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The Journal of Family Practice is a peer-reviewed and indexed journal that provides its 95,000 family physician readers with timely, practical, and evidence-based information that they can immediately put into practice. Research and applied evidence articles, plus patient-oriented departments like Practice Alert, PURLs, and Clinical Inquiries can be found in print and at jfponline.com. The Web site, which logs an average of 125,000 visitors every month, also offers audiocasts by physician specialists and interactive features like Instant Polls and Photo Rounds Friday—a weekly diagnostic puzzle.
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
aeoluser
aeoluses
aeolusing
aeolusly
aeoluss
ahole
aholeed
aholeer
aholees
aholeing
aholely
aholes
alcohol
alcoholed
alcoholer
alcoholes
alcoholing
alcoholly
alcohols
allman
allmaned
allmaner
allmanes
allmaning
allmanly
allmans
alted
altes
alting
altly
alts
analed
analer
anales
analing
anally
analprobe
analprobeed
analprobeer
analprobees
analprobeing
analprobely
analprobes
anals
anilingus
anilingused
anilinguser
anilinguses
anilingusing
anilingusly
anilinguss
anus
anused
anuser
anuses
anusing
anusly
anuss
areola
areolaed
areolaer
areolaes
areolaing
areolaly
areolas
areole
areoleed
areoleer
areolees
areoleing
areolely
areoles
arian
arianed
arianer
arianes
arianing
arianly
arians
aryan
aryaned
aryaner
aryanes
aryaning
aryanly
aryans
asiaed
asiaer
asiaes
asiaing
asialy
asias
ass
ass hole
ass lick
ass licked
ass licker
ass lickes
ass licking
ass lickly
ass licks
assbang
assbanged
assbangeded
assbangeder
assbangedes
assbangeding
assbangedly
assbangeds
assbanger
assbanges
assbanging
assbangly
assbangs
assbangsed
assbangser
assbangses
assbangsing
assbangsly
assbangss
assed
asser
asses
assesed
asseser
asseses
assesing
assesly
assess
assfuck
assfucked
assfucker
assfuckered
assfuckerer
assfuckeres
assfuckering
assfuckerly
assfuckers
assfuckes
assfucking
assfuckly
assfucks
asshat
asshated
asshater
asshates
asshating
asshatly
asshats
assholeed
assholeer
assholees
assholeing
assholely
assholes
assholesed
assholeser
assholeses
assholesing
assholesly
assholess
assing
assly
assmaster
assmastered
assmasterer
assmasteres
assmastering
assmasterly
assmasters
assmunch
assmunched
assmuncher
assmunches
assmunching
assmunchly
assmunchs
asss
asswipe
asswipeed
asswipeer
asswipees
asswipeing
asswipely
asswipes
asswipesed
asswipeser
asswipeses
asswipesing
asswipesly
asswipess
azz
azzed
azzer
azzes
azzing
azzly
azzs
babeed
babeer
babees
babeing
babely
babes
babesed
babeser
babeses
babesing
babesly
babess
ballsac
ballsaced
ballsacer
ballsaces
ballsacing
ballsack
ballsacked
ballsacker
ballsackes
ballsacking
ballsackly
ballsacks
ballsacly
ballsacs
ballsed
ballser
ballses
ballsing
ballsly
ballss
barf
barfed
barfer
barfes
barfing
barfly
barfs
bastard
bastarded
bastarder
bastardes
bastarding
bastardly
bastards
bastardsed
bastardser
bastardses
bastardsing
bastardsly
bastardss
bawdy
bawdyed
bawdyer
bawdyes
bawdying
bawdyly
bawdys
beaner
beanered
beanerer
beaneres
beanering
beanerly
beaners
beardedclam
beardedclamed
beardedclamer
beardedclames
beardedclaming
beardedclamly
beardedclams
beastiality
beastialityed
beastialityer
beastialityes
beastialitying
beastialityly
beastialitys
beatch
beatched
beatcher
beatches
beatching
beatchly
beatchs
beater
beatered
beaterer
beateres
beatering
beaterly
beaters
beered
beerer
beeres
beering
beerly
beeyotch
beeyotched
beeyotcher
beeyotches
beeyotching
beeyotchly
beeyotchs
beotch
beotched
beotcher
beotches
beotching
beotchly
beotchs
biatch
biatched
biatcher
biatches
biatching
biatchly
biatchs
big tits
big titsed
big titser
big titses
big titsing
big titsly
big titss
bigtits
bigtitsed
bigtitser
bigtitses
bigtitsing
bigtitsly
bigtitss
bimbo
bimboed
bimboer
bimboes
bimboing
bimboly
bimbos
bisexualed
bisexualer
bisexuales
bisexualing
bisexually
bisexuals
bitch
bitched
bitcheded
bitcheder
bitchedes
bitcheding
bitchedly
bitcheds
bitcher
bitches
bitchesed
bitcheser
bitcheses
bitchesing
bitchesly
bitchess
bitching
bitchly
bitchs
bitchy
bitchyed
bitchyer
bitchyes
bitchying
bitchyly
bitchys
bleached
bleacher
bleaches
bleaching
bleachly
bleachs
blow job
blow jobed
blow jober
blow jobes
blow jobing
blow jobly
blow jobs
blowed
blower
blowes
blowing
blowjob
blowjobed
blowjober
blowjobes
blowjobing
blowjobly
blowjobs
blowjobsed
blowjobser
blowjobses
blowjobsing
blowjobsly
blowjobss
blowly
blows
boink
boinked
boinker
boinkes
boinking
boinkly
boinks
bollock
bollocked
bollocker
bollockes
bollocking
bollockly
bollocks
bollocksed
bollockser
bollockses
bollocksing
bollocksly
bollockss
bollok
bolloked
bolloker
bollokes
bolloking
bollokly
bolloks
boner
bonered
bonerer
boneres
bonering
bonerly
boners
bonersed
bonerser
bonerses
bonersing
bonersly
bonerss
bong
bonged
bonger
bonges
bonging
bongly
bongs
boob
boobed
boober
boobes
boobies
boobiesed
boobieser
boobieses
boobiesing
boobiesly
boobiess
boobing
boobly
boobs
boobsed
boobser
boobses
boobsing
boobsly
boobss
booby
boobyed
boobyer
boobyes
boobying
boobyly
boobys
booger
boogered
boogerer
boogeres
boogering
boogerly
boogers
bookie
bookieed
bookieer
bookiees
bookieing
bookiely
bookies
bootee
booteeed
booteeer
booteees
booteeing
booteely
bootees
bootie
bootieed
bootieer
bootiees
bootieing
bootiely
booties
booty
bootyed
bootyer
bootyes
bootying
bootyly
bootys
boozeed
boozeer
boozees
boozeing
boozely
boozer
boozered
boozerer
boozeres
boozering
boozerly
boozers
boozes
boozy
boozyed
boozyer
boozyes
boozying
boozyly
boozys
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
bukkakely
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
clitsing
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
cumminer
cummines
cumming
cumminged
cumminger
cumminges
cumminging
cummingly
cummings
cummining
cumminly
cummins
cums
cumshot
cumshoted
cumshoter
cumshotes
cumshoting
cumshotly
cumshots
cumshotsed
cumshotser
cumshotses
cumshotsing
cumshotsly
cumshotss
cumslut
cumsluted
cumsluter
cumslutes
cumsluting
cumslutly
cumsluts
cumstain
cumstained
cumstainer
cumstaines
cumstaining
cumstainly
cumstains
cunilingus
cunilingused
cunilinguser
cunilinguses
cunilingusing
cunilingusly
cunilinguss
cunnilingus
cunnilingused
cunnilinguser
cunnilinguses
cunnilingusing
cunnilingusly
cunnilinguss
cunny
cunnyed
cunnyer
cunnyes
cunnying
cunnyly
cunnys
cunt
cunted
cunter
cuntes
cuntface
cuntfaceed
cuntfaceer
cuntfacees
cuntfaceing
cuntfacely
cuntfaces
cunthunter
cunthuntered
cunthunterer
cunthunteres
cunthuntering
cunthunterly
cunthunters
cunting
cuntlick
cuntlicked
cuntlicker
cuntlickered
cuntlickerer
cuntlickeres
cuntlickering
cuntlickerly
cuntlickers
cuntlickes
cuntlicking
cuntlickly
cuntlicks
cuntly
cunts
cuntsed
cuntser
cuntses
cuntsing
cuntsly
cuntss
dago
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
damnits
damnly
damns
dick
dickbag
dickbaged
dickbager
dickbages
dickbaging
dickbagly
dickbags
dickdipper
dickdippered
dickdipperer
dickdipperes
dickdippering
dickdipperly
dickdippers
dicked
dicker
dickes
dickface
dickfaceed
dickfaceer
dickfacees
dickfaceing
dickfacely
dickfaces
dickflipper
dickflippered
dickflipperer
dickflipperes
dickflippering
dickflipperly
dickflippers
dickhead
dickheaded
dickheader
dickheades
dickheading
dickheadly
dickheads
dickheadsed
dickheadser
dickheadses
dickheadsing
dickheadsly
dickheadss
dicking
dickish
dickished
dickisher
dickishes
dickishing
dickishly
dickishs
dickly
dickripper
dickrippered
dickripperer
dickripperes
dickrippering
dickripperly
dickrippers
dicks
dicksipper
dicksippered
dicksipperer
dicksipperes
dicksippering
dicksipperly
dicksippers
dickweed
dickweeded
dickweeder
dickweedes
dickweeding
dickweedly
dickweeds
dickwhipper
dickwhippered
dickwhipperer
dickwhipperes
dickwhippering
dickwhipperly
dickwhippers
dickzipper
dickzippered
dickzipperer
dickzipperes
dickzippering
dickzipperly
dickzippers
diddle
diddleed
diddleer
diddlees
diddleing
diddlely
diddles
dike
dikeed
dikeer
dikees
dikeing
dikely
dikes
dildo
dildoed
dildoer
dildoes
dildoing
dildoly
dildos
dildosed
dildoser
dildoses
dildosing
dildosly
dildoss
diligaf
diligafed
diligafer
diligafes
diligafing
diligafly
diligafs
dillweed
dillweeded
dillweeder
dillweedes
dillweeding
dillweedly
dillweeds
dimwit
dimwited
dimwiter
dimwites
dimwiting
dimwitly
dimwits
dingle
dingleed
dingleer
dinglees
dingleing
dinglely
dingles
dipship
dipshiped
dipshiper
dipshipes
dipshiping
dipshiply
dipships
dizzyed
dizzyer
dizzyes
dizzying
dizzyly
dizzys
doggiestyleed
doggiestyleer
doggiestylees
doggiestyleing
doggiestylely
doggiestyles
doggystyleed
doggystyleer
doggystylees
doggystyleing
doggystylely
doggystyles
dong
donged
donger
donges
donging
dongly
dongs
doofus
doofused
doofuser
doofuses
doofusing
doofusly
doofuss
doosh
dooshed
doosher
dooshes
dooshing
dooshly
dooshs
dopeyed
dopeyer
dopeyes
dopeying
dopeyly
dopeys
douchebag
douchebaged
douchebager
douchebages
douchebaging
douchebagly
douchebags
douchebagsed
douchebagser
douchebagses
douchebagsing
douchebagsly
douchebagss
doucheed
doucheer
douchees
doucheing
douchely
douches
douchey
doucheyed
doucheyer
doucheyes
doucheying
doucheyly
doucheys
drunk
drunked
drunker
drunkes
drunking
drunkly
drunks
dumass
dumassed
dumasser
dumasses
dumassing
dumassly
dumasss
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
dykes
dykesed
dykeser
dykeses
dykesing
dykesly
dykess
erotic
eroticed
eroticer
erotices
eroticing
eroticly
erotics
extacy
extacyed
extacyer
extacyes
extacying
extacyly
extacys
extasy
extasyed
extasyer
extasyes
extasying
extasyly
extasys
fack
facked
facker
fackes
facking
fackly
facks
fag
faged
fager
fages
fagg
fagged
faggeded
faggeder
faggedes
faggeding
faggedly
faggeds
fagger
fagges
fagging
faggit
faggited
faggiter
faggites
faggiting
faggitly
faggits
faggly
faggot
faggoted
faggoter
faggotes
faggoting
faggotly
faggots
faggs
faging
fagly
fagot
fagoted
fagoter
fagotes
fagoting
fagotly
fagots
fags
fagsed
fagser
fagses
fagsing
fagsly
fagss
faig
faiged
faiger
faiges
faiging
faigly
faigs
faigt
faigted
faigter
faigtes
faigting
faigtly
faigts
fannybandit
fannybandited
fannybanditer
fannybandites
fannybanditing
fannybanditly
fannybandits
farted
farter
fartes
farting
fartknocker
fartknockered
fartknockerer
fartknockeres
fartknockering
fartknockerly
fartknockers
fartly
farts
felch
felched
felcher
felchered
felcherer
felcheres
felchering
felcherly
felchers
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
fuckeres
fuckering
fuckerly
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rumper
rumpes
rumping
rumply
rumprammer
rumprammered
rumprammerer
rumprammeres
rumprammering
rumprammerly
rumprammers
rumps
rums
ruski
ruskied
ruskier
ruskies
ruskiing
ruskily
ruskis
sadism
sadismed
sadismer
sadismes
sadisming
sadismly
sadisms
sadist
sadisted
sadister
sadistes
sadisting
sadistly
sadists
scag
scaged
scager
scages
scaging
scagly
scags
scantily
scantilyed
scantilyer
scantilyes
scantilying
scantilyly
scantilys
schlong
schlonged
schlonger
schlonges
schlonging
schlongly
schlongs
scrog
scroged
scroger
scroges
scroging
scrogly
scrogs
scrot
scrote
scroted
scroteed
scroteer
scrotees
scroteing
scrotely
scroter
scrotes
scroting
scrotly
scrots
scrotum
scrotumed
scrotumer
scrotumes
scrotuming
scrotumly
scrotums
scrud
scruded
scruder
scrudes
scruding
scrudly
scruds
scum
scumed
scumer
scumes
scuming
scumly
scums
seaman
seamaned
seamaner
seamanes
seamaning
seamanly
seamans
seamen
seamened
seamener
seamenes
seamening
seamenly
seamens
seduceed
seduceer
seducees
seduceing
seducely
seduces
semen
semened
semener
semenes
semening
semenly
semens
shamedame
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shamedamely
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shit
shite
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stupidly
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sumofabiatched
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testicle
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thrusted
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toke
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tramp
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transsexualed
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transsexuales
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trashy
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tubgirl
tubgirled
tubgirler
tubgirles
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undies
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valiumed
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valiumes
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venous
virgined
virginer
virgines
virgining
virginly
virgins
vixen
vixened
vixener
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vixens
vodkaed
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voyeur
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wangs
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weenie
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weewee
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weeweeer
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weeweely
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weiner
weinered
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weinerly
weiners
weirdo
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weirdos
wench
wenched
wencher
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wenchly
wenchs
wetback
wetbacked
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wetbackes
wetbacking
wetbackly
wetbacks
whitey
whiteyed
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whiteyes
whiteying
whiteyly
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whiz
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whizly
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whoralicioused
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whoraliciouss
whore
whorealicious
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whorealiciouses
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whored
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whorehouses
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whores
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whoringes
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whoringly
whorings
wigger
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wiggerly
wiggers
woody
woodyed
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woodyes
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woodyly
woodys
wop
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wtf
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wtfly
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xxx
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xxxing
xxxly
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yeasty
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yeastyer
yeastyes
yeastying
yeastyly
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yobbo
yobboed
yobboer
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yobboly
yobbos
zoophile
zoophileed
zoophileer
zoophilees
zoophileing
zoophilely
zoophiles
anal
ass
ass lick
balls
ballsac
bisexual
bleach
causas
cheap
cost of miracles
cunt
display network stats
fart
fda and death
fda AND warn
fda AND warning
fda AND warns
feom
fuck
gfc
humira AND expensive
illegal
madvocate
masturbation
nuccitelli
overdose
porn
shit
snort
texarkana
abbvie
AbbVie
acid
addicted
addiction
adolescent
adult sites
Advocacy
advocacy
agitated states
AJO, postsurgical analgesic, knee, replacement, surgery
alcohol
amphetamine
androgen
antibody
apple cider vinegar
assistance
Assistance
association
at home
attorney
audit
ayurvedic
baby
ban
baricitinib
bed bugs
best
bible
bisexual
black
bleach
blog
bulimia nervosa
buy
cannabis
certificate
certification
certified
cervical cancer, concurrent chemoradiotherapy, intravoxel incoherent motion magnetic resonance imaging, MRI, IVIM, diffusion-weighted MRI, DWI
charlie sheen
cheap
cheapest
child
childhood
childlike
children
chronic fatigue syndrome
Cladribine Tablets
cocaine
cock
combination therapies, synergistic antitumor efficacy, pertuzumab, trastuzumab, ipilimumab, nivolumab, palbociclib, letrozole, lapatinib, docetaxel, trametinib, dabrafenib, carflzomib, lenalidomide
contagious
Cortical Lesions
cream
creams
crime
criminal
cure
dangerous
dangers
dasabuvir
Dasabuvir
dead
deadly
death
dementia
dependence
dependent
depression
dermatillomania
die
diet
Disability
Discount
discount
dog
drink
drug abuse
drug-induced
dying
eastern medicine
eat
ect
eczema
electroconvulsive therapy
electromagnetic therapy
electrotherapy
epa
epilepsy
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fake
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fatal
fatalities
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fibromyalgia
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Financial
fish oil
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free
Gabriel Pardo
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Giancarlo Comi
gilead
Gilead
glaucoma
Glenn S. Williams
Glenn Williams
Gloria Dalla Costa
gonorrhea
Greedy
greedy
guns
hallucinations
harvoni
Harvoni
herbal
herbs
heroin
herpes
Hidradenitis Suppurativa,
holistic
home
home remedies
home remedy
homeopathic
homeopathy
hydrocortisone
ice
image
images
job
kid
kids
kill
killer
laser
lawsuit
lawyer
ledipasvir
Ledipasvir
lesbian
lesions
lights
liver
lupus
marijuana
melancholic
memory loss
menopausal
mental retardation
military
milk
moisturizers
monoamine oxidase inhibitor drugs
MRI
MS
murder
national
natural
natural cure
natural cures
natural medications
natural medicine
natural medicines
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natural treatments
naturally
Needy
needy
Neurology Reviews
neuropathic
nightclub massacre
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oasis
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ombitasvir
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orlando shooting
overactive thyroid gland
overdose
overdosed
Paolo Preziosa
paritaprevir
Paritaprevir
pediatric
pedophile
photo
photos
picture
post partum
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pregnancy
pregnant
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prison
program
Program
Protest
protest
psychedelics
pulse nightclub
puppy
purchase
purchasing
rape
recall
recreational drug
Rehabilitation
Retinal Measurements
retrograde ejaculation
risperdal
ritonavir
Ritonavir
ritonavir with dasabuvir
robin williams
sales
sasquatch
schizophrenia
seizure
seizures
sex
sexual
sexy
shock treatment
silver
sleep disorders
smoking
sociopath
sofosbuvir
Sofosbuvir
sovaldi
ssri
store
sue
suicidal
suicide
supplements
support
Support
Support Path
teen
teenage
teenagers
Telerehabilitation
testosterone
Th17
Th17:FoxP3+Treg cell ratio
Th22
toxic
toxin
tragedy
treatment resistant
V Pak
vagina
velpatasvir
Viekira Pa
Viekira Pak
viekira pak
violence
virgin
vitamin
VPak
weight loss
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xxx
young adult
young adults
zoloft
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sofosbuvir
ritonavir with dasabuvir
discount
support path
program
ritonavir
greedy
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viekira pak
vpak
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needy
protest
abbvie
paritaprevir
ombitasvir
direct-acting antivirals
dasabuvir
gilead
fake-ovir
support
v pak
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harvoni
direct\-acting antivirals
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Anticipating a Problem Pregnancy
An Integrated System for the Recording and Retrieval of Medical Data in a Primary Care Setting: Part 4: Family Folders
Family Process and Family Practice
Publisher's Note
Definition of Family Medicine as an Academic Disipline: A Current Controversy
Rash with hair loss
The FP had never seen a condition like this before, so he used some online resources to come up with a differential diagnosis that included sarcoidosis, leprosy, drug eruption, and mycosis fungoides. Aside from an occasional drug eruption, the other conditions were ones that he had seen in textbooks only.
