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The Journal of Family Practice is a peer-reviewed and indexed journal that provides its 95,000 family physician readers with timely, practical, and evidence-based information that they can immediately put into practice. Research and applied evidence articles, plus patient-oriented departments like Practice Alert, PURLs, and Clinical Inquiries can be found in print and at jfponline.com. The Web site, which logs an average of 125,000 visitors every month, also offers audiocasts by physician specialists and interactive features like Instant Polls and Photo Rounds Friday—a weekly diagnostic puzzle.
gambling
compulsive behaviors
ammunition
assault rifle
black jack
Boko Haram
bondage
child abuse
cocaine
Daech
drug paraphernalia
explosion
gun
human trafficking
ISIL
ISIS
Islamic caliphate
Islamic state
mixed martial arts
MMA
molestation
national rifle association
NRA
nsfw
pedophile
pedophilia
poker
porn
pornography
psychedelic drug
recreational drug
sex slave rings
slot machine
terrorism
terrorist
Texas hold 'em
UFC
substance abuse
abuseed
abuseer
abusees
abuseing
abusely
abuses
aeolus
aeolused
aeoluser
aeoluses
aeolusing
aeolusly
aeoluss
ahole
aholeed
aholeer
aholees
aholeing
aholely
aholes
alcohol
alcoholed
alcoholer
alcoholes
alcoholing
alcoholly
alcohols
allman
allmaned
allmaner
allmanes
allmaning
allmanly
allmans
alted
altes
alting
altly
alts
analed
analer
anales
analing
anally
analprobe
analprobeed
analprobeer
analprobees
analprobeing
analprobely
analprobes
anals
anilingus
anilingused
anilinguser
anilinguses
anilingusing
anilingusly
anilinguss
anus
anused
anuser
anuses
anusing
anusly
anuss
areola
areolaed
areolaer
areolaes
areolaing
areolaly
areolas
areole
areoleed
areoleer
areolees
areoleing
areolely
areoles
arian
arianed
arianer
arianes
arianing
arianly
arians
aryan
aryaned
aryaner
aryanes
aryaning
aryanly
aryans
asiaed
asiaer
asiaes
asiaing
asialy
asias
ass
ass hole
ass lick
ass licked
ass licker
ass lickes
ass licking
ass lickly
ass licks
assbang
assbanged
assbangeded
assbangeder
assbangedes
assbangeding
assbangedly
assbangeds
assbanger
assbanges
assbanging
assbangly
assbangs
assbangsed
assbangser
assbangses
assbangsing
assbangsly
assbangss
assed
asser
asses
assesed
asseser
asseses
assesing
assesly
assess
assfuck
assfucked
assfucker
assfuckered
assfuckerer
assfuckeres
assfuckering
assfuckerly
assfuckers
assfuckes
assfucking
assfuckly
assfucks
asshat
asshated
asshater
asshates
asshating
asshatly
asshats
assholeed
assholeer
assholees
assholeing
assholely
assholes
assholesed
assholeser
assholeses
assholesing
assholesly
assholess
assing
assly
assmaster
assmastered
assmasterer
assmasteres
assmastering
assmasterly
assmasters
assmunch
assmunched
assmuncher
assmunches
assmunching
assmunchly
assmunchs
asss
asswipe
asswipeed
asswipeer
asswipees
asswipeing
asswipely
asswipes
asswipesed
asswipeser
asswipeses
asswipesing
asswipesly
asswipess
azz
azzed
azzer
azzes
azzing
azzly
azzs
babeed
babeer
babees
babeing
babely
babes
babesed
babeser
babeses
babesing
babesly
babess
ballsac
ballsaced
ballsacer
ballsaces
ballsacing
ballsack
ballsacked
ballsacker
ballsackes
ballsacking
ballsackly
ballsacks
ballsacly
ballsacs
ballsed
ballser
ballses
