office or Other Outpatient Services codes 99202-99215

(B) adding new guidelines that are applicable only to Office or Other Outpatient codes (99202-99215); adding a Summary of Guideline Differences table of the differences between the sets of guidelines

(C) revised existing E/M guidelines to ensure there is no conflicting information between the different sets of guidelines

(D) adding definitions of terms associated with the elements of MDM applicable to codes 99202-99215

(E) adding an MDM table that is applicable to codes 99202-99215

(F) defining total time associated with codes 99202-99215

(G) adding guidelines for reporting time when more than one individual performs distinct parts of an E/M service; revision of the MDM table in the Amount and/or Complexity of Data to be Reviewed and Analyzed column:

(1) inserted a dash (-) after the asterisk in the asterisk definition, "* - Each unique test, order, or document may be summed if multiple," to clarify this is the meaning of the asterisk and not an asterisked item itself

(2) for limited amount of data to be reviewed and analyzed (codes 99203/99213), the parenthetical regarding the number of categories for which requirements must be met was revised to state, "¬categories of tests and documents, or independent historian(s)" rather than "categories within tests, documents, or independent historian(s)"

(3) removing the word "or" after each of the bulleted items for limited, moderate (codes 99202/99214), and high (99205/99215) amount and/or complexity of data to be reviewed and analyzed.

Continue to: ACOG is at the helm, with a watchful eye...

 

 

ACOG is at the helm, with a watchful eye

This is a challenging undertaking because E/M codes are used across specialties for office visits and outpatient care. The potential for unintended consequences for all services that include E/M, such as the global obstetrical services or 90-day global surgical services, is substantial. ACOG is intimately involved in this undertaking, watching the developments carefully to ensure that the interests of ObGyns and their patients are protected.

In an effort to reduce burden on physicians and qualified health care professionals, the Centers for Medicare and Medicaid Services ( CMS) has made changes to Evaluation and Management (E/M) documentation requirements and payment policies. Get ready for fairly extensive changes planned for CY 2021. Here we outline already-implemented and future changes and describe the commitment of the American College of Obstetricians and Gynecologists (ACOG) to ObGyn payment in its collaborations with CMS and the American Medical Association (AMA).

E/M services: CMS reduced documentation

Effective January 2019, the CMS made changes to the documentation requirements for E/M services to provide some common-sense relief for physicians facing excessive documentation requirements in their practices. Most physicians agree that modern medical practice, with the use of electronic health records (EHRs), is different now than in the mid-1990s, when the current E/M structures were developed and implemented. Streamlining documentation requirements reduces paperwork burden and some of the time-consuming duplicative work involved in medical practice today.

For instance, when relevant information is already contained in the medical record, it is not necessary to re-document a full medical history. Physicians will now be able to focus their documentation on the interval since the previous visit. Physicians should still review prior data, update as necessary, and indicate in the medical record that they have done so.

Also, for E/M office and outpatient visits for both new and established patients, physicians are no longer required to re-document information that has already been entered in the patient’s record by practice staff or by the patient. If the patient’s chief complaint and history already has been entered by ancillary staff or the beneficiary, the physician should simply indicate in the medical record that the information has been reviewed and verified.

For E/M visits furnished by teaching physicians, CMS has removed the requirement for
potentially duplicative notations that may have been made previously in the medical records by residents or other members of the medical team.

Finally, CMS eliminated the requirement to document the medical necessity of a home visit in lieu of an office visit.

Continue to: Outpatient coding changes for 2021...

 

 

Outpatient coding changes for 2021

Outpatient coding for E/M will continue in its current form for the remainder of 2019 and 2020. However, in 2021, expect substantial changes to take effect. If the CMS rule is instituted, payment for E/M office and outpatient visits will be drastically “simplified.” The current CMS plan for 2021 is to collapse payment for existing E/M Levels 2 through 4 to one payment level for new patients and one payment level for established patients, with optional add-on codes. Level 5 visits will continue at a separate payment level and with continuation of current documentation requirements.

In addition to collapsing the payment in E/M Levels 2, 3, and 4, CMS also will allow flexibility in how those E/M office and outpatient visits are documented. Specifically, documentation may be based on any of the following:

  • current framework (1995 or 1997 guidelines)
  • medical decision making (MDM)
  • time.

When using MDM or the current 1995/1997 framework to document an office visit, Medicare will only require documentation to support a Level 2 E/M outpatient visit code for history, exam, and/or MDM. When time is used as the basis for coding the visit, physicians will document the medical necessity of the visit and that the billing practitioner personally spent the required amount of time face-to-face with the beneficiary.

CMS also has finalized the creation of new add-on codes that describe the additional resources inherent in visits for primary care and particular kinds of nonprocedural specialized medical care (and will not be restricted by physician specialty). These codes would only be reportable with E/M office and outpatient level 2 through 4 visits, and their use generally would not impose new documentation requirements. It is not clear which types of visits would support the use of these add-on codes at this time.

Finally, a new “extended visit” add-on code will be available for use only with E/M Level 2 through 4 visits to account for the additional resources required when spending extended time with a patient.

CMS believes these policies will allow physicians, and all who bill E/M codes, greater flexibility to exercise clinical judgment in their documentation, so that they can focus on what is clinically relevant and medically necessary for the beneficiary.

ACOG’s voice in the process

ACOG strongly opposed several proposals that CMS made during the rule-making process that the agency decided not to finalize. These aspects of the proposal would have:

1. reduced payment by 50% for the least expensive procedure or visit when an E/M office or outpatient visit is furnished on the same day as a procedure by the same physician. These are separately identifiable E/M visits that normally would be reported with a modifier 25.
2. established separate coding and payment for podiatric E/M visits, or
3. standardized the allocation of practice expense relative value units (RVUs) for the codes that describe these services.

CMS has stated that they intend to engage in further discussions with the public and stakeholders to potentially further refine the policies for CY 2021.

Continue to: AMA-CPT and RUC initiative...

 

 

AMA-CPT and RUC initiative

Although the AMA, ACOG, and physicians in general applauded the CMS initiative to reduce the administrative and documentation burden on providers, there was concern about the unintended consequences of the payment changes that are currently scheduled to take effect in 2021. To address these concerns, the AMA convened a work group of physician experts who are knowledgeable in the Current Procedural Terminology (CPT) code development and valuation processes. The charge to the E/M work group is to collaborate across the provider, payer, and coding communities to establish or revise the coding structure and guidelines for outpatient E/M services. The members formed a multispecialty work group representing primary care and surgical specialties and have experience in developing, defining, and valuing codes.

Dr. Barbara Levy, ACOG’s Vice President of Health Policy, co-chaired this expert panel with geriatrician Dr. Peter Hollmann to develop comprehensive consensus-led changes to revise and modernize E/M codes. The work group followed 4 guiding principles to inform their E/M work:

  1. to decrease the administrative burden of documentation and coding
  2. to decrease the need for audits
  3. to decrease unnecessary and redundant documentation in the medical record that is not needed for patient care
  4. to ensure that payment for E/M services is resource based. There is no direct goal for payment redistribution among specialties.

A primary concern expressed by physicians about the CMS proposal was that the collapse of payment for E/M visit across levels 2–4 might lead to a lack of appropriate care for more complex patients since the CMS rule does not provide payment based on the resources required to perform the work of the visit. No one believes that the work needed to care for someone with a sore throat or pink eye is equivalent to the work involved in diagnosing and managing depression, for example.

Beginning in August 2018, the work group met regularly to build consensus. The work group worked at an accelerated pace to develop and value codes that better fit the current medical workflows and meet patient needs.

The work group submitted a code change proposal for E/M codes to the CPT Editorial Panel for consideration during the February 2019 meeting. The next step was the code valuation process through the AMA/Specialty Society RVS Update Committee (RUC) process.

CMS has stated that the 2-year delay to 2021 in implementation of their original proposed changes is to allow time for the E/M code change proposals to move through the development and valuation process and subsequent review by the agency. To date, commercial payers and coders have been supportive of the AMA E/M work group proposals. Dr. Levy, Dr. Hollmann, and AMA staff are meeting with CMS and Department of Health and Human Services staff to provide clarity as they review the CPT proposals. ACOG supports the changes, which would simplify documentation for outpatient E/M codes while retaining differential payments. CMS is closely following the progress of the code changes through the CPT process and RUC code valuation process. We await further rulemaking by CMS in defining and valuing this important code set.

Summary of CPT Editorial Panel actions for office or other outpatient services, February 2019 (Effective Date January 1, 2021)
  • CPT code 99201 to be deleted
  • Revision of codes 99202-99215 as follows:
  • removing history and examination as key components

(A) for selecting the level of service but requiring a medically appropriate history and or examination be performed in order to report codes 99202-99215

(B) making the basis for code selection on either the level of medical decision making (MDM) performed or the total time spent performing the service on the day of the encounter

(C) changing the definition of the time element associated with codes 99202-99215 from typical face-to-face time to total time spent on the day of the encounter and changing the amount of time associated with each code.

  • Revision of the MDM elements associated with codes 99202-99215 as follows:

(i) revising "Number of Diagnoses or Management Options" to "Number and Complexity of Problems Addressed";

(ii) revising "Amount and/or Complexity of Data to be Reviewed" to "Amount and/or Complexity of Data to be Reviewed and Analyzed"; and

(iii) revising "Risk of Complications and/or Morbidity or Mortality" to "Risk of Complications and/or Morbidity or Mortality of Patient Management."

  • Revision of the E/M guidelines by:

(A) restructuring the guidelines into three sections: "Guidelines Common to All E/M Services," "Guidelines for Hospital Observation, Hospital Inpatient, Consultations, Emergency Department, Nursing Facility, Domiciliary, Rest Home or Custodial Care and Home E/M Services," and "Guidelines for Office or Other Outpatient E/M Services" to distinguish the new reporting guidelines for the Office or Other Outpatient Services codes 99202-99215

(B) adding new guidelines that are applicable only to Office or Other Outpatient codes (99202-99215); adding a Summary of Guideline Differences table of the differences between the sets of guidelines

(C) revised existing E/M guidelines to ensure there is no conflicting information between the different sets of guidelines

(D) adding definitions of terms associated with the elements of MDM applicable to codes 99202-99215

(E) adding an MDM table that is applicable to codes 99202-99215

(F) defining total time associated with codes 99202-99215

(G) adding guidelines for reporting time when more than one individual performs distinct parts of an E/M service; revision of the MDM table in the Amount and/or Complexity of Data to be Reviewed and Analyzed column:

(1) inserted a dash (-) after the asterisk in the asterisk definition, "* - Each unique test, order, or document may be summed if multiple," to clarify this is the meaning of the asterisk and not an asterisked item itself

(2) for limited amount of data to be reviewed and analyzed (codes 99203/99213), the parenthetical regarding the number of categories for which requirements must be met was revised to state, "¬categories of tests and documents, or independent historian(s)" rather than "categories within tests, documents, or independent historian(s)"

(3) removing the word "or" after each of the bulleted items for limited, moderate (codes 99202/99214), and high (99205/99215) amount and/or complexity of data to be reviewed and analyzed.

Continue to: ACOG is at the helm, with a watchful eye...

 

 

ACOG is at the helm, with a watchful eye

This is a challenging undertaking because E/M codes are used across specialties for office visits and outpatient care. The potential for unintended consequences for all services that include E/M, such as the global obstetrical services or 90-day global surgical services, is substantial. ACOG is intimately involved in this undertaking, watching the developments carefully to ensure that the interests of ObGyns and their patients are protected.

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Excessive postpartum bleeding is a major cause of maternal morbidity and mortality. Worldwide, obstetric hemorrhage is the most common cause of maternal death.1,2 Medications reported to reduce postpartum bleeding include oxytocin, misoprostol, ergonovine, methylergonovine, carboprost, and tranexamic acid. A recent Cochrane network meta-analysis of 196 trials, including 135,559 women, distilled in 1,361 pages of analysis, reported on the medications associated with the greatest reduction in postpartum bleeding.3 Surprisingly, for preventing blood loss ≥ 500 mL, misoprostol plus oxytocin and ergonovine plus oxytocin were the highest ranked interventions. This evidence is summarized here.

Misoprostol plus oxytocin

After newborn delivery, active management of the third stage of labor, including uterotonic administration, is strongly recommended because it will reduce postpartum blood loss, decreasing the rate of postpartum hemorrhage (PPH).4 Both oxytocin and misoprostol are effective uterotonics. However, the combination of oxytocin plus misoprostol appears to be more effective than oxytocin alone in reducing the frequency of postpartum blood loss greater than 500 mL.3 To understand the clinical efficacy and adverse effects (AEs) of combined oxytocin plus misoprostol a meta-analysis was performed for both vaginal and cesarean deliveries (CDs).

Efficacy and AEs during vaginal delivery. In the meta-analysis, about 6,000 vaginal deliveries were analyzed, with no significant differences for misoprostol plus oxytocin versus oxytocin alone found for the following outcomes: maternal death, intensive care unit admissions, and rate of blood loss ≥ 1,000 mL (1.7% for both uterotonics vs 2.2% for oxytocin alone).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (0.95% vs 2.5%), reduced risk of blood loss ≥ 500 mL (5.9% vs 8.0%), reduced risk of requiring an additional uterotonic (3.6% vs 5.8%), and a smaller decrease in hemoglobin concentration from pre- to postdelivery (-0.89 g/L).3

In my opinion, the difference in hemoglobin concentration, although statistically significant, is not of clinical significance. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (2.4% vs 0.66%), vomiting (3.1% vs 0.86%), and fever (21% vs 3.9%).3 A weakness of this meta-analysis is that the trials used a wide range of misoprostol dosages (200 to 600 µg) and multiple routes of administration, including sublingual (under the tongue), buccal, and rectal. This makes it impossible to identify a best misoprostol dosage and administration route.