Based on that differential diagnosis, the FP decided to do a punch biopsy of the largest nodule, which was near the patient’s mouth. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report came back as folliculotropic mycosis fungoides. The FP researched the diagnosis and determined that this was a cutaneous T-cell lymphoma that involved hair follicles and tended to occur on the head and neck. This explained the patient’s hair loss in his beard and right eyebrow. While the prognosis for mycosis fungoides is quite good, the same cannot be said for the folliculotropic variant.
The FP referred the patient to Dermatology for further evaluation and treatment. In consultation with Hematology, the patient was treated with a potent topical steroid, chemotherapy, and narrowband ultraviolet B light therapy. His condition improved, but ongoing treatment and surveillance were needed.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Chacon G, Nayar A. Cutaneous T-cell lymphoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1124-1131.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
The FP had never seen a condition like this before, so he used some online resources to come up with a differential diagnosis that included sarcoidosis, leprosy, drug eruption, and mycosis fungoides. Aside from an occasional drug eruption, the other conditions were ones that he had seen in textbooks only.
Based on that differential diagnosis, the FP decided to do a punch biopsy of the largest nodule, which was near the patient’s mouth. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report came back as folliculotropic mycosis fungoides. The FP researched the diagnosis and determined that this was a cutaneous T-cell lymphoma that involved hair follicles and tended to occur on the head and neck. This explained the patient’s hair loss in his beard and right eyebrow. While the prognosis for mycosis fungoides is quite good, the same cannot be said for the folliculotropic variant.
The FP referred the patient to Dermatology for further evaluation and treatment. In consultation with Hematology, the patient was treated with a potent topical steroid, chemotherapy, and narrowband ultraviolet B light therapy. His condition improved, but ongoing treatment and surveillance were needed.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Chacon G, Nayar A. Cutaneous T-cell lymphoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1124-1131.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
The FP had never seen a condition like this before, so he used some online resources to come up with a differential diagnosis that included sarcoidosis, leprosy, drug eruption, and mycosis fungoides. Aside from an occasional drug eruption, the other conditions were ones that he had seen in textbooks only.
Based on that differential diagnosis, the FP decided to do a punch biopsy of the largest nodule, which was near the patient’s mouth. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report came back as folliculotropic mycosis fungoides. The FP researched the diagnosis and determined that this was a cutaneous T-cell lymphoma that involved hair follicles and tended to occur on the head and neck. This explained the patient’s hair loss in his beard and right eyebrow. While the prognosis for mycosis fungoides is quite good, the same cannot be said for the folliculotropic variant.
The FP referred the patient to Dermatology for further evaluation and treatment. In consultation with Hematology, the patient was treated with a potent topical steroid, chemotherapy, and narrowband ultraviolet B light therapy. His condition improved, but ongoing treatment and surveillance were needed.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Chacon G, Nayar A. Cutaneous T-cell lymphoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1124-1131.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
Large mass on shoulder
The FP was extremely concerned that this was a large melanoma due the lesion’s chaotic appearance, with multiple colors and an irregular border. Going through the ABCDE criteria, he noted that the lesion was Asymmetric, the Border was irregular, the Colors were varied, the Diameter was > 6 mm, and it was Enlarging by history.
With his dermatoscope attached to his smart phone, the FP looked at the lesion and took a photograph (Figure B). The image revealed a pigment network of the original nevus at 5:00 to 6:00 o’clock and extensions of the tumor due to in-transit metastases. Satellites were visible, especially in the top right and left corners. The FP noted the shiny white lines caused by collagen deposition found in growing tumors. (See “Dermoscopy in family medicine: A primer.”)
The FP knew that the mass needed to be biopsied, but because of its size, the best he could do would be to perform a partial biopsy. So on the day of presentation, the FP performed a 6-mm punch biopsy in the most raised area of the lesion to try and get sufficient depth and breadth for diagnosis and prognosis. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report indicated that the lesion was a nodular melanoma with a Breslow depth of 5.5 mm. This melanoma arose in a nevus, which occurs in about 30% of melanomas. Most melanomas arise de novo.
The FP referred the patient to a surgical oncologist for an excision with 2 cm margins and a sentinel lymph node biopsy. The sentinel node was in the right axilla and was remarkably negative despite the local in-transit metastases/satellites. One year after the original diagnosis was made, there was no evidence of metastatic disease and no new melanomas. The patient follows up with the dermatologist for skin and lymph node surveillance every 3 months.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Melanoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1112-1123.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
The FP was extremely concerned that this was a large melanoma due the lesion’s chaotic appearance, with multiple colors and an irregular border. Going through the ABCDE criteria, he noted that the lesion was Asymmetric, the Border was irregular, the Colors were varied, the Diameter was > 6 mm, and it was Enlarging by history.
With his dermatoscope attached to his smart phone, the FP looked at the lesion and took a photograph (Figure B). The image revealed a pigment network of the original nevus at 5:00 to 6:00 o’clock and extensions of the tumor due to in-transit metastases. Satellites were visible, especially in the top right and left corners. The FP noted the shiny white lines caused by collagen deposition found in growing tumors. (See “Dermoscopy in family medicine: A primer.”)
The FP knew that the mass needed to be biopsied, but because of its size, the best he could do would be to perform a partial biopsy. So on the day of presentation, the FP performed a 6-mm punch biopsy in the most raised area of the lesion to try and get sufficient depth and breadth for diagnosis and prognosis. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report indicated that the lesion was a nodular melanoma with a Breslow depth of 5.5 mm. This melanoma arose in a nevus, which occurs in about 30% of melanomas. Most melanomas arise de novo.
The FP referred the patient to a surgical oncologist for an excision with 2 cm margins and a sentinel lymph node biopsy. The sentinel node was in the right axilla and was remarkably negative despite the local in-transit metastases/satellites. One year after the original diagnosis was made, there was no evidence of metastatic disease and no new melanomas. The patient follows up with the dermatologist for skin and lymph node surveillance every 3 months.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Melanoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1112-1123.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
The FP was extremely concerned that this was a large melanoma due the lesion’s chaotic appearance, with multiple colors and an irregular border. Going through the ABCDE criteria, he noted that the lesion was Asymmetric, the Border was irregular, the Colors were varied, the Diameter was > 6 mm, and it was Enlarging by history.
With his dermatoscope attached to his smart phone, the FP looked at the lesion and took a photograph (Figure B). The image revealed a pigment network of the original nevus at 5:00 to 6:00 o’clock and extensions of the tumor due to in-transit metastases. Satellites were visible, especially in the top right and left corners. The FP noted the shiny white lines caused by collagen deposition found in growing tumors. (See “Dermoscopy in family medicine: A primer.”)
The FP knew that the mass needed to be biopsied, but because of its size, the best he could do would be to perform a partial biopsy. So on the day of presentation, the FP performed a 6-mm punch biopsy in the most raised area of the lesion to try and get sufficient depth and breadth for diagnosis and prognosis. (See the Watch & Learn video on “Punch biopsy.”)
The pathology report indicated that the lesion was a nodular melanoma with a Breslow depth of 5.5 mm. This melanoma arose in a nevus, which occurs in about 30% of melanomas. Most melanomas arise de novo.
The FP referred the patient to a surgical oncologist for an excision with 2 cm margins and a sentinel lymph node biopsy. The sentinel node was in the right axilla and was remarkably negative despite the local in-transit metastases/satellites. One year after the original diagnosis was made, there was no evidence of metastatic disease and no new melanomas. The patient follows up with the dermatologist for skin and lymph node surveillance every 3 months.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Melanoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill;2019:1112-1123.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com
What are the risks of long-term PPI use for GERD symptoms in patients > 65 years?
EVIDENCE SUMMARY
A 2017 meta-analysis of 16 RCTs examined the risk of cardiovascular events in 7540 adult patients taking PPIs for GERD (mean ages 45-55 years).1 The primary outcome was cardiovascular events—including acute myocardial infarction, myocardial ischemia, angina pectoris, cardiac failure, and coronary artery stenosis—and cardiac disorders.
Analysis of pooled data found that PPI use was associated with a 70% increase in cardiovascular risk (relative risk [RR] = 1.7; 95% confidence interval [CI], 1.13-2.56; number needed to harm [NNH] = 241) when compared with controls (placebo, H2 blocker, or surgery). A subgroup analysis found that PPI use for longer than 8 weeks was associated with an even higher risk of adverse cardiovascular events (6 trials, 2296 patients; RR = 2.33; 95% CI, 1.33-4.08; NNH = 67) when compared with controls. The meta-analysis wasn’t limited by heterogeneity (I2 = 0).
C difficile infection risk is higherfor PPI users
A 2016 meta-analysis of 23 observational studies (19 case-control, 4 retrospective cohort; 186,033 patients) examined the risk of hospital-acquired C difficile infections in adults prescribed PPI for any indication.2 PPI exposure varied from use at time of diagnosis or hospitalization to any use within 90 days. Of the 23 studies, 16 reported sufficient data to calculate the mean age for the patients which was 69.9 years.
The risk of C difficile infection was found to be higher with PPI use than no use (pooled odds ratio [OR] = 1.81; 95% CI, 1.52-2.14). Although a significant association was found across a large group, the results were limited by considerable heterogeneity (I2 = 82%).
Risk of community-acquired pneumonia also increases with PPI use
A 2015 systematic review and meta-analysis of 33 trials (18 case-control, 10 cohort, 4 RCTs, and 1 case-crossover study) examined the risk of CAP in adult patients prescribed PPI for any indication for durations ranging from less than 1 month to > 6 months.3 The systematic review was distilled to 26 studies because of overlapping study populations. These 26 studies included 226,769 cases of CAP among 6,351,656 patients. The primary outcome was development of CAP, the secondary outcome was hospitalization for CAP.
PPI use, compared with no use, was associated with an increased risk of developing CAP (pooled OR = 1.49; 95% CI, 1.16-1.92) and an increased risk of hospitalization for CAP (pooled OR = 1.61; 95% CI, 1.12-2.31).
In a subgroup analysis for age, patients older than 65 years were also found to have an increased risk of developing CAP with PPI use (11 trials, total number of patients not provided; OR = 1.33; 95% CI, 1.13-1.58). Despite the significant associations of PPI use with risk revealed in the primary, secondary, and subgroup analyses, the results were limited by marked heterogeneity, with an I2 > 99%.
Continue to: Hip and vertebral fracture risks associated with PPIs
Hip and vertebral fracture riskis associated with PPIs
A 2011 systematic review and meta-analysis investigated the risk of fracture in adult patients taking PPIs for any indication.4 The analysis included 10 observational studies (4 cohort, 6 case-control) with a total of 223,210 fracture cases. The authors examined the incidence of hip, vertebral, and wrist or forearm fractures.
No significant association was found between PPI use and wrist or forearm fracture (3 studies; pooled OR = 1.09; 95% CI, 0.95-1.24). A modest association was noted between PPI use and both hip fractures (9 trials; OR = 1.25; 95% CI, 1.14-1.37) and vertebral fractures (4 trials; OR = 1.5; 95% CI, 1.32-1.72).
Subgroup analysis didn’t reveal evidence of an effect of duration of PPI use on fracture. Investigators didn’t conduct subgroup analysis of different patient ages. Final results were limited by significant heterogeneity with an I2 of 86%.
RECOMMENDATIONS
A 2015 American Geriatrics Society Beers Criteria update recommends limiting PPI use because of increased risk of C difficile infections and fractures. It also recommends against using PPIs for longer than 8 weeks except for high-risk patients (such as patients taking oral corticosteroids or chronic nonsteroidal anti-inflammatory drug users), patients with Barrett’s esophagitis, or patients who need maintenance after failure of a drug discontinuation trial or H2 blockers (quality of evidence, high; SOR, strong).5
Editor’s take
1. Sun S, Cui Z, Zhou M, et al. Proton pump inhibitor monotherapy and the risk of cardiovascular events in patients with gastro-esophageal reflux disease: a meta-analysis. Neurogastroenterol Motil. 2017;29:e12926.
2. Arriola V, Tischendorf J, Musuuza J, et al. Assessing the risk of hospital-acquired clostridium difficile infection with proton pump inhibitor use: a meta-analysis. Infect Control Hosp Epidemiol. 2016;37:1408-1417.
3. Lambert AA, Lam JO, Paik JJ, et al. Risk of community-acquired pneumonia with outpatient proton-pump inhibitor therapy: a systematic review and meta-analysis. PLoS One. 2015;10:e0128004.
4. Ngamruengphong S, Leontiadis GI, Radhi S, et al. Proton pump inhibitors and risk of fracture: a systematic review and meta-analysis of observational studies. Am J Gastroenterol. 2011;106:1209-1218.
5. American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc. 2015;63:2227-2246.
EVIDENCE SUMMARY
A 2017 meta-analysis of 16 RCTs examined the risk of cardiovascular events in 7540 adult patients taking PPIs for GERD (mean ages 45-55 years).1 The primary outcome was cardiovascular events—including acute myocardial infarction, myocardial ischemia, angina pectoris, cardiac failure, and coronary artery stenosis—and cardiac disorders.
Analysis of pooled data found that PPI use was associated with a 70% increase in cardiovascular risk (relative risk [RR] = 1.7; 95% confidence interval [CI], 1.13-2.56; number needed to harm [NNH] = 241) when compared with controls (placebo, H2 blocker, or surgery). A subgroup analysis found that PPI use for longer than 8 weeks was associated with an even higher risk of adverse cardiovascular events (6 trials, 2296 patients; RR = 2.33; 95% CI, 1.33-4.08; NNH = 67) when compared with controls. The meta-analysis wasn’t limited by heterogeneity (I2 = 0).
