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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
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Cancer-survivor pain: What’s the PCP to do?
What to make of the new ACC/AHA high blood pressure guidelines
Resources
- Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. J Am Coll Cardiol. 2017:S0735-S1097.
- James PA, Oparil S, Carter BL, et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
Resources
- Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. J Am Coll Cardiol. 2017:S0735-S1097.
- James PA, Oparil S, Carter BL, et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
Resources
- Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. J Am Coll Cardiol. 2017:S0735-S1097.
- James PA, Oparil S, Carter BL, et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
How do hyaluronic acid and corticosteroid injections compare for knee OA relief?
EVIDENCE SUMMARY
A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.1 At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).
At 3 and 6 months, HA improves pain, but not function, more than CS
Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.2 All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.
Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.
Triamcinolone improves pain, function, but not for long
A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.3 Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.
The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.
Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.
HA (mostly) improves pain, function more than betamethasone
A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.4 Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.
The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).
The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).4
RECOMMENDATIONS
The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.5 They also couldn’t recommend using HA (SOR: strong).
The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.6 In 2014, NICE recommended against offering intra-articular HA injections for managing OA.
The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).7 They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).
1. Bannuru RR, Schmid CH, Kent DM, et al. Comparative effectiveness of pharmacologic interventions for knee osteoarthritis: a systematic review and network meta-analysis. Ann Intern Med. 2015;162:46-54.
2. Wang F, He X. Intra-articular hyaluronic acid and corticosteroids in the treatment of knee osteoarthritis: a meta-analysis. Exp Ther Med. 2015;9:493-500.
3. Tammachote N, Kanitnate S, Yakumpor T, et al. Intra-articular, single-shot Hylan G-F 20 hyaluronic acid injection compared with corticosteroid in knee osteoarthritis: a double-blind, randomized controlled trial. J Bone Joint Surg Am. 2016;98:885-892.
4. Trueba Davalillo CA, Trueba Vasavilbaso C, Navarrete Alvarez JM, et al. Clinical efficacy of intra-articular injections in knee osteoarthritis: a prospective randomized study comparing hyaluronic acid and betamethasone. Open Access Rheumatol Res Rev. 2015;7:9-18.
5. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis of the Knee: Evidence-Based Guideline. 2nd ed. Available at: http://www.aaos.org/cc_files/aaosorg/research/guidelines/treatmentofosteoarthritisofthekneeguideline.pdf. Accessed May 15, 2016.
6. National Institute for Health and Care Excellence. Osteoarthritis: Care and Management. Available at: https://www.nice.org.uk/guidance/cg177/chapter/1-recommendations. Accessed May 15, 2016.
7. United States Department of Veterans Affairs, Department of Defense. VA/DoD Clinical Practice Guideline for the Non-Surgical Management of Hip and Knee Osteoarthritis. Available at: http://www.healthquality.va.gov/guidelines/CD/OA/VADoDOACPGFINAL090214.pdf. Accessed May 15, 2016.
EVIDENCE SUMMARY
A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.1 At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).
At 3 and 6 months, HA improves pain, but not function, more than CS
Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.2 All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.
Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.
Triamcinolone improves pain, function, but not for long
A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.3 Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.
The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.
Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.
HA (mostly) improves pain, function more than betamethasone
A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.4 Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.
The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).
The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).4
RECOMMENDATIONS
The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.5 They also couldn’t recommend using HA (SOR: strong).
The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.6 In 2014, NICE recommended against offering intra-articular HA injections for managing OA.
The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).7 They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).
EVIDENCE SUMMARY
A 2015 network meta-analysis of 137 RCTs with 33,243 patients (ages 45-76 years) with knee OA compared the effectiveness of a variety of treatments including intra-articular CS and HA.1 At 3 months, the effect on pain was not significantly different between the CS and HA groups (12 trials; effect size [ES]=0.02; 95% confidence interval [CI], -0.12 to 0.17). However, a small but significant improvement in function was noted (scoring system not defined) at 3 months favoring HA (ES=0.24; 95% CI, 0.06-0.43; number of trials not specified).
At 3 and 6 months, HA improves pain, but not function, more than CS
Another meta-analysis published in 2015 examined the effectiveness of intra-articular CS and HA in 7 RCTs with 583 patients with knee OA.2 All 7 trials were included in the network meta-analysis and discussed separately to evaluate different time points.
Pain at one month wasn’t significantly different using a visual analog score (VAS) of one to 100 (4 trials; 245 patients; mean difference [MD]=1.66 points; 95% CI, -0.90 to 4.23). At 3 and 6 months, the HA group reported significantly reduced pain compared with the CS group (3 months: 3 trials; 320 patients; MD=12.58 points; 95% CI, -17.76 to -7.40; 6 months: 5 trials; 411 patients; MD=9.01 points; 95% CI, -12.62 to -5.40). There were no significant differences in function outcomes (Index of severity for OA of the knee by Lequesne et al; The Knee Society Clinical Rating System), maximum flexion, or adverse events.
Triamcinolone improves pain, function, but not for long
A 2016 double-blind RCT of 110 patients with knee OA compared intra-articular HA and triamcinolone, assessing pain and function at intervals between 24 hours and 6 months.3 Patients in the HA group received a single injection of 6 mL hylan G-F 20 (Synvisc); patients in the CS group received 1 mL of triamcinolone acetonide 40 mg and 5 mL of 1% lidocaine with epinephrine.
The CS group reported significantly less pain (VAS score 1 to 100) at 24 hours than the HA group (24 points vs 36 points; P=.002); relief lasted as long as one week (14 points vs 23 points; P=.018). After the first week, no difference was seen in pain between groups for as long as 6 months.
Function, assessed by a modified Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC 1 to 100; higher score indicates worse pain, stiffness, and function) showed a significant improvement with CS at 2 weeks (25 points vs 31 points; P=.03), but no difference at any other time point up to 6 months.
HA (mostly) improves pain, function more than betamethasone
A 2015 RCT of 200 patients with knee OA compared the effectiveness of intra-articular HA and betamethasone.4 Evaluators were blinded and assessments were made at 3, 6, 9, and 12 months. The HA group received 2.5 mL of 1% HA (Suprahyal); the CS group received betamethasone dipropionate 5 mg plus betamethasone sodium phosphate 2 mg in 1 mL.
The CS group had significantly less pain (VAS 1 to 10) at 3 months compared with the HA group (2.2 points vs 3.1 points; P=.004), but the HA group had less pain at all other time points (6 months: 3.9 points vs 2.4 points; P=.0001; 9 months: 5.5 points vs 3.6 points; P=.0001; 12 months: 6 points vs 4.1 points; P=.0001).
The WOMAC function subscores (0 to 68; lower indicates more function) were significantly better at all follow-up points in the HA group compared with the CS group (3 months: 19 vs 25; P=.0001; 6 months: 17 vs 29; P=.0001; 9 months: 25 vs 42; P=.0001; 12 months: 28 vs 42; P=.0001).4
RECOMMENDATIONS
The American Academy of Orthopaedic Surgeons 2013 work group couldn’t recommend for or against using intra-articular CS for patients with symptomatic knee OA based on inconclusive evidence.5 They also couldn’t recommend using HA (SOR: strong).
The National Institute for Health and Care Excellence (NICE) stated in 2008 that intra-articular CS injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with OA.6 In 2014, NICE recommended against offering intra-articular HA injections for managing OA.
The US Veterans Administration and Department of Defense have issued guidelines stating that clinicians may consider intra-articular CS injections for patients with symptomatic knee OA (US Preventive Services Task Force [USPSTF] Grade B).7 They report insufficient evidence to recommend for or against the use of intra-articular HA with the caveat that HA may be considered for patients who don’t respond adequately to nonpharmacologic measures and who have an inadequate response, intolerable adverse events, or contraindications to other pharmacologic therapies (USPSTF Grade I).
1. Bannuru RR, Schmid CH, Kent DM, et al. Comparative effectiveness of pharmacologic interventions for knee osteoarthritis: a systematic review and network meta-analysis. Ann Intern Med. 2015;162:46-54.
2. Wang F, He X. Intra-articular hyaluronic acid and corticosteroids in the treatment of knee osteoarthritis: a meta-analysis. Exp Ther Med. 2015;9:493-500.
3. Tammachote N, Kanitnate S, Yakumpor T, et al. Intra-articular, single-shot Hylan G-F 20 hyaluronic acid injection compared with corticosteroid in knee osteoarthritis: a double-blind, randomized controlled trial. J Bone Joint Surg Am. 2016;98:885-892.
4. Trueba Davalillo CA, Trueba Vasavilbaso C, Navarrete Alvarez JM, et al. Clinical efficacy of intra-articular injections in knee osteoarthritis: a prospective randomized study comparing hyaluronic acid and betamethasone. Open Access Rheumatol Res Rev. 2015;7:9-18.
5. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis of the Knee: Evidence-Based Guideline. 2nd ed. Available at: http://www.aaos.org/cc_files/aaosorg/research/guidelines/treatmentofosteoarthritisofthekneeguideline.pdf. Accessed May 15, 2016.
6. National Institute for Health and Care Excellence. Osteoarthritis: Care and Management. Available at: https://www.nice.org.uk/guidance/cg177/chapter/1-recommendations. Accessed May 15, 2016.
7. United States Department of Veterans Affairs, Department of Defense. VA/DoD Clinical Practice Guideline for the Non-Surgical Management of Hip and Knee Osteoarthritis. Available at: http://www.healthquality.va.gov/guidelines/CD/OA/VADoDOACPGFINAL090214.pdf. Accessed May 15, 2016.
1. Bannuru RR, Schmid CH, Kent DM, et al. Comparative effectiveness of pharmacologic interventions for knee osteoarthritis: a systematic review and network meta-analysis. Ann Intern Med. 2015;162:46-54.
2. Wang F, He X. Intra-articular hyaluronic acid and corticosteroids in the treatment of knee osteoarthritis: a meta-analysis. Exp Ther Med. 2015;9:493-500.
3. Tammachote N, Kanitnate S, Yakumpor T, et al. Intra-articular, single-shot Hylan G-F 20 hyaluronic acid injection compared with corticosteroid in knee osteoarthritis: a double-blind, randomized controlled trial. J Bone Joint Surg Am. 2016;98:885-892.
4. Trueba Davalillo CA, Trueba Vasavilbaso C, Navarrete Alvarez JM, et al. Clinical efficacy of intra-articular injections in knee osteoarthritis: a prospective randomized study comparing hyaluronic acid and betamethasone. Open Access Rheumatol Res Rev. 2015;7:9-18.
5. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis of the Knee: Evidence-Based Guideline. 2nd ed. Available at: http://www.aaos.org/cc_files/aaosorg/research/guidelines/treatmentofosteoarthritisofthekneeguideline.pdf. Accessed May 15, 2016.
6. National Institute for Health and Care Excellence. Osteoarthritis: Care and Management. Available at: https://www.nice.org.uk/guidance/cg177/chapter/1-recommendations. Accessed May 15, 2016.
7. United States Department of Veterans Affairs, Department of Defense. VA/DoD Clinical Practice Guideline for the Non-Surgical Management of Hip and Knee Osteoarthritis. Available at: http://www.healthquality.va.gov/guidelines/CD/OA/VADoDOACPGFINAL090214.pdf. Accessed May 15, 2016.
Evidence-based answers from the Family Physicians Inquiries Network
EVIDENCE-BASED ANSWER:
Inconsistent evidence shows a small amount of pain relief early (one week to 3 months) with corticosteroid (CS) injections and an equally small improvement in pain relief and function later (3 to 12 months) with hyaluronic acid (HA) injections (strength of recommendation [SOR]: B, meta-analysis of a randomized controlled trial [RCT] and inconsistent RCTs).
Guidelines state that CS injections can be considered for symptomatic knee osteoarthritis (OA), but that insufficient evidence exists to recommend HA injections (SOR: B, evidence-based guidelines).
Time for another cup of coffee … or two
Nutrition enthusiasts have been saying for years that “we are what we eat.” In this issue of JFP, Drs. Malone and Tsai review the evidence regarding the medicinal properties of certain herbal and botanical supplements. (See here.) Although there are many unfounded claims about the health effects of a wide variety of supplements, increasing evidence from well-conducted randomized trials and large epidemiologic studies demonstrates that certain items we ingest have therapeutic value for a variety of conditions.
However, as Dr. Malone points out, herbal supplements and botanicals are not regulated by the US Food and Drug Administration, so manufacturers are not required to provide proof of effectiveness or safety to market their products. Some of these products have adverse effects. For example, butterbur can cause liver toxicity.1
Because about 38% of Americans use supplements, all primary care clinicians should know which products do—and do not—have evidence of efficacy.2 I suggest you read Dr. Malone’s 2-part article (part 2 is available here), but I can’t resist highlighting several of my favorites:
Coffee. Coffee used to be maligned because of its caffeine content, but more recent evidence suggests it protects against liver disease and has positive effects on cardiovascular disease and even mortality. (See Dr. Malone’s article for references.) There are no randomized trials, however, so we can’t be entirely sure if these associations are causal, but at least I can feel better about the 4 cups of coffee I drink every day!
Tea, especially green tea, appears to have many positive effects on health, including potential roles in reducing the risk of cancer, cardiovascular disease, type 2 diabetes, and even dementia. As with coffee, these associations are based on large observational studies and not randomized trials.
Chamomile. If your coffee gives you too much of a buzz and causes you to feel anxious, calm down with chamomile tea or oil. Evidence from randomized trials indicates it has positive effects on insomnia and anxiety.
Peppermint oil. The data for calming irritable bowel syndrome is fairly strong, and it may be effective in aborting migraines when applied to the forehead. It’s certainly worth a try for these difficult-to-treat conditions.
When patients ask you about botanicals and herbals, a great resource is
Now I will finish my fourth cup of coffee . . .
1. Daniel O, Mauskop A. Nutraceuticals in acute and prophylactic treatment of migraine. Curr Treat Options Neurol. 2016;18:14.
2. National Center for Complementary and Integrative Health. The use of complementary and alternative medicine in the United States. Available at: https://nccih.nih.gov/research/statistics/2007/camsurvey_fs1.htm. Accessed December 14, 2017.
Nutrition enthusiasts have been saying for years that “we are what we eat.” In this issue of JFP, Drs. Malone and Tsai review the evidence regarding the medicinal properties of certain herbal and botanical supplements. (See here.) Although there are many unfounded claims about the health effects of a wide variety of supplements, increasing evidence from well-conducted randomized trials and large epidemiologic studies demonstrates that certain items we ingest have therapeutic value for a variety of conditions.