Efficacy and AEs during CD. In the same meta-analysis about 2,000 CDs were analyzed, with no significant difference for misoprostol plus oxytocin versus oxytocin alone for the following outcomes: maternal death, intensive care unit admissions, and PPH ≥ 1,000 mL blood loss (6.2% vs 6.5%).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (2.6% vs 5.4%), reduced risk of blood loss ≥ 500 mL (32% vs 47%), reduced risk of requiring an additional uterotonic (14% vs 28%), and a smaller decrease in hemoglobin concentration from before to after delivery (-4.0 g/L).3 In my opinion, the statistically significant difference in hemoglobin concentration is not clinically significant. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (12% vs 6.1%), vomiting (8.1% vs 5.4%), shivering (13% vs 7%), and fever (7.7% vs 4.0%).3

Continue to: Ergonovine plus oxytocin...

 

 

Ergonovine plus oxytocin

Ergonovine is an ergot derivative that causes uterine contractions and has been shown to effectively reduce blood loss at delivery. In the United States a methyl-derivative of ergonovine, methylergonovine, is widely available. In a meta-analysis with mostly vaginal deliveries, there were no significant differences for ergonovine plus oxytocin versus oxytocin alone for the following outcomes: death, intensive care unit admission, rate of blood loss ≥ 1,000 mL(2.0% vs 2.7%), blood transfusion, administration of an additional uterotonic, change in hemoglobin from pre- to postdelivery, nausea, hypertension, shivering, and fever.3 However, ergonovine plus oxytocin, compared with oxytocin alone, resulted in a significantly reduced rate of blood loss ≥ 500 mL (8.3% vs 10.2%) and an increased rate of vomiting (8.1% vs 1.6%).3 In these trials women with a blood pressure ≥ 150/100 mm Hg were generally excluded from receiving ergonovine because of its hypertensive effect.

Clinical practice options

Given the Cochrane meta-analysis results, ObGyns have two approaches for optimizing PPH reduction.

Option 1: Use a single uterotonic to reduce postpartum blood loss. If excess bleeding occurs, rapidly administer a second uterotonic agent. Currently, monotherapy with intravenous or intramuscular oxytocin is the standard for reducing postpartum blood loss.5,6 Advantages of this approach compared with dual agent therapy include simplification of care and minimization of AEs. However, oxytocin monotherapy for minimizing postpartum bleeding may be suboptimal. In the largest trial ever performed (involving 29,645 women) when oxytocin was administered postpartum, the rates of estimated blood loss ≥ 500 mL and ≥ 1,000 mL were 9.1% and 1.45%, respectively.5 Is 9% an optimal rate for blood loss ≥ 500 mL following a vaginal delivery? Or should we try to achieve a lower rate?

Given the “high” rate of blood loss ≥ 500 mL with oxytocin alone, it is important for clinicians using the one-uterotonic approach to promptly recognize patients who have excessive bleeding and transition rapidly from prevention to treatment. When PPH cases are reviewed, a common finding is that the clinicians did not timely recognize excess bleeding, delaying transition to treatment with additional uterotonics and other interventions. When routinely using oxytocin monotherapy, lowering the threshold for administering a second uterotonic (methylergonovine, carboprost, misoprostol, or tranexamic acid) may help decrease the frequency of excess postpartum blood loss.

Option 2: Administer two uterotonics to reduce postpartum blood loss at all deliveries. Given the “high” rate of excess postpartum blood loss with oxytocin monotherapy, an alternative is to administer two uterotonics at all births or at births with a high risk of excess blood loss. As discussed, administering two uterotonics, oxytocin plus misoprostol or oxytocin plus ergonovine, has been reported to be more effective than oxytocin alone for reducing postpartum bleeding ≥ 500 mL.3 In the Cochrane meta-analysis, per 1,000 women given oxytocin following a vaginal birth, 122 would have blood loss ≥ 500 mL, compared with 85 given oxytocin plus misoprostol or oxytocin plus ergonovine.3

Misoprostol is administered sublingually, buccally, or rectally, and methylergonovine is administered by intramuscular injection. Although dual uterotonic therapy is more effective than monotherapy, dual therapy is associated with more AEs. As noted, compared with oxytocin monotherapy, the combination of oxytocin plus misoprostol is associated with more nausea, vomiting, shivering, and fever. Oxytocin plus ergonovine is associated with a higher rate of vomiting than oxytocin monotherapy. In my practice I prefer using intramuscular methylergonovine as the second agent to avoid the high rate of fever associated with misoprostol.

For dual agent therapy, one approach is to administer misoprostol 200 µg or 400 µg through the buccal7,8 or sublingual9,10 routes. Higher dosages of misoprostol (600 µg to 800 µg) have been used11,12 but are likely associated with higher rates of nausea, vomiting,shivering, and fever than the lower dosages. Methylergonovine 0.2 mg is administered intramuscularly.

Continue to: The bottom line...

 

 

The bottom line

PPH is a major cause of maternal morbidity, and in low-resource settings, mortality. Oxytocin is the standard for reducing postpartum blood loss, but rates of blood loss ≥ 500 mL are high following this monotherapy. To reduce postpartum blood loss beyond what is possible with oxytocin alone, clinicians can more rapidly transition to administering a second uterotonic when they suspect blood loss is becoming excessive or they can use two uterotonic agents with all births or in those at high risk for excess bleeding. If blood loss does become excessive, clinicians need to pivot rapidly from prevention with oxytocin to treatment with our entire therapeutic armamentarium.

References
  1. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2:e323-e333. 
  2. Slomski A. Why do hundreds of US women die annually in childbirth? JAMA. 2019;321:1239-1241.  
  3. Gallos ID, Papadopoulou A, Man R, et al. Uterotonic agents for preventing postpartum haemorrhage: a network meta-analysis. Cochrane Database Syst Rev. 2018;12:CD011689.  
  4. American College of Obstetricians and Gynecologists. Committee on Practice Bulletins-Obstetrics. Practice Bulletin No. 183: postpartum hemorrhage. Obstet Gynecol. 2017;130:e168-e186. 
  5. Widmer M, Piaggio G, Nguyen TM, et al; WHO Champion Trial Group. Heat-stable carbetocin versus oxytocin to prevent hemorrhage after vaginal birth. N Engl J Med. 2018;379:743-752. 
  6. Adnan N, Conlan-Trant R, McCormick C, et al. Intramuscular versus intravenous oxytocin to prevent postpartum haemorrhage at vaginal delivery: randomised controlled trial. BMJ. 2018;362:k3546. 
  7. Hamm J, Russell Z, Botha T, et al. Buccal misoprostol to prevent hemorrhage at cesarean delivery: a randomized study. Am J Obstet Gynecol. 2005;192:1404-1406. 
  8. Bhullar A, Carlan SJ, Hamm J, et al. Buccal misoprostol to decrease blood loss after vaginal delivery: a randomized trial. Obstet Gynecol. 2004;104:1282-1288. 
  9. Hofmeyr GJ, Fawole B, Mugerwa K, et al. Administration of 400 µg of misoprostol to augment routine active management of the third stage of labor. Int J Gynaecol Obstet. 2011;112:98-102. 
  10. Chaudhuri P, Majumdar A. A randomized trial of sublingual misoprostol to augment routine third-stage management among women at risk of postpartum hemorrhage. Int J Gynaecol Obstet. 2016;132:191-195. 
  11. Winikoff B, Dabash R, Durocher J, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labor: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:210-216. 
  12. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:217-223. 
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Robert L. Barbieri, MD

Editor in Chief, OBG Management 
Chair, Obstetrics and Gynecology
Brigham and Women's Hospital, Boston, Massachusetts 
Kate Macy Ladd Professor of Obstetrics, 
Gynecology and Reproductive Biology 
Harvard Medical School, Boston

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

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Robert L. Barbieri, MD

Editor in Chief, OBG Management 
Chair, Obstetrics and Gynecology
Brigham and Women's Hospital, Boston, Massachusetts 
Kate Macy Ladd Professor of Obstetrics, 
Gynecology and Reproductive Biology 
Harvard Medical School, Boston

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

Author and Disclosure Information

Robert L. Barbieri, MD

Editor in Chief, OBG Management 
Chair, Obstetrics and Gynecology
Brigham and Women's Hospital, Boston, Massachusetts 
Kate Macy Ladd Professor of Obstetrics, 
Gynecology and Reproductive Biology 
Harvard Medical School, Boston

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

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Excessive postpartum bleeding is a major cause of maternal morbidity and mortality. Worldwide, obstetric hemorrhage is the most common cause of maternal death.1,2 Medications reported to reduce postpartum bleeding include oxytocin, misoprostol, ergonovine, methylergonovine, carboprost, and tranexamic acid. A recent Cochrane network meta-analysis of 196 trials, including 135,559 women, distilled in 1,361 pages of analysis, reported on the medications associated with the greatest reduction in postpartum bleeding.3 Surprisingly, for preventing blood loss ≥ 500 mL, misoprostol plus oxytocin and ergonovine plus oxytocin were the highest ranked interventions. This evidence is summarized here.

Misoprostol plus oxytocin

After newborn delivery, active management of the third stage of labor, including uterotonic administration, is strongly recommended because it will reduce postpartum blood loss, decreasing the rate of postpartum hemorrhage (PPH).4 Both oxytocin and misoprostol are effective uterotonics. However, the combination of oxytocin plus misoprostol appears to be more effective than oxytocin alone in reducing the frequency of postpartum blood loss greater than 500 mL.3 To understand the clinical efficacy and adverse effects (AEs) of combined oxytocin plus misoprostol a meta-analysis was performed for both vaginal and cesarean deliveries (CDs).

Efficacy and AEs during vaginal delivery. In the meta-analysis, about 6,000 vaginal deliveries were analyzed, with no significant differences for misoprostol plus oxytocin versus oxytocin alone found for the following outcomes: maternal death, intensive care unit admissions, and rate of blood loss ≥ 1,000 mL (1.7% for both uterotonics vs 2.2% for oxytocin alone).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (0.95% vs 2.5%), reduced risk of blood loss ≥ 500 mL (5.9% vs 8.0%), reduced risk of requiring an additional uterotonic (3.6% vs 5.8%), and a smaller decrease in hemoglobin concentration from pre- to postdelivery (-0.89 g/L).3

In my opinion, the difference in hemoglobin concentration, although statistically significant, is not of clinical significance. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (2.4% vs 0.66%), vomiting (3.1% vs 0.86%), and fever (21% vs 3.9%).3 A weakness of this meta-analysis is that the trials used a wide range of misoprostol dosages (200 to 600 µg) and multiple routes of administration, including sublingual (under the tongue), buccal, and rectal. This makes it impossible to identify a best misoprostol dosage and administration route.

Efficacy and AEs during CD. In the same meta-analysis about 2,000 CDs were analyzed, with no significant difference for misoprostol plus oxytocin versus oxytocin alone for the following outcomes: maternal death, intensive care unit admissions, and PPH ≥ 1,000 mL blood loss (6.2% vs 6.5%).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (2.6% vs 5.4%), reduced risk of blood loss ≥ 500 mL (32% vs 47%), reduced risk of requiring an additional uterotonic (14% vs 28%), and a smaller decrease in hemoglobin concentration from before to after delivery (-4.0 g/L).3 In my opinion, the statistically significant difference in hemoglobin concentration is not clinically significant. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (12% vs 6.1%), vomiting (8.1% vs 5.4%), shivering (13% vs 7%), and fever (7.7% vs 4.0%).3

Continue to: Ergonovine plus oxytocin...

 

 

Ergonovine plus oxytocin

Ergonovine is an ergot derivative that causes uterine contractions and has been shown to effectively reduce blood loss at delivery. In the United States a methyl-derivative of ergonovine, methylergonovine, is widely available. In a meta-analysis with mostly vaginal deliveries, there were no significant differences for ergonovine plus oxytocin versus oxytocin alone for the following outcomes: death, intensive care unit admission, rate of blood loss ≥ 1,000 mL(2.0% vs 2.7%), blood transfusion, administration of an additional uterotonic, change in hemoglobin from pre- to postdelivery, nausea, hypertension, shivering, and fever.3 However, ergonovine plus oxytocin, compared with oxytocin alone, resulted in a significantly reduced rate of blood loss ≥ 500 mL (8.3% vs 10.2%) and an increased rate of vomiting (8.1% vs 1.6%).3 In these trials women with a blood pressure ≥ 150/100 mm Hg were generally excluded from receiving ergonovine because of its hypertensive effect.

Clinical practice options

Given the Cochrane meta-analysis results, ObGyns have two approaches for optimizing PPH reduction.

Option 1: Use a single uterotonic to reduce postpartum blood loss. If excess bleeding occurs, rapidly administer a second uterotonic agent. Currently, monotherapy with intravenous or intramuscular oxytocin is the standard for reducing postpartum blood loss.5,6 Advantages of this approach compared with dual agent therapy include simplification of care and minimization of AEs. However, oxytocin monotherapy for minimizing postpartum bleeding may be suboptimal. In the largest trial ever performed (involving 29,645 women) when oxytocin was administered postpartum, the rates of estimated blood loss ≥ 500 mL and ≥ 1,000 mL were 9.1% and 1.45%, respectively.5 Is 9% an optimal rate for blood loss ≥ 500 mL following a vaginal delivery? Or should we try to achieve a lower rate?

Given the “high” rate of blood loss ≥ 500 mL with oxytocin alone, it is important for clinicians using the one-uterotonic approach to promptly recognize patients who have excessive bleeding and transition rapidly from prevention to treatment. When PPH cases are reviewed, a common finding is that the clinicians did not timely recognize excess bleeding, delaying transition to treatment with additional uterotonics and other interventions. When routinely using oxytocin monotherapy, lowering the threshold for administering a second uterotonic (methylergonovine, carboprost, misoprostol, or tranexamic acid) may help decrease the frequency of excess postpartum blood loss.