C difficile infection risk is higherfor PPI users
A 2016 meta-analysis of 23 observational studies (19 case-control, 4 retrospective cohort; 186,033 patients) examined the risk of hospital-acquired C difficile infections in adults prescribed PPI for any indication.2 PPI exposure varied from use at time of diagnosis or hospitalization to any use within 90 days. Of the 23 studies, 16 reported sufficient data to calculate the mean age for the patients which was 69.9 years.
The risk of C difficile infection was found to be higher with PPI use than no use (pooled odds ratio [OR] = 1.81; 95% CI, 1.52-2.14). Although a significant association was found across a large group, the results were limited by considerable heterogeneity (I2 = 82%).
Risk of community-acquired pneumonia also increases with PPI use
A 2015 systematic review and meta-analysis of 33 trials (18 case-control, 10 cohort, 4 RCTs, and 1 case-crossover study) examined the risk of CAP in adult patients prescribed PPI for any indication for durations ranging from less than 1 month to > 6 months.3 The systematic review was distilled to 26 studies because of overlapping study populations. These 26 studies included 226,769 cases of CAP among 6,351,656 patients. The primary outcome was development of CAP, the secondary outcome was hospitalization for CAP.
PPI use, compared with no use, was associated with an increased risk of developing CAP (pooled OR = 1.49; 95% CI, 1.16-1.92) and an increased risk of hospitalization for CAP (pooled OR = 1.61; 95% CI, 1.12-2.31).
In a subgroup analysis for age, patients older than 65 years were also found to have an increased risk of developing CAP with PPI use (11 trials, total number of patients not provided; OR = 1.33; 95% CI, 1.13-1.58). Despite the significant associations of PPI use with risk revealed in the primary, secondary, and subgroup analyses, the results were limited by marked heterogeneity, with an I2 > 99%.
Continue to: Hip and vertebral fracture risks associated with PPIs
Hip and vertebral fracture riskis associated with PPIs
A 2011 systematic review and meta-analysis investigated the risk of fracture in adult patients taking PPIs for any indication.4 The analysis included 10 observational studies (4 cohort, 6 case-control) with a total of 223,210 fracture cases. The authors examined the incidence of hip, vertebral, and wrist or forearm fractures.
No significant association was found between PPI use and wrist or forearm fracture (3 studies; pooled OR = 1.09; 95% CI, 0.95-1.24). A modest association was noted between PPI use and both hip fractures (9 trials; OR = 1.25; 95% CI, 1.14-1.37) and vertebral fractures (4 trials; OR = 1.5; 95% CI, 1.32-1.72).
Subgroup analysis didn’t reveal evidence of an effect of duration of PPI use on fracture. Investigators didn’t conduct subgroup analysis of different patient ages. Final results were limited by significant heterogeneity with an I2 of 86%.
RECOMMENDATIONS
A 2015 American Geriatrics Society Beers Criteria update recommends limiting PPI use because of increased risk of C difficile infections and fractures. It also recommends against using PPIs for longer than 8 weeks except for high-risk patients (such as patients taking oral corticosteroids or chronic nonsteroidal anti-inflammatory drug users), patients with Barrett’s esophagitis, or patients who need maintenance after failure of a drug discontinuation trial or H2 blockers (quality of evidence, high; SOR, strong).5
Editor’s take
EVIDENCE SUMMARY
A 2017 meta-analysis of 16 RCTs examined the risk of cardiovascular events in 7540 adult patients taking PPIs for GERD (mean ages 45-55 years).1 The primary outcome was cardiovascular events—including acute myocardial infarction, myocardial ischemia, angina pectoris, cardiac failure, and coronary artery stenosis—and cardiac disorders.
Analysis of pooled data found that PPI use was associated with a 70% increase in cardiovascular risk (relative risk [RR] = 1.7; 95% confidence interval [CI], 1.13-2.56; number needed to harm [NNH] = 241) when compared with controls (placebo, H2 blocker, or surgery). A subgroup analysis found that PPI use for longer than 8 weeks was associated with an even higher risk of adverse cardiovascular events (6 trials, 2296 patients; RR = 2.33; 95% CI, 1.33-4.08; NNH = 67) when compared with controls. The meta-analysis wasn’t limited by heterogeneity (I2 = 0).
C difficile infection risk is higherfor PPI users
A 2016 meta-analysis of 23 observational studies (19 case-control, 4 retrospective cohort; 186,033 patients) examined the risk of hospital-acquired C difficile infections in adults prescribed PPI for any indication.2 PPI exposure varied from use at time of diagnosis or hospitalization to any use within 90 days. Of the 23 studies, 16 reported sufficient data to calculate the mean age for the patients which was 69.9 years.
The risk of C difficile infection was found to be higher with PPI use than no use (pooled odds ratio [OR] = 1.81; 95% CI, 1.52-2.14). Although a significant association was found across a large group, the results were limited by considerable heterogeneity (I2 = 82%).
Risk of community-acquired pneumonia also increases with PPI use
A 2015 systematic review and meta-analysis of 33 trials (18 case-control, 10 cohort, 4 RCTs, and 1 case-crossover study) examined the risk of CAP in adult patients prescribed PPI for any indication for durations ranging from less than 1 month to > 6 months.3 The systematic review was distilled to 26 studies because of overlapping study populations. These 26 studies included 226,769 cases of CAP among 6,351,656 patients. The primary outcome was development of CAP, the secondary outcome was hospitalization for CAP.
PPI use, compared with no use, was associated with an increased risk of developing CAP (pooled OR = 1.49; 95% CI, 1.16-1.92) and an increased risk of hospitalization for CAP (pooled OR = 1.61; 95% CI, 1.12-2.31).
In a subgroup analysis for age, patients older than 65 years were also found to have an increased risk of developing CAP with PPI use (11 trials, total number of patients not provided; OR = 1.33; 95% CI, 1.13-1.58). Despite the significant associations of PPI use with risk revealed in the primary, secondary, and subgroup analyses, the results were limited by marked heterogeneity, with an I2 > 99%.
Continue to: Hip and vertebral fracture risks associated with PPIs
Hip and vertebral fracture riskis associated with PPIs
A 2011 systematic review and meta-analysis investigated the risk of fracture in adult patients taking PPIs for any indication.4 The analysis included 10 observational studies (4 cohort, 6 case-control) with a total of 223,210 fracture cases. The authors examined the incidence of hip, vertebral, and wrist or forearm fractures.
No significant association was found between PPI use and wrist or forearm fracture (3 studies; pooled OR = 1.09; 95% CI, 0.95-1.24). A modest association was noted between PPI use and both hip fractures (9 trials; OR = 1.25; 95% CI, 1.14-1.37) and vertebral fractures (4 trials; OR = 1.5; 95% CI, 1.32-1.72).
Subgroup analysis didn’t reveal evidence of an effect of duration of PPI use on fracture. Investigators didn’t conduct subgroup analysis of different patient ages. Final results were limited by significant heterogeneity with an I2 of 86%.
RECOMMENDATIONS
A 2015 American Geriatrics Society Beers Criteria update recommends limiting PPI use because of increased risk of C difficile infections and fractures. It also recommends against using PPIs for longer than 8 weeks except for high-risk patients (such as patients taking oral corticosteroids or chronic nonsteroidal anti-inflammatory drug users), patients with Barrett’s esophagitis, or patients who need maintenance after failure of a drug discontinuation trial or H2 blockers (quality of evidence, high; SOR, strong).5
Editor’s take
1. Sun S, Cui Z, Zhou M, et al. Proton pump inhibitor monotherapy and the risk of cardiovascular events in patients with gastro-esophageal reflux disease: a meta-analysis. Neurogastroenterol Motil. 2017;29:e12926.
2. Arriola V, Tischendorf J, Musuuza J, et al. Assessing the risk of hospital-acquired clostridium difficile infection with proton pump inhibitor use: a meta-analysis. Infect Control Hosp Epidemiol. 2016;37:1408-1417.
3. Lambert AA, Lam JO, Paik JJ, et al. Risk of community-acquired pneumonia with outpatient proton-pump inhibitor therapy: a systematic review and meta-analysis. PLoS One. 2015;10:e0128004.
4. Ngamruengphong S, Leontiadis GI, Radhi S, et al. Proton pump inhibitors and risk of fracture: a systematic review and meta-analysis of observational studies. Am J Gastroenterol. 2011;106:1209-1218.
5. American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc. 2015;63:2227-2246.
1. Sun S, Cui Z, Zhou M, et al. Proton pump inhibitor monotherapy and the risk of cardiovascular events in patients with gastro-esophageal reflux disease: a meta-analysis. Neurogastroenterol Motil. 2017;29:e12926.
2. Arriola V, Tischendorf J, Musuuza J, et al. Assessing the risk of hospital-acquired clostridium difficile infection with proton pump inhibitor use: a meta-analysis. Infect Control Hosp Epidemiol. 2016;37:1408-1417.
3. Lambert AA, Lam JO, Paik JJ, et al. Risk of community-acquired pneumonia with outpatient proton-pump inhibitor therapy: a systematic review and meta-analysis. PLoS One. 2015;10:e0128004.
4. Ngamruengphong S, Leontiadis GI, Radhi S, et al. Proton pump inhibitors and risk of fracture: a systematic review and meta-analysis of observational studies. Am J Gastroenterol. 2011;106:1209-1218.
5. American Geriatrics Society 2015 Beers Criteria Update Expert Panel. American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. J Am Geriatr Soc. 2015;63:2227-2246.
EVIDENCE-BASED ANSWER:
The use of proton pump inhibitors (PPIs) to control gastroesophageal reflux disease (GERD) is significantly associated with an increased risk of cardiovascular events such as acute myocardial infarction and myocardial ischemia, especially with treatment longer than 8 weeks (strength of recommendation [SOR]: A, systematic review of randomized, controlled trials [RCTs]). This summary is based on data extrapolated from studies on all adults because there is limited evidence that specifically addresses patients older than 65 years.
Adults taking PPIs also appear to be at increased risk of Clostridium difficile infection, community-acquired pneumonia (CAP; with use for < 30 days), and fracture (SOR: B, systematic reviews of heterogeneous prospective and retrospective observational studies).
Daily headaches • associated nausea • obesity • Dx?
THE CASE
A 22-year-old woman presented to our office complaining of headaches that started 6 weeks earlier. Initially the headache was throbbing, nonpositional, infrequent, and intermittent, lasting 15 to 45 minutes, often starting in the neck and migrating towards the right frontotemporal region. During the week prior to presentation, the headaches became daily and constant, with brief periods of relief after the patient took ibuprofen 400 mg 4 times a day as needed. The patient reported associated nausea, a sensation of pressure changes in the ears, and intermittent dimming of vision in the right eye (sometimes independent of headache). The patient denied photophobia and phonophobia. Her only medication was an oral contraceptive pill (OCP). She had no prior history of headaches.
Physical examination showed a blood pressure of 148/66 mm Hg, body mass index of 44.38, muscle tenderness in the neck and upper back, and no focal neurological findings. Funduscopic examination was unsuccessful. A working diagnosis of atypical migraine was made, but because of unilateral visual disturbance the patient was referred to Ophthalmology for further evaluation. The following day, ophthalmological consultation found bilateral papilledema and the patient was admitted to our hospitalist service via the Emergency Department. She subsequently was referred to inpatient Neurology.
THE DIAGNOSIS
Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast was unremarkable. Magnetic resonance venography (MRV) with contrast of the brain showed possible stenosis at the junction of the transverse and sigmoid sinuses but no mass lesion nor venous sinus thrombosis. Lumbar puncture (LP) revealed an opening pressure of 650 mm H20 (reference range, 60–250 mm H2O).1 A diagnosis of idiopathic intracranial hypertension (IIH) was made.
DISCUSSION
IIH, previously known as pseudotumor cerebri and benign intracranial hypertension, is defined by signs and symptoms of elevated intracranial pressure (ICP) without obvious cause on neuroimaging (TABLE 12-5). It is well documented that IIH is consequential and can result in vision loss and intractable chronic headaches.5,6 Older terms such as pseudotumor cerebri and benign intracranial hypertension are therefore no longer recommended because they are considered misleading and not reflective of the severity of potential injury caused by the condition3,4,6 IIH is considered a diagnosis of exclusion requiring certain criteria to be met (TABLE 22). Although the etiology of IIH is unclear, associations have been made between IIH and various medications and conditions2-5,7 (TABLE 33,5).
Classically, IIH affects women who are obese and of childbearing age, but studies have shown that this condition also can affect men and children—albeit less frequently.3,5-7 The incidence of IIH in the general population is between 0.03 to 2.36/100,000 people per year, but in women, the incidence is 0.65 to 4.65/100,000 per year.6 Furthermore, females who are obese have an incidence of 2.7 to 19.3/100,000 per year.6
Headache is the most common symptom of IIH. Unfortunately, the differential diagnosis of headache is vast; thus, a careful history is needed to narrow the field3,5-7 (TABLE 42). Associated symptoms of transient visual changes, pulsatile tinnitus, neck and back pain, nausea, vomiting, photo/phonophobia, and findings of abducens nerve palsy or papilledema—while nonspecific— should raise suspicion for elevated ICP and IIH, especially in women who are obese.2-8 Once IIH is suspected, an urgent diagnosis and treatment is necessary to prevent permanent vision loss.3,4,6
Headache with findings of papilledema warrants neuroimaging, preferably with MRI, to rule out intracranial mass and hydrocephalus.1,2,5 MRV also is recommended to assess for intracranial venous thrombosis, an alternate cause for papilledema and increased ICP.1,2,4,5
Continue to: Recently, a classification of IIH...
Recently, a classification of IIH without papilledema has been acknowledged by the International Headache Society.2,8 Specific MRI findings have been suggested to help make this diagnosis5,9 (TABLE 55).
TREATMENT FOR IIH CAN BE MEDICAL OR SURGICAL
Medications associated with IIH should be discontinued.7 The first-line medication for IIH is acetazolamide, a carbonic anhydrase inhibitor that works in the choroid plexus to decrease cerebrospinal fluid (CSF) production and thus, lower ICP.3,6 An adult dose of 1 to 2 g/day3,4,6 is tolerated well, but can be increased to 4 g/day,10 if necessary. Weight loss via diet and exercise or bariatric surgery has been shown to be effective in patients who are obese and have been given a diagnosis of IIH.3,4
Topiramate also has been suggested as a treatment option, based on its usefulness in weight loss and because of its action as a weak carbonic anhydrase inhibitor.3,6 Also, LP has therapeutic merit—although relief is only short-term.3,6 Patients who fail medical therapy and have intractable headache or progressive visual loss appear to benefit from optic nerve sheath fenestration.3,7,8
Our patient experienced notable improvement in her headache after LP. Her OCP was discontinued, a diuretic regimen started, and weight loss counseling was provided. Prior to discharge, the patient was seen by a neuro-ophthalmologist for perimetry, a visual field test that assesses for acute vision loss and establishes a baseline for follow-up monitoring of vision.7
THE TAKEAWAY
Headache is a common condition that may be challenging to correctly diagnose. A thorough history and neurological examination, including fundoscopy, are essential in the evaluation of headache and suspected IIH. In the primary care setting, limited time, lack of mydriatic agents, suboptimal lighting, and practitioner inexperience may pose challenges for funduscopic examination. Ophthalmoscopes incorporating new technology to expand and magnify the examiner’s field of view may facilitate this exam.11 A global rise in the prevalence of obesity underscores a need for primary care providers to be compulsive about their clinical evaluation when symptoms suspicious of IIH are present. Lastly, if IIH cannot be ruled out confidently, recommend a prompt evaluation by an ophthalmologist.
CORRESPONDENCE
Aarti Paltoo, MD, MSc, CCFP, Peel Village Medical Center, 28 Rambler Drive, Brampton, Ontario L6W 1E2 Canada; paltooa@mcmaster.ca
1. Lee SC, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol. 2014;34:278-283.
2. International Headache Society. Idiopathic intracranial hypertension. The International Classification of Headache Disorders. 2nd ed. Oxford, UK: Blackwell Publishing; 2003:1-232.
3. Biousse V, Bruce BB, Newman NJ. Update on the pathophysiology and management of idiopathic intracranial hypertension. J Neurol Neurosurg Psychiatry. 2012;83:488-494.
4. Mollan SP, Markey KA, Benzimra JD, et al. A practical approach to diagnosis, assessment and management of idiopathic intracranial hypertension. Pract Neurol. 2014;14:380-390.
5. Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology. 2013;81:1159-1165.
6. Julayanont P, Karukote A, Ruthirago D, et al. Idiopathic intracranial hypertension: ongoing clinical challenges and future prospects. J Pain Res. 2016;9:87-99.
7. Friedman DI, Digre KB. Headache medicine meets neuro-ophthalmology: exam techniques and challenging cases. Headache. 2013;53:703-716.