ballsing
ballsly
ballss
barf
barfed
barfer
barfes
barfing
barfly
barfs
bastard
bastarded
bastarder
bastardes
bastarding
bastardly
bastards
bastardsed
bastardser
bastardses
bastardsing
bastardsly
bastardss
bawdy
bawdyed
bawdyer
bawdyes
bawdying
bawdyly
bawdys
beaner
beanered
beanerer
beaneres
beanering
beanerly
beaners
beardedclam
beardedclamed
beardedclamer
beardedclames
beardedclaming
beardedclamly
beardedclams
beastiality
beastialityed
beastialityer
beastialityes
beastialitying
beastialityly
beastialitys
beatch
beatched
beatcher
beatches
beatching
beatchly
beatchs
beater
beatered
beaterer
beateres
beatering
beaterly
beaters
beered
beerer
beeres
beering
beerly
beeyotch
beeyotched
beeyotcher
beeyotches
beeyotching
beeyotchly
beeyotchs
beotch
beotched
beotcher
beotches
beotching
beotchly
beotchs
biatch
biatched
biatcher
biatches
biatching
biatchly
biatchs
big tits
big titsed
big titser
big titses
big titsing
big titsly
big titss
bigtits
bigtitsed
bigtitser
bigtitses
bigtitsing
bigtitsly
bigtitss
bimbo
bimboed
bimboer
bimboes
bimboing
bimboly
bimbos
bisexualed
bisexualer
bisexuales
bisexualing
bisexually
bisexuals
bitch
bitched
bitcheded
bitcheder
bitchedes
bitcheding
bitchedly
bitcheds
bitcher
bitches
bitchesed
bitcheser
bitcheses
bitchesing
bitchesly
bitchess
bitching
bitchly
bitchs
bitchy
bitchyed
bitchyer
bitchyes
bitchying
bitchyly
bitchys
bleached
bleacher
bleaches
bleaching
bleachly
bleachs
blow job
blow jobed
blow jober
blow jobes
blow jobing
blow jobly
blow jobs
blowed
blower
blowes
blowing
blowjob
blowjobed
blowjober
blowjobes
blowjobing
blowjobly
blowjobs
blowjobsed
blowjobser
blowjobses
blowjobsing
blowjobsly
blowjobss
blowly
blows
boink
boinked
boinker
boinkes
boinking
boinkly
boinks
bollock
bollocked
bollocker
bollockes
bollocking
bollockly
bollocks
bollocksed
bollockser
bollockses
bollocksing
bollocksly
bollockss
bollok
bolloked
bolloker
bollokes
bolloking
bollokly
bolloks
boner
bonered
bonerer
boneres
bonering
bonerly
boners
bonersed
bonerser
bonerses
bonersing
bonersly
bonerss
bong
bonged
bonger
bonges
bonging
bongly
bongs
boob
boobed
boober
boobes
boobies
boobiesed
boobieser
boobieses
boobiesing
boobiesly
boobiess
boobing
boobly
boobs
boobsed
boobser
boobses
boobsing
boobsly
boobss
booby
boobyed
boobyer
boobyes
boobying
boobyly
boobys
booger
boogered
boogerer
boogeres
boogering
boogerly
boogers
bookie
bookieed
bookieer
bookiees
bookieing
bookiely
bookies
bootee
booteeed
booteeer
booteees
booteeing
booteely
bootees
bootie
bootieed
bootieer
bootiees
bootieing
bootiely
booties
booty
bootyed
bootyer
bootyes
bootying
bootyly
bootys
boozeed
boozeer
boozees
boozeing
boozely
boozer
boozered
boozerer
boozeres
boozering
boozerly
boozers
boozes
boozy
boozyed
boozyer
boozyes
boozying
boozyly
boozys
bosomed
bosomer
bosomes
bosoming
bosomly
bosoms
bosomy
bosomyed
bosomyer
bosomyes
bosomying
bosomyly
bosomys
bugger
buggered
buggerer
buggeres
buggering
buggerly
buggers
bukkake
bukkakeed
bukkakeer
bukkakees
bukkakeing
bukkakely
bukkakes
bull shit
bull shited
bull shiter
bull shites
bull shiting
bull shitly
bull shits
bullshit
bullshited
bullshiter
bullshites
bullshiting
bullshitly
bullshits
bullshitsed
bullshitser
bullshitses
bullshitsing
bullshitsly
bullshitss
bullshitted