However, as Dr. Malone points out, herbal supplements and botanicals are not regulated by the US Food and Drug Administration, so manufacturers are not required to provide proof of effectiveness or safety to market their products. Some of these products have adverse effects. For example, butterbur can cause liver toxicity.1
Because about 38% of Americans use supplements, all primary care clinicians should know which products do—and do not—have evidence of efficacy.2 I suggest you read Dr. Malone’s 2-part article (part 2 is available here), but I can’t resist highlighting several of my favorites:
Coffee. Coffee used to be maligned because of its caffeine content, but more recent evidence suggests it protects against liver disease and has positive effects on cardiovascular disease and even mortality. (See Dr. Malone’s article for references.) There are no randomized trials, however, so we can’t be entirely sure if these associations are causal, but at least I can feel better about the 4 cups of coffee I drink every day!
Tea, especially green tea, appears to have many positive effects on health, including potential roles in reducing the risk of cancer, cardiovascular disease, type 2 diabetes, and even dementia. As with coffee, these associations are based on large observational studies and not randomized trials.
Chamomile. If your coffee gives you too much of a buzz and causes you to feel anxious, calm down with chamomile tea or oil. Evidence from randomized trials indicates it has positive effects on insomnia and anxiety.
Peppermint oil. The data for calming irritable bowel syndrome is fairly strong, and it may be effective in aborting migraines when applied to the forehead. It’s certainly worth a try for these difficult-to-treat conditions.
When patients ask you about botanicals and herbals, a great resource is
Now I will finish my fourth cup of coffee . . .
Nutrition enthusiasts have been saying for years that “we are what we eat.” In this issue of JFP, Drs. Malone and Tsai review the evidence regarding the medicinal properties of certain herbal and botanical supplements. (See here.) Although there are many unfounded claims about the health effects of a wide variety of supplements, increasing evidence from well-conducted randomized trials and large epidemiologic studies demonstrates that certain items we ingest have therapeutic value for a variety of conditions.
However, as Dr. Malone points out, herbal supplements and botanicals are not regulated by the US Food and Drug Administration, so manufacturers are not required to provide proof of effectiveness or safety to market their products. Some of these products have adverse effects. For example, butterbur can cause liver toxicity.1
Because about 38% of Americans use supplements, all primary care clinicians should know which products do—and do not—have evidence of efficacy.2 I suggest you read Dr. Malone’s 2-part article (part 2 is available here), but I can’t resist highlighting several of my favorites:
Coffee. Coffee used to be maligned because of its caffeine content, but more recent evidence suggests it protects against liver disease and has positive effects on cardiovascular disease and even mortality. (See Dr. Malone’s article for references.) There are no randomized trials, however, so we can’t be entirely sure if these associations are causal, but at least I can feel better about the 4 cups of coffee I drink every day!
Tea, especially green tea, appears to have many positive effects on health, including potential roles in reducing the risk of cancer, cardiovascular disease, type 2 diabetes, and even dementia. As with coffee, these associations are based on large observational studies and not randomized trials.
Chamomile. If your coffee gives you too much of a buzz and causes you to feel anxious, calm down with chamomile tea or oil. Evidence from randomized trials indicates it has positive effects on insomnia and anxiety.
Peppermint oil. The data for calming irritable bowel syndrome is fairly strong, and it may be effective in aborting migraines when applied to the forehead. It’s certainly worth a try for these difficult-to-treat conditions.
When patients ask you about botanicals and herbals, a great resource is
Now I will finish my fourth cup of coffee . . .
1. Daniel O, Mauskop A. Nutraceuticals in acute and prophylactic treatment of migraine. Curr Treat Options Neurol. 2016;18:14.
2. National Center for Complementary and Integrative Health. The use of complementary and alternative medicine in the United States. Available at: https://nccih.nih.gov/research/statistics/2007/camsurvey_fs1.htm. Accessed December 14, 2017.
1. Daniel O, Mauskop A. Nutraceuticals in acute and prophylactic treatment of migraine. Curr Treat Options Neurol. 2016;18:14.
2. National Center for Complementary and Integrative Health. The use of complementary and alternative medicine in the United States. Available at: https://nccih.nih.gov/research/statistics/2007/camsurvey_fs1.htm. Accessed December 14, 2017.
Is this hypertension treatment strategy based on SOR “A” evidence?
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al gave an “A” Strength of Recommendation (SOR) rating to the Practice Recommendation that read: “Target a systolic blood pressure (SBP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden.”
As justification for this SBP target, the authors cited a subgroup analysis from the Systolic Blood Pressure Intervention Trial (SPRINT),1 which consisted of patients ≥75 years of age.2 I posit that the inconsistencies of the data cited by Hansell et al contradict an “A” rating, and that the methodology used in SPRINT greatly mitigates the generalizability of the results.
First, Hansell et al admit that no consensus exists on an optimal BP target for older patients. SOR taxonomy requires that the evidence behind an SOR of “A” be based on consistent and good-quality patient-oriented evidence.3 One source cited by the authors states that evidence supporting lower targets is inconsistent,4 while a recent Cochrane review does not support low BP targets.5 Given that the evidence is inconsistent, the SOR should be a “B”, at best.
Second, the evidence to target a systolic BP <120 mm Hg primarily comes from SPRINT.1,2,4 In a Letter to the Editor that appeared in The New England Journal of Medicine, Dr. Marc A. Pfeffer addressed a key methodology issue of that trial: SPRINT protocol called for the withdrawal of antihypertensive therapy in the standard treatment group if a single systolic BP reading was <130 mm Hg, or if readings at 2 or more consecutive visits were <135 mm Hg, regardless of patient symptoms.6
The letter also questioned how frequently this withdrawal occurred, to which the SPRINT authors replied that 87% of participants required at least one reduction in the dose of medication to maintain the treatment target in the standard group, and complete withdrawal of medication was required in <7.5% of participants.7 While this dose adjustment may have been necessary to adequately test the SPRINT hypothesis that lower systolic BP targets are better, routine dose reduction in an asymptomatic patient is not standard practice.
Given the small benefit in absolute risk reduction in SPRINT’s aggressive hypertensive treatment arm of 0.54% per year for the primary composite outcome and 0.37% per year for all-cause mortality,2 the frequent medication dose reductions in the standard treatment arm likely contributed significantly to the statistical benefit seen in the aggressive treatment group in SPRINT.
If an SOR of “A” for BP targets is to be made, the print publication of Hansell et al’s article should communicate the degree of benefit, preferably in terms of absolute risk reduction. Only the online publication of TABLE W1 stated the degree of benefit in the SPRINT subgroup study, but it was stated in terms of relative risk.
Given the current suboptimal rates of hypertension control, primary care physicians would do well to impact morbidity and mortality in older adults by working to achieve standard targets, such as an SBP of <140 mm Hg or <150 mm Hg. Once standard targets are achieved, a conversation could then ensue about the potential benefits and harms of lower BP targets.
Chris Fallert, MD
St. Paul, Minn
1. Williamson JD, Supiano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
2. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
3. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
4. Weiss J, Freeman M, Low A, et al. Benefits and harms of intensive blood pressure treatment in adults aged 60 years or older: a systematic review and meta-analysis. Ann Intern Med. 2017;166:419-429.
5. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
6. Pfeffer MA. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2290.
7. Wright JT Jr, Whelton PK, Reboussin DM. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2294.
Authors’ response:
An SOR of “A” is based on consistent and good-quality patient-oriented evidence, which is further defined for treatment, prevention, and screening studies as (a) systematic reviews/meta-analyses of randomized controlled trials (RCTs) with consistent findings or (b) a high-quality individual RCT.1 The recommendation to “target a systolic blood pressure (BP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden” meets level 1 evidence based on both (a) and (b).
While a Cochrane review of hypertension did not support a systolic BP target <120 mm Hg, the populations evaluated included a variety of ages; the studies did not specifically focus on those ≥75 years of age with inherently high cardiovascular risk while excluding patients with diabetes.2 The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial results,3 which are often viewed as inconsistent with SPRINT,4 included patients with diabetes and patients of a younger average age than SPRINT. Although no overall mortality benefit of intensive BP control was found in the ACCORD trial, there was significant reduction in stroke, as well as additional benefit in the ACCORD standard glycemia group.3,5
The American College of Cardiology/American Heart Association 2017 BP guidelines summarize several meta-analyses that consistently support tighter BP control with recommendations for a lower BP target of <130 mm Hg systolic.5,6 They selected a target of <130 mm Hg, rather than <120 mm Hg, assuming that general health care providers cannot be as efficacious at lowering BP as researchers in efficacy trials.5
With regard to medication withdrawal as a flaw in the SPRINT design,4 an accepted geriatric principle is reduction in polypharmacy whenever possible. Medication reduction or withdrawal when a patient is too far below target is prudent. The 2 different target groups in an RCT have to be statistically different to draw conclusions about the differences. This strategy has been employed in other BP trials. Medication withdrawal is an appropriate means to achieve targets, which the SPRINT investigators did successfully with a least-square mean systolic BP for patients ≥75 years of age in the control group of 134.8 mm Hg and 123.4 mm Hg in the intensive group.4 Even with reduction in polypharmacy in the standard group, SPRINT demonstrated cardiovascular and mortality benefit with tighter control.4
With regard to Dr. Fallert’s comments about a small absolute risk reduction for the entire SPRINT study population, our article in JFP specifically pertains to adults ≥75 years of age. The numbers needed to treat for composite cardiovascular outcomes and all-cause mortality in the ≥75 SPRINT group are 27 (95% confidence interval [CI], 19-61) and 41 (95% CI, 27-145), respectively.4
We agree that there is suboptimal hypertension control at present. However, physicians should not only focus on this modifiable risk factor to reduce CVD risk and mortality in appropriate patients, but they should focus on doing it to the evidence-based goal.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
2. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
3. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
4. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
5. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
6. Reboussin DM, Allen NB, Griswold ME, et al. Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Available at: http://hyper.ahajournals.org/content/early/2017/11/10/HYP.0000000000000067. Accessed December 12, 2017.
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al gave an “A” Strength of Recommendation (SOR) rating to the Practice Recommendation that read: “Target a systolic blood pressure (SBP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden.”
As justification for this SBP target, the authors cited a subgroup analysis from the Systolic Blood Pressure Intervention Trial (SPRINT),1 which consisted of patients ≥75 years of age.2 I posit that the inconsistencies of the data cited by Hansell et al contradict an “A” rating, and that the methodology used in SPRINT greatly mitigates the generalizability of the results.
First, Hansell et al admit that no consensus exists on an optimal BP target for older patients. SOR taxonomy requires that the evidence behind an SOR of “A” be based on consistent and good-quality patient-oriented evidence.3 One source cited by the authors states that evidence supporting lower targets is inconsistent,4 while a recent Cochrane review does not support low BP targets.5 Given that the evidence is inconsistent, the SOR should be a “B”, at best.
Second, the evidence to target a systolic BP <120 mm Hg primarily comes from SPRINT.1,2,4 In a Letter to the Editor that appeared in The New England Journal of Medicine, Dr. Marc A. Pfeffer addressed a key methodology issue of that trial: SPRINT protocol called for the withdrawal of antihypertensive therapy in the standard treatment group if a single systolic BP reading was <130 mm Hg, or if readings at 2 or more consecutive visits were <135 mm Hg, regardless of patient symptoms.6
The letter also questioned how frequently this withdrawal occurred, to which the SPRINT authors replied that 87% of participants required at least one reduction in the dose of medication to maintain the treatment target in the standard group, and complete withdrawal of medication was required in <7.5% of participants.7 While this dose adjustment may have been necessary to adequately test the SPRINT hypothesis that lower systolic BP targets are better, routine dose reduction in an asymptomatic patient is not standard practice.
Given the small benefit in absolute risk reduction in SPRINT’s aggressive hypertensive treatment arm of 0.54% per year for the primary composite outcome and 0.37% per year for all-cause mortality,2 the frequent medication dose reductions in the standard treatment arm likely contributed significantly to the statistical benefit seen in the aggressive treatment group in SPRINT.
If an SOR of “A” for BP targets is to be made, the print publication of Hansell et al’s article should communicate the degree of benefit, preferably in terms of absolute risk reduction. Only the online publication of TABLE W1 stated the degree of benefit in the SPRINT subgroup study, but it was stated in terms of relative risk.
Given the current suboptimal rates of hypertension control, primary care physicians would do well to impact morbidity and mortality in older adults by working to achieve standard targets, such as an SBP of <140 mm Hg or <150 mm Hg. Once standard targets are achieved, a conversation could then ensue about the potential benefits and harms of lower BP targets.
Chris Fallert, MD
St. Paul, Minn
1. Williamson JD, Supiano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
2. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
3. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
4. Weiss J, Freeman M, Low A, et al. Benefits and harms of intensive blood pressure treatment in adults aged 60 years or older: a systematic review and meta-analysis. Ann Intern Med. 2017;166:419-429.
5. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
6. Pfeffer MA. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2290.
7. Wright JT Jr, Whelton PK, Reboussin DM. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2294.
Authors’ response:
An SOR of “A” is based on consistent and good-quality patient-oriented evidence, which is further defined for treatment, prevention, and screening studies as (a) systematic reviews/meta-analyses of randomized controlled trials (RCTs) with consistent findings or (b) a high-quality individual RCT.1 The recommendation to “target a systolic blood pressure (BP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden” meets level 1 evidence based on both (a) and (b).