8. Digre KB, Nakamoto BK, Warner JE, et al. A comparison of idiopathic intracranaial hypertension with and without papilledema. Headache. 2009;49:185-193.
9. Digre KB. Imaging characteristics of IIH: are they reliable? Cephalagia. 2013;33:1067-1069.
10. Horton J. Acetazolamide for pseudotumor cerebri--evidence from the NORDIC trial. JAMA. 2014;311:1618-1619.
11. Petrushkin H, Barsam A, Mavrakakis M, et al. Optic disc assessment in the emergency department: a comparative study between the PanOptic and direct ophthalmoscopes. Emerg Med J. 2012;29:1007-1008.
THE CASE
A 22-year-old woman presented to our office complaining of headaches that started 6 weeks earlier. Initially the headache was throbbing, nonpositional, infrequent, and intermittent, lasting 15 to 45 minutes, often starting in the neck and migrating towards the right frontotemporal region. During the week prior to presentation, the headaches became daily and constant, with brief periods of relief after the patient took ibuprofen 400 mg 4 times a day as needed. The patient reported associated nausea, a sensation of pressure changes in the ears, and intermittent dimming of vision in the right eye (sometimes independent of headache). The patient denied photophobia and phonophobia. Her only medication was an oral contraceptive pill (OCP). She had no prior history of headaches.
Physical examination showed a blood pressure of 148/66 mm Hg, body mass index of 44.38, muscle tenderness in the neck and upper back, and no focal neurological findings. Funduscopic examination was unsuccessful. A working diagnosis of atypical migraine was made, but because of unilateral visual disturbance the patient was referred to Ophthalmology for further evaluation. The following day, ophthalmological consultation found bilateral papilledema and the patient was admitted to our hospitalist service via the Emergency Department. She subsequently was referred to inpatient Neurology.
THE DIAGNOSIS
Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast was unremarkable. Magnetic resonance venography (MRV) with contrast of the brain showed possible stenosis at the junction of the transverse and sigmoid sinuses but no mass lesion nor venous sinus thrombosis. Lumbar puncture (LP) revealed an opening pressure of 650 mm H20 (reference range, 60–250 mm H2O).1 A diagnosis of idiopathic intracranial hypertension (IIH) was made.
DISCUSSION
IIH, previously known as pseudotumor cerebri and benign intracranial hypertension, is defined by signs and symptoms of elevated intracranial pressure (ICP) without obvious cause on neuroimaging (TABLE 12-5). It is well documented that IIH is consequential and can result in vision loss and intractable chronic headaches.5,6 Older terms such as pseudotumor cerebri and benign intracranial hypertension are therefore no longer recommended because they are considered misleading and not reflective of the severity of potential injury caused by the condition3,4,6 IIH is considered a diagnosis of exclusion requiring certain criteria to be met (TABLE 22). Although the etiology of IIH is unclear, associations have been made between IIH and various medications and conditions2-5,7 (TABLE 33,5).
Classically, IIH affects women who are obese and of childbearing age, but studies have shown that this condition also can affect men and children—albeit less frequently.3,5-7 The incidence of IIH in the general population is between 0.03 to 2.36/100,000 people per year, but in women, the incidence is 0.65 to 4.65/100,000 per year.6 Furthermore, females who are obese have an incidence of 2.7 to 19.3/100,000 per year.6
Headache is the most common symptom of IIH. Unfortunately, the differential diagnosis of headache is vast; thus, a careful history is needed to narrow the field3,5-7 (TABLE 42). Associated symptoms of transient visual changes, pulsatile tinnitus, neck and back pain, nausea, vomiting, photo/phonophobia, and findings of abducens nerve palsy or papilledema—while nonspecific— should raise suspicion for elevated ICP and IIH, especially in women who are obese.2-8 Once IIH is suspected, an urgent diagnosis and treatment is necessary to prevent permanent vision loss.3,4,6
Headache with findings of papilledema warrants neuroimaging, preferably with MRI, to rule out intracranial mass and hydrocephalus.1,2,5 MRV also is recommended to assess for intracranial venous thrombosis, an alternate cause for papilledema and increased ICP.1,2,4,5
Continue to: Recently, a classification of IIH...
Recently, a classification of IIH without papilledema has been acknowledged by the International Headache Society.2,8 Specific MRI findings have been suggested to help make this diagnosis5,9 (TABLE 55).
TREATMENT FOR IIH CAN BE MEDICAL OR SURGICAL
Medications associated with IIH should be discontinued.7 The first-line medication for IIH is acetazolamide, a carbonic anhydrase inhibitor that works in the choroid plexus to decrease cerebrospinal fluid (CSF) production and thus, lower ICP.3,6 An adult dose of 1 to 2 g/day3,4,6 is tolerated well, but can be increased to 4 g/day,10 if necessary. Weight loss via diet and exercise or bariatric surgery has been shown to be effective in patients who are obese and have been given a diagnosis of IIH.3,4
Topiramate also has been suggested as a treatment option, based on its usefulness in weight loss and because of its action as a weak carbonic anhydrase inhibitor.3,6 Also, LP has therapeutic merit—although relief is only short-term.3,6 Patients who fail medical therapy and have intractable headache or progressive visual loss appear to benefit from optic nerve sheath fenestration.3,7,8
Our patient experienced notable improvement in her headache after LP. Her OCP was discontinued, a diuretic regimen started, and weight loss counseling was provided. Prior to discharge, the patient was seen by a neuro-ophthalmologist for perimetry, a visual field test that assesses for acute vision loss and establishes a baseline for follow-up monitoring of vision.7
THE TAKEAWAY
Headache is a common condition that may be challenging to correctly diagnose. A thorough history and neurological examination, including fundoscopy, are essential in the evaluation of headache and suspected IIH. In the primary care setting, limited time, lack of mydriatic agents, suboptimal lighting, and practitioner inexperience may pose challenges for funduscopic examination. Ophthalmoscopes incorporating new technology to expand and magnify the examiner’s field of view may facilitate this exam.11 A global rise in the prevalence of obesity underscores a need for primary care providers to be compulsive about their clinical evaluation when symptoms suspicious of IIH are present. Lastly, if IIH cannot be ruled out confidently, recommend a prompt evaluation by an ophthalmologist.
CORRESPONDENCE
Aarti Paltoo, MD, MSc, CCFP, Peel Village Medical Center, 28 Rambler Drive, Brampton, Ontario L6W 1E2 Canada; paltooa@mcmaster.ca
THE CASE
A 22-year-old woman presented to our office complaining of headaches that started 6 weeks earlier. Initially the headache was throbbing, nonpositional, infrequent, and intermittent, lasting 15 to 45 minutes, often starting in the neck and migrating towards the right frontotemporal region. During the week prior to presentation, the headaches became daily and constant, with brief periods of relief after the patient took ibuprofen 400 mg 4 times a day as needed. The patient reported associated nausea, a sensation of pressure changes in the ears, and intermittent dimming of vision in the right eye (sometimes independent of headache). The patient denied photophobia and phonophobia. Her only medication was an oral contraceptive pill (OCP). She had no prior history of headaches.
Physical examination showed a blood pressure of 148/66 mm Hg, body mass index of 44.38, muscle tenderness in the neck and upper back, and no focal neurological findings. Funduscopic examination was unsuccessful. A working diagnosis of atypical migraine was made, but because of unilateral visual disturbance the patient was referred to Ophthalmology for further evaluation. The following day, ophthalmological consultation found bilateral papilledema and the patient was admitted to our hospitalist service via the Emergency Department. She subsequently was referred to inpatient Neurology.
THE DIAGNOSIS
Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast was unremarkable. Magnetic resonance venography (MRV) with contrast of the brain showed possible stenosis at the junction of the transverse and sigmoid sinuses but no mass lesion nor venous sinus thrombosis. Lumbar puncture (LP) revealed an opening pressure of 650 mm H20 (reference range, 60–250 mm H2O).1 A diagnosis of idiopathic intracranial hypertension (IIH) was made.
DISCUSSION
IIH, previously known as pseudotumor cerebri and benign intracranial hypertension, is defined by signs and symptoms of elevated intracranial pressure (ICP) without obvious cause on neuroimaging (TABLE 12-5). It is well documented that IIH is consequential and can result in vision loss and intractable chronic headaches.5,6 Older terms such as pseudotumor cerebri and benign intracranial hypertension are therefore no longer recommended because they are considered misleading and not reflective of the severity of potential injury caused by the condition3,4,6 IIH is considered a diagnosis of exclusion requiring certain criteria to be met (TABLE 22). Although the etiology of IIH is unclear, associations have been made between IIH and various medications and conditions2-5,7 (TABLE 33,5).
Classically, IIH affects women who are obese and of childbearing age, but studies have shown that this condition also can affect men and children—albeit less frequently.3,5-7 The incidence of IIH in the general population is between 0.03 to 2.36/100,000 people per year, but in women, the incidence is 0.65 to 4.65/100,000 per year.6 Furthermore, females who are obese have an incidence of 2.7 to 19.3/100,000 per year.6
Headache is the most common symptom of IIH. Unfortunately, the differential diagnosis of headache is vast; thus, a careful history is needed to narrow the field3,5-7 (TABLE 42). Associated symptoms of transient visual changes, pulsatile tinnitus, neck and back pain, nausea, vomiting, photo/phonophobia, and findings of abducens nerve palsy or papilledema—while nonspecific— should raise suspicion for elevated ICP and IIH, especially in women who are obese.2-8 Once IIH is suspected, an urgent diagnosis and treatment is necessary to prevent permanent vision loss.3,4,6
Headache with findings of papilledema warrants neuroimaging, preferably with MRI, to rule out intracranial mass and hydrocephalus.1,2,5 MRV also is recommended to assess for intracranial venous thrombosis, an alternate cause for papilledema and increased ICP.1,2,4,5
Continue to: Recently, a classification of IIH...
Recently, a classification of IIH without papilledema has been acknowledged by the International Headache Society.2,8 Specific MRI findings have been suggested to help make this diagnosis5,9 (TABLE 55).
TREATMENT FOR IIH CAN BE MEDICAL OR SURGICAL
Medications associated with IIH should be discontinued.7 The first-line medication for IIH is acetazolamide, a carbonic anhydrase inhibitor that works in the choroid plexus to decrease cerebrospinal fluid (CSF) production and thus, lower ICP.3,6 An adult dose of 1 to 2 g/day3,4,6 is tolerated well, but can be increased to 4 g/day,10 if necessary. Weight loss via diet and exercise or bariatric surgery has been shown to be effective in patients who are obese and have been given a diagnosis of IIH.3,4
Topiramate also has been suggested as a treatment option, based on its usefulness in weight loss and because of its action as a weak carbonic anhydrase inhibitor.3,6 Also, LP has therapeutic merit—although relief is only short-term.3,6 Patients who fail medical therapy and have intractable headache or progressive visual loss appear to benefit from optic nerve sheath fenestration.3,7,8
Our patient experienced notable improvement in her headache after LP. Her OCP was discontinued, a diuretic regimen started, and weight loss counseling was provided. Prior to discharge, the patient was seen by a neuro-ophthalmologist for perimetry, a visual field test that assesses for acute vision loss and establishes a baseline for follow-up monitoring of vision.7
THE TAKEAWAY
Headache is a common condition that may be challenging to correctly diagnose. A thorough history and neurological examination, including fundoscopy, are essential in the evaluation of headache and suspected IIH. In the primary care setting, limited time, lack of mydriatic agents, suboptimal lighting, and practitioner inexperience may pose challenges for funduscopic examination. Ophthalmoscopes incorporating new technology to expand and magnify the examiner’s field of view may facilitate this exam.11 A global rise in the prevalence of obesity underscores a need for primary care providers to be compulsive about their clinical evaluation when symptoms suspicious of IIH are present. Lastly, if IIH cannot be ruled out confidently, recommend a prompt evaluation by an ophthalmologist.
CORRESPONDENCE
Aarti Paltoo, MD, MSc, CCFP, Peel Village Medical Center, 28 Rambler Drive, Brampton, Ontario L6W 1E2 Canada; paltooa@mcmaster.ca
1. Lee SC, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol. 2014;34:278-283.
2. International Headache Society. Idiopathic intracranial hypertension. The International Classification of Headache Disorders. 2nd ed. Oxford, UK: Blackwell Publishing; 2003:1-232.
3. Biousse V, Bruce BB, Newman NJ. Update on the pathophysiology and management of idiopathic intracranial hypertension. J Neurol Neurosurg Psychiatry. 2012;83:488-494.
4. Mollan SP, Markey KA, Benzimra JD, et al. A practical approach to diagnosis, assessment and management of idiopathic intracranial hypertension. Pract Neurol. 2014;14:380-390.
5. Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology. 2013;81:1159-1165.
6. Julayanont P, Karukote A, Ruthirago D, et al. Idiopathic intracranial hypertension: ongoing clinical challenges and future prospects. J Pain Res. 2016;9:87-99.
7. Friedman DI, Digre KB. Headache medicine meets neuro-ophthalmology: exam techniques and challenging cases. Headache. 2013;53:703-716.
8. Digre KB, Nakamoto BK, Warner JE, et al. A comparison of idiopathic intracranaial hypertension with and without papilledema. Headache. 2009;49:185-193.
9. Digre KB. Imaging characteristics of IIH: are they reliable? Cephalagia. 2013;33:1067-1069.
10. Horton J. Acetazolamide for pseudotumor cerebri--evidence from the NORDIC trial. JAMA. 2014;311:1618-1619.
11. Petrushkin H, Barsam A, Mavrakakis M, et al. Optic disc assessment in the emergency department: a comparative study between the PanOptic and direct ophthalmoscopes. Emerg Med J. 2012;29:1007-1008.
1. Lee SC, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol. 2014;34:278-283.
2. International Headache Society. Idiopathic intracranial hypertension. The International Classification of Headache Disorders. 2nd ed. Oxford, UK: Blackwell Publishing; 2003:1-232.
3. Biousse V, Bruce BB, Newman NJ. Update on the pathophysiology and management of idiopathic intracranial hypertension. J Neurol Neurosurg Psychiatry. 2012;83:488-494.
4. Mollan SP, Markey KA, Benzimra JD, et al. A practical approach to diagnosis, assessment and management of idiopathic intracranial hypertension. Pract Neurol. 2014;14:380-390.
5. Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. Neurology. 2013;81:1159-1165.
6. Julayanont P, Karukote A, Ruthirago D, et al. Idiopathic intracranial hypertension: ongoing clinical challenges and future prospects. J Pain Res. 2016;9:87-99.
7. Friedman DI, Digre KB. Headache medicine meets neuro-ophthalmology: exam techniques and challenging cases. Headache. 2013;53:703-716.
8. Digre KB, Nakamoto BK, Warner JE, et al. A comparison of idiopathic intracranaial hypertension with and without papilledema. Headache. 2009;49:185-193.
9. Digre KB. Imaging characteristics of IIH: are they reliable? Cephalagia. 2013;33:1067-1069.
10. Horton J. Acetazolamide for pseudotumor cerebri--evidence from the NORDIC trial. JAMA. 2014;311:1618-1619.
11. Petrushkin H, Barsam A, Mavrakakis M, et al. Optic disc assessment in the emergency department: a comparative study between the PanOptic and direct ophthalmoscopes. Emerg Med J. 2012;29:1007-1008.
High ankle sprains: Easy to miss, so follow these tips
CASE
A 19-year-old college football player presents to your outpatient family practice clinic after suffering a right ankle injury during a football game over the weekend. He reports having his right ankle planted on the turf with his foot externally rotated when an opponent fell onto his posterior right lower extremity. He reports having felt immediate pain in the area of the right ankle and requiring assistance off of the field, as he had difficulty walking. The patient was taken to the emergency department where x-rays of the right foot and ankle did not show any signs of acute fracture or dislocation. The patient was diagnosed with a lateral ankle sprain, placed in a pneumatic ankle walking brace, and given crutches.