bullshitteded
bullshitteder
bullshittedes
bullshitteding
bullshittedly
bullshitteds
bullturds
bullturdsed
bullturdser
bullturdses
bullturdsing
bullturdsly
bullturdss
bung
bunged
bunger
bunges
bunging
bungly
bungs
busty
bustyed
bustyer
bustyes
bustying
bustyly
bustys
butt
butt fuck
butt fucked
butt fucker
butt fuckes
butt fucking
butt fuckly
butt fucks
butted
buttes
buttfuck
buttfucked
buttfucker
buttfuckered
buttfuckerer
buttfuckeres
buttfuckering
buttfuckerly
buttfuckers
buttfuckes
buttfucking
buttfuckly
buttfucks
butting
buttly
buttplug
buttpluged
buttpluger
buttpluges
buttpluging
buttplugly
buttplugs
butts
caca
cacaed
cacaer
cacaes
cacaing
cacaly
cacas
cahone
cahoneed
cahoneer
cahonees
cahoneing
cahonely
cahones
cameltoe
cameltoeed
cameltoeer
cameltoees
cameltoeing
cameltoely
cameltoes
carpetmuncher
carpetmunchered
carpetmuncherer
carpetmuncheres
carpetmunchering
carpetmuncherly
carpetmunchers
cawk
cawked
cawker
cawkes
cawking
cawkly
cawks
chinc
chinced
chincer
chinces
chincing
chincly
chincs
chincsed
chincser
chincses
chincsing
chincsly
chincss
chink
chinked
chinker
chinkes
chinking
chinkly
chinks
chode
chodeed
chodeer
chodees
chodeing
chodely
chodes
chodesed
chodeser
chodeses
chodesing
chodesly
chodess
clit
clited
cliter
clites
cliting
clitly
clitoris
clitorised
clitoriser
clitorises
clitorising
clitorisly
clitoriss
clitorus
clitorused
clitoruser
clitoruses
clitorusing
clitorusly
clitoruss
clits
clitsed
clitser
clitses
clitsing
clitsly
clitss
clitty
clittyed
clittyer
clittyes
clittying
clittyly
clittys
cocain
cocaine
cocained
cocaineed
cocaineer
cocainees
cocaineing
cocainely
cocainer
cocaines
cocaining
cocainly
cocains
cock
cock sucker
cock suckered
cock suckerer
cock suckeres
cock suckering
cock suckerly
cock suckers
cockblock
cockblocked
cockblocker
cockblockes
cockblocking
cockblockly
cockblocks
cocked
cocker
cockes
cockholster
cockholstered
cockholsterer
cockholsteres
cockholstering
cockholsterly
cockholsters
cocking
cockknocker
cockknockered
cockknockerer
cockknockeres
cockknockering
cockknockerly
cockknockers
cockly
cocks
cocksed
cockser
cockses
cocksing
cocksly
cocksmoker
cocksmokered
cocksmokerer
cocksmokeres
cocksmokering
cocksmokerly
cocksmokers
cockss
cocksucker
cocksuckered
cocksuckerer
cocksuckeres
cocksuckering
cocksuckerly
cocksuckers
coital
coitaled
coitaler
coitales
coitaling
coitally
coitals
commie
commieed
commieer
commiees
commieing
commiely
commies
condomed
condomer
condomes
condoming
condomly
condoms
coon
cooned
cooner
coones
cooning
coonly
coons
coonsed
coonser
coonses
coonsing
coonsly
coonss
corksucker
corksuckered
corksuckerer
corksuckeres
corksuckering
corksuckerly
corksuckers
cracked
crackwhore
crackwhoreed
crackwhoreer
crackwhorees
crackwhoreing
crackwhorely
crackwhores
crap
craped
craper
crapes
craping
craply
crappy
crappyed
crappyer
crappyes
crappying
crappyly
crappys
cum
cumed
cumer
cumes
cuming
cumly
cummin
cummined
cumminer
cummines
cumming
cumminged
cumminger
cumminges
cumminging
cummingly
cummings
cummining
cumminly
cummins
cums
cumshot
cumshoted
cumshoter
cumshotes
cumshoting
cumshotly
cumshots
cumshotsed
cumshotser
cumshotses
cumshotsing
cumshotsly
cumshotss
cumslut
cumsluted
cumsluter
cumslutes
cumsluting
cumslutly
cumsluts
cumstain
cumstained