Option 2: Administer two uterotonics to reduce postpartum blood loss at all deliveries. Given the “high” rate of excess postpartum blood loss with oxytocin monotherapy, an alternative is to administer two uterotonics at all births or at births with a high risk of excess blood loss. As discussed, administering two uterotonics, oxytocin plus misoprostol or oxytocin plus ergonovine, has been reported to be more effective than oxytocin alone for reducing postpartum bleeding ≥ 500 mL.3 In the Cochrane meta-analysis, per 1,000 women given oxytocin following a vaginal birth, 122 would have blood loss ≥ 500 mL, compared with 85 given oxytocin plus misoprostol or oxytocin plus ergonovine.3

Misoprostol is administered sublingually, buccally, or rectally, and methylergonovine is administered by intramuscular injection. Although dual uterotonic therapy is more effective than monotherapy, dual therapy is associated with more AEs. As noted, compared with oxytocin monotherapy, the combination of oxytocin plus misoprostol is associated with more nausea, vomiting, shivering, and fever. Oxytocin plus ergonovine is associated with a higher rate of vomiting than oxytocin monotherapy. In my practice I prefer using intramuscular methylergonovine as the second agent to avoid the high rate of fever associated with misoprostol.

For dual agent therapy, one approach is to administer misoprostol 200 µg or 400 µg through the buccal7,8 or sublingual9,10 routes. Higher dosages of misoprostol (600 µg to 800 µg) have been used11,12 but are likely associated with higher rates of nausea, vomiting,shivering, and fever than the lower dosages. Methylergonovine 0.2 mg is administered intramuscularly.

Continue to: The bottom line...

 

 

The bottom line

PPH is a major cause of maternal morbidity, and in low-resource settings, mortality. Oxytocin is the standard for reducing postpartum blood loss, but rates of blood loss ≥ 500 mL are high following this monotherapy. To reduce postpartum blood loss beyond what is possible with oxytocin alone, clinicians can more rapidly transition to administering a second uterotonic when they suspect blood loss is becoming excessive or they can use two uterotonic agents with all births or in those at high risk for excess bleeding. If blood loss does become excessive, clinicians need to pivot rapidly from prevention with oxytocin to treatment with our entire therapeutic armamentarium.

Excessive postpartum bleeding is a major cause of maternal morbidity and mortality. Worldwide, obstetric hemorrhage is the most common cause of maternal death.1,2 Medications reported to reduce postpartum bleeding include oxytocin, misoprostol, ergonovine, methylergonovine, carboprost, and tranexamic acid. A recent Cochrane network meta-analysis of 196 trials, including 135,559 women, distilled in 1,361 pages of analysis, reported on the medications associated with the greatest reduction in postpartum bleeding.3 Surprisingly, for preventing blood loss ≥ 500 mL, misoprostol plus oxytocin and ergonovine plus oxytocin were the highest ranked interventions. This evidence is summarized here.

Misoprostol plus oxytocin

After newborn delivery, active management of the third stage of labor, including uterotonic administration, is strongly recommended because it will reduce postpartum blood loss, decreasing the rate of postpartum hemorrhage (PPH).4 Both oxytocin and misoprostol are effective uterotonics. However, the combination of oxytocin plus misoprostol appears to be more effective than oxytocin alone in reducing the frequency of postpartum blood loss greater than 500 mL.3 To understand the clinical efficacy and adverse effects (AEs) of combined oxytocin plus misoprostol a meta-analysis was performed for both vaginal and cesarean deliveries (CDs).

Efficacy and AEs during vaginal delivery. In the meta-analysis, about 6,000 vaginal deliveries were analyzed, with no significant differences for misoprostol plus oxytocin versus oxytocin alone found for the following outcomes: maternal death, intensive care unit admissions, and rate of blood loss ≥ 1,000 mL (1.7% for both uterotonics vs 2.2% for oxytocin alone).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (0.95% vs 2.5%), reduced risk of blood loss ≥ 500 mL (5.9% vs 8.0%), reduced risk of requiring an additional uterotonic (3.6% vs 5.8%), and a smaller decrease in hemoglobin concentration from pre- to postdelivery (-0.89 g/L).3

In my opinion, the difference in hemoglobin concentration, although statistically significant, is not of clinical significance. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (2.4% vs 0.66%), vomiting (3.1% vs 0.86%), and fever (21% vs 3.9%).3 A weakness of this meta-analysis is that the trials used a wide range of misoprostol dosages (200 to 600 µg) and multiple routes of administration, including sublingual (under the tongue), buccal, and rectal. This makes it impossible to identify a best misoprostol dosage and administration route.

Efficacy and AEs during CD. In the same meta-analysis about 2,000 CDs were analyzed, with no significant difference for misoprostol plus oxytocin versus oxytocin alone for the following outcomes: maternal death, intensive care unit admissions, and PPH ≥ 1,000 mL blood loss (6.2% vs 6.5%).3 Misoprostol plus oxytocin was significantly superior to oxytocin alone for the following outcomes: reduced risk of blood transfusion (2.6% vs 5.4%), reduced risk of blood loss ≥ 500 mL (32% vs 47%), reduced risk of requiring an additional uterotonic (14% vs 28%), and a smaller decrease in hemoglobin concentration from before to after delivery (-4.0 g/L).3 In my opinion, the statistically significant difference in hemoglobin concentration is not clinically significant. However, compared with oxytocin alone, misoprostol plus oxytocin caused significantly more nausea (12% vs 6.1%), vomiting (8.1% vs 5.4%), shivering (13% vs 7%), and fever (7.7% vs 4.0%).3

Continue to: Ergonovine plus oxytocin...

 

 

Ergonovine plus oxytocin

Ergonovine is an ergot derivative that causes uterine contractions and has been shown to effectively reduce blood loss at delivery. In the United States a methyl-derivative of ergonovine, methylergonovine, is widely available. In a meta-analysis with mostly vaginal deliveries, there were no significant differences for ergonovine plus oxytocin versus oxytocin alone for the following outcomes: death, intensive care unit admission, rate of blood loss ≥ 1,000 mL(2.0% vs 2.7%), blood transfusion, administration of an additional uterotonic, change in hemoglobin from pre- to postdelivery, nausea, hypertension, shivering, and fever.3 However, ergonovine plus oxytocin, compared with oxytocin alone, resulted in a significantly reduced rate of blood loss ≥ 500 mL (8.3% vs 10.2%) and an increased rate of vomiting (8.1% vs 1.6%).3 In these trials women with a blood pressure ≥ 150/100 mm Hg were generally excluded from receiving ergonovine because of its hypertensive effect.

Clinical practice options

Given the Cochrane meta-analysis results, ObGyns have two approaches for optimizing PPH reduction.

Option 1: Use a single uterotonic to reduce postpartum blood loss. If excess bleeding occurs, rapidly administer a second uterotonic agent. Currently, monotherapy with intravenous or intramuscular oxytocin is the standard for reducing postpartum blood loss.5,6 Advantages of this approach compared with dual agent therapy include simplification of care and minimization of AEs. However, oxytocin monotherapy for minimizing postpartum bleeding may be suboptimal. In the largest trial ever performed (involving 29,645 women) when oxytocin was administered postpartum, the rates of estimated blood loss ≥ 500 mL and ≥ 1,000 mL were 9.1% and 1.45%, respectively.5 Is 9% an optimal rate for blood loss ≥ 500 mL following a vaginal delivery? Or should we try to achieve a lower rate?

Given the “high” rate of blood loss ≥ 500 mL with oxytocin alone, it is important for clinicians using the one-uterotonic approach to promptly recognize patients who have excessive bleeding and transition rapidly from prevention to treatment. When PPH cases are reviewed, a common finding is that the clinicians did not timely recognize excess bleeding, delaying transition to treatment with additional uterotonics and other interventions. When routinely using oxytocin monotherapy, lowering the threshold for administering a second uterotonic (methylergonovine, carboprost, misoprostol, or tranexamic acid) may help decrease the frequency of excess postpartum blood loss.

Option 2: Administer two uterotonics to reduce postpartum blood loss at all deliveries. Given the “high” rate of excess postpartum blood loss with oxytocin monotherapy, an alternative is to administer two uterotonics at all births or at births with a high risk of excess blood loss. As discussed, administering two uterotonics, oxytocin plus misoprostol or oxytocin plus ergonovine, has been reported to be more effective than oxytocin alone for reducing postpartum bleeding ≥ 500 mL.3 In the Cochrane meta-analysis, per 1,000 women given oxytocin following a vaginal birth, 122 would have blood loss ≥ 500 mL, compared with 85 given oxytocin plus misoprostol or oxytocin plus ergonovine.3

Misoprostol is administered sublingually, buccally, or rectally, and methylergonovine is administered by intramuscular injection. Although dual uterotonic therapy is more effective than monotherapy, dual therapy is associated with more AEs. As noted, compared with oxytocin monotherapy, the combination of oxytocin plus misoprostol is associated with more nausea, vomiting, shivering, and fever. Oxytocin plus ergonovine is associated with a higher rate of vomiting than oxytocin monotherapy. In my practice I prefer using intramuscular methylergonovine as the second agent to avoid the high rate of fever associated with misoprostol.

For dual agent therapy, one approach is to administer misoprostol 200 µg or 400 µg through the buccal7,8 or sublingual9,10 routes. Higher dosages of misoprostol (600 µg to 800 µg) have been used11,12 but are likely associated with higher rates of nausea, vomiting,shivering, and fever than the lower dosages. Methylergonovine 0.2 mg is administered intramuscularly.

Continue to: The bottom line...

 

 

The bottom line

PPH is a major cause of maternal morbidity, and in low-resource settings, mortality. Oxytocin is the standard for reducing postpartum blood loss, but rates of blood loss ≥ 500 mL are high following this monotherapy. To reduce postpartum blood loss beyond what is possible with oxytocin alone, clinicians can more rapidly transition to administering a second uterotonic when they suspect blood loss is becoming excessive or they can use two uterotonic agents with all births or in those at high risk for excess bleeding. If blood loss does become excessive, clinicians need to pivot rapidly from prevention with oxytocin to treatment with our entire therapeutic armamentarium.

References
  1. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2:e323-e333. 
  2. Slomski A. Why do hundreds of US women die annually in childbirth? JAMA. 2019;321:1239-1241.  
  3. Gallos ID, Papadopoulou A, Man R, et al. Uterotonic agents for preventing postpartum haemorrhage: a network meta-analysis. Cochrane Database Syst Rev. 2018;12:CD011689.  
  4. American College of Obstetricians and Gynecologists. Committee on Practice Bulletins-Obstetrics. Practice Bulletin No. 183: postpartum hemorrhage. Obstet Gynecol. 2017;130:e168-e186. 
  5. Widmer M, Piaggio G, Nguyen TM, et al; WHO Champion Trial Group. Heat-stable carbetocin versus oxytocin to prevent hemorrhage after vaginal birth. N Engl J Med. 2018;379:743-752. 
  6. Adnan N, Conlan-Trant R, McCormick C, et al. Intramuscular versus intravenous oxytocin to prevent postpartum haemorrhage at vaginal delivery: randomised controlled trial. BMJ. 2018;362:k3546. 
  7. Hamm J, Russell Z, Botha T, et al. Buccal misoprostol to prevent hemorrhage at cesarean delivery: a randomized study. Am J Obstet Gynecol. 2005;192:1404-1406. 
  8. Bhullar A, Carlan SJ, Hamm J, et al. Buccal misoprostol to decrease blood loss after vaginal delivery: a randomized trial. Obstet Gynecol. 2004;104:1282-1288. 
  9. Hofmeyr GJ, Fawole B, Mugerwa K, et al. Administration of 400 µg of misoprostol to augment routine active management of the third stage of labor. Int J Gynaecol Obstet. 2011;112:98-102. 
  10. Chaudhuri P, Majumdar A. A randomized trial of sublingual misoprostol to augment routine third-stage management among women at risk of postpartum hemorrhage. Int J Gynaecol Obstet. 2016;132:191-195. 
  11. Winikoff B, Dabash R, Durocher J, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labor: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:210-216. 
  12. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:217-223. 
References
  1. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2:e323-e333. 
  2. Slomski A. Why do hundreds of US women die annually in childbirth? JAMA. 2019;321:1239-1241.  
  3. Gallos ID, Papadopoulou A, Man R, et al. Uterotonic agents for preventing postpartum haemorrhage: a network meta-analysis. Cochrane Database Syst Rev. 2018;12:CD011689.  
  4. American College of Obstetricians and Gynecologists. Committee on Practice Bulletins-Obstetrics. Practice Bulletin No. 183: postpartum hemorrhage. Obstet Gynecol. 2017;130:e168-e186. 
  5. Widmer M, Piaggio G, Nguyen TM, et al; WHO Champion Trial Group. Heat-stable carbetocin versus oxytocin to prevent hemorrhage after vaginal birth. N Engl J Med. 2018;379:743-752. 
  6. Adnan N, Conlan-Trant R, McCormick C, et al. Intramuscular versus intravenous oxytocin to prevent postpartum haemorrhage at vaginal delivery: randomised controlled trial. BMJ. 2018;362:k3546. 
  7. Hamm J, Russell Z, Botha T, et al. Buccal misoprostol to prevent hemorrhage at cesarean delivery: a randomized study. Am J Obstet Gynecol. 2005;192:1404-1406. 
  8. Bhullar A, Carlan SJ, Hamm J, et al. Buccal misoprostol to decrease blood loss after vaginal delivery: a randomized trial. Obstet Gynecol. 2004;104:1282-1288. 
  9. Hofmeyr GJ, Fawole B, Mugerwa K, et al. Administration of 400 µg of misoprostol to augment routine active management of the third stage of labor. Int J Gynaecol Obstet. 2011;112:98-102. 
  10. Chaudhuri P, Majumdar A. A randomized trial of sublingual misoprostol to augment routine third-stage management among women at risk of postpartum hemorrhage. Int J Gynaecol Obstet. 2016;132:191-195. 
  11. Winikoff B, Dabash R, Durocher J, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labor: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:210-216. 
  12. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double-blind, randomised, non-inferiority trial. Lancet. 2010;375:217-223. 
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In women with late preterm mild hypertensive disorders, does immediate delivery versus expectant management differ in terms of neonatal neurodevelopmental outcomes?