A high ankle sprain, or distal tibiofibular syndesmotic injury, can be an elusive diagnosis and is often mistaken for the more common lateral ankle sprain. Syndesmotic injuries have been documented to occur in approximately 1% to 10% of all ankle sprains.1-3 The highest number of these injuries occurs between the ages of 18 and 34 years, and they are more frequently seen in athletes than in nonathletes, particularly those who play collision sports, such as football, ice hockey, rugby, wrestling, and lacrosse.1-9 In one study by Hunt et al,10 syndesmotic injuries accounted for 24.6% of all ankle injuries in National Collegiate Athletic Association (NCAA) football players. Incidence continues to grow as recognition of high ankle sprains increases among medical professionals.1,5 Identification of syndesmotic injury is critical, as lack of detection can lead to extensive time missed from athletic participation and chronic ankle dysfunction, including pain and instability.2,4,6,11
Back to basics: A brief anatomy review
Stability in the distal tibiofibular joint is maintained by the syndesmotic ligaments, which include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the transverse ligament, and the interosseous ligament.3-6,8 This complex of ligaments stabilizes the fibula within the incisura of the tibia and maintains a stable ankle mortise.1,4,5,11 The deep portion of the deltoid ligament also adds stability to the syndesmosis and may be disrupted by a syndesmotic injury.2,5-7,11
Mechanisms of injury: From most common to less likely
The distal tibiofibular syndesmosis is disrupted when an injury forces apart the distal tibiofibular joint. The most commonly reported means of injury is external rotation with hyper-dorsiflexion of the ankle.1-3,5,6,11 With excessive external rotation of the forefoot, the talus is forced against the medial aspect of the fibula, resulting in separation of the distal tibia and fibula and injury to the syndesmotic ligaments.2,3,5,6 Injuries associated with external rotation are commonly seen in sports that immobilize the ankle within a rigid boot, such as skiing and ice hockey.1,2,5 Some authors have suggested that a planovalgus foot alignment may place athletes at inherent risk for an external rotation ankle injury.5,6
Syndesmotic injury may also occur with hyper-dorsiflexion, as the anterior, widest portion of the talus rotates into the ankle mortise, wedging the tibia and fibula apart.2,3,5 There have also been reports of syndesmotic injuries associated with internal rotation, plantar flexion, inversion, and eversion.3,5,11 Therefore, physicians should maintain a high index of suspicion for injury to the distal tibiofibular joint, regardless of the mechanism of injury.
Presentation and evaluation
Observation of the patient and visualization of the affected ankle can provide many clues. Many patients will have difficulty walking after suffering a syndesmotic injury and may require the use of an assistive device.5 The inability to bear weight after an ankle injury points to a more severe diagnosis, such as an ankle fracture or syndesmotic injury, as opposed to a simple lateral ankle sprain. Patients may report anterior ankle pain, a sensation of instability with weight bearing on the affected ankle, or have persistent symptoms despite a course of conservative treatment. Also, they can have a variable amount of edema and ecchymosis associated with their injury; a minimal extent of swelling or ecchymosis does not exclude syndesmotic injury.3
A large percentage of patients will present with a concomitant sprain of the lateral ligaments associated with lateral swelling and bruising. One study found that 91% of syndesmotic injuries involved at least 1 of the lateral collateral ligaments (anterior talofibular ligament [ATFL], calcaneofibular ligament [CFL], or posterior talofibular ligament [PTFL]).12 Patients may have pain or a sensation of instability when pushing off with the toes,5 and patients with syndesmotic injuries often have tenderness to palpation over the distal anterolateral ankle or syndesmotic ligaments.7
Continue to: A thorough examination...
A thorough examination of the ankle, including palpation of common fracture sites, is important. Employ the Ottawa Ankle Rules (see http://www.theottawarules.ca/ankle_rules) to investigate for: tenderness to palpation over the posterior 6 cm of the posterior aspects of the distal medial and lateral malleoli; tenderness over the navicular; tenderness over the base of the fifth metatarsal; and/or the inability to bear weight on the affected lower extremity immediately after injury or upon evaluation in the physician’s office. Any of these findings should raise concern for a possible fracture (see “Adult foot fractures: A guide”) and require an x-ray(s) for further evaluation.13
Perform range-of-motion and strength testing with regard to ankle dorsiflexion, plantar flexion, abduction, adduction, inversion, and eversion. Palpate the ATFL, CFL, and PTFL for tenderness, as these structures may be involved to varying degrees in lateral ankle sprains. An anterior drawer test (see https://www.youtube.com/watch?v=vAcBEYZKcto) may be positive with injury to the ATFL. This test is performed by stabilizing the distal tibia with one hand and using the other hand to grasp the posterior aspect of the calcaneus and apply an anterior force. The test is positive if the talus translates forward, which correlates with laxity or rupture of the ATFL.13 The examiner should also palpate the Achilles tendon, peroneal tendons just posterior to the lateral malleolus, and the tibialis posterior tendon just posterior to the medial malleolus to inspect for tenderness or defects that may be signs of injury to these tendons.
An associated Weber B or C fracture? Trauma causing ankle syndesmosis injuries may be associated with Weber B or Weber C distal fibula fractures.7 Weber B fractures occur in the distal fibula at the level of the ankle joint (see FIGURE 1). These types of fractures are typically associated with external rotation injuries and are usually not associated with disruption of the interosseous membrane.
Weber C fractures are distal fibular fractures occurring above the level of the ankle joint. These fractures are also typically associated with external ankle rotation injuries and include disruption of the syndesmosis and deltoid ligament.14
Also pay special attention to the proximal fibula, as syndesmotic injuries are commonly associated with a Maisonneuve fracture, which is a proximal fibula fracture associated with external rotation forces of the ankle (see FIGURE 1).1,2,4,11,14,15 Further workup should occur in any patient with the possibility of a Weber- or Maisonneuve-type fracture.
Continue to: Multiple tests...
Multiple tests are available to investigate the possibility of a syndesmotic injury and to assess return-to-sport readiness, including the External Rotation Test, the Squeeze Test, the Crossed-Leg Test, the Dorsiflexion Compression Test, the Cotton Test, the Stabilization Test, the Fibular Translation Test, and the Single Leg Hop Test (see TABLE1-3,5,6,16,17). The External Rotation Test is noted by some authors to have the highest interobserver reliability, and is our preferred test.2 The Squeeze Test also has moderate interobserver reliability.2 There is a significant degree of variation among the sensitivity and specificity of these diagnostic tests, and no single test is sufficiently reliable or accurate to diagnose a syndesmotic ankle injury. Therefore, it is recommended to use multiple physical exam maneuvers, the history and mechanism of injury, and findings on imaging studies in conjunction to make the diagnosis of a syndesmotic injury.1,16
Imaging: Which modes and when?
The initial workup should include ankle x-rays when evaluating for the possibility of a distal tibiofibular syndesmosis injury. While the Ottawa Ankle Rules are helpful in providing guidance with regard to x-rays, suspicion of a syndesmotic injury mandates x-rays to determine the stability of the joint and rule out fracture. The European Society of Sports Traumatology, Knee Surgery and Arthroscopy–European Foot and Ankle Associates (ESSKA-AFAS) recommend, at a minimum, obtaining anteroposterior (AP)- and mortise-view ankle x-rays to investigate the tibiofibular clear space, medial clear space, and tibiofibular overlap.7 Most physicians also include a lateral ankle x-ray.
If possible, images should be performed while the patient is bearing weight to further evaluate stability. Radiographic findings that support the diagnosis of syndesmotic injury include a tibiofibular clear space > 6 mm on AP view, medial clear space > 4 mm on mortise view, or tibiofibular overlap < 6 mm on AP view or < 1 mm on mortise view (see FIGURES 2 and 3).1,3,5,8 Additionally, if you suspect a proximal fibular fracture, obtain an x-ray series of the proximal tibia and fibula to investigate the possibility of a Maisonneuve injury.1,2,4,11
If you continue to suspect a syndesmotic injury despite normal x-rays, obtain stress x-rays, in addition to the AP and mortise views, to ensure stability. These x-rays include AP and mortise ankle views with manual external rotation of the ankle joint, which may demonstrate abnormalities not seen on standard x-rays. Bilateral imaging can also be useful to further assess when mild abnormalities vs symmetric anatomic variants are in question.1,7
If there is concern for an unstable injury, refer the patient to a foot and ankle surgeon, who may pursue magnetic resonance imaging (MRI) or standing computed tomography (CT).1,2,5,7 MRI is the recommended choice for further evaluation of a syndesmotic injury, as it is proven to be accurate in evaluating the integrity of the syndesmotic ligaments (see FIGURES 4 and 5).18 MRI has demonstrated 100% sensitivity for detecting AITFL and PITFL injuries, as well as 93% and 100% specificity for AITFL and PITFL tears, respectively.8 A weight-bearing CT scan, particularly axial views, can also be a useful adjunct, as it is more sensitive than standard x-rays for assessing for mild diastasis. Although CT can provide an assessment of bony structures, it is not able to evaluate soft tissue structures, limiting its utility in evaluation of syndesmotic injuries.1,7
Continue to: Although not the standard of care...
Although not the standard of care, ultrasonography (US) is gaining traction as a means of investigating the integrity of the syndesmotic ligaments. US is inexpensive, readily available in many clinics, allows for dynamic testing, and avoids radiation exposure.7 However, US requires a skilled sonographer with experience in the ankle joint for an accurate diagnosis. If the workup with advanced imaging is inconclusive, but a high degree of suspicion remains for an unstable syndesmotic injury, consider arthroscopy to directly visualize and assess the syndesmotic structures.1,2,5,7,8
Grading the severity of the injury and pursuing appropriate Tx
Typically, the severity of a syndesmotic injury is classified as fitting into 1 of 3 categories: Grade I and II injuries are the most common, each accounting for 40% of syndesmotic injuries, while 20% of high ankle sprains are classified as Grade III.12
A Grade I injury consists of a stable syndesmotic joint without abnormal radiographic findings. There may be associated tenderness to palpation over the distal tibiofibular joint, and provocative testing may be subtle or normal. These injuries are often minor and able to be treated conservatively.
A Grade II injury is associated with a partial syndesmotic disruption, typically with partial tearing of the AITFL and interosseous ligament. These injuries may be stable or accompanied by mild instability, and provocative testing is usually positive. X-rays are typically normal with Grade II injuries, but may display subtle radiographic findings suggestive of a syndesmotic injury. Treatment of Grade II injuries is somewhat controversial and should be an individualized decision based upon the patient’s age, activity level, clinical exam, and imaging findings. Therefore, treatment of Grade II syndesmotic injuries may include a trial of conservative management or surgical intervention.
A Grade III injury represents inherent instability of the distal tibiofibular joint with complete disruption of all syndesmotic ligaments, with or without involvement of the deltoid ligament. X-rays will be positive in Grade III syndesmotic injuries because of the complete disruption of syndesmotic ligaments. All Grade III injuries require surgical intervention with a syndesmotic screw or other stabilization procedure.1,6-8,15
Continue to: A 3-stage rehabilitation protocol
A 3-stage rehabilitation protocol
When conservative management is deemed appropriate for a stable syndesmotic sprain, a 3-stage rehabilitation protocol is typically utilized.
The acute phase focuses on protection, pain control, and decreasing inflammation. The patient’s ankle is often immobilized in a cast or controlled ankle movement (CAM) boot. The patient is typically allowed to bear weight in the immobilizer during this phase as long as he/she is pain-free. If pain is present with weight bearing despite immobilization, non-weight bearing is recommended. The patient is instructed to elevate the lower extremity, take anti-inflammatory medication, and ice the affected ankle. Additionally, physical therapy modalities may be utilized to help with edema and pain. Joint immobilization is typically employed for 1 to 3 weeks post-injury. In the acute phase, the patient may also work with a physical therapist or athletic trainer on passive range of motion (ROM), progressing to active ROM as tolerated.1,5,7,8,19
The patient can transition from the CAM boot to a lace-up ankle brace when he/she is able to bear full weight and can navigate stairs without pain, which typically occurs around 3 to 6 weeks post-injury.1,5,7 A pneumatic walking brace may also be used as a transition device to provide added stabilization.
In the sub-acute phase, rehabilitation may progress to increase ankle mobility, strengthening, neuromuscular control, and to allow the patient to perform activities of daily living.5-7
The advanced training phase includes continued neuromuscular control, increased strengthening, plyometrics, agility, and sports-specific drills.5 Athletes are allowed to return to full participation when they have regained full ROM, are able to perform sport-specific agility drills without pain or instability, and have near-normal strength.5-7 Some authors also advocate that a Single Leg Hop Test should be included in the physical exam, and that it should be pain free prior to allowing an athlete to return to competition.20 Both progression in physical rehabilitation and return to sport should be individualized based upon injury severity, patient functionality, and physical exam findings.
Continue to: Outcomes forecast
Outcomes forecast: Variable
The resolution of symptoms and return to competition after a syndesmotic injury is variable. In one cohort study of cadets (N = 614) at the United States Military Academy, the average time lost from a syndesmotic ankle sprain was 9.82 days (range 3-21 days).9 In a retrospective review of National Hockey League players, average time to return to competition after a syndesmotic ankle injury sprain (n = 14) was 45 days (range 6-137 days) vs 1.4 days (range 0-6 days) for lateral ankle sprains (n = 5).21 In another study, National Football League players with syndesmotic sprains (n = 36) had a mean time loss from play of 15.4 days (± 11.1 days) vs 6.5 days (± 6.5 days) of time loss from play in those with lateral ankle sprains (n = 53).22
Although there is a fair amount of variability among studies, most authors agree that the average athlete can expect to return to sport 4 to 8 weeks post-injury with conservative management.19 At least 1 study suggests that the average time to return to sport in patients with Grade III syndesmotic injuries who undergo surgical treatment with a syndesmotic screw is 41 days (range 32-48).23 The differences in return to sport may be related to severity of injury and/or type of activity.
Persistent symptoms are relatively common after conservative management of syndesmotic injuries. One case series found that 36% of patients treated conservatively had complaints of persistent mild-to-moderate ankle stiffness, 23% had mild-to-moderate pain, and 18% had mild-to-moderate ankle swelling.24 Despite these symptoms, 86% of the patients rated their ankle function as good after conservative treatment.24 In patients with persistent symptoms, other possible etiologies should be considered including neurologic injury, complex regional pain syndrome, osteochondral defect, loose body, or other sources that may be contributing to pain, swelling, or delayed recovery.
At least 1 randomized controlled trial (RCT) investigated the utility of platelet rich plasma (PRP) injections around the injured AITFL in the setting of an acute syndesmotic injury. The study showed promising results, including quicker return to play, restabilization of the syndesmotic joint, and less residual pain;25 however, the study population was relatively small (N = 16), and the authors believed that more research is required on the benefits of PRP therapy in syndesmotic injuries before recommendations can be made.
An ounce of preventionis worth a pound of cure
Although injury is not always avoidable, there are measures that can help prevent ankle sprains and facilitate return to play after injury. As previously mentioned, athletes should be able to demonstrate the ability to run, cut, jump, and perform sport-specific activities without limitations prior to being allowed to return to sport after injury.5-7,26 Additionally, issues with biomechanics and functional deficits should be analyzed and addressed. By targeting specific strength deficits, focusing on proprioceptive awareness, and working on neuromuscular control, injury rates and recurrent injuries can be minimized. One RCT showed a 35% reduction in the recurrence rate of lateral ankle sprains with the use of an unsupervised home-based proprioceptive training program.27
Continue to: Strength training...
Strength training, proprioceptive and neuromuscular control activities, and low-risk activities such as jogging, biking, and swimming do not necessarily require the use of prophylactic bracing. However, because syndesmotic injuries are associated with recurrent ankle injuries, prophylactic bracing should be used during high-risk activities that involve agility maneuvers and jumping. Substantial evidence demonstrates that the use of ankle taping or ankle bracing decreases the incidence of ankle injuries, particularly in those who have had previous ankle injuries.26 In one study (N = 450), only 3% of athletes with a history of prior ankle injuries suffered a recurrent ankle sprain when using an ankle orthosis compared with a 17% injury rate in the control group.28
More recently, 2 separate studies by McGuine et al demonstrated that the use of lace-up ankle braces led to a reduction in the incidence of acute ankle injuries by 61% among 2081 high-school football players, and resulted in a significant reduction in acute ankle injuries in a study of 1460 male and female high-school basketball players, compared with the control groups.29,30
CASE
Ten days after injuring himself, the patient returns for a follow-up exam. Despite using the walking brace and crutches, he is still having significant difficulty bearing weight. He reports a sensation of instability in the right ankle. On exam, you note visible edema of the right ankle and ecchymosis over the lateral ankle, as well as moderate tenderness to palpation over the area of the ATFL and deltoid ligament. Tenderness over the medial malleolus, lateral malleolus, fifth metatarsal, and navicular is absent. Pain is reproducible with external rotation, and a Squeeze Test is positive. There is no tenderness over the proximal tibia or fibula. The patient is neurovascularly intact.
You order stress x-rays, which show widening of the medial clear space. The patient is placed in a CAM boot, instructed to continue non–weight-bearing on the ankle, and referred to a local foot and ankle surgeon for consideration of surgical fixation.
CORRESPONDENCE
John T. Nickless, MD, Division of Primary Care Sports Medicine, Department of Orthopedic Surgery, Rush University Medical Center, 1611 W. Harrison Street, Suite 200, Chicago, IL, 60612; jack.nickless@rushortho.com.
1. Switaj PJ, Mendoza M, Kadakia AR. Acute and chronic Injuries to the syndesmosis. Clin Sports Med. 2015;34:643-677.
2. Scheyerer MJ, Helfet DL, Wirth S, et al. Diagnostics in suspicion of ankle syndesmotic injury. Am J Orthop. 2011;40:192-197.
3. Smith KM, Kovacich-Smith KJ, Witt M. Evaluation and management of high ankle sprains. Clin Podiatr Med Surg. 2001;18:443-456.