While a Cochrane review of hypertension did not support a systolic BP target <120 mm Hg, the populations evaluated included a variety of ages; the studies did not specifically focus on those ≥75 years of age with inherently high cardiovascular risk while excluding patients with diabetes.2 The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial results,3 which are often viewed as inconsistent with SPRINT,4 included patients with diabetes and patients of a younger average age than SPRINT. Although no overall mortality benefit of intensive BP control was found in the ACCORD trial, there was significant reduction in stroke, as well as additional benefit in the ACCORD standard glycemia group.3,5
The American College of Cardiology/American Heart Association 2017 BP guidelines summarize several meta-analyses that consistently support tighter BP control with recommendations for a lower BP target of <130 mm Hg systolic.5,6 They selected a target of <130 mm Hg, rather than <120 mm Hg, assuming that general health care providers cannot be as efficacious at lowering BP as researchers in efficacy trials.5
With regard to medication withdrawal as a flaw in the SPRINT design,4 an accepted geriatric principle is reduction in polypharmacy whenever possible. Medication reduction or withdrawal when a patient is too far below target is prudent. The 2 different target groups in an RCT have to be statistically different to draw conclusions about the differences. This strategy has been employed in other BP trials. Medication withdrawal is an appropriate means to achieve targets, which the SPRINT investigators did successfully with a least-square mean systolic BP for patients ≥75 years of age in the control group of 134.8 mm Hg and 123.4 mm Hg in the intensive group.4 Even with reduction in polypharmacy in the standard group, SPRINT demonstrated cardiovascular and mortality benefit with tighter control.4
With regard to Dr. Fallert’s comments about a small absolute risk reduction for the entire SPRINT study population, our article in JFP specifically pertains to adults ≥75 years of age. The numbers needed to treat for composite cardiovascular outcomes and all-cause mortality in the ≥75 SPRINT group are 27 (95% confidence interval [CI], 19-61) and 41 (95% CI, 27-145), respectively.4
We agree that there is suboptimal hypertension control at present. However, physicians should not only focus on this modifiable risk factor to reduce CVD risk and mortality in appropriate patients, but they should focus on doing it to the evidence-based goal.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
2. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
3. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
4. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
5. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
6. Reboussin DM, Allen NB, Griswold ME, et al. Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Available at: http://hyper.ahajournals.org/content/early/2017/11/10/HYP.0000000000000067. Accessed December 12, 2017.
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al gave an “A” Strength of Recommendation (SOR) rating to the Practice Recommendation that read: “Target a systolic blood pressure (SBP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden.”
As justification for this SBP target, the authors cited a subgroup analysis from the Systolic Blood Pressure Intervention Trial (SPRINT),1 which consisted of patients ≥75 years of age.2 I posit that the inconsistencies of the data cited by Hansell et al contradict an “A” rating, and that the methodology used in SPRINT greatly mitigates the generalizability of the results.
First, Hansell et al admit that no consensus exists on an optimal BP target for older patients. SOR taxonomy requires that the evidence behind an SOR of “A” be based on consistent and good-quality patient-oriented evidence.3 One source cited by the authors states that evidence supporting lower targets is inconsistent,4 while a recent Cochrane review does not support low BP targets.5 Given that the evidence is inconsistent, the SOR should be a “B”, at best.
Second, the evidence to target a systolic BP <120 mm Hg primarily comes from SPRINT.1,2,4 In a Letter to the Editor that appeared in The New England Journal of Medicine, Dr. Marc A. Pfeffer addressed a key methodology issue of that trial: SPRINT protocol called for the withdrawal of antihypertensive therapy in the standard treatment group if a single systolic BP reading was <130 mm Hg, or if readings at 2 or more consecutive visits were <135 mm Hg, regardless of patient symptoms.6
The letter also questioned how frequently this withdrawal occurred, to which the SPRINT authors replied that 87% of participants required at least one reduction in the dose of medication to maintain the treatment target in the standard group, and complete withdrawal of medication was required in <7.5% of participants.7 While this dose adjustment may have been necessary to adequately test the SPRINT hypothesis that lower systolic BP targets are better, routine dose reduction in an asymptomatic patient is not standard practice.
Given the small benefit in absolute risk reduction in SPRINT’s aggressive hypertensive treatment arm of 0.54% per year for the primary composite outcome and 0.37% per year for all-cause mortality,2 the frequent medication dose reductions in the standard treatment arm likely contributed significantly to the statistical benefit seen in the aggressive treatment group in SPRINT.
If an SOR of “A” for BP targets is to be made, the print publication of Hansell et al’s article should communicate the degree of benefit, preferably in terms of absolute risk reduction. Only the online publication of TABLE W1 stated the degree of benefit in the SPRINT subgroup study, but it was stated in terms of relative risk.
Given the current suboptimal rates of hypertension control, primary care physicians would do well to impact morbidity and mortality in older adults by working to achieve standard targets, such as an SBP of <140 mm Hg or <150 mm Hg. Once standard targets are achieved, a conversation could then ensue about the potential benefits and harms of lower BP targets.
Chris Fallert, MD
St. Paul, Minn
1. Williamson JD, Supiano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
2. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
3. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
4. Weiss J, Freeman M, Low A, et al. Benefits and harms of intensive blood pressure treatment in adults aged 60 years or older: a systematic review and meta-analysis. Ann Intern Med. 2017;166:419-429.
5. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
6. Pfeffer MA. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2290.
7. Wright JT Jr, Whelton PK, Reboussin DM. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2016;374:2294.
Authors’ response:
An SOR of “A” is based on consistent and good-quality patient-oriented evidence, which is further defined for treatment, prevention, and screening studies as (a) systematic reviews/meta-analyses of randomized controlled trials (RCTs) with consistent findings or (b) a high-quality individual RCT.1 The recommendation to “target a systolic blood pressure (BP) <120 mm Hg in community-dwelling, nondiabetic patients ≥75 years of age if it is achievable without undue burden” meets level 1 evidence based on both (a) and (b).
While a Cochrane review of hypertension did not support a systolic BP target <120 mm Hg, the populations evaluated included a variety of ages; the studies did not specifically focus on those ≥75 years of age with inherently high cardiovascular risk while excluding patients with diabetes.2 The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial results,3 which are often viewed as inconsistent with SPRINT,4 included patients with diabetes and patients of a younger average age than SPRINT. Although no overall mortality benefit of intensive BP control was found in the ACCORD trial, there was significant reduction in stroke, as well as additional benefit in the ACCORD standard glycemia group.3,5
The American College of Cardiology/American Heart Association 2017 BP guidelines summarize several meta-analyses that consistently support tighter BP control with recommendations for a lower BP target of <130 mm Hg systolic.5,6 They selected a target of <130 mm Hg, rather than <120 mm Hg, assuming that general health care providers cannot be as efficacious at lowering BP as researchers in efficacy trials.5
With regard to medication withdrawal as a flaw in the SPRINT design,4 an accepted geriatric principle is reduction in polypharmacy whenever possible. Medication reduction or withdrawal when a patient is too far below target is prudent. The 2 different target groups in an RCT have to be statistically different to draw conclusions about the differences. This strategy has been employed in other BP trials. Medication withdrawal is an appropriate means to achieve targets, which the SPRINT investigators did successfully with a least-square mean systolic BP for patients ≥75 years of age in the control group of 134.8 mm Hg and 123.4 mm Hg in the intensive group.4 Even with reduction in polypharmacy in the standard group, SPRINT demonstrated cardiovascular and mortality benefit with tighter control.4
With regard to Dr. Fallert’s comments about a small absolute risk reduction for the entire SPRINT study population, our article in JFP specifically pertains to adults ≥75 years of age. The numbers needed to treat for composite cardiovascular outcomes and all-cause mortality in the ≥75 SPRINT group are 27 (95% confidence interval [CI], 19-61) and 41 (95% CI, 27-145), respectively.4
We agree that there is suboptimal hypertension control at present. However, physicians should not only focus on this modifiable risk factor to reduce CVD risk and mortality in appropriate patients, but they should focus on doing it to the evidence-based goal.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Ebell MH, Siwek J, Weiss BD, et al. Strength of recommendation taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician. 2004;69:548-556.
2. Garrison SR, Kolber MR, Korownyk CS, et al. Blood pressure targets for hypertension in older adults. Cochrane Database Syst Rev. 2017;8:CD011575.
3. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
4. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
5. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
6. Reboussin DM, Allen NB, Griswold ME, et al. Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Available at: http://hyper.ahajournals.org/content/early/2017/11/10/HYP.0000000000000067. Accessed December 12, 2017.
Let’s recognize Dr. John Geyman, too
Thank you for your tribute to David Warfield Stires, The Journal of Family Practice’s founding publisher (J Fam Pract. 2017;66:654-655). The real hero of the story, however, is Dr. John Geyman, who had the vision to found a research journal at the birth of our specialty. This was no easy task, as John faced a challenging chicken-and-egg problem: how to establish a research journal when academic family medicine was just getting underway and had no track record of generating a steady stream of quality research. The latter problem was due, in part, to the lack of a research journal devoted to promoting and publishing research in the field.
Yet, John did it, putting family medicine research on the publishing map. His groundbreaking work set the stage for future journals, including the Journal of the American Board of Family Medicine, the American Medical Association’s now-defunct Archives of Family Medicine, and the American Academy of Family Physicians’ Annals of Family Medicine.
As a family medicine resident in the 1970s, I remember coveting JFP so much that I managed to collect every issue from Volume 1, Issue 1, through the turn of the century. And as a young faculty member at Georgetown University Medical Center in the 1980s, I painstakingly created an annotated bibliography of the then-published content of JFP to use for teaching, research, and administration.
When I became editor of American Family Physician in 1988, I made a pilgrimage to the University of Washington School of Medicine in Seattle, where John was chairman of the Department of Family Medicine. I wanted to seek his advice, learn from his vast experience, and pay tribute to all that he’d done for our specialty. Over the past 30 years, John has continued to leave his mark. (See http://www.johngeymanmd.org/bio.html.)
A tribute to David Warfield Stires is incomplete without a corresponding acknowledgement and celebration of John’s decades-long visionary leadership in family medicine.
Jay Siwek, MD
Washington, DC
Thank you for your tribute to David Warfield Stires, The Journal of Family Practice’s founding publisher (J Fam Pract. 2017;66:654-655). The real hero of the story, however, is Dr. John Geyman, who had the vision to found a research journal at the birth of our specialty. This was no easy task, as John faced a challenging chicken-and-egg problem: how to establish a research journal when academic family medicine was just getting underway and had no track record of generating a steady stream of quality research. The latter problem was due, in part, to the lack of a research journal devoted to promoting and publishing research in the field.
Yet, John did it, putting family medicine research on the publishing map. His groundbreaking work set the stage for future journals, including the Journal of the American Board of Family Medicine, the American Medical Association’s now-defunct Archives of Family Medicine, and the American Academy of Family Physicians’ Annals of Family Medicine.
As a family medicine resident in the 1970s, I remember coveting JFP so much that I managed to collect every issue from Volume 1, Issue 1, through the turn of the century. And as a young faculty member at Georgetown University Medical Center in the 1980s, I painstakingly created an annotated bibliography of the then-published content of JFP to use for teaching, research, and administration.
When I became editor of American Family Physician in 1988, I made a pilgrimage to the University of Washington School of Medicine in Seattle, where John was chairman of the Department of Family Medicine. I wanted to seek his advice, learn from his vast experience, and pay tribute to all that he’d done for our specialty. Over the past 30 years, John has continued to leave his mark. (See http://www.johngeymanmd.org/bio.html.)
A tribute to David Warfield Stires is incomplete without a corresponding acknowledgement and celebration of John’s decades-long visionary leadership in family medicine.
Jay Siwek, MD
Washington, DC
Thank you for your tribute to David Warfield Stires, The Journal of Family Practice’s founding publisher (J Fam Pract. 2017;66:654-655). The real hero of the story, however, is Dr. John Geyman, who had the vision to found a research journal at the birth of our specialty. This was no easy task, as John faced a challenging chicken-and-egg problem: how to establish a research journal when academic family medicine was just getting underway and had no track record of generating a steady stream of quality research. The latter problem was due, in part, to the lack of a research journal devoted to promoting and publishing research in the field.
Yet, John did it, putting family medicine research on the publishing map. His groundbreaking work set the stage for future journals, including the Journal of the American Board of Family Medicine, the American Medical Association’s now-defunct Archives of Family Medicine, and the American Academy of Family Physicians’ Annals of Family Medicine.
As a family medicine resident in the 1970s, I remember coveting JFP so much that I managed to collect every issue from Volume 1, Issue 1, through the turn of the century. And as a young faculty member at Georgetown University Medical Center in the 1980s, I painstakingly created an annotated bibliography of the then-published content of JFP to use for teaching, research, and administration.
When I became editor of American Family Physician in 1988, I made a pilgrimage to the University of Washington School of Medicine in Seattle, where John was chairman of the Department of Family Medicine. I wanted to seek his advice, learn from his vast experience, and pay tribute to all that he’d done for our specialty. Over the past 30 years, John has continued to leave his mark. (See http://www.johngeymanmd.org/bio.html.)
A tribute to David Warfield Stires is incomplete without a corresponding acknowledgement and celebration of John’s decades-long visionary leadership in family medicine.
Jay Siwek, MD
Washington, DC
Utilize guidelines, but customize BP treatment in older patients
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al recommend a systolic blood pressure (SBP) treatment target of <120 mm Hg for community-dwelling, nondiabetic patients ≥75 years of age. This recommendation is not supported by the authors’ cited guidelines, and we have serious concerns about the risk of harm from such overly stringent BP control in this population.
While Hansell et al acknowledge that no consensus exists regarding an optimal BP target for older patients, the authors cite the Eighth Joint National Committee (JNC 8), the American College of Physicians (ACP), the Systolic Blood Pressure Intervention Trial (SPRINT) subgroup analysis, and the BP arm of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial to justify their recommendation. But as the authors mention, JNC 8 conducted a comprehensive review of the available evidence and determined that a BP target of <150/90 mm Hg for hypertensive patients ≥60 years of age is appropriate.1
The authors also state that ACP recommends an SBP target of <140 mm Hg, while, in fact, the recommendations from ACP (which are joint guidelines published with the American Academy of Family Physicians) say that high-quality evidence strongly supports an SBP target of <150 mm Hg to reduce the risk for mortality, stroke, and cardiac events in adults ≥60 years of age.2
SPRINT does support Hansell et al’s recommended SBP target of <120 mm Hg, but this trial provided only composite data of adults ≥75 years of age and did not differentiate between the outcomes in otherwise healthy adults ≥75 years of age vs those with cardiovascular conditions.3 As Hansell et al point out, the SPRINT trial was halted prematurely, which compromises the validity of their findings.
Lastly, the ACCORD trial did not find benefit to treating SBP <120 mm Hg compared with <140 mm Hg in adults with diabetes, but it did find substantial harms in the <120 mm Hg group, including an increased risk of renal impairment and hypokalemia.4
Hansel et al’s overreliance on the SPRINT subgroup analysis represents a significant flaw in the assertion that an SBP target <120 mm Hg is reasonable for all community-dwelling, non-diabetic adults ≥75 years of age. While the authors made the allowance that a higher target (<140 mm Hg) is acceptable if a target of <120 mm Hg places undue burden on the patient, the guidelines they cited, when considered together, suggest that starting at a higher target is not only sufficient to prevent complications, but also reduces overtreatment.