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Zwertbroek EF, Franssen MT, Broekhuijsen K, et al; HYPITAT-II Study Group. Neonatal developmental and behavioral outcomes of immediate delivery versus expectant monitoring of mild hypertensive disorders of pregnancy: 2-year outcomes of the HYPITAT-II trial. Am J Obstet Gynecol. doi:10.1016/j.ajog.2019.03.024.

EXPERT COMMENTARY

In women with mild hypertensive disorders in the preterm period, the maternal benefits of delivery should be weighed against the consequences of preterm birth for the neonate. In a recent study, Zwertbroek and colleagues sought to evaluate the long-term neurodevelopmental effects of this decision on the offspring.

 

Details of the study

The authors conducted a follow-up study of the randomized, controlled Hypertension and Preeclampsia Intervention Trial At Term II (HYPITAT-II), in which 704 women diagnosed with late preterm (34–37 weeks) hypertensive disorders in pregnancy (gestational hypertension, chronic hypertension, or mild preeclampsia) were randomly assigned to immediate delivery or expectant management.

Expectant management consisted of close monitoring until 37 weeks or until an indication for delivery occurred, whichever came first. Children born to those mothers were eligible for this study (women enrolled during 2011–2015) when they reached 2 years of age; 342 children were included in this analysis. Of note, children from the expectant management group had been delivered at a more advanced gestational age (median, 37.0 vs 36.1 weeks; P<.001) than those in the immediate-delivery group.

Survey tools. Parents completed 2 response surveys, the Ages and Stages Questionnaire (ASQ) and the Child Behavior Checklist (CBCL), between 23 and 26 months’ corrected age. The ASQ is designed to detect developmental delay, while the CBCL assesses behavioral and emotional problems. The primary outcome was an abnormal result on either screen.

Results. Based on 330 returned questionnaires, the authors found more abnormal ASQ scores (45 of 162 [28%] vs 27 of 148 [18%] children; P = .045) in the immediate-delivery group versus the expectant management group, most pronounced in the fine motor domain. They found no difference in the CBCL scores. The authors concluded that immediate delivery for women with late preterm mild hypertensive disorders in pregnancy increases the risk of developmental delay in the children.

Study strengths and limitations

This study is unique as a planned follow-up to a randomized, controlled trial, allowing for 2-year outcomes to be assessed on children of enrolled women with mild hypertensive disorders in the late preterm period. The authors used validated surveys that are known to predict long-term neurodevelopmental outcomes.

Continue to: This work has several limitations...

 

 

This work has several limitations, however. Randomization was not truly maintained given the less than 50% response rate of original participants. Additionally, parents completed the surveys and provider confirmation of developmental concerns or diagnoses was not obtained. Further, assessments at 2 years of age may be too early to detect subtle differences, with evaluations at 5 years more predictive of long-term outcomes; the authors stated that these data already are being collected.

Finally, while these data importantly reinforce the conclusions of the parent HYPITAT-II trial, which support expectant management for mild hypertensive disorders in the late preterm period,1 clinicians must always take care to individualize decisions in the face of worsening maternal disease.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
This follow-up study of the HYPITAT-II randomized, controlled trial demonstrates poorer neurodevelopmental outcomes in offspring of late preterm mild hypertensives who undergo immediate delivery. These data support current practice recommendations to expectantly manage women with late preterm mild hypertensive disease until 37 weeks or signs of clinical worsening, whichever comes first.

 

References
  1. Broekjuijsen K, van Baaren GJ, van Pampus MG, et al; HYPITAT-II Study Group. Immediate delivery versus expectant monitoring for hypertensive disorders of pregnancy between 34 and 37 weeks of gestation (HYPITAT-II): an open-label, randomised controlled trial. Lancet. 2015;385:2492-2501.
     
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Rebecca F. Hamm, MD, is a Maternal and Fetal Medicine Fellow, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine, Philadelphia.

Sindhu K. Srinivas, MD, MSCE, is Associate Professor of Obstetrics and Gynecology, Division of Maternal and Fetal Medicine, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine.

The authors report no financial relationships related to this article. 

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Rebecca F. Hamm, MD, is a Maternal and Fetal Medicine Fellow, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine, Philadelphia.

Sindhu K. Srinivas, MD, MSCE, is Associate Professor of Obstetrics and Gynecology, Division of Maternal and Fetal Medicine, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine.

The authors report no financial relationships related to this article. 

Author and Disclosure Information

Rebecca F. Hamm, MD, is a Maternal and Fetal Medicine Fellow, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine, Philadelphia.

Sindhu K. Srinivas, MD, MSCE, is Associate Professor of Obstetrics and Gynecology, Division of Maternal and Fetal Medicine, Department of Obstetrics and Gynecology, University of Pennsylvania Perelman School of Medicine.

The authors report no financial relationships related to this article. 

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Zwertbroek EF, Franssen MT, Broekhuijsen K, et al; HYPITAT-II Study Group. Neonatal developmental and behavioral outcomes of immediate delivery versus expectant monitoring of mild hypertensive disorders of pregnancy: 2-year outcomes of the HYPITAT-II trial. Am J Obstet Gynecol. doi:10.1016/j.ajog.2019.03.024.

EXPERT COMMENTARY

In women with mild hypertensive disorders in the preterm period, the maternal benefits of delivery should be weighed against the consequences of preterm birth for the neonate. In a recent study, Zwertbroek and colleagues sought to evaluate the long-term neurodevelopmental effects of this decision on the offspring.

 

Details of the study

The authors conducted a follow-up study of the randomized, controlled Hypertension and Preeclampsia Intervention Trial At Term II (HYPITAT-II), in which 704 women diagnosed with late preterm (34–37 weeks) hypertensive disorders in pregnancy (gestational hypertension, chronic hypertension, or mild preeclampsia) were randomly assigned to immediate delivery or expectant management.

Expectant management consisted of close monitoring until 37 weeks or until an indication for delivery occurred, whichever came first. Children born to those mothers were eligible for this study (women enrolled during 2011–2015) when they reached 2 years of age; 342 children were included in this analysis. Of note, children from the expectant management group had been delivered at a more advanced gestational age (median, 37.0 vs 36.1 weeks; P<.001) than those in the immediate-delivery group.

Survey tools. Parents completed 2 response surveys, the Ages and Stages Questionnaire (ASQ) and the Child Behavior Checklist (CBCL), between 23 and 26 months’ corrected age. The ASQ is designed to detect developmental delay, while the CBCL assesses behavioral and emotional problems. The primary outcome was an abnormal result on either screen.

Results. Based on 330 returned questionnaires, the authors found more abnormal ASQ scores (45 of 162 [28%] vs 27 of 148 [18%] children; P = .045) in the immediate-delivery group versus the expectant management group, most pronounced in the fine motor domain. They found no difference in the CBCL scores. The authors concluded that immediate delivery for women with late preterm mild hypertensive disorders in pregnancy increases the risk of developmental delay in the children.

Study strengths and limitations

This study is unique as a planned follow-up to a randomized, controlled trial, allowing for 2-year outcomes to be assessed on children of enrolled women with mild hypertensive disorders in the late preterm period. The authors used validated surveys that are known to predict long-term neurodevelopmental outcomes.

Continue to: This work has several limitations...

 

 

This work has several limitations, however. Randomization was not truly maintained given the less than 50% response rate of original participants. Additionally, parents completed the surveys and provider confirmation of developmental concerns or diagnoses was not obtained. Further, assessments at 2 years of age may be too early to detect subtle differences, with evaluations at 5 years more predictive of long-term outcomes; the authors stated that these data already are being collected.

Finally, while these data importantly reinforce the conclusions of the parent HYPITAT-II trial, which support expectant management for mild hypertensive disorders in the late preterm period,1 clinicians must always take care to individualize decisions in the face of worsening maternal disease.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
This follow-up study of the HYPITAT-II randomized, controlled trial demonstrates poorer neurodevelopmental outcomes in offspring of late preterm mild hypertensives who undergo immediate delivery. These data support current practice recommendations to expectantly manage women with late preterm mild hypertensive disease until 37 weeks or signs of clinical worsening, whichever comes first.

 

Zwertbroek EF, Franssen MT, Broekhuijsen K, et al; HYPITAT-II Study Group. Neonatal developmental and behavioral outcomes of immediate delivery versus expectant monitoring of mild hypertensive disorders of pregnancy: 2-year outcomes of the HYPITAT-II trial. Am J Obstet Gynecol. doi:10.1016/j.ajog.2019.03.024.

EXPERT COMMENTARY

In women with mild hypertensive disorders in the preterm period, the maternal benefits of delivery should be weighed against the consequences of preterm birth for the neonate. In a recent study, Zwertbroek and colleagues sought to evaluate the long-term neurodevelopmental effects of this decision on the offspring.

 

Details of the study

The authors conducted a follow-up study of the randomized, controlled Hypertension and Preeclampsia Intervention Trial At Term II (HYPITAT-II), in which 704 women diagnosed with late preterm (34–37 weeks) hypertensive disorders in pregnancy (gestational hypertension, chronic hypertension, or mild preeclampsia) were randomly assigned to immediate delivery or expectant management.

Expectant management consisted of close monitoring until 37 weeks or until an indication for delivery occurred, whichever came first. Children born to those mothers were eligible for this study (women enrolled during 2011–2015) when they reached 2 years of age; 342 children were included in this analysis. Of note, children from the expectant management group had been delivered at a more advanced gestational age (median, 37.0 vs 36.1 weeks; P<.001) than those in the immediate-delivery group.

Survey tools. Parents completed 2 response surveys, the Ages and Stages Questionnaire (ASQ) and the Child Behavior Checklist (CBCL), between 23 and 26 months’ corrected age. The ASQ is designed to detect developmental delay, while the CBCL assesses behavioral and emotional problems. The primary outcome was an abnormal result on either screen.

Results. Based on 330 returned questionnaires, the authors found more abnormal ASQ scores (45 of 162 [28%] vs 27 of 148 [18%] children; P = .045) in the immediate-delivery group versus the expectant management group, most pronounced in the fine motor domain. They found no difference in the CBCL scores. The authors concluded that immediate delivery for women with late preterm mild hypertensive disorders in pregnancy increases the risk of developmental delay in the children.

Study strengths and limitations

This study is unique as a planned follow-up to a randomized, controlled trial, allowing for 2-year outcomes to be assessed on children of enrolled women with mild hypertensive disorders in the late preterm period. The authors used validated surveys that are known to predict long-term neurodevelopmental outcomes.

Continue to: This work has several limitations...

 

 

This work has several limitations, however. Randomization was not truly maintained given the less than 50% response rate of original participants. Additionally, parents completed the surveys and provider confirmation of developmental concerns or diagnoses was not obtained. Further, assessments at 2 years of age may be too early to detect subtle differences, with evaluations at 5 years more predictive of long-term outcomes; the authors stated that these data already are being collected.

Finally, while these data importantly reinforce the conclusions of the parent HYPITAT-II trial, which support expectant management for mild hypertensive disorders in the late preterm period,1 clinicians must always take care to individualize decisions in the face of worsening maternal disease.

WHAT THIS EVIDENCE MEANS FOR PRACTICE
This follow-up study of the HYPITAT-II randomized, controlled trial demonstrates poorer neurodevelopmental outcomes in offspring of late preterm mild hypertensives who undergo immediate delivery. These data support current practice recommendations to expectantly manage women with late preterm mild hypertensive disease until 37 weeks or signs of clinical worsening, whichever comes first.

 

References
  1. Broekjuijsen K, van Baaren GJ, van Pampus MG, et al; HYPITAT-II Study Group. Immediate delivery versus expectant monitoring for hypertensive disorders of pregnancy between 34 and 37 weeks of gestation (HYPITAT-II): an open-label, randomised controlled trial. Lancet. 2015;385:2492-2501.
     
References
  1. Broekjuijsen K, van Baaren GJ, van Pampus MG, et al; HYPITAT-II Study Group. Immediate delivery versus expectant monitoring for hypertensive disorders of pregnancy between 34 and 37 weeks of gestation (HYPITAT-II): an open-label, randomised controlled trial. Lancet. 2015;385:2492-2501.
     
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What to do when a patient presents with breast pain

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Changed
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Breast pain is one of the most common breast-related patient complaints and is found to affect at least 50% of the female population.1 Most cases are self-limiting and are related to hormonal and normal fibrocystic changes. The median age of onset of symptoms is 36 years, with most women experiencing pain for 5 to 12 years.2 Because the cause of breast pain is not always clear, its presence can produce anxiety in patients and physicians over the possibility of underlying malignancy. Although breast cancer is not associated with breast pain, many patients presenting with pain are referred for diagnostic imaging (usually with negative results). The majority of women with mastalgia and normal clinical examination findings can be reassured with education about the many benign causes of breast pain.

What are causes of breast pain without an imaging abnormality?

Hormones. Mastalgia can be focal or generalized and is mostly due to hormonal changes. Elevated estrogen can stimulate the growth of breast tissue, which is known as epithelial hyperplasia.3 Fluctuations in hormone levels can occur in perimenopausal women in their forties and can result in new symptoms of breast pain.4 Sometimes starting a new contraceptive medication or hormone replacement therapy can exacerbate the pain. Switching brands or medications may help. Another cause of mastalgia may be elevated prolactin levels, with hypothalamic-pituitary dysfunction.5,6

Diet. There is evidence to link a high-fat diet with breast pain. The pain has been shown to improve when lipid intake is reduced and high- and low-density lipoprotein cholesterol levels are normalized. As estrogen is a steroid hormone that can be synthesized from lipids and fatty acids, elevated lipid metabolism can increase estrogen levels and exacerbate breast pain symptoms.7,8 Essential fatty acids, such as evening primrose oil and vitamin E, have been used to treat mastalgia because they reduce inflammation in fatty breast tissue through the prostaglandin pathway.9,10

Caffeine. Methylxanthines can be found in coffee, tea, and chocolate and can aggravate mastalgia by enhancing the cyclin adenosine monophosphate (cAMP) pathway. This pathway stimulates cellular proliferation and fibrocystic changes which in turn can exacerbate breast pain.11

Smoking. In my clinical practice I have clearly noted a higher incidence of breast pain in patients who smoke. The pain tends to improve significantly when the patient quits or even cuts back on smoking. The exact reasons for smoking’s effects on breast pain are not well known; however, they are thought to be related to acceleration of the cAMP pathway.