cumstainer
cumstaines
cumstaining
cumstainly
cumstains
cunilingus
cunilingused
cunilinguser
cunilinguses
cunilingusing
cunilingusly
cunilinguss
cunnilingus
cunnilingused
cunnilinguser
cunnilinguses
cunnilingusing
cunnilingusly
cunnilinguss
cunny
cunnyed
cunnyer
cunnyes
cunnying
cunnyly
cunnys
cunt
cunted
cunter
cuntes
cuntface
cuntfaceed
cuntfaceer
cuntfacees
cuntfaceing
cuntfacely
cuntfaces
cunthunter
cunthuntered
cunthunterer
cunthunteres
cunthuntering
cunthunterly
cunthunters
cunting
cuntlick
cuntlicked
cuntlicker
cuntlickered
cuntlickerer
cuntlickeres
cuntlickering
cuntlickerly
cuntlickers
cuntlickes
cuntlicking
cuntlickly
cuntlicks
cuntly
cunts
cuntsed
cuntser
cuntses
cuntsing
cuntsly
cuntss
dago
dagoed
dagoer
dagoes
dagoing
dagoly
dagos
dagosed
dagoser
dagoses
dagosing
dagosly
dagoss
dammit
dammited
dammiter
dammites
dammiting
dammitly
dammits
damn
damned
damneded
damneder
damnedes
damneding
damnedly
damneds
damner
damnes
damning
damnit
damnited
damniter
damnites
damniting
damnitly
damnits
damnly
damns
dick
dickbag
dickbaged
dickbager
dickbages
dickbaging
dickbagly
dickbags
dickdipper
dickdippered
dickdipperer
dickdipperes
dickdippering
dickdipperly
dickdippers
dicked
dicker
dickes
dickface
dickfaceed
dickfaceer
dickfacees
dickfaceing
dickfacely
dickfaces
dickflipper
dickflippered
dickflipperer
dickflipperes
dickflippering
dickflipperly
dickflippers
dickhead
dickheaded
dickheader
dickheades
dickheading
dickheadly
dickheads
dickheadsed
dickheadser
dickheadses
dickheadsing
dickheadsly
dickheadss
dicking
dickish
dickished
dickisher
dickishes
dickishing
dickishly
dickishs
dickly
dickripper
dickrippered
dickripperer
dickripperes
dickrippering
dickripperly
dickrippers
dicks
dicksipper
dicksippered
dicksipperer
dicksipperes
dicksippering
dicksipperly
dicksippers
dickweed
dickweeded
dickweeder
dickweedes
dickweeding
dickweedly
dickweeds
dickwhipper
dickwhippered
dickwhipperer
dickwhipperes
dickwhippering
dickwhipperly
dickwhippers
dickzipper
dickzippered
dickzipperer
dickzipperes
dickzippering
dickzipperly
dickzippers
diddle
diddleed
diddleer
diddlees
diddleing
diddlely
diddles
dike
dikeed
dikeer
dikees
dikeing
dikely
dikes
dildo
dildoed
dildoer
dildoes
dildoing
dildoly
dildos
dildosed
dildoser
dildoses
dildosing
dildosly
dildoss
diligaf
diligafed
diligafer
diligafes
diligafing
diligafly
diligafs
dillweed
dillweeded
dillweeder
dillweedes
dillweeding
dillweedly
dillweeds
dimwit
dimwited
dimwiter
dimwites
dimwiting
dimwitly
dimwits
dingle
dingleed
dingleer
dinglees
dingleing
dinglely
dingles
dipship
dipshiped
dipshiper
dipshipes
dipshiping
dipshiply
dipships
dizzyed
dizzyer
dizzyes
dizzying
dizzyly
dizzys
doggiestyleed
doggiestyleer
doggiestylees
doggiestyleing
doggiestylely
doggiestyles
doggystyleed
doggystyleer
doggystylees
doggystyleing
doggystylely
doggystyles
dong
donged
donger
donges
donging
dongly
dongs
doofus
doofused
doofuser
doofuses
doofusing
doofusly
doofuss
doosh
dooshed
doosher
dooshes
dooshing
dooshly
dooshs
dopeyed
dopeyer
dopeyes
dopeying
dopeyly
dopeys
douchebag
douchebaged
douchebager
douchebages
douchebaging
douchebagly
douchebags
douchebagsed
douchebagser
douchebagses
douchebagsing
douchebagsly
douchebagss
doucheed
doucheer
douchees
doucheing
douchely