Adults ≥75 years of age are a diverse group regarding disease conditions, life expectancy, and personal priorities. While it is tempting to make generalizations about BP treatment targets, we owe it to our patients to understand the nuances of applicable guidelines so that we can tailor BP treatment targets to each patient’s unique clinical situation and personal priorities. Applying a blanket recommendation to this heterogeneous population may result in significant harms from overtreatment.
Jennifer L. Middleton, MD, MPH, FAAFP; Miriam Chan, PharmD, CDE
Columbus, Ohio
1. James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
2. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
3. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
4. ACCORD Study Group, Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010;362:1575-1585.
Authors’ response:
We agree with the title of this letter, “Utilize guidelines, but customize BP treatment in older patients.” Our recommendations are not limited to targeting a systolic BP <120 mm Hg for community-dwelling, nondiabetic adults ≥75 years of age, but include consideration for “undue burden.” Our third practice recommendation, which recommends that one consider cognitive function, polypharmacy, multimorbidity, and frailty, is an equally—if not more—important recommendation.
With regard to the specific concerns about the current guidelines:
- The American College of Physicians and American Academy of Family Physicians’ “Recommendation 1” advocates a systolic BP goal <150 mm Hg for adults ≥60 years of age. However, “Recommendation 3” endorses intensifying treatment in adults ≥60 years of age at high cardiovascular (CV) risk. Based on Framingham criteria, all adults ≥75 years of age are considered at high risk for CV disease, as stated in our article. Therefore, “Recommendation 3” for a target of <140 mm Hg is applicable for the population addressed in our article.1
- The Eighth Joint National Committee (JNC 8) does recommend a BP target <150 mm Hg for adults ≥60 years of age, but does not take into account recent data, which is why we wanted to highlight that data for physicians.2
- Since submission of our article, The American College of Cardiology/American Heart Association (ACC/AHA) has published its first set of guidelines since 2003, which lowered BP target to <130 mm Hg in patients with high CV risk. Those guidelines outline the validity of SPRINT and the consistency of the existing evidence, including the linear relationship of BP and mortality.3
- SPRINT was halted early specifically because of the mortality benefit in the intensive treatment group, which is ethically appropriate.4 It is unclear to us how this compromises the validity of the trial. There is often concern for bias from early cessation in small trials, but this was a large, well-powered trial.
- The ACC/AHA guidelines also address some of the nuances of ACCORD, which is specific to patients with diabetes (whom we excluded from our first Practice Recommendation). Although no overall mortality benefit was found, there was stroke reduction in this group and additional benefit in the standard glycemia group.3,5 A meta-analysis of SPRINT and ACCORD showed CV disease reduction with a BP target <120 mm Hg.6
Although we do believe that SPRINT is a landmark trial contributing a great deal to our recommendations, we strongly emphasized that comorbidities, frailty, and dementia greatly impact treatment decisions. We stressed that prescribers use caution and slow titration because of adverse effects. Geriatric medicine is a complex art, and one of the goals of our article was to highlight this complexity and emphasize the importance of considering goals of care, comorbidity, frailty, and cognitive function when choosing optimal BP targets.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
2. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
3. Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
4. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
5. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
6. Perkovic V, Rodgers A. Redefining blood-pressure targets—SPRINT starts the marathon. N Engl Med. 2015;373:2175-2178.
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al recommend a systolic blood pressure (SBP) treatment target of <120 mm Hg for community-dwelling, nondiabetic patients ≥75 years of age. This recommendation is not supported by the authors’ cited guidelines, and we have serious concerns about the risk of harm from such overly stringent BP control in this population.
While Hansell et al acknowledge that no consensus exists regarding an optimal BP target for older patients, the authors cite the Eighth Joint National Committee (JNC 8), the American College of Physicians (ACP), the Systolic Blood Pressure Intervention Trial (SPRINT) subgroup analysis, and the BP arm of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial to justify their recommendation. But as the authors mention, JNC 8 conducted a comprehensive review of the available evidence and determined that a BP target of <150/90 mm Hg for hypertensive patients ≥60 years of age is appropriate.1
The authors also state that ACP recommends an SBP target of <140 mm Hg, while, in fact, the recommendations from ACP (which are joint guidelines published with the American Academy of Family Physicians) say that high-quality evidence strongly supports an SBP target of <150 mm Hg to reduce the risk for mortality, stroke, and cardiac events in adults ≥60 years of age.2
SPRINT does support Hansell et al’s recommended SBP target of <120 mm Hg, but this trial provided only composite data of adults ≥75 years of age and did not differentiate between the outcomes in otherwise healthy adults ≥75 years of age vs those with cardiovascular conditions.3 As Hansell et al point out, the SPRINT trial was halted prematurely, which compromises the validity of their findings.
Lastly, the ACCORD trial did not find benefit to treating SBP <120 mm Hg compared with <140 mm Hg in adults with diabetes, but it did find substantial harms in the <120 mm Hg group, including an increased risk of renal impairment and hypokalemia.4
Hansel et al’s overreliance on the SPRINT subgroup analysis represents a significant flaw in the assertion that an SBP target <120 mm Hg is reasonable for all community-dwelling, non-diabetic adults ≥75 years of age. While the authors made the allowance that a higher target (<140 mm Hg) is acceptable if a target of <120 mm Hg places undue burden on the patient, the guidelines they cited, when considered together, suggest that starting at a higher target is not only sufficient to prevent complications, but also reduces overtreatment.
Adults ≥75 years of age are a diverse group regarding disease conditions, life expectancy, and personal priorities. While it is tempting to make generalizations about BP treatment targets, we owe it to our patients to understand the nuances of applicable guidelines so that we can tailor BP treatment targets to each patient’s unique clinical situation and personal priorities. Applying a blanket recommendation to this heterogeneous population may result in significant harms from overtreatment.
Jennifer L. Middleton, MD, MPH, FAAFP; Miriam Chan, PharmD, CDE
Columbus, Ohio
1. James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
2. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
3. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
4. ACCORD Study Group, Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010;362:1575-1585.
Authors’ response:
We agree with the title of this letter, “Utilize guidelines, but customize BP treatment in older patients.” Our recommendations are not limited to targeting a systolic BP <120 mm Hg for community-dwelling, nondiabetic adults ≥75 years of age, but include consideration for “undue burden.” Our third practice recommendation, which recommends that one consider cognitive function, polypharmacy, multimorbidity, and frailty, is an equally—if not more—important recommendation.
With regard to the specific concerns about the current guidelines:
- The American College of Physicians and American Academy of Family Physicians’ “Recommendation 1” advocates a systolic BP goal <150 mm Hg for adults ≥60 years of age. However, “Recommendation 3” endorses intensifying treatment in adults ≥60 years of age at high cardiovascular (CV) risk. Based on Framingham criteria, all adults ≥75 years of age are considered at high risk for CV disease, as stated in our article. Therefore, “Recommendation 3” for a target of <140 mm Hg is applicable for the population addressed in our article.1
- The Eighth Joint National Committee (JNC 8) does recommend a BP target <150 mm Hg for adults ≥60 years of age, but does not take into account recent data, which is why we wanted to highlight that data for physicians.2
- Since submission of our article, The American College of Cardiology/American Heart Association (ACC/AHA) has published its first set of guidelines since 2003, which lowered BP target to <130 mm Hg in patients with high CV risk. Those guidelines outline the validity of SPRINT and the consistency of the existing evidence, including the linear relationship of BP and mortality.3
- SPRINT was halted early specifically because of the mortality benefit in the intensive treatment group, which is ethically appropriate.4 It is unclear to us how this compromises the validity of the trial. There is often concern for bias from early cessation in small trials, but this was a large, well-powered trial.
- The ACC/AHA guidelines also address some of the nuances of ACCORD, which is specific to patients with diabetes (whom we excluded from our first Practice Recommendation). Although no overall mortality benefit was found, there was stroke reduction in this group and additional benefit in the standard glycemia group.3,5 A meta-analysis of SPRINT and ACCORD showed CV disease reduction with a BP target <120 mm Hg.6
Although we do believe that SPRINT is a landmark trial contributing a great deal to our recommendations, we strongly emphasized that comorbidities, frailty, and dementia greatly impact treatment decisions. We stressed that prescribers use caution and slow titration because of adverse effects. Geriatric medicine is a complex art, and one of the goals of our article was to highlight this complexity and emphasize the importance of considering goals of care, comorbidity, frailty, and cognitive function when choosing optimal BP targets.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
2. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
3. Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
4. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
5. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
6. Perkovic V, Rodgers A. Redefining blood-pressure targets—SPRINT starts the marathon. N Engl Med. 2015;373:2175-2178.
In the article, “Hypertension treatment strategies for older adults” (J Fam Pract. 2017;66:546-554), Hansell et al recommend a systolic blood pressure (SBP) treatment target of <120 mm Hg for community-dwelling, nondiabetic patients ≥75 years of age. This recommendation is not supported by the authors’ cited guidelines, and we have serious concerns about the risk of harm from such overly stringent BP control in this population.
While Hansell et al acknowledge that no consensus exists regarding an optimal BP target for older patients, the authors cite the Eighth Joint National Committee (JNC 8), the American College of Physicians (ACP), the Systolic Blood Pressure Intervention Trial (SPRINT) subgroup analysis, and the BP arm of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial to justify their recommendation. But as the authors mention, JNC 8 conducted a comprehensive review of the available evidence and determined that a BP target of <150/90 mm Hg for hypertensive patients ≥60 years of age is appropriate.1
The authors also state that ACP recommends an SBP target of <140 mm Hg, while, in fact, the recommendations from ACP (which are joint guidelines published with the American Academy of Family Physicians) say that high-quality evidence strongly supports an SBP target of <150 mm Hg to reduce the risk for mortality, stroke, and cardiac events in adults ≥60 years of age.2
SPRINT does support Hansell et al’s recommended SBP target of <120 mm Hg, but this trial provided only composite data of adults ≥75 years of age and did not differentiate between the outcomes in otherwise healthy adults ≥75 years of age vs those with cardiovascular conditions.3 As Hansell et al point out, the SPRINT trial was halted prematurely, which compromises the validity of their findings.
Lastly, the ACCORD trial did not find benefit to treating SBP <120 mm Hg compared with <140 mm Hg in adults with diabetes, but it did find substantial harms in the <120 mm Hg group, including an increased risk of renal impairment and hypokalemia.4
Hansel et al’s overreliance on the SPRINT subgroup analysis represents a significant flaw in the assertion that an SBP target <120 mm Hg is reasonable for all community-dwelling, non-diabetic adults ≥75 years of age. While the authors made the allowance that a higher target (<140 mm Hg) is acceptable if a target of <120 mm Hg places undue burden on the patient, the guidelines they cited, when considered together, suggest that starting at a higher target is not only sufficient to prevent complications, but also reduces overtreatment.
Adults ≥75 years of age are a diverse group regarding disease conditions, life expectancy, and personal priorities. While it is tempting to make generalizations about BP treatment targets, we owe it to our patients to understand the nuances of applicable guidelines so that we can tailor BP treatment targets to each patient’s unique clinical situation and personal priorities. Applying a blanket recommendation to this heterogeneous population may result in significant harms from overtreatment.
Jennifer L. Middleton, MD, MPH, FAAFP; Miriam Chan, PharmD, CDE
Columbus, Ohio
1. James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
2. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
3. Williamson JD, Suplano MA, Applegate WB, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA. 2016;315:2673-2682.
4. ACCORD Study Group, Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010;362:1575-1585.
Authors’ response:
We agree with the title of this letter, “Utilize guidelines, but customize BP treatment in older patients.” Our recommendations are not limited to targeting a systolic BP <120 mm Hg for community-dwelling, nondiabetic adults ≥75 years of age, but include consideration for “undue burden.” Our third practice recommendation, which recommends that one consider cognitive function, polypharmacy, multimorbidity, and frailty, is an equally—if not more—important recommendation.
With regard to the specific concerns about the current guidelines:
- The American College of Physicians and American Academy of Family Physicians’ “Recommendation 1” advocates a systolic BP goal <150 mm Hg for adults ≥60 years of age. However, “Recommendation 3” endorses intensifying treatment in adults ≥60 years of age at high cardiovascular (CV) risk. Based on Framingham criteria, all adults ≥75 years of age are considered at high risk for CV disease, as stated in our article. Therefore, “Recommendation 3” for a target of <140 mm Hg is applicable for the population addressed in our article.1
- The Eighth Joint National Committee (JNC 8) does recommend a BP target <150 mm Hg for adults ≥60 years of age, but does not take into account recent data, which is why we wanted to highlight that data for physicians.2
- Since submission of our article, The American College of Cardiology/American Heart Association (ACC/AHA) has published its first set of guidelines since 2003, which lowered BP target to <130 mm Hg in patients with high CV risk. Those guidelines outline the validity of SPRINT and the consistency of the existing evidence, including the linear relationship of BP and mortality.3
- SPRINT was halted early specifically because of the mortality benefit in the intensive treatment group, which is ethically appropriate.4 It is unclear to us how this compromises the validity of the trial. There is often concern for bias from early cessation in small trials, but this was a large, well-powered trial.
- The ACC/AHA guidelines also address some of the nuances of ACCORD, which is specific to patients with diabetes (whom we excluded from our first Practice Recommendation). Although no overall mortality benefit was found, there was stroke reduction in this group and additional benefit in the standard glycemia group.3,5 A meta-analysis of SPRINT and ACCORD showed CV disease reduction with a BP target <120 mm Hg.6
Although we do believe that SPRINT is a landmark trial contributing a great deal to our recommendations, we strongly emphasized that comorbidities, frailty, and dementia greatly impact treatment decisions. We stressed that prescribers use caution and slow titration because of adverse effects. Geriatric medicine is a complex art, and one of the goals of our article was to highlight this complexity and emphasize the importance of considering goals of care, comorbidity, frailty, and cognitive function when choosing optimal BP targets.
Maggie W. Hansell, MD; Emily M. Mann, MD; Julienne K. Kirk, PharmD
Winston-Salem, NC
1. Qaseem A, Wilt TJ, Rich R, et al. Pharmacological treatment of hypertension in adults aged 60 years or older to higher versus lower blood pressure targets: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2017;166:430-437.
2. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507-520.
3. Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Available at: http://hyper.ahajournals.org/content/hypertensionaha/early/2017/11/10/HYP.0000000000000066.full.pdf. Accessed December 12, 2017.
4. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2106.
5. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of intensive blood-pressure control in type 2 diabetes. N Engl J Med. 2010;362:1575-1585.
6. Perkovic V, Rodgers A. Redefining blood-pressure targets—SPRINT starts the marathon. N Engl Med. 2015;373:2175-2178.
Weakness with left elbow flexion • left anterior shoulder pain • Dx?
THE CASE
A 41-year-old, right-hand dominant man sought care at our facility one day after trying to pull his boat out of the water. He’d tried to lift the boat with his hands while his forearms were fully supinated and his elbows were flexed to about 90°. He then felt a sharp burning sensation in his left anterior shoulder and was unable to lift the boat. The patient denied feeling a popping sensation at the time of the injury. He had mild pain at night, but was able to sleep. He said that he had mild diminished strength with elbow flexion, but denied having any numbness, tingling, or discoloration of his skin.
The patient said he did weightlifting and strength training of his upper and lower extremities 4 times/week. He was in good general health, was not taking any medications or supplements, and denied smoking or using illicit drugs. His surgical history was significant for a Bankart repair 8 years ago.
On physical examination, the patient had a scar from the previous surgery, a hollow area in his left anterior shoulder, and a prominent biceps muscle belly (FIGURE). His shoulder range of motion was normal. Left shoulder Neer, Hawkins-Kennedy, drop-arm, cross-arm, empty can, and apprehension tests were negative. A left Speed’s test (resisted elbow flexion when elbow is flexed 20° to 30° with the forearm in supination and the arm in about 60° of flexion) was positive for mild anterior shoulder pain. So, too, was a Yergason’s test (resisted forearm supination and elbow flexion when forearm is pronated and elbow is flexed to 90°). The patient’s elbow flexion strength was 4 out of 5, and his supination strength was 5 out of 5. Neurovascular and sensory examinations of his upper extremities, including radial and ulnar pulses, were normal.
THE DIAGNOSIS
A diagnostic musculoskeletal ultrasound revealed an empty tendon sheath of the long head of the biceps in the bicipital groove and a retracted echogenic stump with associated hematoma at the proximal musculotendinous junction. Based on the patient’s history, physical examination, and ultrasound, a diagnosis of an acute rupture of the left long head of the biceps brachii tendon was made.
DISCUSSION
Diagnosis of acute rupture is often made clinically based on a visually apparent defect proximally and a bulbous mass distally (“Popeye deformity”).1 Ultrasound and magnetic resonance imaging (MRI) may aid in the diagnosis by demonstrating an absence of the long head in the bicipital groove or at its insertion.
The biceps brachii tendon functions in flexion and supination of the forearm. The long head of the biceps also plays a stabilizing role in the glenohumeral joint during elbow flexion and supination.2 Injury to the biceps most often occurs in middle-aged men following a traumatic sudden eccentric bicipital contraction event, during which most patients describe a snapping or popping sensation.3,4
Rupture of the proximal biceps tendon represents about 90% of all biceps ruptures, which almost exclusively involve the long head of the biceps.3,5,6 Risk factors for tendon rupture include obesity, smoking, steroid injection in or around the tendon, and previous tendinopathy.7-10
Functional limitations. It is generally thought that functional limitations following a proximal biceps rupture are relatively minimal, due to the work of other flexors and supinators, including the brachialis and brachioradialis. However, because strength and endurance of the muscle can decrease by about 25%, physical laborers and high-demand athletes may notice a degree of residual weakness with supination and elbow flexion.11,12
Surgery is suitable for some, but not all
Surgical repair is recommended for acute ruptures in patients with high physical demands and for whom a slight loss of flexion and supination strength would not be well tolerated.13 Tenotomy and tenodesis are the main techniques used to surgically repair a rupture of the long head of the biceps brachii tendon. Although there is no consensus on which technique is superior, it seems that there is less cosmetic deformity and better post-surgery biomechanical strength with tenodesis compared with tenotomy.14 However, tenodesis is associated with a higher likelihood of bicipital pain,14 and recent case reports have suggested it is associated with an increased risk of humeral fracture.15 Therefore, each patient should be treated on an individual case basis, taking into account age, activity level, and physical demand.14
For most patients, treatment remains conservative with typically excellent outcomes. Nonoperative management includes gentle range-of-motion exercises for the prevention of contractures of the elbow and shoulder. Such exercises can be started almost immediately after injury. In one study, nonoperative management was recommended for patients with sedentary work, injury in the non-dominant arm, and acceptable cosmetic deformity. Researchers noted that patients who opt for a nonsurgical treatment generally do well with a home exercise program and rarely have stiffness.1
If the patient is a young athlete, if cosmetic deformity is unacceptable, or if the injury is in the dominant arm of a laborer, then the patient may want to consider tenodesis.1 Tangari et al found that in high-demand athletes, biceps tenodesis resulted in excellent functional and cosmetic results with no clinically significant decrease in strength after an average follow-up of 7.6 years.13 In a case s
Our patient elected to proceed with a tenodesis procedure. Two months after the surgery, he had fully recovered.
THE TAKEAWAY
Rupture of the biceps brachii tendon is relatively uncommon. In the vast majority of cases, it happens in the long head of the dominant arm of middle-aged men. Diagnosis is mainly clinical; however, ultrasound and MRI can confirm the diagnosis when there is doubt. Nonoperative management is appropriate for the majority of patients. Young athletes, patients who are concerned with cosmetic appearance, and labor workers with injury to their dominant arm should be referred to an orthopedic surgeon for possible surgery.
1. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38:117-125.
2. Payne LZ, Deng XH, Craig EV, et al. The combined dynamic and static contributions to subacromial impingement. A biomechanical analysis. Am J Sports Med. 1997;25:801-808.
3. Jayamoorthy T, Field JR, Costi JJ, et al. Biceps tenodesis: a biomechanical study of fixation methods. J Shoulder Elbow Surg. 2004;13:160-164.
4. Mazzocca AD, Spang JT, Arciero RA. Distal biceps rupture. Orthop Clin North Am. 2008;39:237-249, vii.
5. Carter AN, Erickson SM. Proximal biceps tendon rupture: primarily an injury of middle age. Phys Sportsmed. 1999;27:95-101.
6. Elser F, Braun S, Dewing CB, et al. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27:581-592.
7. Kelly MP, Perkinson SG, Ablove RH, et al. Distal biceps tendon ruptures: an epidemiological analysis using a large population database. Am J Sports Med. 2015;43:2012-2017.
8. Schneider A, Bennett JM, O’Connor DP, et al. Bilateral ruptures of the distal biceps brachii tendon. J Shoulder Elbow Surg. 2009;18:804-807.
9. Sethi N, Wright R, Yamaguchi K. Disorders of the long head of the biceps tendon. J Shoulder Elbow Surg. 1999;8:644-654.
10. The Physician and Sportsmedicine. Complete rupture of large tendons. Risk factors, signs, and definitive treatment. Available at: https://orthony.com/directory/uploads/flik_complete-rupture-of-large-tendons.pdf. Accessed December 8, 2017.
11. Pearl ML, Bessos K, Wong K. Strength deficits related to distal biceps tendon rupture and repair. A case report. Am J Sports Med. 1998;26:295-296.
12. Deutch SR, Gelineck J, Johannsen HV, et al. Permanent disabilities in the displaced muscle from rupture of the long head tendon of the biceps. Scand J Med Sci Sports. 2005;15:159-162.
13. Tangari M, Carbone S, Gallo M, et al. Long head of the biceps tendon rupture in professional wrestlers: treatment with a mini-open tenodesis. J Shoulder Elbow Surg. 2011;20:409-413.
14. Hsu AR, Ghodadra NS, Provencher MT, et al. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20:326-332.
15. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20:e7-e11.
THE CASE
A 41-year-old, right-hand dominant man sought care at our facility one day after trying to pull his boat out of the water. He’d tried to lift the boat with his hands while his forearms were fully supinated and his elbows were flexed to about 90°. He then felt a sharp burning sensation in his left anterior shoulder and was unable to lift the boat. The patient denied feeling a popping sensation at the time of the injury. He had mild pain at night, but was able to sleep. He said that he had mild diminished strength with elbow flexion, but denied having any numbness, tingling, or discoloration of his skin.
The patient said he did weightlifting and strength training of his upper and lower extremities 4 times/week. He was in good general health, was not taking any medications or supplements, and denied smoking or using illicit drugs. His surgical history was significant for a Bankart repair 8 years ago.
On physical examination, the patient had a scar from the previous surgery, a hollow area in his left anterior shoulder, and a prominent biceps muscle belly (FIGURE). His shoulder range of motion was normal. Left shoulder Neer, Hawkins-Kennedy, drop-arm, cross-arm, empty can, and apprehension tests were negative. A left Speed’s test (resisted elbow flexion when elbow is flexed 20° to 30° with the forearm in supination and the arm in about 60° of flexion) was positive for mild anterior shoulder pain. So, too, was a Yergason’s test (resisted forearm supination and elbow flexion when forearm is pronated and elbow is flexed to 90°). The patient’s elbow flexion strength was 4 out of 5, and his supination strength was 5 out of 5. Neurovascular and sensory examinations of his upper extremities, including radial and ulnar pulses, were normal.
THE DIAGNOSIS
A diagnostic musculoskeletal ultrasound revealed an empty tendon sheath of the long head of the biceps in the bicipital groove and a retracted echogenic stump with associated hematoma at the proximal musculotendinous junction. Based on the patient’s history, physical examination, and ultrasound, a diagnosis of an acute rupture of the left long head of the biceps brachii tendon was made.
DISCUSSION
Diagnosis of acute rupture is often made clinically based on a visually apparent defect proximally and a bulbous mass distally (“Popeye deformity”).1 Ultrasound and magnetic resonance imaging (MRI) may aid in the diagnosis by demonstrating an absence of the long head in the bicipital groove or at its insertion.
The biceps brachii tendon functions in flexion and supination of the forearm. The long head of the biceps also plays a stabilizing role in the glenohumeral joint during elbow flexion and supination.2 Injury to the biceps most often occurs in middle-aged men following a traumatic sudden eccentric bicipital contraction event, during which most patients describe a snapping or popping sensation.3,4
Rupture of the proximal biceps tendon represents about 90% of all biceps ruptures, which almost exclusively involve the long head of the biceps.3,5,6 Risk factors for tendon rupture include obesity, smoking, steroid injection in or around the tendon, and previous tendinopathy.7-10
Functional limitations. It is generally thought that functional limitations following a proximal biceps rupture are relatively minimal, due to the work of other flexors and supinators, including the brachialis and brachioradialis. However, because strength and endurance of the muscle can decrease by about 25%, physical laborers and high-demand athletes may notice a degree of residual weakness with supination and elbow flexion.11,12
Surgery is suitable for some, but not all
Surgical repair is recommended for acute ruptures in patients with high physical demands and for whom a slight loss of flexion and supination strength would not be well tolerated.13 Tenotomy and tenodesis are the main techniques used to surgically repair a rupture of the long head of the biceps brachii tendon. Although there is no consensus on which technique is superior, it seems that there is less cosmetic deformity and better post-surgery biomechanical strength with tenodesis compared with tenotomy.14 However, tenodesis is associated with a higher likelihood of bicipital pain,14 and recent case reports have suggested it is associated with an increased risk of humeral fracture.15 Therefore, each patient should be treated on an individual case basis, taking into account age, activity level, and physical demand.14
For most patients, treatment remains conservative with typically excellent outcomes. Nonoperative management includes gentle range-of-motion exercises for the prevention of contractures of the elbow and shoulder. Such exercises can be started almost immediately after injury. In one study, nonoperative management was recommended for patients with sedentary work, injury in the non-dominant arm, and acceptable cosmetic deformity. Researchers noted that patients who opt for a nonsurgical treatment generally do well with a home exercise program and rarely have stiffness.1
If the patient is a young athlete, if cosmetic deformity is unacceptable, or if the injury is in the dominant arm of a laborer, then the patient may want to consider tenodesis.1 Tangari et al found that in high-demand athletes, biceps tenodesis resulted in excellent functional and cosmetic results with no clinically significant decrease in strength after an average follow-up of 7.6 years.13 In a case s
Our patient elected to proceed with a tenodesis procedure. Two months after the surgery, he had fully recovered.
THE TAKEAWAY
Rupture of the biceps brachii tendon is relatively uncommon. In the vast majority of cases, it happens in the long head of the dominant arm of middle-aged men. Diagnosis is mainly clinical; however, ultrasound and MRI can confirm the diagnosis when there is doubt. Nonoperative management is appropriate for the majority of patients. Young athletes, patients who are concerned with cosmetic appearance, and labor workers with injury to their dominant arm should be referred to an orthopedic surgeon for possible surgery.
THE CASE
A 41-year-old, right-hand dominant man sought care at our facility one day after trying to pull his boat out of the water. He’d tried to lift the boat with his hands while his forearms were fully supinated and his elbows were flexed to about 90°. He then felt a sharp burning sensation in his left anterior shoulder and was unable to lift the boat. The patient denied feeling a popping sensation at the time of the injury. He had mild pain at night, but was able to sleep. He said that he had mild diminished strength with elbow flexion, but denied having any numbness, tingling, or discoloration of his skin.
The patient said he did weightlifting and strength training of his upper and lower extremities 4 times/week. He was in good general health, was not taking any medications or supplements, and denied smoking or using illicit drugs. His surgical history was significant for a Bankart repair 8 years ago.
On physical examination, the patient had a scar from the previous surgery, a hollow area in his left anterior shoulder, and a prominent biceps muscle belly (FIGURE). His shoulder range of motion was normal. Left shoulder Neer, Hawkins-Kennedy, drop-arm, cross-arm, empty can, and apprehension tests were negative. A left Speed’s test (resisted elbow flexion when elbow is flexed 20° to 30° with the forearm in supination and the arm in about 60° of flexion) was positive for mild anterior shoulder pain. So, too, was a Yergason’s test (resisted forearm supination and elbow flexion when forearm is pronated and elbow is flexed to 90°). The patient’s elbow flexion strength was 4 out of 5, and his supination strength was 5 out of 5. Neurovascular and sensory examinations of his upper extremities, including radial and ulnar pulses, were normal.