Large breast size. Very large breasts will strain and weaken the suspensory ligaments, leading to pain and discomfort. It has been shown that wearing a supportive sports bra during episodes of breast pain is effective.

Types of breast pain

Cyclical

Women with fibrocystic breasts tend to experience more breast pain. Breast sensitivity can be localized to the upper outer quadrants or to the nipple and sub-areolar area. It also can be generalized. The pain tends to peak with ovulation, improve with menses, and to recur every few weeks. Patients who have had partial hysterectomy (with ovaries in situ) or endometrial ablation will be unable to correlate their symptoms to menstruation. Therefore, women are encouraged to keep a diary or calendar of their symptoms to detect any correlation with their ovarian cycle. Such correlation is reassuring.

Continue to: Noncyclical...

 

 

Noncyclical

Noncyclical breast pain is not associated with the menstrual cycle and can be unilateral or bilateral. Providers should perform a good history of patients presenting with noncyclicalbreast pain, to include character, onset, duration, location, radiation, alleviating, and aggravating factors. A physical examination may elicit point tenderness at the chest by pushing the breast tissue off of the chest wall while the patient is in supine position and pressing directly over the ribs. Lack of tenderness on palpation of the breast parenchyma, but pain on the chest wall, points to a musculoskeletal etiology. Chest wall pain may be related to muscle spasm or muscle strain, trauma, rib fracture, or costochondritis (Tietze syndrome). Finally, based on history of review of systems and physical examination, referred pain from biliary or cardiac etiology should be considered.

When breast pain occurs with skin changes

Skin changes usually have an underlying pathology. Infectious processes, such as infected epidermal inclusion cyst, hidradenitis of the cleavage and inframammary crease, or breast abscess will present with pain and induration with an acute onset of 5 to 10 days. Large pendulous breasts may develop yeast infection at the inframammary crease. Chronic infectious irritation can lead to hyperpigmentation of that area. Eczema or contact dermatitis frequently can affect the areola and become confused with Paget disease (ductal carcinoma in situ of the nipple). With Paget, the excoriation always starts at the nipple and can then spread to the areola. However, with dermatitis, the rash begins on the peri-areolar skin, without affecting the nipple itself.

When breast pain occurs with nipple discharge

Breast pain with nipple discharge usually is bilateral and more common in patients with significant fibrocystic changes who smoke. If the nipple discharge is bilateral, serous and non-bloody, and multiduct, it is considered benign and physiologic. Physiologic nipple discharge can be multifactorial and hormonal. It may be related to thyroid disorders or medications such as antidepressants, selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, or antipsychotics. The only nipple discharge that is considered pathologic is unilateral spontaneous bloody discharge for which diagnostic imaging and breast surgeon referral is indicated. Women should be discouraged from self-expressing their nipples, as 80% will experience serous nipple discharge upon manual self-expression.

Should I order breast imaging for my patient with breast pain and a normal clinical breast exam?

Breast pain is not associated with breast cancer. Most breast cancers do not hurt; they present as firm, painless masses. However, when a woman notices pain in her breast, her first concern is breast cancer. This concern is re-enforced by the medical provider whose first impulse is to order diagnostic imaging. Yet less than 3% of breast cancers are associated with breast pain.

There have been multiple published retrospective and prospective radiologic studies about the utility of breast imaging in women with breast pain without a palpable mass. All of the studies have demonstrated that breast imaging with mammography and ultrasonography in these patients yields mostly negative or benign findings. The incidence of breast cancer during imaging work-up in women with breast pain and no clinical abnormality is only 0.4% to 1.8%.1-3 Some patients may develop future subsequent breast cancer in the symptomatic breast. But this is considered incidental and possibly related to increased cell turnover related to fibrocystic changes. Breast imaging for evaluation of breast pain only provides reassurance to the physician. The patient's reassurance will come from a medical explanation for the symptoms and advice on symptom management from the provider.

Researchers from MD Anderson Cancer Center reported imaging findings and cost analysis for 799 patients presenting with breast pain from 3 large network community-based breast imaging centers in 2014. Breast ultrasound was the initial imaging modality for women younger than age 30. Digital mammography (sometimes with tomosynthesis) was used for those older than age 30 that had not had a mammogram in the last 6 months. Breast magnetic resonance imaging was performed only when ordered by the referring physician. Most of the patients presented for diagnostic imaging, and 95% had negative findings and 5% had a benign finding. Only 1 patient was found to have an incidental cancer in the contralateral breast, which was detected by tomosynthesis. The cost of breast imaging was $87,322 in younger women and $152,732 in women older than age 40, representing overutilization of health care resources and no association between breast pain and breast cancer.4

References

  1. Chetlan AL, Kapoor MM, Watts MR. Mastalgia: imaging work-up appropriateness. Acad Radiol. 2017;24:345-349.
  2. Arslan M, Kücükerdem HS, Can H, et al. Retrospective analysis of women with only mastalgia. J Breast Health. 2016;12:151-154.
  3. Noroozian M, Stein LF, Gaetke-Udager K, et al. Long-term clinical outcomes in women with breast pain in the absence of additional clinical findings: Mammography remains indicated. Breast Cancer Res Treat. 2015;149:417-424.
  4. Kushwaha AC, Shin K, Kalambo M, et al. Overutilization of health care resources for breast pain. AJR Am J Roentgenol. 2018; 211:217-223.
 

Management of mastalgia

Appropriate breast pain management begins with a good history and physical examination. The decision to perform imaging should depend on clinical exam findings and not on symptoms of breast pain. If there is a palpable mass, then breast imaging and possible biopsy is appropriate. However, if clinical exam is normal, there is no indication for breast imaging in low-risk women under the age of 40 whose only symptom is breast pain. Women older than age 40 can undergo diagnostic imaging, if they have not had a negative screening mammogram in the past year.

Breast pain with abnormal clinical exam

In the patient who is younger than age 30 with a palpable mass. For this patient order targeted breast ultrasound (US) (FIGURE 1). If results are negative, repeat the clinical examination 1 week after menses. If the mass is persistent, refer the patient to a breast surgeon. If diagnostic imaging results are negative, consider breast MRI, especially if there is a strong family history of breast cancer.

In the patient who is aged 30 and older with a palpable mass. For this patient, bilateral diagnostic mammogram and US are in order. The testing is best performed 1 week after menses to reduce false-positive findings. If imaging is negative and the patient still has a clinically suspicious finding or mass, refer her to a breast surgeon and consider breast MRI. At this point if there is a persistent firm dominant mass, a biopsy is indicated as part of the triple test. If the mass resolves with menses, the patient can be reassured that the cause is most likely benign, with clinical examination repeated in 3 months.

Continue to: Breast pain and normal clinical exam...

 

 

Breast pain and normal clinical exam

When women who report breast pain have normal clinical examination findings (and have a negative screening mammogram in the past 12 months if older than age 40), there are several management strategies you can offer (FIGURE 2).

Reassurance and education. The majority of women with breast pain can be managed with reassurance and education, which are often sufficient to reduce their anxieties.

Supportive bra. The most effective intervention is to wear and sleep in a well-fitted supportive sports bra for 4 to 12 weeks. In a nonrandomized single-center trial of danazol versus sports bra, 85% of women reported relief of their breast pain with bra alone (vs 58% with danazol).12 A supportive bra is the first-line management of mastalgia (Level II evidence).

Symptom diary/calendar. Many women do not know whether or not their symptoms correspond to their ovarian cycle or are related to hormonal fluctuations. Therefore, it is reassuring and informative for them to keep a calendar or a diary of their symptoms to determine whether their symptoms occur or are exacerbated in a cyclical pattern.

Diet and lifestyle modification. Women should avoid caffeine (especially when having pain). Studies on methylxanthines have demonstrated some symptom relief with reducing caffeine intake.11,13 One cup of coffee or tea per day most likely will not make a difference. However, if a woman is drinking large quantities of caffeinated beverages throughout the day, it will very likely improve her breast pain if she cuts back. This is especially true during the times of exacerbated pain prior to her menses.

In addition, recommend reduced dietary fat (overall good health). This is good advice for any patient. There were 2 small studies that showed improvement in breast pain with a 15% reduction in dietary fat.7,8

Finally, advise that patients stop smoking. Smoking aggravates and exacerbates fibrocystic changes, and these will lead to more breast pain.

Medical management. Over-the-counter medications that are found in the vitamin section of a local drug store are vitamin E and evening primrose oil. There are no significant adverse effects with these treatments. Their efficacy is theoretical, however; 3 randomized controlled trials demonstrated no significant clinical benefit with evening primrose oil versus placebo for treatment of mastalgia.14

Topical or oral nonsteroidal anti-inflammatory drugs (NSAIDs; Voltaren gel, topical compound pain creams) are useful as second-line management after using a supportive bra. Three randomized controlled trials have demonstrated up to 90% improvement of mastalgia with topical NSAIDs.15-17

Tamoxifen is a selective estrogen-receptor modulator (SERM), which is an antagonist to the estrogen receptor (ER) in the breast and an agonist to the ER in the endometrium. Tamoxifen has been found to reduce symptoms of mastalgia by 70% even at a lower dosage of 10-mg per day (for 6 months), or as a topical gel (afimoxifene). The oral form can have some adverse effects, including hot flashes, and has a low risk for thromboembolic events and endometrial neoplasia.18-20

Danazol is very effective in reducing breast pain symptoms (by 80%), with a higher relapse after stopping the medication. Danazol is less tolerated due to its androgenic effects, such as hirsutism, acne, menorrhagia, and voice changes. Both danazol and tamoxifen can be teratogenic and should be used with caution in women of child-bearing age.21

Finally, bromocriptine inhibits serum prolactin and has been reported to provide 65% improvement in breast pain. Its use for breast pain is not US Food and Drug Administration–approved and adverse effects include nausea, dizziness, and hypotension.22

Tamoxifen, danazol, and bromocriptine can be considered as third-line management options for severe treatment-resistant mastalgia.

Continue to: FIGURE 2 Treatment algorithm for breast pain...

 

 

In summary

Evaluation and counseling for breast pain should be managed by women’s health care providers in a primary care setting. Most patients need reassurance and medical explanation of their symptoms. They should be educated that more than 95% of the time breast pain is not caused by an underlying malignancy but rather due to hormonal and fibrocystic changes, which can be managed conservatively. If the clinical breast examination and recent screening mammogram (in women over age 40) results are negative, patients should be educated that their pain is benign and undergo a trial of conservative measures: wear and sleep in a supporting bra; keep a calendar of symptoms to determine any relation to cyclical changes; and avoid nicotine, caffeine, and fatty food. Topical pain creams with diclofenac and evening primrose oil also can be effective in ameliorating the symptoms. Breast pain is not a surgical disease; referral to a surgical specialist and diagnostic imaging can be unnecessary and expensive.

 

References
  1. Scurr J, Hedger W, Morris P, et al.  The prevalence, severity, and impact of breast pain in the general population. Breast J. 2014;20:508-513. 
  2. Davies EL, Gateley CA, Miers M, et al. The long-term course of mastalgia. J R Soc Med. 1998;91:462-464. 
  3. Singletary SE, Robb GL, Hortobagy GN. Advanced Therapy of Breast Disease. 2nd ed.  Ontario, Canada: BC Decker Inc.; 2004.  
  4. Gong C, Song E, Jia W, et al. A double-blind randomized controlled trial of toremifen therapy for mastaglia. Arch Surg. 2006;141:43-47. 
  5. Kumar S, Mansel RE, Scanlon MF, et al. Altered responses of prolactin, luteinizing hormone and follicle stimulating hormone secretion to thyrotrophin releasing hormone/gonadotrophin releasing hormone stimulation in cyclical mastalgia. Br J Surg. 1984;71:870-873.  
  6. Mansel RE, Dogliotti L.  European multicentre trial of bromocriptine in cyclical mastalgia. Lancet. 1990;335:190-193. 
  7. Rose DP, Boyar AP, Cohen C, et al. Effect of a low-fat diet on hormone levels in women with cystic breast disease. I. Serum steroids and gonadotropins. J Natl Cancer Inst. 1987;78:623-626. 
  8. Goodwin JP, Miller A, Del Giudice ME, et al. Elevated high-density lipoprotein cholesterol and dietary fat intake in women with cyclic mastopathy. Am J Obstet Gynecol. 1998;179:430-437. 
  9. Goyal A, Mansel RE. Efamast Study Group. A randomized multicenter study of gamolenic acid (Efamast) with and without antioxidant vitamins and minerals in the management of mastalgia. Breast J. 2005;11(1):41-47. 
  10. Parsay S, Olfati F, Nahidi S. Therapeutic effects of vitamin E on cyclic mastalgia. Breast J.  2009;15:510-514. 
  11. Allen SS, Froberg DG. The effect of decreased caffeine consumption on benign proliferative breast disease: a randomized clinical trial. Surgery. 1987;101:720-730. 
  12. Hadi MS. Sports brassiere: is it a solution for mastalgia? Breast J. 2000;6:407-409. 
  13. Russell LC.  Caffeine restriction as initial treatment for breast pain. Nurse Pract. 1989; 14(2): 36-7. 
  14. Srivastava A, Mansel RE, Arvind N, et al. Evidence-based management of mastalgia: a meta-analysis of randomised trials. Breast. 2007;16:503-512. 
  15. Irving AD, Morrison SL. Effectiveness of topical non-steroidal anti-inflammatory drugs in the management of breast pain. J R Coll Surg Edinb. 1998;43:158-159. 
  16. Colak T, Ipek T, Kanik A, et al. Efficiency of topical nonsteroidal anti-inflammatory drugs in mastalgia treatment. J Am Coll Surg. 2003;196(4):525-530. 
  17. Kaviani A, Mehrdad N, Najafi M, et al. Comparison of naproxen with placebo for the management of noncyclical breast pain: a randomized, double-blind, controlled trial. World J Surg. 2008;32:2464-2470. 
  18. Fentiman IS, Caleffi M, Brame K, et al. Double-blind controlled trial of tamoxifen therapy for mastalgia. Lancet. 1986;1:287-288. 
  19. Jain BK, Bansal A, Choudhary D, et al. Centchroman vs tamoxifen for regression of mastalgia: a randomized controlled trial. Intl J Surg. 2015;15:11-16. 
  20. Mansel R, Goyal A, Le Nestour EL, et al; Afimoxifene (4-OHT) Breast Pain Research group. A phase II trial of Afimoxifene (4-hydroxyamoxifen gel) for cyclical mastalgia in premenopausal women. Breast Cancer Res Treat. 2007;106:389-397. 
  21. O'Brien PM, Abukhalil IE. Randomized controlled trial of the management of premenstrual syndrome and premenstrual mastalgia using luteal phase-only danazol. Am J Obstet Gynecol. 1999;180:18-23. 
  22. Blichert-Toft M, Andersen AN, Henriksen OB, et al. Treatment of mastalgia with bromocriptine: a double-blind cross-over study. Br Med J. 1979;1:237.
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Breast pain is one of the most common breast-related patient complaints and is found to affect at least 50% of the female population.1 Most cases are self-limiting and are related to hormonal and normal fibrocystic changes. The median age of onset of symptoms is 36 years, with most women experiencing pain for 5 to 12 years.2 Because the cause of breast pain is not always clear, its presence can produce anxiety in patients and physicians over the possibility of underlying malignancy. Although breast cancer is not associated with breast pain, many patients presenting with pain are referred for diagnostic imaging (usually with negative results). The majority of women with mastalgia and normal clinical examination findings can be reassured with education about the many benign causes of breast pain.