douches
douchey
doucheyed
doucheyer
doucheyes
doucheying
doucheyly
doucheys
drunk
drunked
drunker
drunkes
drunking
drunkly
drunks
dumass
dumassed
dumasser
dumasses
dumassing
dumassly
dumasss
dumbass
dumbassed
dumbasser
dumbasses
dumbassesed
dumbasseser
dumbasseses
dumbassesing
dumbassesly
dumbassess
dumbassing
dumbassly
dumbasss
dummy
dummyed
dummyer
dummyes
dummying
dummyly
dummys
dyke
dykeed
dykeer
dykees
dykeing
dykely
dykes
dykesed
dykeser
dykeses
dykesing
dykesly
dykess
erotic
eroticed
eroticer
erotices
eroticing
eroticly
erotics
extacy
extacyed
extacyer
extacyes
extacying
extacyly
extacys
extasy
extasyed
extasyer
extasyes
extasying
extasyly
extasys
fack
facked
facker
fackes
facking
fackly
facks
fag
faged
fager
fages
fagg
fagged
faggeded
faggeder
faggedes
faggeding
faggedly
faggeds
fagger
fagges
fagging
faggit
faggited
faggiter
faggites
faggiting
faggitly
faggits
faggly
faggot
faggoted
faggoter
faggotes
faggoting
faggotly
faggots
faggs
faging
fagly
fagot
fagoted
fagoter
fagotes
fagoting
fagotly
fagots
fags
fagsed
fagser
fagses
fagsing
fagsly
fagss
faig
faiged
faiger
faiges
faiging
faigly
faigs
faigt
faigted
faigter
faigtes
faigting
faigtly
faigts
fannybandit
fannybandited
fannybanditer
fannybandites
fannybanditing
fannybanditly
fannybandits
farted
farter
fartes
farting
fartknocker
fartknockered
fartknockerer
fartknockeres
fartknockering
fartknockerly
fartknockers
fartly
farts
felch
felched
felcher
felchered
felcherer
felcheres
felchering
felcherly
felchers
felches
felching
felchinged
felchinger
felchinges
felchinging
felchingly
felchings
felchly
felchs
fellate
fellateed
fellateer
fellatees
fellateing
fellately
fellates
fellatio
fellatioed
fellatioer
fellatioes
fellatioing
fellatioly
fellatios
feltch
feltched
feltcher
feltchered
feltcherer
feltcheres
feltchering
feltcherly
feltchers
feltches
feltching
feltchly
feltchs
feom
feomed
feomer
feomes
feoming
feomly
feoms
fisted
fisteded
fisteder
fistedes
fisteding
fistedly
fisteds
fisting
fistinged
fistinger
fistinges
fistinging
fistingly
fistings
fisty
fistyed
fistyer
fistyes
fistying
fistyly
fistys
floozy
floozyed
floozyer
floozyes
floozying
floozyly
floozys
foad
foaded
foader
foades
foading
foadly
foads
fondleed
fondleer
fondlees
fondleing
fondlely
fondles
foobar
foobared
foobarer
foobares
foobaring
foobarly
foobars
freex
freexed
freexer
freexes
freexing
freexly
freexs
frigg
frigga
friggaed
friggaer
friggaes
friggaing
friggaly
friggas
frigged
frigger
frigges
frigging
friggly
friggs
fubar
fubared
fubarer
fubares
fubaring
fubarly
fubars
fuck
fuckass
fuckassed
fuckasser
fuckasses
fuckassing
fuckassly
fuckasss
fucked
fuckeded
fuckeder
fuckedes
fuckeding
fuckedly
fuckeds
fucker
fuckered
fuckerer
fuckeres
fuckering
fuckerly
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rumper
rumpes
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Advocacy
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AJO, postsurgical analgesic, knee, replacement, surgery
alcohol
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apple cider vinegar
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Psoriasis
THE COMPARISON
A Elbow and forearm with erythematous, well-demarcated, pink plaques with mild micaceous scale in a 42-year-old White woman.