4. Reissig J, Bitterman A, Lee S. Common foot and ankle injuries: what not to miss and how best to manage. J Am Osteopath Assoc. 2017;117:98-104.
5. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2:460-470.
6. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35:1197-1207.
7. Vopat ML, Vopat BG, Lubberts B, et al. Current trends in the diagnosis and management of syndesmotic injury. Curr Rev Musculoskelet Med. 2017;10:94-103.
8. Mak MF, Gartner L, Pearce CJ. Management of syndesmosis injuries in the elite athlete. Foot Ankle Clin. 2013;18:195-214.
9. Waterman BR, Belmont PJ, Cameron KL, et al. Epidemiology of ankle sprain at the United States Military Academy. Am J Sports Med. 2010;38:797-803.
10. Hunt KJ, George E, Harris AHS, et al. Epidemiology of syndesmosis injuries in intercollegiate football: incidence and risk factors from National Collegiate Athletic Association injury surveillance system data from 2004-2005 to 2008-2009. Clin J Sport Med. 2013;23:278-282.
11. Schnetzke M, Vetter SY, Beisemann N, et al. Management of syndesmotic injuries: what is the evidence? World J Orthop. 2016;7:718-725.
12. de César PC, Ávila EM, de Abreu MR. Comparison of magnetic resonance imaging to physical examination for syndesmotic injury after lateral ankle sprain. Foot Ankle Int. 2011;32:1110-1114.
13. Ivins D. Acute ankle sprain: an update. Am Fam Physician. 2006;74:1714-1720.
14. Porter D, Rund A, Barnes AF, et al. Optimal management of ankle syndesmosis injuries. Open Access J Sports Med. 2014;5:173-182.
15. Press CM, Gupta A, Hutchinson MR. Management of ankle syndesmosis injuries in the athlete. Curr Sports Med Rep. 2009;8:228-233.
16. Sman AD, Hiller CE, Rae K, et al. Diagnostic accuracy of clinical tests for ankle syndesmosis injury. Br J Sports Med. 2015;49:323-329.
17. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14:232-236.
18. Hunt KJ. Syndesmosis injuries. Curr Rev Musculoskelet Med. 2013;6:304-312.
19. Miller TL, Skalak T. Evaluation and treatment recommendations for acute injuries to the ankle syndesmosis without associated fracture. Sports Med. 2014;44:179-188.
20. Miller BS, Downie BK, Johnson PD, et al. Time to return to play after high ankle sprains in collegiate football players: a prediction model. Sports Health. 2012;4:504-509.
21. Wright RW, Barile RJ, Surprenant DA, et al. Ankle syndesmosis sprains in National Hockey League players. Am J Sports Med. 2016;32:1941-1945.
22. Osbahr DC, Drakos MC, O’Loughlin PF, et al. Syndesmosis and lateral ankle sprains in the National Football League. Orthopedics. 2013;36:e1378-e1384.
23. Taylor DC, Tenuta JJ, Uhorchak JM, et al. Aggressive surgical treatment and early return to sports in athletes with grade III syndesmosis sprains. Am J Sports Med. 2007;35:1133-1138.
24. Taylor DC, Englehardt DL, Bassett FH. Syndesmosis sprains of the ankle: the influence of heterotopic ossification. Am J Sports Med. 1992;20:146-150.
25. Laver L, Carmont MR, McConkey MO, et al. Plasma rich in growth factors (PRGF) as a treatment for high ankle sprain in elite athletes: a randomized control trial. Knee Surg Sports Traumatol Arthrosc. 2014;23:3383-3392.
26. Kaminski TW, Hertel J, Amendola N, et al. National Athletic Trainers’ Association position statement: conservative management and prevention of ankle sprains in athletes. J Athl Train. 2013;48:528-545.
27. Hupperets MDW, Verhagen EALM, van Mechelen W. Effect of unsupervised home based proprioceptive training on recurrences of ankle sprain: randomised controlled trial. BMJ. 2009;339:b2684.
28. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985;13:259-262.
29. McGuine TA, Brooks A, Hetzel S. The effect of lace-up ankle braces on injury rates in high school basketball players. Am J Sports Med. 2011;39:1840-1848.
30. McGuine TA, Hetzel S, Wilson J, et al. The effect of lace-up ankle braces on injury rates in high school football players. Am J Sports Med. 2012;40:49-57.
CASE
A 19-year-old college football player presents to your outpatient family practice clinic after suffering a right ankle injury during a football game over the weekend. He reports having his right ankle planted on the turf with his foot externally rotated when an opponent fell onto his posterior right lower extremity. He reports having felt immediate pain in the area of the right ankle and requiring assistance off of the field, as he had difficulty walking. The patient was taken to the emergency department where x-rays of the right foot and ankle did not show any signs of acute fracture or dislocation. The patient was diagnosed with a lateral ankle sprain, placed in a pneumatic ankle walking brace, and given crutches.
A high ankle sprain, or distal tibiofibular syndesmotic injury, can be an elusive diagnosis and is often mistaken for the more common lateral ankle sprain. Syndesmotic injuries have been documented to occur in approximately 1% to 10% of all ankle sprains.1-3 The highest number of these injuries occurs between the ages of 18 and 34 years, and they are more frequently seen in athletes than in nonathletes, particularly those who play collision sports, such as football, ice hockey, rugby, wrestling, and lacrosse.1-9 In one study by Hunt et al,10 syndesmotic injuries accounted for 24.6% of all ankle injuries in National Collegiate Athletic Association (NCAA) football players. Incidence continues to grow as recognition of high ankle sprains increases among medical professionals.1,5 Identification of syndesmotic injury is critical, as lack of detection can lead to extensive time missed from athletic participation and chronic ankle dysfunction, including pain and instability.2,4,6,11
Back to basics: A brief anatomy review
Stability in the distal tibiofibular joint is maintained by the syndesmotic ligaments, which include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the transverse ligament, and the interosseous ligament.3-6,8 This complex of ligaments stabilizes the fibula within the incisura of the tibia and maintains a stable ankle mortise.1,4,5,11 The deep portion of the deltoid ligament also adds stability to the syndesmosis and may be disrupted by a syndesmotic injury.2,5-7,11
Mechanisms of injury: From most common to less likely
The distal tibiofibular syndesmosis is disrupted when an injury forces apart the distal tibiofibular joint. The most commonly reported means of injury is external rotation with hyper-dorsiflexion of the ankle.1-3,5,6,11 With excessive external rotation of the forefoot, the talus is forced against the medial aspect of the fibula, resulting in separation of the distal tibia and fibula and injury to the syndesmotic ligaments.2,3,5,6 Injuries associated with external rotation are commonly seen in sports that immobilize the ankle within a rigid boot, such as skiing and ice hockey.1,2,5 Some authors have suggested that a planovalgus foot alignment may place athletes at inherent risk for an external rotation ankle injury.5,6
Syndesmotic injury may also occur with hyper-dorsiflexion, as the anterior, widest portion of the talus rotates into the ankle mortise, wedging the tibia and fibula apart.2,3,5 There have also been reports of syndesmotic injuries associated with internal rotation, plantar flexion, inversion, and eversion.3,5,11 Therefore, physicians should maintain a high index of suspicion for injury to the distal tibiofibular joint, regardless of the mechanism of injury.
Presentation and evaluation
Observation of the patient and visualization of the affected ankle can provide many clues. Many patients will have difficulty walking after suffering a syndesmotic injury and may require the use of an assistive device.5 The inability to bear weight after an ankle injury points to a more severe diagnosis, such as an ankle fracture or syndesmotic injury, as opposed to a simple lateral ankle sprain. Patients may report anterior ankle pain, a sensation of instability with weight bearing on the affected ankle, or have persistent symptoms despite a course of conservative treatment. Also, they can have a variable amount of edema and ecchymosis associated with their injury; a minimal extent of swelling or ecchymosis does not exclude syndesmotic injury.3
A large percentage of patients will present with a concomitant sprain of the lateral ligaments associated with lateral swelling and bruising. One study found that 91% of syndesmotic injuries involved at least 1 of the lateral collateral ligaments (anterior talofibular ligament [ATFL], calcaneofibular ligament [CFL], or posterior talofibular ligament [PTFL]).12 Patients may have pain or a sensation of instability when pushing off with the toes,5 and patients with syndesmotic injuries often have tenderness to palpation over the distal anterolateral ankle or syndesmotic ligaments.7
Continue to: A thorough examination...
A thorough examination of the ankle, including palpation of common fracture sites, is important. Employ the Ottawa Ankle Rules (see http://www.theottawarules.ca/ankle_rules) to investigate for: tenderness to palpation over the posterior 6 cm of the posterior aspects of the distal medial and lateral malleoli; tenderness over the navicular; tenderness over the base of the fifth metatarsal; and/or the inability to bear weight on the affected lower extremity immediately after injury or upon evaluation in the physician’s office. Any of these findings should raise concern for a possible fracture (see “Adult foot fractures: A guide”) and require an x-ray(s) for further evaluation.13
Perform range-of-motion and strength testing with regard to ankle dorsiflexion, plantar flexion, abduction, adduction, inversion, and eversion. Palpate the ATFL, CFL, and PTFL for tenderness, as these structures may be involved to varying degrees in lateral ankle sprains. An anterior drawer test (see https://www.youtube.com/watch?v=vAcBEYZKcto) may be positive with injury to the ATFL. This test is performed by stabilizing the distal tibia with one hand and using the other hand to grasp the posterior aspect of the calcaneus and apply an anterior force. The test is positive if the talus translates forward, which correlates with laxity or rupture of the ATFL.13 The examiner should also palpate the Achilles tendon, peroneal tendons just posterior to the lateral malleolus, and the tibialis posterior tendon just posterior to the medial malleolus to inspect for tenderness or defects that may be signs of injury to these tendons.
An associated Weber B or C fracture? Trauma causing ankle syndesmosis injuries may be associated with Weber B or Weber C distal fibula fractures.7 Weber B fractures occur in the distal fibula at the level of the ankle joint (see FIGURE 1). These types of fractures are typically associated with external rotation injuries and are usually not associated with disruption of the interosseous membrane.
Weber C fractures are distal fibular fractures occurring above the level of the ankle joint. These fractures are also typically associated with external ankle rotation injuries and include disruption of the syndesmosis and deltoid ligament.14
Also pay special attention to the proximal fibula, as syndesmotic injuries are commonly associated with a Maisonneuve fracture, which is a proximal fibula fracture associated with external rotation forces of the ankle (see FIGURE 1).1,2,4,11,14,15 Further workup should occur in any patient with the possibility of a Weber- or Maisonneuve-type fracture.
Continue to: Multiple tests...
Multiple tests are available to investigate the possibility of a syndesmotic injury and to assess return-to-sport readiness, including the External Rotation Test, the Squeeze Test, the Crossed-Leg Test, the Dorsiflexion Compression Test, the Cotton Test, the Stabilization Test, the Fibular Translation Test, and the Single Leg Hop Test (see TABLE1-3,5,6,16,17). The External Rotation Test is noted by some authors to have the highest interobserver reliability, and is our preferred test.2 The Squeeze Test also has moderate interobserver reliability.2 There is a significant degree of variation among the sensitivity and specificity of these diagnostic tests, and no single test is sufficiently reliable or accurate to diagnose a syndesmotic ankle injury. Therefore, it is recommended to use multiple physical exam maneuvers, the history and mechanism of injury, and findings on imaging studies in conjunction to make the diagnosis of a syndesmotic injury.1,16
Imaging: Which modes and when?
The initial workup should include ankle x-rays when evaluating for the possibility of a distal tibiofibular syndesmosis injury. While the Ottawa Ankle Rules are helpful in providing guidance with regard to x-rays, suspicion of a syndesmotic injury mandates x-rays to determine the stability of the joint and rule out fracture. The European Society of Sports Traumatology, Knee Surgery and Arthroscopy–European Foot and Ankle Associates (ESSKA-AFAS) recommend, at a minimum, obtaining anteroposterior (AP)- and mortise-view ankle x-rays to investigate the tibiofibular clear space, medial clear space, and tibiofibular overlap.7 Most physicians also include a lateral ankle x-ray.
If possible, images should be performed while the patient is bearing weight to further evaluate stability. Radiographic findings that support the diagnosis of syndesmotic injury include a tibiofibular clear space > 6 mm on AP view, medial clear space > 4 mm on mortise view, or tibiofibular overlap < 6 mm on AP view or < 1 mm on mortise view (see FIGURES 2 and 3).1,3,5,8 Additionally, if you suspect a proximal fibular fracture, obtain an x-ray series of the proximal tibia and fibula to investigate the possibility of a Maisonneuve injury.1,2,4,11
If you continue to suspect a syndesmotic injury despite normal x-rays, obtain stress x-rays, in addition to the AP and mortise views, to ensure stability. These x-rays include AP and mortise ankle views with manual external rotation of the ankle joint, which may demonstrate abnormalities not seen on standard x-rays. Bilateral imaging can also be useful to further assess when mild abnormalities vs symmetric anatomic variants are in question.1,7
If there is concern for an unstable injury, refer the patient to a foot and ankle surgeon, who may pursue magnetic resonance imaging (MRI) or standing computed tomography (CT).1,2,5,7 MRI is the recommended choice for further evaluation of a syndesmotic injury, as it is proven to be accurate in evaluating the integrity of the syndesmotic ligaments (see FIGURES 4 and 5).18 MRI has demonstrated 100% sensitivity for detecting AITFL and PITFL injuries, as well as 93% and 100% specificity for AITFL and PITFL tears, respectively.8 A weight-bearing CT scan, particularly axial views, can also be a useful adjunct, as it is more sensitive than standard x-rays for assessing for mild diastasis. Although CT can provide an assessment of bony structures, it is not able to evaluate soft tissue structures, limiting its utility in evaluation of syndesmotic injuries.1,7
Continue to: Although not the standard of care...
Although not the standard of care, ultrasonography (US) is gaining traction as a means of investigating the integrity of the syndesmotic ligaments. US is inexpensive, readily available in many clinics, allows for dynamic testing, and avoids radiation exposure.7 However, US requires a skilled sonographer with experience in the ankle joint for an accurate diagnosis. If the workup with advanced imaging is inconclusive, but a high degree of suspicion remains for an unstable syndesmotic injury, consider arthroscopy to directly visualize and assess the syndesmotic structures.1,2,5,7,8
Grading the severity of the injury and pursuing appropriate Tx
Typically, the severity of a syndesmotic injury is classified as fitting into 1 of 3 categories: Grade I and II injuries are the most common, each accounting for 40% of syndesmotic injuries, while 20% of high ankle sprains are classified as Grade III.12
A Grade I injury consists of a stable syndesmotic joint without abnormal radiographic findings. There may be associated tenderness to palpation over the distal tibiofibular joint, and provocative testing may be subtle or normal. These injuries are often minor and able to be treated conservatively.
A Grade II injury is associated with a partial syndesmotic disruption, typically with partial tearing of the AITFL and interosseous ligament. These injuries may be stable or accompanied by mild instability, and provocative testing is usually positive. X-rays are typically normal with Grade II injuries, but may display subtle radiographic findings suggestive of a syndesmotic injury. Treatment of Grade II injuries is somewhat controversial and should be an individualized decision based upon the patient’s age, activity level, clinical exam, and imaging findings. Therefore, treatment of Grade II syndesmotic injuries may include a trial of conservative management or surgical intervention.
A Grade III injury represents inherent instability of the distal tibiofibular joint with complete disruption of all syndesmotic ligaments, with or without involvement of the deltoid ligament. X-rays will be positive in Grade III syndesmotic injuries because of the complete disruption of syndesmotic ligaments. All Grade III injuries require surgical intervention with a syndesmotic screw or other stabilization procedure.1,6-8,15
Continue to: A 3-stage rehabilitation protocol
A 3-stage rehabilitation protocol
When conservative management is deemed appropriate for a stable syndesmotic sprain, a 3-stage rehabilitation protocol is typically utilized.
The acute phase focuses on protection, pain control, and decreasing inflammation. The patient’s ankle is often immobilized in a cast or controlled ankle movement (CAM) boot. The patient is typically allowed to bear weight in the immobilizer during this phase as long as he/she is pain-free. If pain is present with weight bearing despite immobilization, non-weight bearing is recommended. The patient is instructed to elevate the lower extremity, take anti-inflammatory medication, and ice the affected ankle. Additionally, physical therapy modalities may be utilized to help with edema and pain. Joint immobilization is typically employed for 1 to 3 weeks post-injury. In the acute phase, the patient may also work with a physical therapist or athletic trainer on passive range of motion (ROM), progressing to active ROM as tolerated.1,5,7,8,19
The patient can transition from the CAM boot to a lace-up ankle brace when he/she is able to bear full weight and can navigate stairs without pain, which typically occurs around 3 to 6 weeks post-injury.1,5,7 A pneumatic walking brace may also be used as a transition device to provide added stabilization.