THE DIAGNOSIS
A diagnostic musculoskeletal ultrasound revealed an empty tendon sheath of the long head of the biceps in the bicipital groove and a retracted echogenic stump with associated hematoma at the proximal musculotendinous junction. Based on the patient’s history, physical examination, and ultrasound, a diagnosis of an acute rupture of the left long head of the biceps brachii tendon was made.
DISCUSSION
Diagnosis of acute rupture is often made clinically based on a visually apparent defect proximally and a bulbous mass distally (“Popeye deformity”).1 Ultrasound and magnetic resonance imaging (MRI) may aid in the diagnosis by demonstrating an absence of the long head in the bicipital groove or at its insertion.
The biceps brachii tendon functions in flexion and supination of the forearm. The long head of the biceps also plays a stabilizing role in the glenohumeral joint during elbow flexion and supination.2 Injury to the biceps most often occurs in middle-aged men following a traumatic sudden eccentric bicipital contraction event, during which most patients describe a snapping or popping sensation.3,4
Rupture of the proximal biceps tendon represents about 90% of all biceps ruptures, which almost exclusively involve the long head of the biceps.3,5,6 Risk factors for tendon rupture include obesity, smoking, steroid injection in or around the tendon, and previous tendinopathy.7-10
Functional limitations. It is generally thought that functional limitations following a proximal biceps rupture are relatively minimal, due to the work of other flexors and supinators, including the brachialis and brachioradialis. However, because strength and endurance of the muscle can decrease by about 25%, physical laborers and high-demand athletes may notice a degree of residual weakness with supination and elbow flexion.11,12
Surgery is suitable for some, but not all
Surgical repair is recommended for acute ruptures in patients with high physical demands and for whom a slight loss of flexion and supination strength would not be well tolerated.13 Tenotomy and tenodesis are the main techniques used to surgically repair a rupture of the long head of the biceps brachii tendon. Although there is no consensus on which technique is superior, it seems that there is less cosmetic deformity and better post-surgery biomechanical strength with tenodesis compared with tenotomy.14 However, tenodesis is associated with a higher likelihood of bicipital pain,14 and recent case reports have suggested it is associated with an increased risk of humeral fracture.15 Therefore, each patient should be treated on an individual case basis, taking into account age, activity level, and physical demand.14
For most patients, treatment remains conservative with typically excellent outcomes. Nonoperative management includes gentle range-of-motion exercises for the prevention of contractures of the elbow and shoulder. Such exercises can be started almost immediately after injury. In one study, nonoperative management was recommended for patients with sedentary work, injury in the non-dominant arm, and acceptable cosmetic deformity. Researchers noted that patients who opt for a nonsurgical treatment generally do well with a home exercise program and rarely have stiffness.1
If the patient is a young athlete, if cosmetic deformity is unacceptable, or if the injury is in the dominant arm of a laborer, then the patient may want to consider tenodesis.1 Tangari et al found that in high-demand athletes, biceps tenodesis resulted in excellent functional and cosmetic results with no clinically significant decrease in strength after an average follow-up of 7.6 years.13 In a case s
Our patient elected to proceed with a tenodesis procedure. Two months after the surgery, he had fully recovered.
THE TAKEAWAY
Rupture of the biceps brachii tendon is relatively uncommon. In the vast majority of cases, it happens in the long head of the dominant arm of middle-aged men. Diagnosis is mainly clinical; however, ultrasound and MRI can confirm the diagnosis when there is doubt. Nonoperative management is appropriate for the majority of patients. Young athletes, patients who are concerned with cosmetic appearance, and labor workers with injury to their dominant arm should be referred to an orthopedic surgeon for possible surgery.
1. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38:117-125.
2. Payne LZ, Deng XH, Craig EV, et al. The combined dynamic and static contributions to subacromial impingement. A biomechanical analysis. Am J Sports Med. 1997;25:801-808.
3. Jayamoorthy T, Field JR, Costi JJ, et al. Biceps tenodesis: a biomechanical study of fixation methods. J Shoulder Elbow Surg. 2004;13:160-164.
4. Mazzocca AD, Spang JT, Arciero RA. Distal biceps rupture. Orthop Clin North Am. 2008;39:237-249, vii.
5. Carter AN, Erickson SM. Proximal biceps tendon rupture: primarily an injury of middle age. Phys Sportsmed. 1999;27:95-101.
6. Elser F, Braun S, Dewing CB, et al. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27:581-592.
7. Kelly MP, Perkinson SG, Ablove RH, et al. Distal biceps tendon ruptures: an epidemiological analysis using a large population database. Am J Sports Med. 2015;43:2012-2017.
8. Schneider A, Bennett JM, O’Connor DP, et al. Bilateral ruptures of the distal biceps brachii tendon. J Shoulder Elbow Surg. 2009;18:804-807.
9. Sethi N, Wright R, Yamaguchi K. Disorders of the long head of the biceps tendon. J Shoulder Elbow Surg. 1999;8:644-654.
10. The Physician and Sportsmedicine. Complete rupture of large tendons. Risk factors, signs, and definitive treatment. Available at: https://orthony.com/directory/uploads/flik_complete-rupture-of-large-tendons.pdf. Accessed December 8, 2017.
11. Pearl ML, Bessos K, Wong K. Strength deficits related to distal biceps tendon rupture and repair. A case report. Am J Sports Med. 1998;26:295-296.
12. Deutch SR, Gelineck J, Johannsen HV, et al. Permanent disabilities in the displaced muscle from rupture of the long head tendon of the biceps. Scand J Med Sci Sports. 2005;15:159-162.
13. Tangari M, Carbone S, Gallo M, et al. Long head of the biceps tendon rupture in professional wrestlers: treatment with a mini-open tenodesis. J Shoulder Elbow Surg. 2011;20:409-413.
14. Hsu AR, Ghodadra NS, Provencher MT, et al. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20:326-332.
15. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20:e7-e11.
1. Geaney LE, Mazzocca AD. Biceps brachii tendon ruptures: a review of diagnosis and treatment of proximal and distal biceps tendon ruptures. Phys Sportsmed. 2010;38:117-125.
2. Payne LZ, Deng XH, Craig EV, et al. The combined dynamic and static contributions to subacromial impingement. A biomechanical analysis. Am J Sports Med. 1997;25:801-808.
3. Jayamoorthy T, Field JR, Costi JJ, et al. Biceps tenodesis: a biomechanical study of fixation methods. J Shoulder Elbow Surg. 2004;13:160-164.
4. Mazzocca AD, Spang JT, Arciero RA. Distal biceps rupture. Orthop Clin North Am. 2008;39:237-249, vii.
5. Carter AN, Erickson SM. Proximal biceps tendon rupture: primarily an injury of middle age. Phys Sportsmed. 1999;27:95-101.
6. Elser F, Braun S, Dewing CB, et al. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27:581-592.
7. Kelly MP, Perkinson SG, Ablove RH, et al. Distal biceps tendon ruptures: an epidemiological analysis using a large population database. Am J Sports Med. 2015;43:2012-2017.
8. Schneider A, Bennett JM, O’Connor DP, et al. Bilateral ruptures of the distal biceps brachii tendon. J Shoulder Elbow Surg. 2009;18:804-807.
9. Sethi N, Wright R, Yamaguchi K. Disorders of the long head of the biceps tendon. J Shoulder Elbow Surg. 1999;8:644-654.
10. The Physician and Sportsmedicine. Complete rupture of large tendons. Risk factors, signs, and definitive treatment. Available at: https://orthony.com/directory/uploads/flik_complete-rupture-of-large-tendons.pdf. Accessed December 8, 2017.
11. Pearl ML, Bessos K, Wong K. Strength deficits related to distal biceps tendon rupture and repair. A case report. Am J Sports Med. 1998;26:295-296.
12. Deutch SR, Gelineck J, Johannsen HV, et al. Permanent disabilities in the displaced muscle from rupture of the long head tendon of the biceps. Scand J Med Sci Sports. 2005;15:159-162.
13. Tangari M, Carbone S, Gallo M, et al. Long head of the biceps tendon rupture in professional wrestlers: treatment with a mini-open tenodesis. J Shoulder Elbow Surg. 2011;20:409-413.
14. Hsu AR, Ghodadra NS, Provencher MT, et al. Biceps tenotomy versus tenodesis: a review of clinical outcomes and biomechanical results. J Shoulder Elbow Surg. 2011;20:326-332.
15. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20:e7-e11.
Painful jaw lesion
A 48-year-old Chinese woman was referred to our center with a 7-month history of a painful lesion on her left jaw that had been gradually increasing in size. The patient noted occasional purulent and bloody discharge from the lesion. She denied having a toothache.
An examination revealed an erythematous nodule with perilesional puckering superior to the left body of the mandible, measuring 7 × 8 mm, with no discharge or surrounding inflammation (FIGURE 1). There was no cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Odontogenic sinus tract
Further examination on the inside of the patient’s mouth revealed root stumps of the left inferior molars (FIGURE 2). Based on the appearance of the lesion and molar involvement, we diagnosed odontogenic sinus tract (OST). OST, also known as odontogenic fistula or dental sinus, is a clinical diagnosis.
Symptoms such as odontalgia may be present in only 50% of patients with OST; thus, patients often initially consult their physician, rather than their dentist.1 If OST is suspected, evaluation should begin with a thorough history focusing on any recent facial trauma or past dental diseases. Dental panoramic or periapical radiography can be performed to confirm the extent of dental disease, and pulp vitality testing can determine if a diseased tooth is restorable.
A biopsy of the sinus tract is not required, as it would only reveal granulation tissue. Bimanual palpation of the oral cavity may reveal a cord-like structure from the cutaneous sinus to the underlying alveolar bone. (This structure was palpated in our patient.)
The pathogenesis of OST begins with dental caries, which progress to degeneration of the pulp and formation of periapical abscesses and root stumps. Progressive suppuration causes local destruction and subsequent tract formation through the alveolar bone and mandible. The build-up in pressure within this tract results in an eruption through the skin, manifesting as a sinus with extrusion of pus. The most common site of OST is at the angle of the mandible.2
The differential Dx is limited
There are a small number of other cutaneous conditions that may arise in the region of the mandible, but they have clinical features that distinguish them from OST.
Pyogenic granuloma presents as an erythematous papule that bleeds on contact. It usually develops rapidly following antecedent trauma.
Actinomycosis usually appears as an indolent plaque, with draining sinuses that extrude yellow grains on pressure. It may result from an underlying dental infection.
Squamous cell carcinoma of the skin often presents as a scaly plaque or non-healing ulcer with irregular margins and everted edges.
A furuncle is a tender, erythematous papule or nodule centered on a hair follicle. It is commonly associated with Staphylococcus aureus infection.
Treating OST
Treatment requires endodontic referral for root canal therapy, after which most cases resolve within a few weeks. OST can heal with post-inflammatory hyper- or hypopigmentation as a result of melanocyte damage. Systemic antibiotic administration is not necessary.3
We referred our patient to a dentist, who removed the root stumps and provided root canal treatment. The OST healed within several weeks. The patient had residual hypopigmentation after the OST healed, but was satisfied with the outcome.
CORRESPONDENCE
Hua-Liang Joel Lim, MBBS, MMed, National Skin Centre, 1 Mandalay Rd, Singapore 308205; [email protected].
1. Cioffi GA, Terezhalmy GT, Parlette HL. Cutaneous draining sinus tract: an odontogenic etiology. J Am Acad Dermatol. 1986;14:94-100.
2. Brown RS, Jones R, Feimster T, et al. Cutaneous sinus tracts (or emerging sinus tracts) of odontogenic origin: a report of 3 cases. Clin Cosmet Investig Dent. 2010;2:63-67.
3. Susic M, Krakar N, Borcic J, et al. Odontogenic sinus tract to the neck skin: a case report. J Dermatol. 2004;31:920-922.
A 48-year-old Chinese woman was referred to our center with a 7-month history of a painful lesion on her left jaw that had been gradually increasing in size. The patient noted occasional purulent and bloody discharge from the lesion. She denied having a toothache.
An examination revealed an erythematous nodule with perilesional puckering superior to the left body of the mandible, measuring 7 × 8 mm, with no discharge or surrounding inflammation (FIGURE 1). There was no cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Odontogenic sinus tract
Further examination on the inside of the patient’s mouth revealed root stumps of the left inferior molars (FIGURE 2). Based on the appearance of the lesion and molar involvement, we diagnosed odontogenic sinus tract (OST). OST, also known as odontogenic fistula or dental sinus, is a clinical diagnosis.
Symptoms such as odontalgia may be present in only 50% of patients with OST; thus, patients often initially consult their physician, rather than their dentist.1 If OST is suspected, evaluation should begin with a thorough history focusing on any recent facial trauma or past dental diseases. Dental panoramic or periapical radiography can be performed to confirm the extent of dental disease, and pulp vitality testing can determine if a diseased tooth is restorable.
A biopsy of the sinus tract is not required, as it would only reveal granulation tissue. Bimanual palpation of the oral cavity may reveal a cord-like structure from the cutaneous sinus to the underlying alveolar bone. (This structure was palpated in our patient.)
The pathogenesis of OST begins with dental caries, which progress to degeneration of the pulp and formation of periapical abscesses and root stumps. Progressive suppuration causes local destruction and subsequent tract formation through the alveolar bone and mandible. The build-up in pressure within this tract results in an eruption through the skin, manifesting as a sinus with extrusion of pus. The most common site of OST is at the angle of the mandible.2
The differential Dx is limited
There are a small number of other cutaneous conditions that may arise in the region of the mandible, but they have clinical features that distinguish them from OST.
Pyogenic granuloma presents as an erythematous papule that bleeds on contact. It usually develops rapidly following antecedent trauma.
Actinomycosis usually appears as an indolent plaque, with draining sinuses that extrude yellow grains on pressure. It may result from an underlying dental infection.
Squamous cell carcinoma of the skin often presents as a scaly plaque or non-healing ulcer with irregular margins and everted edges.
A furuncle is a tender, erythematous papule or nodule centered on a hair follicle. It is commonly associated with Staphylococcus aureus infection.