B Elbow and forearm with violaceous, well-demarcated plaques with micaceous scale and hyperpigmented patches around the active plaques in a 58-year-old Black man.
Epidemiology
Psoriasis prevalence in the United States has been estimated at 3.7%.1-3 If broken down by race or ethnicity, the prevalence of psoriasis varies: 2.5% to 3.7% in White adults1-4; 1.3% to 2% in Black adults1-4; 1.6% in Hispanics/other adults1-3; 1% in children overall; 0.29% in White children1,5; and 0.06% in Black children.1,5
Key clinical features in people with darker skin tones include:
- plaques that may appear more violaceous in color instead of pink or erythematous
- higher body surface area of involvement4 and thicker, more scaly plaques6
- increased likelihood of postinflammatory hyperpigmentation (PIH).
Worth noting
Although individuals of all skin tones may experience the psychosocial impact of psoriasis, quality-of-life measures have been found to be worse in those with skin of color (SOC) compared to White patients. 1,4 This may be due to the lingering PIH and hypopigmentation that occurs even after inflammatory plaques are treated. Of course, lack of access to care contributes to greater disease burden and more devastating psychological impact.
Health disparity highlight
Psoriasis may be underreported and underdiagnosed in individuals with SOC, as factors contributing to health care disparities may play a role, such as access to health care in general,1,7 and access to clinicians proficient in diagnosing cutaneous diseases in SOC may be delayed.8
Biologic medications are used less often in Black patients than in White patients, despite biologic medications being very efficacious for treatment of psoriasis.1,9,10
1. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
2. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70:512-516.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Gelfand JM, Stern RS, Nijsten T, et al. The prevalence of psoriasis in African Americans: results from a population-based study. J Am Acad Dermatol. 2005;52:23-26.
5. Wu JJ, Black MH, Smith N, et al. Low prevalence of psoriasis among children and adolescents in a large multiethnic cohort in southern California. J Am Acad Dermatol. 2011;65:957-964.
6. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
7. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
8. Mundluru SN, Ramalingam ND, Tran HN. Addressing internal medicine residents’ discomfort with basic dermatology in persons of color in the primary care clinic. Am J Med Qual. 2019;34:513-513.
9. Kerr GS, Qaiyumi S, Richards J, et al. Psoriasis and psoriatic arthritis in African-American patients—the need to measure disease burden. Clin Rheumatol. 2015;34:1753-1759.
10. Takeshita J, Gelfand JM, Li P, et al. Psoriasis in the US Medicare population: prevalence, treatment, and factors associated with biologic use. J Invest Dermatol. 2015;135:2955-2963.
THE COMPARISON
A Elbow and forearm with erythematous, well-demarcated, pink plaques with mild micaceous scale in a 42-year-old White woman.
B Elbow and forearm with violaceous, well-demarcated plaques with micaceous scale and hyperpigmented patches around the active plaques in a 58-year-old Black man.
Epidemiology
Psoriasis prevalence in the United States has been estimated at 3.7%.1-3 If broken down by race or ethnicity, the prevalence of psoriasis varies: 2.5% to 3.7% in White adults1-4; 1.3% to 2% in Black adults1-4; 1.6% in Hispanics/other adults1-3; 1% in children overall; 0.29% in White children1,5; and 0.06% in Black children.1,5
Key clinical features in people with darker skin tones include:
- plaques that may appear more violaceous in color instead of pink or erythematous
- higher body surface area of involvement4 and thicker, more scaly plaques6
- increased likelihood of postinflammatory hyperpigmentation (PIH).