What are causes of breast pain without an imaging abnormality?

Hormones. Mastalgia can be focal or generalized and is mostly due to hormonal changes. Elevated estrogen can stimulate the growth of breast tissue, which is known as epithelial hyperplasia.3 Fluctuations in hormone levels can occur in perimenopausal women in their forties and can result in new symptoms of breast pain.4 Sometimes starting a new contraceptive medication or hormone replacement therapy can exacerbate the pain. Switching brands or medications may help. Another cause of mastalgia may be elevated prolactin levels, with hypothalamic-pituitary dysfunction.5,6

Diet. There is evidence to link a high-fat diet with breast pain. The pain has been shown to improve when lipid intake is reduced and high- and low-density lipoprotein cholesterol levels are normalized. As estrogen is a steroid hormone that can be synthesized from lipids and fatty acids, elevated lipid metabolism can increase estrogen levels and exacerbate breast pain symptoms.7,8 Essential fatty acids, such as evening primrose oil and vitamin E, have been used to treat mastalgia because they reduce inflammation in fatty breast tissue through the prostaglandin pathway.9,10

Caffeine. Methylxanthines can be found in coffee, tea, and chocolate and can aggravate mastalgia by enhancing the cyclin adenosine monophosphate (cAMP) pathway. This pathway stimulates cellular proliferation and fibrocystic changes which in turn can exacerbate breast pain.11

Smoking. In my clinical practice I have clearly noted a higher incidence of breast pain in patients who smoke. The pain tends to improve significantly when the patient quits or even cuts back on smoking. The exact reasons for smoking’s effects on breast pain are not well known; however, they are thought to be related to acceleration of the cAMP pathway.

Large breast size. Very large breasts will strain and weaken the suspensory ligaments, leading to pain and discomfort. It has been shown that wearing a supportive sports bra during episodes of breast pain is effective.

Types of breast pain

Cyclical

Women with fibrocystic breasts tend to experience more breast pain. Breast sensitivity can be localized to the upper outer quadrants or to the nipple and sub-areolar area. It also can be generalized. The pain tends to peak with ovulation, improve with menses, and to recur every few weeks. Patients who have had partial hysterectomy (with ovaries in situ) or endometrial ablation will be unable to correlate their symptoms to menstruation. Therefore, women are encouraged to keep a diary or calendar of their symptoms to detect any correlation with their ovarian cycle. Such correlation is reassuring.

Continue to: Noncyclical...

 

 

Noncyclical

Noncyclical breast pain is not associated with the menstrual cycle and can be unilateral or bilateral. Providers should perform a good history of patients presenting with noncyclicalbreast pain, to include character, onset, duration, location, radiation, alleviating, and aggravating factors. A physical examination may elicit point tenderness at the chest by pushing the breast tissue off of the chest wall while the patient is in supine position and pressing directly over the ribs. Lack of tenderness on palpation of the breast parenchyma, but pain on the chest wall, points to a musculoskeletal etiology. Chest wall pain may be related to muscle spasm or muscle strain, trauma, rib fracture, or costochondritis (Tietze syndrome). Finally, based on history of review of systems and physical examination, referred pain from biliary or cardiac etiology should be considered.

When breast pain occurs with skin changes

Skin changes usually have an underlying pathology. Infectious processes, such as infected epidermal inclusion cyst, hidradenitis of the cleavage and inframammary crease, or breast abscess will present with pain and induration with an acute onset of 5 to 10 days. Large pendulous breasts may develop yeast infection at the inframammary crease. Chronic infectious irritation can lead to hyperpigmentation of that area. Eczema or contact dermatitis frequently can affect the areola and become confused with Paget disease (ductal carcinoma in situ of the nipple). With Paget, the excoriation always starts at the nipple and can then spread to the areola. However, with dermatitis, the rash begins on the peri-areolar skin, without affecting the nipple itself.

When breast pain occurs with nipple discharge

Breast pain with nipple discharge usually is bilateral and more common in patients with significant fibrocystic changes who smoke. If the nipple discharge is bilateral, serous and non-bloody, and multiduct, it is considered benign and physiologic. Physiologic nipple discharge can be multifactorial and hormonal. It may be related to thyroid disorders or medications such as antidepressants, selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, or antipsychotics. The only nipple discharge that is considered pathologic is unilateral spontaneous bloody discharge for which diagnostic imaging and breast surgeon referral is indicated. Women should be discouraged from self-expressing their nipples, as 80% will experience serous nipple discharge upon manual self-expression.

Should I order breast imaging for my patient with breast pain and a normal clinical breast exam?

Breast pain is not associated with breast cancer. Most breast cancers do not hurt; they present as firm, painless masses. However, when a woman notices pain in her breast, her first concern is breast cancer. This concern is re-enforced by the medical provider whose first impulse is to order diagnostic imaging. Yet less than 3% of breast cancers are associated with breast pain.

There have been multiple published retrospective and prospective radiologic studies about the utility of breast imaging in women with breast pain without a palpable mass. All of the studies have demonstrated that breast imaging with mammography and ultrasonography in these patients yields mostly negative or benign findings. The incidence of breast cancer during imaging work-up in women with breast pain and no clinical abnormality is only 0.4% to 1.8%.1-3 Some patients may develop future subsequent breast cancer in the symptomatic breast. But this is considered incidental and possibly related to increased cell turnover related to fibrocystic changes. Breast imaging for evaluation of breast pain only provides reassurance to the physician. The patient's reassurance will come from a medical explanation for the symptoms and advice on symptom management from the provider.

Researchers from MD Anderson Cancer Center reported imaging findings and cost analysis for 799 patients presenting with breast pain from 3 large network community-based breast imaging centers in 2014. Breast ultrasound was the initial imaging modality for women younger than age 30. Digital mammography (sometimes with tomosynthesis) was used for those older than age 30 that had not had a mammogram in the last 6 months. Breast magnetic resonance imaging was performed only when ordered by the referring physician. Most of the patients presented for diagnostic imaging, and 95% had negative findings and 5% had a benign finding. Only 1 patient was found to have an incidental cancer in the contralateral breast, which was detected by tomosynthesis. The cost of breast imaging was $87,322 in younger women and $152,732 in women older than age 40, representing overutilization of health care resources and no association between breast pain and breast cancer.4

References

  1. Chetlan AL, Kapoor MM, Watts MR. Mastalgia: imaging work-up appropriateness. Acad Radiol. 2017;24:345-349.
  2. Arslan M, Kücükerdem HS, Can H, et al. Retrospective analysis of women with only mastalgia. J Breast Health. 2016;12:151-154.
  3. Noroozian M, Stein LF, Gaetke-Udager K, et al. Long-term clinical outcomes in women with breast pain in the absence of additional clinical findings: Mammography remains indicated. Breast Cancer Res Treat. 2015;149:417-424.
  4. Kushwaha AC, Shin K, Kalambo M, et al. Overutilization of health care resources for breast pain. AJR Am J Roentgenol. 2018; 211:217-223.
 

Management of mastalgia

Appropriate breast pain management begins with a good history and physical examination. The decision to perform imaging should depend on clinical exam findings and not on symptoms of breast pain. If there is a palpable mass, then breast imaging and possible biopsy is appropriate. However, if clinical exam is normal, there is no indication for breast imaging in low-risk women under the age of 40 whose only symptom is breast pain. Women older than age 40 can undergo diagnostic imaging, if they have not had a negative screening mammogram in the past year.

Breast pain with abnormal clinical exam

In the patient who is younger than age 30 with a palpable mass. For this patient order targeted breast ultrasound (US) (FIGURE 1). If results are negative, repeat the clinical examination 1 week after menses. If the mass is persistent, refer the patient to a breast surgeon. If diagnostic imaging results are negative, consider breast MRI, especially if there is a strong family history of breast cancer.

In the patient who is aged 30 and older with a palpable mass. For this patient, bilateral diagnostic mammogram and US are in order. The testing is best performed 1 week after menses to reduce false-positive findings. If imaging is negative and the patient still has a clinically suspicious finding or mass, refer her to a breast surgeon and consider breast MRI. At this point if there is a persistent firm dominant mass, a biopsy is indicated as part of the triple test. If the mass resolves with menses, the patient can be reassured that the cause is most likely benign, with clinical examination repeated in 3 months.

Continue to: Breast pain and normal clinical exam...

 

 

Breast pain and normal clinical exam

When women who report breast pain have normal clinical examination findings (and have a negative screening mammogram in the past 12 months if older than age 40), there are several management strategies you can offer (FIGURE 2).

Reassurance and education. The majority of women with breast pain can be managed with reassurance and education, which are often sufficient to reduce their anxieties.

Supportive bra. The most effective intervention is to wear and sleep in a well-fitted supportive sports bra for 4 to 12 weeks. In a nonrandomized single-center trial of danazol versus sports bra, 85% of women reported relief of their breast pain with bra alone (vs 58% with danazol).12 A supportive bra is the first-line management of mastalgia (Level II evidence).

Symptom diary/calendar. Many women do not know whether or not their symptoms correspond to their ovarian cycle or are related to hormonal fluctuations. Therefore, it is reassuring and informative for them to keep a calendar or a diary of their symptoms to determine whether their symptoms occur or are exacerbated in a cyclical pattern.

Diet and lifestyle modification. Women should avoid caffeine (especially when having pain). Studies on methylxanthines have demonstrated some symptom relief with reducing caffeine intake.11,13 One cup of coffee or tea per day most likely will not make a difference. However, if a woman is drinking large quantities of caffeinated beverages throughout the day, it will very likely improve her breast pain if she cuts back. This is especially true during the times of exacerbated pain prior to her menses.

In addition, recommend reduced dietary fat (overall good health). This is good advice for any patient. There were 2 small studies that showed improvement in breast pain with a 15% reduction in dietary fat.7,8

Finally, advise that patients stop smoking. Smoking aggravates and exacerbates fibrocystic changes, and these will lead to more breast pain.

Medical management. Over-the-counter medications that are found in the vitamin section of a local drug store are vitamin E and evening primrose oil. There are no significant adverse effects with these treatments. Their efficacy is theoretical, however; 3 randomized controlled trials demonstrated no significant clinical benefit with evening primrose oil versus placebo for treatment of mastalgia.14

Topical or oral nonsteroidal anti-inflammatory drugs (NSAIDs; Voltaren gel, topical compound pain creams) are useful as second-line management after using a supportive bra. Three randomized controlled trials have demonstrated up to 90% improvement of mastalgia with topical NSAIDs.15-17

Tamoxifen is a selective estrogen-receptor modulator (SERM), which is an antagonist to the estrogen receptor (ER) in the breast and an agonist to the ER in the endometrium. Tamoxifen has been found to reduce symptoms of mastalgia by 70% even at a lower dosage of 10-mg per day (for 6 months), or as a topical gel (afimoxifene). The oral form can have some adverse effects, including hot flashes, and has a low risk for thromboembolic events and endometrial neoplasia.18-20

Danazol is very effective in reducing breast pain symptoms (by 80%), with a higher relapse after stopping the medication. Danazol is less tolerated due to its androgenic effects, such as hirsutism, acne, menorrhagia, and voice changes. Both danazol and tamoxifen can be teratogenic and should be used with caution in women of child-bearing age.21

Finally, bromocriptine inhibits serum prolactin and has been reported to provide 65% improvement in breast pain. Its use for breast pain is not US Food and Drug Administration–approved and adverse effects include nausea, dizziness, and hypotension.22

Tamoxifen, danazol, and bromocriptine can be considered as third-line management options for severe treatment-resistant mastalgia.

Continue to: FIGURE 2 Treatment algorithm for breast pain...