Treating OST
Treatment requires endodontic referral for root canal therapy, after which most cases resolve within a few weeks. OST can heal with post-inflammatory hyper- or hypopigmentation as a result of melanocyte damage. Systemic antibiotic administration is not necessary.3
We referred our patient to a dentist, who removed the root stumps and provided root canal treatment. The OST healed within several weeks. The patient had residual hypopigmentation after the OST healed, but was satisfied with the outcome.
CORRESPONDENCE
Hua-Liang Joel Lim, MBBS, MMed, National Skin Centre, 1 Mandalay Rd, Singapore 308205; [email protected].
A 48-year-old Chinese woman was referred to our center with a 7-month history of a painful lesion on her left jaw that had been gradually increasing in size. The patient noted occasional purulent and bloody discharge from the lesion. She denied having a toothache.
An examination revealed an erythematous nodule with perilesional puckering superior to the left body of the mandible, measuring 7 × 8 mm, with no discharge or surrounding inflammation (FIGURE 1). There was no cervical lymphadenopathy.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Odontogenic sinus tract
Further examination on the inside of the patient’s mouth revealed root stumps of the left inferior molars (FIGURE 2). Based on the appearance of the lesion and molar involvement, we diagnosed odontogenic sinus tract (OST). OST, also known as odontogenic fistula or dental sinus, is a clinical diagnosis.
Symptoms such as odontalgia may be present in only 50% of patients with OST; thus, patients often initially consult their physician, rather than their dentist.1 If OST is suspected, evaluation should begin with a thorough history focusing on any recent facial trauma or past dental diseases. Dental panoramic or periapical radiography can be performed to confirm the extent of dental disease, and pulp vitality testing can determine if a diseased tooth is restorable.
A biopsy of the sinus tract is not required, as it would only reveal granulation tissue. Bimanual palpation of the oral cavity may reveal a cord-like structure from the cutaneous sinus to the underlying alveolar bone. (This structure was palpated in our patient.)
The pathogenesis of OST begins with dental caries, which progress to degeneration of the pulp and formation of periapical abscesses and root stumps. Progressive suppuration causes local destruction and subsequent tract formation through the alveolar bone and mandible. The build-up in pressure within this tract results in an eruption through the skin, manifesting as a sinus with extrusion of pus. The most common site of OST is at the angle of the mandible.2
The differential Dx is limited
There are a small number of other cutaneous conditions that may arise in the region of the mandible, but they have clinical features that distinguish them from OST.
Pyogenic granuloma presents as an erythematous papule that bleeds on contact. It usually develops rapidly following antecedent trauma.
Actinomycosis usually appears as an indolent plaque, with draining sinuses that extrude yellow grains on pressure. It may result from an underlying dental infection.
Squamous cell carcinoma of the skin often presents as a scaly plaque or non-healing ulcer with irregular margins and everted edges.
A furuncle is a tender, erythematous papule or nodule centered on a hair follicle. It is commonly associated with Staphylococcus aureus infection.
Treating OST
Treatment requires endodontic referral for root canal therapy, after which most cases resolve within a few weeks. OST can heal with post-inflammatory hyper- or hypopigmentation as a result of melanocyte damage. Systemic antibiotic administration is not necessary.3
We referred our patient to a dentist, who removed the root stumps and provided root canal treatment. The OST healed within several weeks. The patient had residual hypopigmentation after the OST healed, but was satisfied with the outcome.
CORRESPONDENCE
Hua-Liang Joel Lim, MBBS, MMed, National Skin Centre, 1 Mandalay Rd, Singapore 308205; [email protected].
1. Cioffi GA, Terezhalmy GT, Parlette HL. Cutaneous draining sinus tract: an odontogenic etiology. J Am Acad Dermatol. 1986;14:94-100.
2. Brown RS, Jones R, Feimster T, et al. Cutaneous sinus tracts (or emerging sinus tracts) of odontogenic origin: a report of 3 cases. Clin Cosmet Investig Dent. 2010;2:63-67.
3. Susic M, Krakar N, Borcic J, et al. Odontogenic sinus tract to the neck skin: a case report. J Dermatol. 2004;31:920-922.
1. Cioffi GA, Terezhalmy GT, Parlette HL. Cutaneous draining sinus tract: an odontogenic etiology. J Am Acad Dermatol. 1986;14:94-100.
2. Brown RS, Jones R, Feimster T, et al. Cutaneous sinus tracts (or emerging sinus tracts) of odontogenic origin: a report of 3 cases. Clin Cosmet Investig Dent. 2010;2:63-67.
3. Susic M, Krakar N, Borcic J, et al. Odontogenic sinus tract to the neck skin: a case report. J Dermatol. 2004;31:920-922.
Worsening dyspnea
A 62-year-old woman presented with a 2- to 3-week history of fatigue, nonproductive cough, dyspnea on exertion, and intermittent fever/chills. Her past medical history was significant for rheumatoid arthritis (RA) that had been treated with methotrexate and prednisone for the past 6 years. The patient was currently smoking half a pack a day with a 40-pack year history. The patient was a lifelong resident of Arizona and had previously worked in a stone mine.
On physical examination she appeared comfortable without any increased work of breathing. Her vital signs included a temperature of 36.6° C, a blood pressure of 110/54 mm Hg, a pulse of 90 beats/min, respirations of 16/min, and room-air oxygen saturation of 87%. Pulmonary examination revealed scattered wheezes with fine bibasilar crackles. The remainder of her physical exam was normal. Because she was hypoxic, she was admitted to the hospital.
At the hospital, a chest x-ray showed diffuse, bilateral interstitial changes (FIGURE 1). Laboratory tests revealed a white blood cell count of 13,800/mcL (normal: 4500-10,500/mcL) with 73% neutrophils (normal: 40%-60%), 3% bands (normal: 0-3%), 14% monocytes (normal: 2%-8%), 6% eosinophils (normal: 1%-4%), and 3% lymphocytes (normal: 20%-30%). Community-acquired pneumonia was suspected, and the patient was started on levofloxacin. Over the next 2 days, her dyspnea worsened. She became tachycardic, and her oxygen requirement increased to 15 L/min via a non-rebreather mask. She was transferred to the intensive care unit.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Interstitial lung disease
Given the patient’s worsening respiratory status, a computed tomography (CT) scan was ordered (FIGURE 2). Review of the CT scan showed ground-glass opacification, mild subpleural honeycombing, reticularity, and traction bronchiectasis bilaterally at the lung bases. Bronchoscopy with lavage was performed to rule out infectious etiologies and was negative. These findings, along with the patient’s medical history of RA and use of methotrexate, led us to diagnose interstitial lung disease (ILD) in this patient.
ILD refers to a group of disorders that primarily affects the pulmonary interstitium, rather than the alveolar spaces or pleura.1 The most common causes of ILD seen in primary care are idiopathic pulmonary fibrosis, connective tissue disease, and hypersensitivity pneumonitis secondary to drugs (such as methotrexate, citalopram, fluoxetine, nitrofurantoin, and cephalosporins), radiation, or occupational exposures. (Textile, metal, and plastic workers are at a heightened risk, as are painters and individuals who work with animals.)1 In 2010, idiopathic pulmonary fibrosis had a prevalence of 18.2 cases per 100,000 people.2 Determining the underlying cause of ILD is important, as it may influence prognosis and treatment decisions.
The most common presenting symptoms of ILD are exertional dyspnea, cough with insidious onset, fatigue, and weakness.1,3 Bear in mind, however, that patients with ILD associated with a connective tissue disease may have more subtle manifestations of exertional dyspnea, such as a change in activity level or low resting oxygen saturations. The pulmonary exam can be normal or can reveal fine end-inspiratory crackles, and may include high-pitched, inspiratory rhonchi, or “squeaks.”1
When a diagnosis of ILD is suspected, investigation should begin with high-resolution CT (HRCT).1.3-5 In patients for whom a potential cause of ILD is not identified or who have more than one potential cause, specific patterns seen on the HRCT can help determine the most likely etiology.5 Chest x-ray has low sensitivity and specificity for ILD and can frequently be misinterpreted, as occurred with our patient.1
Rule out other causes of dyspnea
The differential diagnosis for dyspnea includes:
Heart failure. Congestive heart failure can present with acutely worsening dyspnea and cough, but is also commonly associated with orthopnea and/or paroxysmal nocturnal dyspnea. On physical examination, findings of volume overload such as pulmonary crackles, lower extremity edema, and elevated jugular venous pressure are additional signs that heart failure is present.
Pulmonary embolism (PE). Patients with PE commonly present with acute dyspnea, chest pain, and may also have a cough. Additional risk factors for PE (prolonged immobility, fracture, recent hospitalization) may also be present. A Wells score and a D-dimer test can be used to determine the probability of a patient having PE.
Asthma/chronic obstructive pulmonary disease. COPD exacerbations commonly present with a productive cough and worsening dyspnea. Pulmonary exam findings include wheezing, tachypnea, increased respiratory effort, and poor air movement.
Infection (including coccidioidomycosis in the desert southwest, where this patient lived). Our patient was initially treated for pneumonia because she had reported fevers associated with dyspnea and cough along with an elevated white blood cell count. Chest x-ray findings in patients with pneumonia can reveal either lobar consolidation or interstitial infiltrates.
Failure to respond to treatment of the more common causes of dyspnea, as occurred with our patient, should prompt consideration of ILD, particularly in those who have a history of connective tissue disease. Once a diagnosis of ILD is made, referral to a pulmonary specialist is advised.1,3
A poor prognosis and a focus on quality of life
Immunosuppressive therapy is currently the standard treatment for ILD, although there is little evidence to support this practice.1,3,4 Therapy usually includes corticosteroids with or without the addition of a second immunosuppressive agent such as azathioprine, mycophenolate mofetil, or cyclophosphamide.1,4
In addition to drug therapy, the American College of Chest Physicians recommends routine assessment of quality-of-life (QOL) concerns in patients with ILD (TABLE).6,7 Additional QOL tools available to physicians include the Medical Outcomes Study Short-Form 36-Item Instrument8 and the St. George’s Respiratory Questionnaire.9
The prognosis is poor, even with treatment. Patients with ILD have a life expectancy that averages 2 to 4 years from diagnosis.6 Patients with ILD are frequently distressed about worsening control of dyspnea and becoming a burden to family members; they also have anxiety about dying.6 It’s important to allocate sufficient time for end-of-life discussions, as studies have shown that patients would like their physicians to address the issue more thoroughly.10
Our patient was started on high-flow oxygen and high-dose steroids. Azathioprine was later added. The patient’s methotrexate was stopped, in light of its association with ILD. Unfortunately, the treatments were not successful and the patient’s respiratory status continued to deteriorate. A family meeting was held with the patient to discuss end-of-life wishes, and the patient expressed a preference for hospice care. She died a few days after hospice enrollment.
CORRESPONDENCE
Karyn B. Kolman, MD, University of Arizona College of Medicine at South Campus Family Medicine Residency, 2800 E Ajo Way, Room 3006, Tucson, AZ 85713; [email protected].
1. Wallis A, Spinks K. The diagnosis and management of interstial lung disease. BMJ. 2015;350:h2072.
2. Raghu G, Chen SY, Hou Q, et al. Incidence and prevalence of idiopathic pulmonary fibrosis in US adults 18-64 years old. Eur Respir J. 2016;48:179-186.
3. Yunt ZX, Solomon JJ. Lung disease in rheumatoid arthritis. Rheum Dis Clin North Am. 2015;41:225-236.
4. Vij R, Strek ME. Diagnosis and treatment of connective tissue disease-associated interstitial lung disease. Chest. 2013;143:814-824.
5. Nair A, Walsh SL, Desai SR. Imaging of pulmonary involvement in rheumatic disease. Rheum Dis Clin North Am. 2015;41:167-196.
6. Gilbert CR, Smith CM. Advanced parenchymal lung disease: quality of life and palliative care. Mt Sinai J Med. 2009;76:63-70.
7. Swigris JJ, Stewart AL, Gould MK, et al. Patients’ perspectives on how idiopathic pulmonary fibrosis affects the quality of their lives. Health Qual Life Outcomes. 2005;3:61.
8. RAND. Medical Outcomes Study 36-Item Short Form Survey (SF-36). Available at: http://www.rand.org/health/surveys_tools/mos/mos_core_36item.html. Accessed May 27, 2016.
9. St George’s Respiratory Questionnaire. Available at: http://www.healthstatus.sgul.ac.uk/. Accessed May 27, 2016.
10. Bajwah S, Koffman J, Higginson IJ, et. al. ‘I wish I knew more…’ the end-of-life planning and information needs for end-stage fibrotic interstitial lung disease: views of patients, carers, and health professionals. BMJ Support Palliat Care. 2013;3;84-90.
A 62-year-old woman presented with a 2- to 3-week history of fatigue, nonproductive cough, dyspnea on exertion, and intermittent fever/chills. Her past medical history was significant for rheumatoid arthritis (RA) that had been treated with methotrexate and prednisone for the past 6 years. The patient was currently smoking half a pack a day with a 40-pack year history. The patient was a lifelong resident of Arizona and had previously worked in a stone mine.
On physical examination she appeared comfortable without any increased work of breathing. Her vital signs included a temperature of 36.6° C, a blood pressure of 110/54 mm Hg, a pulse of 90 beats/min, respirations of 16/min, and room-air oxygen saturation of 87%. Pulmonary examination revealed scattered wheezes with fine bibasilar crackles. The remainder of her physical exam was normal. Because she was hypoxic, she was admitted to the hospital.
At the hospital, a chest x-ray showed diffuse, bilateral interstitial changes (FIGURE 1). Laboratory tests revealed a white blood cell count of 13,800/mcL (normal: 4500-10,500/mcL) with 73% neutrophils (normal: 40%-60%), 3% bands (normal: 0-3%), 14% monocytes (normal: 2%-8%), 6% eosinophils (normal: 1%-4%), and 3% lymphocytes (normal: 20%-30%). Community-acquired pneumonia was suspected, and the patient was started on levofloxacin. Over the next 2 days, her dyspnea worsened. She became tachycardic, and her oxygen requirement increased to 15 L/min via a non-rebreather mask. She was transferred to the intensive care unit.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Interstitial lung disease
Given the patient’s worsening respiratory status, a computed tomography (CT) scan was ordered (FIGURE 2). Review of the CT scan showed ground-glass opacification, mild subpleural honeycombing, reticularity, and traction bronchiectasis bilaterally at the lung bases. Bronchoscopy with lavage was performed to rule out infectious etiologies and was negative. These findings, along with the patient’s medical history of RA and use of methotrexate, led us to diagnose interstitial lung disease (ILD) in this patient.