In the sub-acute phase, rehabilitation may progress to increase ankle mobility, strengthening, neuromuscular control, and to allow the patient to perform activities of daily living.5-7
The advanced training phase includes continued neuromuscular control, increased strengthening, plyometrics, agility, and sports-specific drills.5 Athletes are allowed to return to full participation when they have regained full ROM, are able to perform sport-specific agility drills without pain or instability, and have near-normal strength.5-7 Some authors also advocate that a Single Leg Hop Test should be included in the physical exam, and that it should be pain free prior to allowing an athlete to return to competition.20 Both progression in physical rehabilitation and return to sport should be individualized based upon injury severity, patient functionality, and physical exam findings.
Continue to: Outcomes forecast
Outcomes forecast: Variable
The resolution of symptoms and return to competition after a syndesmotic injury is variable. In one cohort study of cadets (N = 614) at the United States Military Academy, the average time lost from a syndesmotic ankle sprain was 9.82 days (range 3-21 days).9 In a retrospective review of National Hockey League players, average time to return to competition after a syndesmotic ankle injury sprain (n = 14) was 45 days (range 6-137 days) vs 1.4 days (range 0-6 days) for lateral ankle sprains (n = 5).21 In another study, National Football League players with syndesmotic sprains (n = 36) had a mean time loss from play of 15.4 days (± 11.1 days) vs 6.5 days (± 6.5 days) of time loss from play in those with lateral ankle sprains (n = 53).22
Although there is a fair amount of variability among studies, most authors agree that the average athlete can expect to return to sport 4 to 8 weeks post-injury with conservative management.19 At least 1 study suggests that the average time to return to sport in patients with Grade III syndesmotic injuries who undergo surgical treatment with a syndesmotic screw is 41 days (range 32-48).23 The differences in return to sport may be related to severity of injury and/or type of activity.
Persistent symptoms are relatively common after conservative management of syndesmotic injuries. One case series found that 36% of patients treated conservatively had complaints of persistent mild-to-moderate ankle stiffness, 23% had mild-to-moderate pain, and 18% had mild-to-moderate ankle swelling.24 Despite these symptoms, 86% of the patients rated their ankle function as good after conservative treatment.24 In patients with persistent symptoms, other possible etiologies should be considered including neurologic injury, complex regional pain syndrome, osteochondral defect, loose body, or other sources that may be contributing to pain, swelling, or delayed recovery.
At least 1 randomized controlled trial (RCT) investigated the utility of platelet rich plasma (PRP) injections around the injured AITFL in the setting of an acute syndesmotic injury. The study showed promising results, including quicker return to play, restabilization of the syndesmotic joint, and less residual pain;25 however, the study population was relatively small (N = 16), and the authors believed that more research is required on the benefits of PRP therapy in syndesmotic injuries before recommendations can be made.
An ounce of preventionis worth a pound of cure
Although injury is not always avoidable, there are measures that can help prevent ankle sprains and facilitate return to play after injury. As previously mentioned, athletes should be able to demonstrate the ability to run, cut, jump, and perform sport-specific activities without limitations prior to being allowed to return to sport after injury.5-7,26 Additionally, issues with biomechanics and functional deficits should be analyzed and addressed. By targeting specific strength deficits, focusing on proprioceptive awareness, and working on neuromuscular control, injury rates and recurrent injuries can be minimized. One RCT showed a 35% reduction in the recurrence rate of lateral ankle sprains with the use of an unsupervised home-based proprioceptive training program.27
Continue to: Strength training...
Strength training, proprioceptive and neuromuscular control activities, and low-risk activities such as jogging, biking, and swimming do not necessarily require the use of prophylactic bracing. However, because syndesmotic injuries are associated with recurrent ankle injuries, prophylactic bracing should be used during high-risk activities that involve agility maneuvers and jumping. Substantial evidence demonstrates that the use of ankle taping or ankle bracing decreases the incidence of ankle injuries, particularly in those who have had previous ankle injuries.26 In one study (N = 450), only 3% of athletes with a history of prior ankle injuries suffered a recurrent ankle sprain when using an ankle orthosis compared with a 17% injury rate in the control group.28
More recently, 2 separate studies by McGuine et al demonstrated that the use of lace-up ankle braces led to a reduction in the incidence of acute ankle injuries by 61% among 2081 high-school football players, and resulted in a significant reduction in acute ankle injuries in a study of 1460 male and female high-school basketball players, compared with the control groups.29,30
CASE
Ten days after injuring himself, the patient returns for a follow-up exam. Despite using the walking brace and crutches, he is still having significant difficulty bearing weight. He reports a sensation of instability in the right ankle. On exam, you note visible edema of the right ankle and ecchymosis over the lateral ankle, as well as moderate tenderness to palpation over the area of the ATFL and deltoid ligament. Tenderness over the medial malleolus, lateral malleolus, fifth metatarsal, and navicular is absent. Pain is reproducible with external rotation, and a Squeeze Test is positive. There is no tenderness over the proximal tibia or fibula. The patient is neurovascularly intact.
You order stress x-rays, which show widening of the medial clear space. The patient is placed in a CAM boot, instructed to continue non–weight-bearing on the ankle, and referred to a local foot and ankle surgeon for consideration of surgical fixation.
CORRESPONDENCE
John T. Nickless, MD, Division of Primary Care Sports Medicine, Department of Orthopedic Surgery, Rush University Medical Center, 1611 W. Harrison Street, Suite 200, Chicago, IL, 60612; jack.nickless@rushortho.com.
CASE
A 19-year-old college football player presents to your outpatient family practice clinic after suffering a right ankle injury during a football game over the weekend. He reports having his right ankle planted on the turf with his foot externally rotated when an opponent fell onto his posterior right lower extremity. He reports having felt immediate pain in the area of the right ankle and requiring assistance off of the field, as he had difficulty walking. The patient was taken to the emergency department where x-rays of the right foot and ankle did not show any signs of acute fracture or dislocation. The patient was diagnosed with a lateral ankle sprain, placed in a pneumatic ankle walking brace, and given crutches.
A high ankle sprain, or distal tibiofibular syndesmotic injury, can be an elusive diagnosis and is often mistaken for the more common lateral ankle sprain. Syndesmotic injuries have been documented to occur in approximately 1% to 10% of all ankle sprains.1-3 The highest number of these injuries occurs between the ages of 18 and 34 years, and they are more frequently seen in athletes than in nonathletes, particularly those who play collision sports, such as football, ice hockey, rugby, wrestling, and lacrosse.1-9 In one study by Hunt et al,10 syndesmotic injuries accounted for 24.6% of all ankle injuries in National Collegiate Athletic Association (NCAA) football players. Incidence continues to grow as recognition of high ankle sprains increases among medical professionals.1,5 Identification of syndesmotic injury is critical, as lack of detection can lead to extensive time missed from athletic participation and chronic ankle dysfunction, including pain and instability.2,4,6,11
Back to basics: A brief anatomy review
Stability in the distal tibiofibular joint is maintained by the syndesmotic ligaments, which include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the transverse ligament, and the interosseous ligament.3-6,8 This complex of ligaments stabilizes the fibula within the incisura of the tibia and maintains a stable ankle mortise.1,4,5,11 The deep portion of the deltoid ligament also adds stability to the syndesmosis and may be disrupted by a syndesmotic injury.2,5-7,11
Mechanisms of injury: From most common to less likely
The distal tibiofibular syndesmosis is disrupted when an injury forces apart the distal tibiofibular joint. The most commonly reported means of injury is external rotation with hyper-dorsiflexion of the ankle.1-3,5,6,11 With excessive external rotation of the forefoot, the talus is forced against the medial aspect of the fibula, resulting in separation of the distal tibia and fibula and injury to the syndesmotic ligaments.2,3,5,6 Injuries associated with external rotation are commonly seen in sports that immobilize the ankle within a rigid boot, such as skiing and ice hockey.1,2,5 Some authors have suggested that a planovalgus foot alignment may place athletes at inherent risk for an external rotation ankle injury.5,6
Syndesmotic injury may also occur with hyper-dorsiflexion, as the anterior, widest portion of the talus rotates into the ankle mortise, wedging the tibia and fibula apart.2,3,5 There have also been reports of syndesmotic injuries associated with internal rotation, plantar flexion, inversion, and eversion.3,5,11 Therefore, physicians should maintain a high index of suspicion for injury to the distal tibiofibular joint, regardless of the mechanism of injury.
Presentation and evaluation
Observation of the patient and visualization of the affected ankle can provide many clues. Many patients will have difficulty walking after suffering a syndesmotic injury and may require the use of an assistive device.5 The inability to bear weight after an ankle injury points to a more severe diagnosis, such as an ankle fracture or syndesmotic injury, as opposed to a simple lateral ankle sprain. Patients may report anterior ankle pain, a sensation of instability with weight bearing on the affected ankle, or have persistent symptoms despite a course of conservative treatment. Also, they can have a variable amount of edema and ecchymosis associated with their injury; a minimal extent of swelling or ecchymosis does not exclude syndesmotic injury.3
A large percentage of patients will present with a concomitant sprain of the lateral ligaments associated with lateral swelling and bruising. One study found that 91% of syndesmotic injuries involved at least 1 of the lateral collateral ligaments (anterior talofibular ligament [ATFL], calcaneofibular ligament [CFL], or posterior talofibular ligament [PTFL]).12 Patients may have pain or a sensation of instability when pushing off with the toes,5 and patients with syndesmotic injuries often have tenderness to palpation over the distal anterolateral ankle or syndesmotic ligaments.7
Continue to: A thorough examination...
A thorough examination of the ankle, including palpation of common fracture sites, is important. Employ the Ottawa Ankle Rules (see http://www.theottawarules.ca/ankle_rules) to investigate for: tenderness to palpation over the posterior 6 cm of the posterior aspects of the distal medial and lateral malleoli; tenderness over the navicular; tenderness over the base of the fifth metatarsal; and/or the inability to bear weight on the affected lower extremity immediately after injury or upon evaluation in the physician’s office. Any of these findings should raise concern for a possible fracture (see “Adult foot fractures: A guide”) and require an x-ray(s) for further evaluation.13
Perform range-of-motion and strength testing with regard to ankle dorsiflexion, plantar flexion, abduction, adduction, inversion, and eversion. Palpate the ATFL, CFL, and PTFL for tenderness, as these structures may be involved to varying degrees in lateral ankle sprains. An anterior drawer test (see https://www.youtube.com/watch?v=vAcBEYZKcto) may be positive with injury to the ATFL. This test is performed by stabilizing the distal tibia with one hand and using the other hand to grasp the posterior aspect of the calcaneus and apply an anterior force. The test is positive if the talus translates forward, which correlates with laxity or rupture of the ATFL.13 The examiner should also palpate the Achilles tendon, peroneal tendons just posterior to the lateral malleolus, and the tibialis posterior tendon just posterior to the medial malleolus to inspect for tenderness or defects that may be signs of injury to these tendons.
An associated Weber B or C fracture? Trauma causing ankle syndesmosis injuries may be associated with Weber B or Weber C distal fibula fractures.7 Weber B fractures occur in the distal fibula at the level of the ankle joint (see FIGURE 1). These types of fractures are typically associated with external rotation injuries and are usually not associated with disruption of the interosseous membrane.
Weber C fractures are distal fibular fractures occurring above the level of the ankle joint. These fractures are also typically associated with external ankle rotation injuries and include disruption of the syndesmosis and deltoid ligament.14
Also pay special attention to the proximal fibula, as syndesmotic injuries are commonly associated with a Maisonneuve fracture, which is a proximal fibula fracture associated with external rotation forces of the ankle (see FIGURE 1).1,2,4,11,14,15 Further workup should occur in any patient with the possibility of a Weber- or Maisonneuve-type fracture.
Continue to: Multiple tests...
Multiple tests are available to investigate the possibility of a syndesmotic injury and to assess return-to-sport readiness, including the External Rotation Test, the Squeeze Test, the Crossed-Leg Test, the Dorsiflexion Compression Test, the Cotton Test, the Stabilization Test, the Fibular Translation Test, and the Single Leg Hop Test (see TABLE1-3,5,6,16,17). The External Rotation Test is noted by some authors to have the highest interobserver reliability, and is our preferred test.2 The Squeeze Test also has moderate interobserver reliability.2 There is a significant degree of variation among the sensitivity and specificity of these diagnostic tests, and no single test is sufficiently reliable or accurate to diagnose a syndesmotic ankle injury. Therefore, it is recommended to use multiple physical exam maneuvers, the history and mechanism of injury, and findings on imaging studies in conjunction to make the diagnosis of a syndesmotic injury.1,16
Imaging: Which modes and when?
The initial workup should include ankle x-rays when evaluating for the possibility of a distal tibiofibular syndesmosis injury. While the Ottawa Ankle Rules are helpful in providing guidance with regard to x-rays, suspicion of a syndesmotic injury mandates x-rays to determine the stability of the joint and rule out fracture. The European Society of Sports Traumatology, Knee Surgery and Arthroscopy–European Foot and Ankle Associates (ESSKA-AFAS) recommend, at a minimum, obtaining anteroposterior (AP)- and mortise-view ankle x-rays to investigate the tibiofibular clear space, medial clear space, and tibiofibular overlap.7 Most physicians also include a lateral ankle x-ray.
If possible, images should be performed while the patient is bearing weight to further evaluate stability. Radiographic findings that support the diagnosis of syndesmotic injury include a tibiofibular clear space > 6 mm on AP view, medial clear space > 4 mm on mortise view, or tibiofibular overlap < 6 mm on AP view or < 1 mm on mortise view (see FIGURES 2 and 3).1,3,5,8 Additionally, if you suspect a proximal fibular fracture, obtain an x-ray series of the proximal tibia and fibula to investigate the possibility of a Maisonneuve injury.1,2,4,11
If you continue to suspect a syndesmotic injury despite normal x-rays, obtain stress x-rays, in addition to the AP and mortise views, to ensure stability. These x-rays include AP and mortise ankle views with manual external rotation of the ankle joint, which may demonstrate abnormalities not seen on standard x-rays. Bilateral imaging can also be useful to further assess when mild abnormalities vs symmetric anatomic variants are in question.1,7
If there is concern for an unstable injury, refer the patient to a foot and ankle surgeon, who may pursue magnetic resonance imaging (MRI) or standing computed tomography (CT).1,2,5,7 MRI is the recommended choice for further evaluation of a syndesmotic injury, as it is proven to be accurate in evaluating the integrity of the syndesmotic ligaments (see FIGURES 4 and 5).18 MRI has demonstrated 100% sensitivity for detecting AITFL and PITFL injuries, as well as 93% and 100% specificity for AITFL and PITFL tears, respectively.8 A weight-bearing CT scan, particularly axial views, can also be a useful adjunct, as it is more sensitive than standard x-rays for assessing for mild diastasis. Although CT can provide an assessment of bony structures, it is not able to evaluate soft tissue structures, limiting its utility in evaluation of syndesmotic injuries.1,7
Continue to: Although not the standard of care...
Although not the standard of care, ultrasonography (US) is gaining traction as a means of investigating the integrity of the syndesmotic ligaments. US is inexpensive, readily available in many clinics, allows for dynamic testing, and avoids radiation exposure.7 However, US requires a skilled sonographer with experience in the ankle joint for an accurate diagnosis. If the workup with advanced imaging is inconclusive, but a high degree of suspicion remains for an unstable syndesmotic injury, consider arthroscopy to directly visualize and assess the syndesmotic structures.1,2,5,7,8
Grading the severity of the injury and pursuing appropriate Tx
Typically, the severity of a syndesmotic injury is classified as fitting into 1 of 3 categories: Grade I and II injuries are the most common, each accounting for 40% of syndesmotic injuries, while 20% of high ankle sprains are classified as Grade III.12
A Grade I injury consists of a stable syndesmotic joint without abnormal radiographic findings. There may be associated tenderness to palpation over the distal tibiofibular joint, and provocative testing may be subtle or normal. These injuries are often minor and able to be treated conservatively.
A Grade II injury is associated with a partial syndesmotic disruption, typically with partial tearing of the AITFL and interosseous ligament. These injuries may be stable or accompanied by mild instability, and provocative testing is usually positive. X-rays are typically normal with Grade II injuries, but may display subtle radiographic findings suggestive of a syndesmotic injury. Treatment of Grade II injuries is somewhat controversial and should be an individualized decision based upon the patient’s age, activity level, clinical exam, and imaging findings. Therefore, treatment of Grade II syndesmotic injuries may include a trial of conservative management or surgical intervention.
A Grade III injury represents inherent instability of the distal tibiofibular joint with complete disruption of all syndesmotic ligaments, with or without involvement of the deltoid ligament. X-rays will be positive in Grade III syndesmotic injuries because of the complete disruption of syndesmotic ligaments. All Grade III injuries require surgical intervention with a syndesmotic screw or other stabilization procedure.1,6-8,15
Continue to: A 3-stage rehabilitation protocol
A 3-stage rehabilitation protocol
When conservative management is deemed appropriate for a stable syndesmotic sprain, a 3-stage rehabilitation protocol is typically utilized.