 

 

In summary

Evaluation and counseling for breast pain should be managed by women’s health care providers in a primary care setting. Most patients need reassurance and medical explanation of their symptoms. They should be educated that more than 95% of the time breast pain is not caused by an underlying malignancy but rather due to hormonal and fibrocystic changes, which can be managed conservatively. If the clinical breast examination and recent screening mammogram (in women over age 40) results are negative, patients should be educated that their pain is benign and undergo a trial of conservative measures: wear and sleep in a supporting bra; keep a calendar of symptoms to determine any relation to cyclical changes; and avoid nicotine, caffeine, and fatty food. Topical pain creams with diclofenac and evening primrose oil also can be effective in ameliorating the symptoms. Breast pain is not a surgical disease; referral to a surgical specialist and diagnostic imaging can be unnecessary and expensive.

 

Breast pain is one of the most common breast-related patient complaints and is found to affect at least 50% of the female population.1 Most cases are self-limiting and are related to hormonal and normal fibrocystic changes. The median age of onset of symptoms is 36 years, with most women experiencing pain for 5 to 12 years.2 Because the cause of breast pain is not always clear, its presence can produce anxiety in patients and physicians over the possibility of underlying malignancy. Although breast cancer is not associated with breast pain, many patients presenting with pain are referred for diagnostic imaging (usually with negative results). The majority of women with mastalgia and normal clinical examination findings can be reassured with education about the many benign causes of breast pain.

What are causes of breast pain without an imaging abnormality?

Hormones. Mastalgia can be focal or generalized and is mostly due to hormonal changes. Elevated estrogen can stimulate the growth of breast tissue, which is known as epithelial hyperplasia.3 Fluctuations in hormone levels can occur in perimenopausal women in their forties and can result in new symptoms of breast pain.4 Sometimes starting a new contraceptive medication or hormone replacement therapy can exacerbate the pain. Switching brands or medications may help. Another cause of mastalgia may be elevated prolactin levels, with hypothalamic-pituitary dysfunction.5,6

Diet. There is evidence to link a high-fat diet with breast pain. The pain has been shown to improve when lipid intake is reduced and high- and low-density lipoprotein cholesterol levels are normalized. As estrogen is a steroid hormone that can be synthesized from lipids and fatty acids, elevated lipid metabolism can increase estrogen levels and exacerbate breast pain symptoms.7,8 Essential fatty acids, such as evening primrose oil and vitamin E, have been used to treat mastalgia because they reduce inflammation in fatty breast tissue through the prostaglandin pathway.9,10

Caffeine. Methylxanthines can be found in coffee, tea, and chocolate and can aggravate mastalgia by enhancing the cyclin adenosine monophosphate (cAMP) pathway. This pathway stimulates cellular proliferation and fibrocystic changes which in turn can exacerbate breast pain.11

Smoking. In my clinical practice I have clearly noted a higher incidence of breast pain in patients who smoke. The pain tends to improve significantly when the patient quits or even cuts back on smoking. The exact reasons for smoking’s effects on breast pain are not well known; however, they are thought to be related to acceleration of the cAMP pathway.

Large breast size. Very large breasts will strain and weaken the suspensory ligaments, leading to pain and discomfort. It has been shown that wearing a supportive sports bra during episodes of breast pain is effective.

Types of breast pain

Cyclical

Women with fibrocystic breasts tend to experience more breast pain. Breast sensitivity can be localized to the upper outer quadrants or to the nipple and sub-areolar area. It also can be generalized. The pain tends to peak with ovulation, improve with menses, and to recur every few weeks. Patients who have had partial hysterectomy (with ovaries in situ) or endometrial ablation will be unable to correlate their symptoms to menstruation. Therefore, women are encouraged to keep a diary or calendar of their symptoms to detect any correlation with their ovarian cycle. Such correlation is reassuring.

Continue to: Noncyclical...

 

 

Noncyclical

Noncyclical breast pain is not associated with the menstrual cycle and can be unilateral or bilateral. Providers should perform a good history of patients presenting with noncyclicalbreast pain, to include character, onset, duration, location, radiation, alleviating, and aggravating factors. A physical examination may elicit point tenderness at the chest by pushing the breast tissue off of the chest wall while the patient is in supine position and pressing directly over the ribs. Lack of tenderness on palpation of the breast parenchyma, but pain on the chest wall, points to a musculoskeletal etiology. Chest wall pain may be related to muscle spasm or muscle strain, trauma, rib fracture, or costochondritis (Tietze syndrome). Finally, based on history of review of systems and physical examination, referred pain from biliary or cardiac etiology should be considered.

When breast pain occurs with skin changes

Skin changes usually have an underlying pathology. Infectious processes, such as infected epidermal inclusion cyst, hidradenitis of the cleavage and inframammary crease, or breast abscess will present with pain and induration with an acute onset of 5 to 10 days. Large pendulous breasts may develop yeast infection at the inframammary crease. Chronic infectious irritation can lead to hyperpigmentation of that area. Eczema or contact dermatitis frequently can affect the areola and become confused with Paget disease (ductal carcinoma in situ of the nipple). With Paget, the excoriation always starts at the nipple and can then spread to the areola. However, with dermatitis, the rash begins on the peri-areolar skin, without affecting the nipple itself.

When breast pain occurs with nipple discharge

Breast pain with nipple discharge usually is bilateral and more common in patients with significant fibrocystic changes who smoke. If the nipple discharge is bilateral, serous and non-bloody, and multiduct, it is considered benign and physiologic. Physiologic nipple discharge can be multifactorial and hormonal. It may be related to thyroid disorders or medications such as antidepressants, selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, or antipsychotics. The only nipple discharge that is considered pathologic is unilateral spontaneous bloody discharge for which diagnostic imaging and breast surgeon referral is indicated. Women should be discouraged from self-expressing their nipples, as 80% will experience serous nipple discharge upon manual self-expression.

Should I order breast imaging for my patient with breast pain and a normal clinical breast exam?

Breast pain is not associated with breast cancer. Most breast cancers do not hurt; they present as firm, painless masses. However, when a woman notices pain in her breast, her first concern is breast cancer. This concern is re-enforced by the medical provider whose first impulse is to order diagnostic imaging. Yet less than 3% of breast cancers are associated with breast pain.

There have been multiple published retrospective and prospective radiologic studies about the utility of breast imaging in women with breast pain without a palpable mass. All of the studies have demonstrated that breast imaging with mammography and ultrasonography in these patients yields mostly negative or benign findings. The incidence of breast cancer during imaging work-up in women with breast pain and no clinical abnormality is only 0.4% to 1.8%.1-3 Some patients may develop future subsequent breast cancer in the symptomatic breast. But this is considered incidental and possibly related to increased cell turnover related to fibrocystic changes. Breast imaging for evaluation of breast pain only provides reassurance to the physician. The patient's reassurance will come from a medical explanation for the symptoms and advice on symptom management from the provider.

Researchers from MD Anderson Cancer Center reported imaging findings and cost analysis for 799 patients presenting with breast pain from 3 large network community-based breast imaging centers in 2014. Breast ultrasound was the initial imaging modality for women younger than age 30. Digital mammography (sometimes with tomosynthesis) was used for those older than age 30 that had not had a mammogram in the last 6 months. Breast magnetic resonance imaging was performed only when ordered by the referring physician. Most of the patients presented for diagnostic imaging, and 95% had negative findings and 5% had a benign finding. Only 1 patient was found to have an incidental cancer in the contralateral breast, which was detected by tomosynthesis. The cost of breast imaging was $87,322 in younger women and $152,732 in women older than age 40, representing overutilization of health care resources and no association between breast pain and breast cancer.4

References

  1. Chetlan AL, Kapoor MM, Watts MR. Mastalgia: imaging work-up appropriateness. Acad Radiol. 2017;24:345-349.
  2. Arslan M, Kücükerdem HS, Can H, et al. Retrospective analysis of women with only mastalgia. J Breast Health. 2016;12:151-154.
  3. Noroozian M, Stein LF, Gaetke-Udager K, et al. Long-term clinical outcomes in women with breast pain in the absence of additional clinical findings: Mammography remains indicated. Breast Cancer Res Treat. 2015;149:417-424.
  4. Kushwaha AC, Shin K, Kalambo M, et al. Overutilization of health care resources for breast pain. AJR Am J Roentgenol. 2018; 211:217-223.
 

Management of mastalgia

Appropriate breast pain management begins with a good history and physical examination. The decision to perform imaging should depend on clinical exam findings and not on symptoms of breast pain. If there is a palpable mass, then breast imaging and possible biopsy is appropriate. However, if clinical exam is normal, there is no indication for breast imaging in low-risk women under the age of 40 whose only symptom is breast pain. Women older than age 40 can undergo diagnostic imaging, if they have not had a negative screening mammogram in the past year.

Breast pain with abnormal clinical exam

In the patient who is younger than age 30 with a palpable mass. For this patient order targeted breast ultrasound (US) (FIGURE 1). If results are negative, repeat the clinical examination 1 week after menses. If the mass is persistent, refer the patient to a breast surgeon. If diagnostic imaging results are negative, consider breast MRI, especially if there is a strong family history of breast cancer.

In the patient who is aged 30 and older with a palpable mass. For this patient, bilateral diagnostic mammogram and US are in order. The testing is best performed 1 week after menses to reduce false-positive findings. If imaging is negative and the patient still has a clinically suspicious finding or mass, refer her to a breast surgeon and consider breast MRI. At this point if there is a persistent firm dominant mass, a biopsy is indicated as part of the triple test. If the mass resolves with menses, the patient can be reassured that the cause is most likely benign, with clinical examination repeated in 3 months.

Continue to: Breast pain and normal clinical exam...

 

 

Breast pain and normal clinical exam

When women who report breast pain have normal clinical examination findings (and have a negative screening mammogram in the past 12 months if older than age 40), there are several management strategies you can offer (FIGURE 2).

Reassurance and education. The majority of women with breast pain can be managed with reassurance and education, which are often sufficient to reduce their anxieties.

Supportive bra. The most effective intervention is to wear and sleep in a well-fitted supportive sports bra for 4 to 12 weeks. In a nonrandomized single-center trial of danazol versus sports bra, 85% of women reported relief of their breast pain with bra alone (vs 58% with danazol).12 A supportive bra is the first-line management of mastalgia (Level II evidence).

Symptom diary/calendar. Many women do not know whether or not their symptoms correspond to their ovarian cycle or are related to hormonal fluctuations. Therefore, it is reassuring and informative for them to keep a calendar or a diary of their symptoms to determine whether their symptoms occur or are exacerbated in a cyclical pattern.

Diet and lifestyle modification. Women should avoid caffeine (especially when having pain). Studies on methylxanthines have demonstrated some symptom relief with reducing caffeine intake.11,13 One cup of coffee or tea per day most likely will not make a difference. However, if a woman is drinking large quantities of caffeinated beverages throughout the day, it will very likely improve her breast pain if she cuts back. This is especially true during the times of exacerbated pain prior to her menses.

In addition, recommend reduced dietary fat (overall good health). This is good advice for any patient. There were 2 small studies that showed improvement in breast pain with a 15% reduction in dietary fat.7,8

Finally, advise that patients stop smoking. Smoking aggravates and exacerbates fibrocystic changes, and these will lead to more breast pain.

Medical management. Over-the-counter medications that are found in the vitamin section of a local drug store are vitamin E and evening primrose oil. There are no significant adverse effects with these treatments. Their efficacy is theoretical, however; 3 randomized controlled trials demonstrated no significant clinical benefit with evening primrose oil versus placebo for treatment of mastalgia.14

Topical or oral nonsteroidal anti-inflammatory drugs (NSAIDs; Voltaren gel, topical compound pain creams) are useful as second-line management after using a supportive bra. Three randomized controlled trials have demonstrated up to 90% improvement of mastalgia with topical NSAIDs.15-17

Tamoxifen is a selective estrogen-receptor modulator (SERM), which is an antagonist to the estrogen receptor (ER) in the breast and an agonist to the ER in the endometrium. Tamoxifen has been found to reduce symptoms of mastalgia by 70% even at a lower dosage of 10-mg per day (for 6 months), or as a topical gel (afimoxifene). The oral form can have some adverse effects, including hot flashes, and has a low risk for thromboembolic events and endometrial neoplasia.18-20

Danazol is very effective in reducing breast pain symptoms (by 80%), with a higher relapse after stopping the medication. Danazol is less tolerated due to its androgenic effects, such as hirsutism, acne, menorrhagia, and voice changes. Both danazol and tamoxifen can be teratogenic and should be used with caution in women of child-bearing age.21

Finally, bromocriptine inhibits serum prolactin and has been reported to provide 65% improvement in breast pain. Its use for breast pain is not US Food and Drug Administration–approved and adverse effects include nausea, dizziness, and hypotension.22

Tamoxifen, danazol, and bromocriptine can be considered as third-line management options for severe treatment-resistant mastalgia.

Continue to: FIGURE 2 Treatment algorithm for breast pain...

 

 

In summary

Evaluation and counseling for breast pain should be managed by women’s health care providers in a primary care setting. Most patients need reassurance and medical explanation of their symptoms. They should be educated that more than 95% of the time breast pain is not caused by an underlying malignancy but rather due to hormonal and fibrocystic changes, which can be managed conservatively. If the clinical breast examination and recent screening mammogram (in women over age 40) results are negative, patients should be educated that their pain is benign and undergo a trial of conservative measures: wear and sleep in a supporting bra; keep a calendar of symptoms to determine any relation to cyclical changes; and avoid nicotine, caffeine, and fatty food. Topical pain creams with diclofenac and evening primrose oil also can be effective in ameliorating the symptoms. Breast pain is not a surgical disease; referral to a surgical specialist and diagnostic imaging can be unnecessary and expensive.