ILD refers to a group of disorders that primarily affects the pulmonary interstitium, rather than the alveolar spaces or pleura.1 The most common causes of ILD seen in primary care are idiopathic pulmonary fibrosis, connective tissue disease, and hypersensitivity pneumonitis secondary to drugs (such as methotrexate, citalopram, fluoxetine, nitrofurantoin, and cephalosporins), radiation, or occupational exposures. (Textile, metal, and plastic workers are at a heightened risk, as are painters and individuals who work with animals.)1 In 2010, idiopathic pulmonary fibrosis had a prevalence of 18.2 cases per 100,000 people.2 Determining the underlying cause of ILD is important, as it may influence prognosis and treatment decisions.
The most common presenting symptoms of ILD are exertional dyspnea, cough with insidious onset, fatigue, and weakness.1,3 Bear in mind, however, that patients with ILD associated with a connective tissue disease may have more subtle manifestations of exertional dyspnea, such as a change in activity level or low resting oxygen saturations. The pulmonary exam can be normal or can reveal fine end-inspiratory crackles, and may include high-pitched, inspiratory rhonchi, or “squeaks.”1
When a diagnosis of ILD is suspected, investigation should begin with high-resolution CT (HRCT).1.3-5 In patients for whom a potential cause of ILD is not identified or who have more than one potential cause, specific patterns seen on the HRCT can help determine the most likely etiology.5 Chest x-ray has low sensitivity and specificity for ILD and can frequently be misinterpreted, as occurred with our patient.1
Rule out other causes of dyspnea
The differential diagnosis for dyspnea includes:
Heart failure. Congestive heart failure can present with acutely worsening dyspnea and cough, but is also commonly associated with orthopnea and/or paroxysmal nocturnal dyspnea. On physical examination, findings of volume overload such as pulmonary crackles, lower extremity edema, and elevated jugular venous pressure are additional signs that heart failure is present.
Pulmonary embolism (PE). Patients with PE commonly present with acute dyspnea, chest pain, and may also have a cough. Additional risk factors for PE (prolonged immobility, fracture, recent hospitalization) may also be present. A Wells score and a D-dimer test can be used to determine the probability of a patient having PE.
Asthma/chronic obstructive pulmonary disease. COPD exacerbations commonly present with a productive cough and worsening dyspnea. Pulmonary exam findings include wheezing, tachypnea, increased respiratory effort, and poor air movement.
Infection (including coccidioidomycosis in the desert southwest, where this patient lived). Our patient was initially treated for pneumonia because she had reported fevers associated with dyspnea and cough along with an elevated white blood cell count. Chest x-ray findings in patients with pneumonia can reveal either lobar consolidation or interstitial infiltrates.
Failure to respond to treatment of the more common causes of dyspnea, as occurred with our patient, should prompt consideration of ILD, particularly in those who have a history of connective tissue disease. Once a diagnosis of ILD is made, referral to a pulmonary specialist is advised.1,3
A poor prognosis and a focus on quality of life
Immunosuppressive therapy is currently the standard treatment for ILD, although there is little evidence to support this practice.1,3,4 Therapy usually includes corticosteroids with or without the addition of a second immunosuppressive agent such as azathioprine, mycophenolate mofetil, or cyclophosphamide.1,4
In addition to drug therapy, the American College of Chest Physicians recommends routine assessment of quality-of-life (QOL) concerns in patients with ILD (TABLE).6,7 Additional QOL tools available to physicians include the Medical Outcomes Study Short-Form 36-Item Instrument8 and the St. George’s Respiratory Questionnaire.9
The prognosis is poor, even with treatment. Patients with ILD have a life expectancy that averages 2 to 4 years from diagnosis.6 Patients with ILD are frequently distressed about worsening control of dyspnea and becoming a burden to family members; they also have anxiety about dying.6 It’s important to allocate sufficient time for end-of-life discussions, as studies have shown that patients would like their physicians to address the issue more thoroughly.10
Our patient was started on high-flow oxygen and high-dose steroids. Azathioprine was later added. The patient’s methotrexate was stopped, in light of its association with ILD. Unfortunately, the treatments were not successful and the patient’s respiratory status continued to deteriorate. A family meeting was held with the patient to discuss end-of-life wishes, and the patient expressed a preference for hospice care. She died a few days after hospice enrollment.
CORRESPONDENCE
Karyn B. Kolman, MD, University of Arizona College of Medicine at South Campus Family Medicine Residency, 2800 E Ajo Way, Room 3006, Tucson, AZ 85713; [email protected].
A 62-year-old woman presented with a 2- to 3-week history of fatigue, nonproductive cough, dyspnea on exertion, and intermittent fever/chills. Her past medical history was significant for rheumatoid arthritis (RA) that had been treated with methotrexate and prednisone for the past 6 years. The patient was currently smoking half a pack a day with a 40-pack year history. The patient was a lifelong resident of Arizona and had previously worked in a stone mine.
On physical examination she appeared comfortable without any increased work of breathing. Her vital signs included a temperature of 36.6° C, a blood pressure of 110/54 mm Hg, a pulse of 90 beats/min, respirations of 16/min, and room-air oxygen saturation of 87%. Pulmonary examination revealed scattered wheezes with fine bibasilar crackles. The remainder of her physical exam was normal. Because she was hypoxic, she was admitted to the hospital.
At the hospital, a chest x-ray showed diffuse, bilateral interstitial changes (FIGURE 1). Laboratory tests revealed a white blood cell count of 13,800/mcL (normal: 4500-10,500/mcL) with 73% neutrophils (normal: 40%-60%), 3% bands (normal: 0-3%), 14% monocytes (normal: 2%-8%), 6% eosinophils (normal: 1%-4%), and 3% lymphocytes (normal: 20%-30%). Community-acquired pneumonia was suspected, and the patient was started on levofloxacin. Over the next 2 days, her dyspnea worsened. She became tachycardic, and her oxygen requirement increased to 15 L/min via a non-rebreather mask. She was transferred to the intensive care unit.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Interstitial lung disease
Given the patient’s worsening respiratory status, a computed tomography (CT) scan was ordered (FIGURE 2). Review of the CT scan showed ground-glass opacification, mild subpleural honeycombing, reticularity, and traction bronchiectasis bilaterally at the lung bases. Bronchoscopy with lavage was performed to rule out infectious etiologies and was negative. These findings, along with the patient’s medical history of RA and use of methotrexate, led us to diagnose interstitial lung disease (ILD) in this patient.
ILD refers to a group of disorders that primarily affects the pulmonary interstitium, rather than the alveolar spaces or pleura.1 The most common causes of ILD seen in primary care are idiopathic pulmonary fibrosis, connective tissue disease, and hypersensitivity pneumonitis secondary to drugs (such as methotrexate, citalopram, fluoxetine, nitrofurantoin, and cephalosporins), radiation, or occupational exposures. (Textile, metal, and plastic workers are at a heightened risk, as are painters and individuals who work with animals.)1 In 2010, idiopathic pulmonary fibrosis had a prevalence of 18.2 cases per 100,000 people.2 Determining the underlying cause of ILD is important, as it may influence prognosis and treatment decisions.
The most common presenting symptoms of ILD are exertional dyspnea, cough with insidious onset, fatigue, and weakness.1,3 Bear in mind, however, that patients with ILD associated with a connective tissue disease may have more subtle manifestations of exertional dyspnea, such as a change in activity level or low resting oxygen saturations. The pulmonary exam can be normal or can reveal fine end-inspiratory crackles, and may include high-pitched, inspiratory rhonchi, or “squeaks.”1
When a diagnosis of ILD is suspected, investigation should begin with high-resolution CT (HRCT).1.3-5 In patients for whom a potential cause of ILD is not identified or who have more than one potential cause, specific patterns seen on the HRCT can help determine the most likely etiology.5 Chest x-ray has low sensitivity and specificity for ILD and can frequently be misinterpreted, as occurred with our patient.1
Rule out other causes of dyspnea
The differential diagnosis for dyspnea includes:
Heart failure. Congestive heart failure can present with acutely worsening dyspnea and cough, but is also commonly associated with orthopnea and/or paroxysmal nocturnal dyspnea. On physical examination, findings of volume overload such as pulmonary crackles, lower extremity edema, and elevated jugular venous pressure are additional signs that heart failure is present.
Pulmonary embolism (PE). Patients with PE commonly present with acute dyspnea, chest pain, and may also have a cough. Additional risk factors for PE (prolonged immobility, fracture, recent hospitalization) may also be present. A Wells score and a D-dimer test can be used to determine the probability of a patient having PE.
Asthma/chronic obstructive pulmonary disease. COPD exacerbations commonly present with a productive cough and worsening dyspnea. Pulmonary exam findings include wheezing, tachypnea, increased respiratory effort, and poor air movement.
Infection (including coccidioidomycosis in the desert southwest, where this patient lived). Our patient was initially treated for pneumonia because she had reported fevers associated with dyspnea and cough along with an elevated white blood cell count. Chest x-ray findings in patients with pneumonia can reveal either lobar consolidation or interstitial infiltrates.
Failure to respond to treatment of the more common causes of dyspnea, as occurred with our patient, should prompt consideration of ILD, particularly in those who have a history of connective tissue disease. Once a diagnosis of ILD is made, referral to a pulmonary specialist is advised.1,3
A poor prognosis and a focus on quality of life
Immunosuppressive therapy is currently the standard treatment for ILD, although there is little evidence to support this practice.1,3,4 Therapy usually includes corticosteroids with or without the addition of a second immunosuppressive agent such as azathioprine, mycophenolate mofetil, or cyclophosphamide.1,4
In addition to drug therapy, the American College of Chest Physicians recommends routine assessment of quality-of-life (QOL) concerns in patients with ILD (TABLE).6,7 Additional QOL tools available to physicians include the Medical Outcomes Study Short-Form 36-Item Instrument8 and the St. George’s Respiratory Questionnaire.9
The prognosis is poor, even with treatment. Patients with ILD have a life expectancy that averages 2 to 4 years from diagnosis.6 Patients with ILD are frequently distressed about worsening control of dyspnea and becoming a burden to family members; they also have anxiety about dying.6 It’s important to allocate sufficient time for end-of-life discussions, as studies have shown that patients would like their physicians to address the issue more thoroughly.10
Our patient was started on high-flow oxygen and high-dose steroids. Azathioprine was later added. The patient’s methotrexate was stopped, in light of its association with ILD. Unfortunately, the treatments were not successful and the patient’s respiratory status continued to deteriorate. A family meeting was held with the patient to discuss end-of-life wishes, and the patient expressed a preference for hospice care. She died a few days after hospice enrollment.
CORRESPONDENCE
Karyn B. Kolman, MD, University of Arizona College of Medicine at South Campus Family Medicine Residency, 2800 E Ajo Way, Room 3006, Tucson, AZ 85713; [email protected].
1. Wallis A, Spinks K. The diagnosis and management of interstial lung disease. BMJ. 2015;350:h2072.
2. Raghu G, Chen SY, Hou Q, et al. Incidence and prevalence of idiopathic pulmonary fibrosis in US adults 18-64 years old. Eur Respir J. 2016;48:179-186.
3. Yunt ZX, Solomon JJ. Lung disease in rheumatoid arthritis. Rheum Dis Clin North Am. 2015;41:225-236.
4. Vij R, Strek ME. Diagnosis and treatment of connective tissue disease-associated interstitial lung disease. Chest. 2013;143:814-824.
5. Nair A, Walsh SL, Desai SR. Imaging of pulmonary involvement in rheumatic disease. Rheum Dis Clin North Am. 2015;41:167-196.
6. Gilbert CR, Smith CM. Advanced parenchymal lung disease: quality of life and palliative care. Mt Sinai J Med. 2009;76:63-70.
7. Swigris JJ, Stewart AL, Gould MK, et al. Patients’ perspectives on how idiopathic pulmonary fibrosis affects the quality of their lives. Health Qual Life Outcomes. 2005;3:61.
8. RAND. Medical Outcomes Study 36-Item Short Form Survey (SF-36). Available at: http://www.rand.org/health/surveys_tools/mos/mos_core_36item.html. Accessed May 27, 2016.
9. St George’s Respiratory Questionnaire. Available at: http://www.healthstatus.sgul.ac.uk/. Accessed May 27, 2016.
10. Bajwah S, Koffman J, Higginson IJ, et. al. ‘I wish I knew more…’ the end-of-life planning and information needs for end-stage fibrotic interstitial lung disease: views of patients, carers, and health professionals. BMJ Support Palliat Care. 2013;3;84-90.
1. Wallis A, Spinks K. The diagnosis and management of interstial lung disease. BMJ. 2015;350:h2072.
2. Raghu G, Chen SY, Hou Q, et al. Incidence and prevalence of idiopathic pulmonary fibrosis in US adults 18-64 years old. Eur Respir J. 2016;48:179-186.
3. Yunt ZX, Solomon JJ. Lung disease in rheumatoid arthritis. Rheum Dis Clin North Am. 2015;41:225-236.
4. Vij R, Strek ME. Diagnosis and treatment of connective tissue disease-associated interstitial lung disease. Chest. 2013;143:814-824.
5. Nair A, Walsh SL, Desai SR. Imaging of pulmonary involvement in rheumatic disease. Rheum Dis Clin North Am. 2015;41:167-196.
6. Gilbert CR, Smith CM. Advanced parenchymal lung disease: quality of life and palliative care. Mt Sinai J Med. 2009;76:63-70.
7. Swigris JJ, Stewart AL, Gould MK, et al. Patients’ perspectives on how idiopathic pulmonary fibrosis affects the quality of their lives. Health Qual Life Outcomes. 2005;3:61.
8. RAND. Medical Outcomes Study 36-Item Short Form Survey (SF-36). Available at: http://www.rand.org/health/surveys_tools/mos/mos_core_36item.html. Accessed May 27, 2016.
9. St George’s Respiratory Questionnaire. Available at: http://www.healthstatus.sgul.ac.uk/. Accessed May 27, 2016.
10. Bajwah S, Koffman J, Higginson IJ, et. al. ‘I wish I knew more…’ the end-of-life planning and information needs for end-stage fibrotic interstitial lung disease: views of patients, carers, and health professionals. BMJ Support Palliat Care. 2013;3;84-90.