The acute phase focuses on protection, pain control, and decreasing inflammation. The patient’s ankle is often immobilized in a cast or controlled ankle movement (CAM) boot. The patient is typically allowed to bear weight in the immobilizer during this phase as long as he/she is pain-free. If pain is present with weight bearing despite immobilization, non-weight bearing is recommended. The patient is instructed to elevate the lower extremity, take anti-inflammatory medication, and ice the affected ankle. Additionally, physical therapy modalities may be utilized to help with edema and pain. Joint immobilization is typically employed for 1 to 3 weeks post-injury. In the acute phase, the patient may also work with a physical therapist or athletic trainer on passive range of motion (ROM), progressing to active ROM as tolerated.1,5,7,8,19
The patient can transition from the CAM boot to a lace-up ankle brace when he/she is able to bear full weight and can navigate stairs without pain, which typically occurs around 3 to 6 weeks post-injury.1,5,7 A pneumatic walking brace may also be used as a transition device to provide added stabilization.
In the sub-acute phase, rehabilitation may progress to increase ankle mobility, strengthening, neuromuscular control, and to allow the patient to perform activities of daily living.5-7
The advanced training phase includes continued neuromuscular control, increased strengthening, plyometrics, agility, and sports-specific drills.5 Athletes are allowed to return to full participation when they have regained full ROM, are able to perform sport-specific agility drills without pain or instability, and have near-normal strength.5-7 Some authors also advocate that a Single Leg Hop Test should be included in the physical exam, and that it should be pain free prior to allowing an athlete to return to competition.20 Both progression in physical rehabilitation and return to sport should be individualized based upon injury severity, patient functionality, and physical exam findings.
Continue to: Outcomes forecast
Outcomes forecast: Variable
The resolution of symptoms and return to competition after a syndesmotic injury is variable. In one cohort study of cadets (N = 614) at the United States Military Academy, the average time lost from a syndesmotic ankle sprain was 9.82 days (range 3-21 days).9 In a retrospective review of National Hockey League players, average time to return to competition after a syndesmotic ankle injury sprain (n = 14) was 45 days (range 6-137 days) vs 1.4 days (range 0-6 days) for lateral ankle sprains (n = 5).21 In another study, National Football League players with syndesmotic sprains (n = 36) had a mean time loss from play of 15.4 days (± 11.1 days) vs 6.5 days (± 6.5 days) of time loss from play in those with lateral ankle sprains (n = 53).22
Although there is a fair amount of variability among studies, most authors agree that the average athlete can expect to return to sport 4 to 8 weeks post-injury with conservative management.19 At least 1 study suggests that the average time to return to sport in patients with Grade III syndesmotic injuries who undergo surgical treatment with a syndesmotic screw is 41 days (range 32-48).23 The differences in return to sport may be related to severity of injury and/or type of activity.
Persistent symptoms are relatively common after conservative management of syndesmotic injuries. One case series found that 36% of patients treated conservatively had complaints of persistent mild-to-moderate ankle stiffness, 23% had mild-to-moderate pain, and 18% had mild-to-moderate ankle swelling.24 Despite these symptoms, 86% of the patients rated their ankle function as good after conservative treatment.24 In patients with persistent symptoms, other possible etiologies should be considered including neurologic injury, complex regional pain syndrome, osteochondral defect, loose body, or other sources that may be contributing to pain, swelling, or delayed recovery.
At least 1 randomized controlled trial (RCT) investigated the utility of platelet rich plasma (PRP) injections around the injured AITFL in the setting of an acute syndesmotic injury. The study showed promising results, including quicker return to play, restabilization of the syndesmotic joint, and less residual pain;25 however, the study population was relatively small (N = 16), and the authors believed that more research is required on the benefits of PRP therapy in syndesmotic injuries before recommendations can be made.
An ounce of preventionis worth a pound of cure
Although injury is not always avoidable, there are measures that can help prevent ankle sprains and facilitate return to play after injury. As previously mentioned, athletes should be able to demonstrate the ability to run, cut, jump, and perform sport-specific activities without limitations prior to being allowed to return to sport after injury.5-7,26 Additionally, issues with biomechanics and functional deficits should be analyzed and addressed. By targeting specific strength deficits, focusing on proprioceptive awareness, and working on neuromuscular control, injury rates and recurrent injuries can be minimized. One RCT showed a 35% reduction in the recurrence rate of lateral ankle sprains with the use of an unsupervised home-based proprioceptive training program.27
Continue to: Strength training...
Strength training, proprioceptive and neuromuscular control activities, and low-risk activities such as jogging, biking, and swimming do not necessarily require the use of prophylactic bracing. However, because syndesmotic injuries are associated with recurrent ankle injuries, prophylactic bracing should be used during high-risk activities that involve agility maneuvers and jumping. Substantial evidence demonstrates that the use of ankle taping or ankle bracing decreases the incidence of ankle injuries, particularly in those who have had previous ankle injuries.26 In one study (N = 450), only 3% of athletes with a history of prior ankle injuries suffered a recurrent ankle sprain when using an ankle orthosis compared with a 17% injury rate in the control group.28
More recently, 2 separate studies by McGuine et al demonstrated that the use of lace-up ankle braces led to a reduction in the incidence of acute ankle injuries by 61% among 2081 high-school football players, and resulted in a significant reduction in acute ankle injuries in a study of 1460 male and female high-school basketball players, compared with the control groups.29,30
CASE
Ten days after injuring himself, the patient returns for a follow-up exam. Despite using the walking brace and crutches, he is still having significant difficulty bearing weight. He reports a sensation of instability in the right ankle. On exam, you note visible edema of the right ankle and ecchymosis over the lateral ankle, as well as moderate tenderness to palpation over the area of the ATFL and deltoid ligament. Tenderness over the medial malleolus, lateral malleolus, fifth metatarsal, and navicular is absent. Pain is reproducible with external rotation, and a Squeeze Test is positive. There is no tenderness over the proximal tibia or fibula. The patient is neurovascularly intact.
You order stress x-rays, which show widening of the medial clear space. The patient is placed in a CAM boot, instructed to continue non–weight-bearing on the ankle, and referred to a local foot and ankle surgeon for consideration of surgical fixation.
CORRESPONDENCE
John T. Nickless, MD, Division of Primary Care Sports Medicine, Department of Orthopedic Surgery, Rush University Medical Center, 1611 W. Harrison Street, Suite 200, Chicago, IL, 60612; jack.nickless@rushortho.com.
1. Switaj PJ, Mendoza M, Kadakia AR. Acute and chronic Injuries to the syndesmosis. Clin Sports Med. 2015;34:643-677.
2. Scheyerer MJ, Helfet DL, Wirth S, et al. Diagnostics in suspicion of ankle syndesmotic injury. Am J Orthop. 2011;40:192-197.
3. Smith KM, Kovacich-Smith KJ, Witt M. Evaluation and management of high ankle sprains. Clin Podiatr Med Surg. 2001;18:443-456.
4. Reissig J, Bitterman A, Lee S. Common foot and ankle injuries: what not to miss and how best to manage. J Am Osteopath Assoc. 2017;117:98-104.
5. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2:460-470.
6. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35:1197-1207.
7. Vopat ML, Vopat BG, Lubberts B, et al. Current trends in the diagnosis and management of syndesmotic injury. Curr Rev Musculoskelet Med. 2017;10:94-103.
8. Mak MF, Gartner L, Pearce CJ. Management of syndesmosis injuries in the elite athlete. Foot Ankle Clin. 2013;18:195-214.
9. Waterman BR, Belmont PJ, Cameron KL, et al. Epidemiology of ankle sprain at the United States Military Academy. Am J Sports Med. 2010;38:797-803.
10. Hunt KJ, George E, Harris AHS, et al. Epidemiology of syndesmosis injuries in intercollegiate football: incidence and risk factors from National Collegiate Athletic Association injury surveillance system data from 2004-2005 to 2008-2009. Clin J Sport Med. 2013;23:278-282.
11. Schnetzke M, Vetter SY, Beisemann N, et al. Management of syndesmotic injuries: what is the evidence? World J Orthop. 2016;7:718-725.
12. de César PC, Ávila EM, de Abreu MR. Comparison of magnetic resonance imaging to physical examination for syndesmotic injury after lateral ankle sprain. Foot Ankle Int. 2011;32:1110-1114.
13. Ivins D. Acute ankle sprain: an update. Am Fam Physician. 2006;74:1714-1720.
14. Porter D, Rund A, Barnes AF, et al. Optimal management of ankle syndesmosis injuries. Open Access J Sports Med. 2014;5:173-182.
15. Press CM, Gupta A, Hutchinson MR. Management of ankle syndesmosis injuries in the athlete. Curr Sports Med Rep. 2009;8:228-233.
16. Sman AD, Hiller CE, Rae K, et al. Diagnostic accuracy of clinical tests for ankle syndesmosis injury. Br J Sports Med. 2015;49:323-329.
17. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14:232-236.
18. Hunt KJ. Syndesmosis injuries. Curr Rev Musculoskelet Med. 2013;6:304-312.
19. Miller TL, Skalak T. Evaluation and treatment recommendations for acute injuries to the ankle syndesmosis without associated fracture. Sports Med. 2014;44:179-188.
20. Miller BS, Downie BK, Johnson PD, et al. Time to return to play after high ankle sprains in collegiate football players: a prediction model. Sports Health. 2012;4:504-509.
21. Wright RW, Barile RJ, Surprenant DA, et al. Ankle syndesmosis sprains in National Hockey League players. Am J Sports Med. 2016;32:1941-1945.
22. Osbahr DC, Drakos MC, O’Loughlin PF, et al. Syndesmosis and lateral ankle sprains in the National Football League. Orthopedics. 2013;36:e1378-e1384.
23. Taylor DC, Tenuta JJ, Uhorchak JM, et al. Aggressive surgical treatment and early return to sports in athletes with grade III syndesmosis sprains. Am J Sports Med. 2007;35:1133-1138.
24. Taylor DC, Englehardt DL, Bassett FH. Syndesmosis sprains of the ankle: the influence of heterotopic ossification. Am J Sports Med. 1992;20:146-150.
25. Laver L, Carmont MR, McConkey MO, et al. Plasma rich in growth factors (PRGF) as a treatment for high ankle sprain in elite athletes: a randomized control trial. Knee Surg Sports Traumatol Arthrosc. 2014;23:3383-3392.
26. Kaminski TW, Hertel J, Amendola N, et al. National Athletic Trainers’ Association position statement: conservative management and prevention of ankle sprains in athletes. J Athl Train. 2013;48:528-545.
27. Hupperets MDW, Verhagen EALM, van Mechelen W. Effect of unsupervised home based proprioceptive training on recurrences of ankle sprain: randomised controlled trial. BMJ. 2009;339:b2684.
28. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985;13:259-262.
29. McGuine TA, Brooks A, Hetzel S. The effect of lace-up ankle braces on injury rates in high school basketball players. Am J Sports Med. 2011;39:1840-1848.
30. McGuine TA, Hetzel S, Wilson J, et al. The effect of lace-up ankle braces on injury rates in high school football players. Am J Sports Med. 2012;40:49-57.
1. Switaj PJ, Mendoza M, Kadakia AR. Acute and chronic Injuries to the syndesmosis. Clin Sports Med. 2015;34:643-677.
2. Scheyerer MJ, Helfet DL, Wirth S, et al. Diagnostics in suspicion of ankle syndesmotic injury. Am J Orthop. 2011;40:192-197.
3. Smith KM, Kovacich-Smith KJ, Witt M. Evaluation and management of high ankle sprains. Clin Podiatr Med Surg. 2001;18:443-456.
4. Reissig J, Bitterman A, Lee S. Common foot and ankle injuries: what not to miss and how best to manage. J Am Osteopath Assoc. 2017;117:98-104.
5. Williams GN, Allen EJ. Rehabilitation of syndesmotic (high) ankle sprains. Sports Health. 2010;2:460-470.
6. Williams GN, Jones MH, Amendola A. Syndesmotic ankle sprains in athletes. Am J Sports Med. 2007;35:1197-1207.
7. Vopat ML, Vopat BG, Lubberts B, et al. Current trends in the diagnosis and management of syndesmotic injury. Curr Rev Musculoskelet Med. 2017;10:94-103.
8. Mak MF, Gartner L, Pearce CJ. Management of syndesmosis injuries in the elite athlete. Foot Ankle Clin. 2013;18:195-214.
9. Waterman BR, Belmont PJ, Cameron KL, et al. Epidemiology of ankle sprain at the United States Military Academy. Am J Sports Med. 2010;38:797-803.
10. Hunt KJ, George E, Harris AHS, et al. Epidemiology of syndesmosis injuries in intercollegiate football: incidence and risk factors from National Collegiate Athletic Association injury surveillance system data from 2004-2005 to 2008-2009. Clin J Sport Med. 2013;23:278-282.
11. Schnetzke M, Vetter SY, Beisemann N, et al. Management of syndesmotic injuries: what is the evidence? World J Orthop. 2016;7:718-725.
12. de César PC, Ávila EM, de Abreu MR. Comparison of magnetic resonance imaging to physical examination for syndesmotic injury after lateral ankle sprain. Foot Ankle Int. 2011;32:1110-1114.
13. Ivins D. Acute ankle sprain: an update. Am Fam Physician. 2006;74:1714-1720.
14. Porter D, Rund A, Barnes AF, et al. Optimal management of ankle syndesmosis injuries. Open Access J Sports Med. 2014;5:173-182.
15. Press CM, Gupta A, Hutchinson MR. Management of ankle syndesmosis injuries in the athlete. Curr Sports Med Rep. 2009;8:228-233.
16. Sman AD, Hiller CE, Rae K, et al. Diagnostic accuracy of clinical tests for ankle syndesmosis injury. Br J Sports Med. 2015;49:323-329.
17. Amendola A, Williams G, Foster D. Evidence-based approach to treatment of acute traumatic syndesmosis (high ankle) sprains. Sports Med Arthrosc. 2006;14:232-236.
18. Hunt KJ. Syndesmosis injuries. Curr Rev Musculoskelet Med. 2013;6:304-312.
19. Miller TL, Skalak T. Evaluation and treatment recommendations for acute injuries to the ankle syndesmosis without associated fracture. Sports Med. 2014;44:179-188.
20. Miller BS, Downie BK, Johnson PD, et al. Time to return to play after high ankle sprains in collegiate football players: a prediction model. Sports Health. 2012;4:504-509.
21. Wright RW, Barile RJ, Surprenant DA, et al. Ankle syndesmosis sprains in National Hockey League players. Am J Sports Med. 2016;32:1941-1945.
22. Osbahr DC, Drakos MC, O’Loughlin PF, et al. Syndesmosis and lateral ankle sprains in the National Football League. Orthopedics. 2013;36:e1378-e1384.
23. Taylor DC, Tenuta JJ, Uhorchak JM, et al. Aggressive surgical treatment and early return to sports in athletes with grade III syndesmosis sprains. Am J Sports Med. 2007;35:1133-1138.
24. Taylor DC, Englehardt DL, Bassett FH. Syndesmosis sprains of the ankle: the influence of heterotopic ossification. Am J Sports Med. 1992;20:146-150.
25. Laver L, Carmont MR, McConkey MO, et al. Plasma rich in growth factors (PRGF) as a treatment for high ankle sprain in elite athletes: a randomized control trial. Knee Surg Sports Traumatol Arthrosc. 2014;23:3383-3392.
26. Kaminski TW, Hertel J, Amendola N, et al. National Athletic Trainers’ Association position statement: conservative management and prevention of ankle sprains in athletes. J Athl Train. 2013;48:528-545.
27. Hupperets MDW, Verhagen EALM, van Mechelen W. Effect of unsupervised home based proprioceptive training on recurrences of ankle sprain: randomised controlled trial. BMJ. 2009;339:b2684.
28. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985;13:259-262.
29. McGuine TA, Brooks A, Hetzel S. The effect of lace-up ankle braces on injury rates in high school basketball players. Am J Sports Med. 2011;39:1840-1848.
30. McGuine TA, Hetzel S, Wilson J, et al. The effect of lace-up ankle braces on injury rates in high school football players. Am J Sports Med. 2012;40:49-57.
PRACTICE RECOMMENDATIONS
› Maintain a high level of suspicion for syndesmotic injury in any athlete describing an external rotation or hyper-dorsiflexion ankle injury. A
› Obtain weight-bearing anteroposterior- and mortise-view ankle x-rays in all cases of suspected syndesmotic injuries. A
› Consider stress x-rays of the affected ankle, contralateral ankle x-rays for comparison views, or advanced imaging with magnetic resonance imaging (MRI) or computed tomography if initial x-rays are unrevealing. A
› Treat stable syndesmotic injuries with conservative measures and rehabilitation. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series