 

References
  1. Scurr J, Hedger W, Morris P, et al.  The prevalence, severity, and impact of breast pain in the general population. Breast J. 2014;20:508-513. 
  2. Davies EL, Gateley CA, Miers M, et al. The long-term course of mastalgia. J R Soc Med. 1998;91:462-464. 
  3. Singletary SE, Robb GL, Hortobagy GN. Advanced Therapy of Breast Disease. 2nd ed.  Ontario, Canada: BC Decker Inc.; 2004.  
  4. Gong C, Song E, Jia W, et al. A double-blind randomized controlled trial of toremifen therapy for mastaglia. Arch Surg. 2006;141:43-47. 
  5. Kumar S, Mansel RE, Scanlon MF, et al. Altered responses of prolactin, luteinizing hormone and follicle stimulating hormone secretion to thyrotrophin releasing hormone/gonadotrophin releasing hormone stimulation in cyclical mastalgia. Br J Surg. 1984;71:870-873.  
  6. Mansel RE, Dogliotti L.  European multicentre trial of bromocriptine in cyclical mastalgia. Lancet. 1990;335:190-193. 
  7. Rose DP, Boyar AP, Cohen C, et al. Effect of a low-fat diet on hormone levels in women with cystic breast disease. I. Serum steroids and gonadotropins. J Natl Cancer Inst. 1987;78:623-626. 
  8. Goodwin JP, Miller A, Del Giudice ME, et al. Elevated high-density lipoprotein cholesterol and dietary fat intake in women with cyclic mastopathy. Am J Obstet Gynecol. 1998;179:430-437. 
  9. Goyal A, Mansel RE. Efamast Study Group. A randomized multicenter study of gamolenic acid (Efamast) with and without antioxidant vitamins and minerals in the management of mastalgia. Breast J. 2005;11(1):41-47. 
  10. Parsay S, Olfati F, Nahidi S. Therapeutic effects of vitamin E on cyclic mastalgia. Breast J.  2009;15:510-514. 
  11. Allen SS, Froberg DG. The effect of decreased caffeine consumption on benign proliferative breast disease: a randomized clinical trial. Surgery. 1987;101:720-730. 
  12. Hadi MS. Sports brassiere: is it a solution for mastalgia? Breast J. 2000;6:407-409. 
  13. Russell LC.  Caffeine restriction as initial treatment for breast pain. Nurse Pract. 1989; 14(2): 36-7. 
  14. Srivastava A, Mansel RE, Arvind N, et al. Evidence-based management of mastalgia: a meta-analysis of randomised trials. Breast. 2007;16:503-512. 
  15. Irving AD, Morrison SL. Effectiveness of topical non-steroidal anti-inflammatory drugs in the management of breast pain. J R Coll Surg Edinb. 1998;43:158-159. 
  16. Colak T, Ipek T, Kanik A, et al. Efficiency of topical nonsteroidal anti-inflammatory drugs in mastalgia treatment. J Am Coll Surg. 2003;196(4):525-530. 
  17. Kaviani A, Mehrdad N, Najafi M, et al. Comparison of naproxen with placebo for the management of noncyclical breast pain: a randomized, double-blind, controlled trial. World J Surg. 2008;32:2464-2470. 
  18. Fentiman IS, Caleffi M, Brame K, et al. Double-blind controlled trial of tamoxifen therapy for mastalgia. Lancet. 1986;1:287-288. 
  19. Jain BK, Bansal A, Choudhary D, et al. Centchroman vs tamoxifen for regression of mastalgia: a randomized controlled trial. Intl J Surg. 2015;15:11-16. 
  20. Mansel R, Goyal A, Le Nestour EL, et al; Afimoxifene (4-OHT) Breast Pain Research group. A phase II trial of Afimoxifene (4-hydroxyamoxifen gel) for cyclical mastalgia in premenopausal women. Breast Cancer Res Treat. 2007;106:389-397. 
  21. O'Brien PM, Abukhalil IE. Randomized controlled trial of the management of premenstrual syndrome and premenstrual mastalgia using luteal phase-only danazol. Am J Obstet Gynecol. 1999;180:18-23. 
  22. Blichert-Toft M, Andersen AN, Henriksen OB, et al. Treatment of mastalgia with bromocriptine: a double-blind cross-over study. Br Med J. 1979;1:237.
References
  1. Scurr J, Hedger W, Morris P, et al.  The prevalence, severity, and impact of breast pain in the general population. Breast J. 2014;20:508-513. 
  2. Davies EL, Gateley CA, Miers M, et al. The long-term course of mastalgia. J R Soc Med. 1998;91:462-464. 
  3. Singletary SE, Robb GL, Hortobagy GN. Advanced Therapy of Breast Disease. 2nd ed.  Ontario, Canada: BC Decker Inc.; 2004.  
  4. Gong C, Song E, Jia W, et al. A double-blind randomized controlled trial of toremifen therapy for mastaglia. Arch Surg. 2006;141:43-47. 
  5. Kumar S, Mansel RE, Scanlon MF, et al. Altered responses of prolactin, luteinizing hormone and follicle stimulating hormone secretion to thyrotrophin releasing hormone/gonadotrophin releasing hormone stimulation in cyclical mastalgia. Br J Surg. 1984;71:870-873.  
  6. Mansel RE, Dogliotti L.  European multicentre trial of bromocriptine in cyclical mastalgia. Lancet. 1990;335:190-193. 
  7. Rose DP, Boyar AP, Cohen C, et al. Effect of a low-fat diet on hormone levels in women with cystic breast disease. I. Serum steroids and gonadotropins. J Natl Cancer Inst. 1987;78:623-626. 
  8. Goodwin JP, Miller A, Del Giudice ME, et al. Elevated high-density lipoprotein cholesterol and dietary fat intake in women with cyclic mastopathy. Am J Obstet Gynecol. 1998;179:430-437. 
  9. Goyal A, Mansel RE. Efamast Study Group. A randomized multicenter study of gamolenic acid (Efamast) with and without antioxidant vitamins and minerals in the management of mastalgia. Breast J. 2005;11(1):41-47. 
  10. Parsay S, Olfati F, Nahidi S. Therapeutic effects of vitamin E on cyclic mastalgia. Breast J.  2009;15:510-514. 
  11. Allen SS, Froberg DG. The effect of decreased caffeine consumption on benign proliferative breast disease: a randomized clinical trial. Surgery. 1987;101:720-730. 
  12. Hadi MS. Sports brassiere: is it a solution for mastalgia? Breast J. 2000;6:407-409. 
  13. Russell LC.  Caffeine restriction as initial treatment for breast pain. Nurse Pract. 1989; 14(2): 36-7. 
  14. Srivastava A, Mansel RE, Arvind N, et al. Evidence-based management of mastalgia: a meta-analysis of randomised trials. Breast. 2007;16:503-512. 
  15. Irving AD, Morrison SL. Effectiveness of topical non-steroidal anti-inflammatory drugs in the management of breast pain. J R Coll Surg Edinb. 1998;43:158-159. 
  16. Colak T, Ipek T, Kanik A, et al. Efficiency of topical nonsteroidal anti-inflammatory drugs in mastalgia treatment. J Am Coll Surg. 2003;196(4):525-530. 
  17. Kaviani A, Mehrdad N, Najafi M, et al. Comparison of naproxen with placebo for the management of noncyclical breast pain: a randomized, double-blind, controlled trial. World J Surg. 2008;32:2464-2470. 
  18. Fentiman IS, Caleffi M, Brame K, et al. Double-blind controlled trial of tamoxifen therapy for mastalgia. Lancet. 1986;1:287-288. 
  19. Jain BK, Bansal A, Choudhary D, et al. Centchroman vs tamoxifen for regression of mastalgia: a randomized controlled trial. Intl J Surg. 2015;15:11-16. 
  20. Mansel R, Goyal A, Le Nestour EL, et al; Afimoxifene (4-OHT) Breast Pain Research group. A phase II trial of Afimoxifene (4-hydroxyamoxifen gel) for cyclical mastalgia in premenopausal women. Breast Cancer Res Treat. 2007;106:389-397. 
  21. O'Brien PM, Abukhalil IE. Randomized controlled trial of the management of premenstrual syndrome and premenstrual mastalgia using luteal phase-only danazol. Am J Obstet Gynecol. 1999;180:18-23. 
  22. Blichert-Toft M, Andersen AN, Henriksen OB, et al. Treatment of mastalgia with bromocriptine: a double-blind cross-over study. Br Med J. 1979;1:237.
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Maternal mortality: Critical next steps in addressing the crisis

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As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).1 It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.1

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.2 Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.2

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.3 Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.2 Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).3 Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”3 This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.6 Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

 

 

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

  • Expand Medicaid coverage to 1 year postpartum.
  • Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
  • Ensure the sharing of best practices of care across hospital systems.
  • Focus on culturally-competent care to address implicit bias among health care workers.
  • Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

References
  1. The Centers for Disease Control and Prevention. Pregnancy Mortality Surveillance System, Trends in Pregnancy-Related Deaths. https://www.cdc.gov/reproductivehealth/maternalinfanthealth/pregnancy-mortality-surveillance-system.htm. Accessed May 29, 2019.
  2. Stuebe A, Moore JE, Mittal P, et al. Extending medicaid coverage for postpartum moms. May 6, 2019. https://www.healthaffairs.org/do/10.1377/hblog20190501.254675/full/. Accessed May 29, 2019.
  3. Building U.S. Capacity to Review and Prevent Maternal Deaths. Report from nine maternal mortality review committees. 2018. Color/Word_R17_G85_B204http://reviewtoaction.org/Report_from_Nine_MMRCs. Accessed May 29, 2019.
  4. MacDorman MF, Declercq E, Cabral H, et al. Recent increases in the U.S. maternal mortality rate: disentangling trends from measurement issues. Obstet Gynecol. 2016;128:447-455.
  5. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2016. Natl Vital Stat Rep. 2018;67:1-55.
  6. Vestal C. For addicted women, the year after childbirth is the deadliest. August 14, 2018. https://www.pewtrusts.org/en/research-and-analysis/blogs/stateline/2018/08/14/for-addicted-women-the-year-after-childbirth-is-the-deadliest. Accessed May 29, 2019.
Author and Disclosure Information

Dr. Vainer is Resident, Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts.

Dr. Evans is Assistant Professor, Tufts University School of Medicine, and Associate Program Director, Department of Obstetrics and Gynecology, Tufts Medical Center.

The authors report no financial relationships relevant to this article.

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Dr. Vainer is Resident, Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts.

Dr. Evans is Assistant Professor, Tufts University School of Medicine, and Associate Program Director, Department of Obstetrics and Gynecology, Tufts Medical Center.

The authors report no financial relationships relevant to this article.

Author and Disclosure Information

Dr. Vainer is Resident, Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts.

Dr. Evans is Assistant Professor, Tufts University School of Medicine, and Associate Program Director, Department of Obstetrics and Gynecology, Tufts Medical Center.

The authors report no financial relationships relevant to this article.

As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).1 It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.1

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.2 Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.2

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.3 Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.2 Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).3 Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”3 This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.6 Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

 

 

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

  • Expand Medicaid coverage to 1 year postpartum.
  • Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
  • Ensure the sharing of best practices of care across hospital systems.
  • Focus on culturally-competent care to address implicit bias among health care workers.
  • Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).1 It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.1

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.2 Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.2

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.3 Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.2 Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).3 Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”3 This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.6 Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

 

 

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

  • Expand Medicaid coverage to 1 year postpartum.
  • Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
  • Ensure the sharing of best practices of care across hospital systems.
  • Focus on culturally-competent care to address implicit bias among health care workers.
  • Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

References
  1. The Centers for Disease Control and Prevention. Pregnancy Mortality Surveillance System, Trends in Pregnancy-Related Deaths. https://www.cdc.gov/reproductivehealth/maternalinfanthealth/pregnancy-mortality-surveillance-system.htm. Accessed May 29, 2019.
  2. Stuebe A, Moore JE, Mittal P, et al. Extending medicaid coverage for postpartum moms. May 6, 2019. https://www.healthaffairs.org/do/10.1377/hblog20190501.254675/full/. Accessed May 29, 2019.
  3. Building U.S. Capacity to Review and Prevent Maternal Deaths. Report from nine maternal mortality review committees. 2018. Color/Word_R17_G85_B204http://reviewtoaction.org/Report_from_Nine_MMRCs. Accessed May 29, 2019.
  4. MacDorman MF, Declercq E, Cabral H, et al. Recent increases in the U.S. maternal mortality rate: disentangling trends from measurement issues. Obstet Gynecol. 2016;128:447-455.
  5. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2016. Natl Vital Stat Rep. 2018;67:1-55.
  6. Vestal C. For addicted women, the year after childbirth is the deadliest. August 14, 2018. https://www.pewtrusts.org/en/research-and-analysis/blogs/stateline/2018/08/14/for-addicted-women-the-year-after-childbirth-is-the-deadliest. Accessed May 29, 2019.
References
  1. The Centers for Disease Control and Prevention. Pregnancy Mortality Surveillance System, Trends in Pregnancy-Related Deaths. https://www.cdc.gov/reproductivehealth/maternalinfanthealth/pregnancy-mortality-surveillance-system.htm. Accessed May 29, 2019.
  2. Stuebe A, Moore JE, Mittal P, et al. Extending medicaid coverage for postpartum moms. May 6, 2019. https://www.healthaffairs.org/do/10.1377/hblog20190501.254675/full/. Accessed May 29, 2019.
  3. Building U.S. Capacity to Review and Prevent Maternal Deaths. Report from nine maternal mortality review committees. 2018. Color/Word_R17_G85_B204http://reviewtoaction.org/Report_from_Nine_MMRCs. Accessed May 29, 2019.
  4. MacDorman MF, Declercq E, Cabral H, et al. Recent increases in the U.S. maternal mortality rate: disentangling trends from measurement issues. Obstet Gynecol. 2016;128:447-455.
  5. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2016. Natl Vital Stat Rep. 2018;67:1-55.
  6. Vestal C. For addicted women, the year after childbirth is the deadliest. August 14, 2018. https://www.pewtrusts.org/en/research-and-analysis/blogs/stateline/2018/08/14/for-addicted-women-the-year-after-childbirth-is-the-deadliest. Accessed May 29, 2019.
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