Worth noting
Although individuals of all skin tones may experience the psychosocial impact of psoriasis, quality-of-life measures have been found to be worse in those with skin of color (SOC) compared to White patients. 1,4 This may be due to the lingering PIH and hypopigmentation that occurs even after inflammatory plaques are treated. Of course, lack of access to care contributes to greater disease burden and more devastating psychological impact.
Health disparity highlight
Psoriasis may be underreported and underdiagnosed in individuals with SOC, as factors contributing to health care disparities may play a role, such as access to health care in general,1,7 and access to clinicians proficient in diagnosing cutaneous diseases in SOC may be delayed.8
Biologic medications are used less often in Black patients than in White patients, despite biologic medications being very efficacious for treatment of psoriasis.1,9,10
THE COMPARISON
A Elbow and forearm with erythematous, well-demarcated, pink plaques with mild micaceous scale in a 42-year-old White woman.
B Elbow and forearm with violaceous, well-demarcated plaques with micaceous scale and hyperpigmented patches around the active plaques in a 58-year-old Black man.
Epidemiology
Psoriasis prevalence in the United States has been estimated at 3.7%.1-3 If broken down by race or ethnicity, the prevalence of psoriasis varies: 2.5% to 3.7% in White adults1-4; 1.3% to 2% in Black adults1-4; 1.6% in Hispanics/other adults1-3; 1% in children overall; 0.29% in White children1,5; and 0.06% in Black children.1,5
Key clinical features in people with darker skin tones include:
- plaques that may appear more violaceous in color instead of pink or erythematous
- higher body surface area of involvement4 and thicker, more scaly plaques6
- increased likelihood of postinflammatory hyperpigmentation (PIH).
Worth noting
Although individuals of all skin tones may experience the psychosocial impact of psoriasis, quality-of-life measures have been found to be worse in those with skin of color (SOC) compared to White patients. 1,4 This may be due to the lingering PIH and hypopigmentation that occurs even after inflammatory plaques are treated. Of course, lack of access to care contributes to greater disease burden and more devastating psychological impact.
Health disparity highlight
Psoriasis may be underreported and underdiagnosed in individuals with SOC, as factors contributing to health care disparities may play a role, such as access to health care in general,1,7 and access to clinicians proficient in diagnosing cutaneous diseases in SOC may be delayed.8
Biologic medications are used less often in Black patients than in White patients, despite biologic medications being very efficacious for treatment of psoriasis.1,9,10
1. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
2. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70:512-516.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Gelfand JM, Stern RS, Nijsten T, et al. The prevalence of psoriasis in African Americans: results from a population-based study. J Am Acad Dermatol. 2005;52:23-26.
5. Wu JJ, Black MH, Smith N, et al. Low prevalence of psoriasis among children and adolescents in a large multiethnic cohort in southern California. J Am Acad Dermatol. 2011;65:957-964.
6. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
7. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
8. Mundluru SN, Ramalingam ND, Tran HN. Addressing internal medicine residents’ discomfort with basic dermatology in persons of color in the primary care clinic. Am J Med Qual. 2019;34:513-513.
9. Kerr GS, Qaiyumi S, Richards J, et al. Psoriasis and psoriatic arthritis in African-American patients—the need to measure disease burden. Clin Rheumatol. 2015;34:1753-1759.
10. Takeshita J, Gelfand JM, Li P, et al. Psoriasis in the US Medicare population: prevalence, treatment, and factors associated with biologic use. J Invest Dermatol. 2015;135:2955-2963.
1. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
2. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70:512-516.
3. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47:37-45.
4. Gelfand JM, Stern RS, Nijsten T, et al. The prevalence of psoriasis in African Americans: results from a population-based study. J Am Acad Dermatol. 2005;52:23-26.
5. Wu JJ, Black MH, Smith N, et al. Low prevalence of psoriasis among children and adolescents in a large multiethnic cohort in southern California. J Am Acad Dermatol. 2011;65:957-964.
6. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
7. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
8. Mundluru SN, Ramalingam ND, Tran HN. Addressing internal medicine residents’ discomfort with basic dermatology in persons of color in the primary care clinic. Am J Med Qual. 2019;34:513-513.
9. Kerr GS, Qaiyumi S, Richards J, et al. Psoriasis and psoriatic arthritis in African-American patients—the need to measure disease burden. Clin Rheumatol. 2015;34:1753-1759.
10. Takeshita J, Gelfand JM, Li P, et al. Psoriasis in the US Medicare population: prevalence, treatment, and factors associated with biologic use. J Invest Dermatol. 2015;135:2955-2963.
This is not the time to modify a HTN regimen
ILLUSTRATIVE CASE
A 67-year-old man with hypertension that is well controlled on hydrochlorothiazide 25 mg po daily was admitted to the family medicine inpatient service for community-acquired pneumonia requiring antibiotic therapy and oxygen support. Despite improvement in his overall condition, his blood pressure was consistently > 160/90 mm Hg during his hospitalization. He was treated with lisinopril 10 mg po daily in addition to his home medications, which helped achieve recommended blood pressure goals.
Prior to discharge, his blood pressure was noted to be 108/62 mm Hg. He asks if it is necessary to continue this new blood pressure medicine, as his home blood pressure readings had been within the goal set by his primary care physician. Should you continue this new antihypertensive agent at discharge?
Outpatient antihypertensive medication regimens are commonly intensified at hospital discharge in response to transient short-term elevations in blood pressure during inpatient encounters for noncardiac conditions.1,2 This is typically a reflexive response during a hospitalization, despite the unknown long-term, patient-oriented clinical outcomes. These short-term, in-hospital blood pressure elevations may be due to numerous temporary causes, such as stress/anxiety, a pain response, agitation, a medication adverse effect, or volume overload.3
The transition from inpatient to outpatient care is a high-risk period, especially for older adults, as functional status is generally worse at hospital discharge than prehospitalization baseline.4 To compound this problem, adverse drug reactions are a common cause of hospitalization for older adults. Changing blood pressure medications in response to acute physiologic changes during illness may contribute to patient harm. Although observational studies of adverse drug reactions related to blood pressure medications are numerous, researchers have only evaluated adverse drug reactions pertaining to hospital admissions.5-8 This study sought to evaluate the clinical outcomes associated with intensification of antihypertensive regimens at discharge among older adults.
STUDY SUMMARY
Increased risk of readmission, adverse events after intensification at discharge
This retrospective cohort study, which was conducted across multiple
Antihypertensive medication changes at discharge were evaluated using information pulled from VHA pharmacies, combined with clinical data merged from VHA and Medicare claims. Intensification was defined as either adding a new blood pressure medication or a dose increase of more than 20% on a previously prescribed antihypertensive medication. Patients were excluded if they were discharged with a secondary diagnosis that required modifications to a blood pressure medication (such as atrial fibrillation, acute coronary syndrome, or stroke), were hospitalized in the previous 30 days, were admitted from a skilled nursing facility, or received more than 20% of their care (including filling prescriptions) outside the VHA system.
Primary outcomes included hospital readmission or SAEs (falls, syncope, hypotension, serious electrolyte abnormalities, or acute kidney injury) within 30 days or having a cardiovascular event within 1 year of hospital discharge. Secondary outcomes included the change in systolic blood pressure (SBP) within 1 year after discharge. Propensity score matching was used as a balancing factor to create a matched-pairs cohort to compare those receiving blood pressure medication intensification at hospital discharge with those who did not.
Continue to: Intensification of the blood pressure...
Intensification of the blood pressure regimen at hospital discharge was associated with an increased risk in 30-day hospital readmission (hazard ratio [HR] = 1.23; 95% CI, 1.07–1.42; number needed to harm [NNH] = 27) and SAEs (HR = 1.41; 95% CI, 1.06–1.88; NNH = 63). There was no associated reduction in cardiovascular events (HR = 1.18; 95% CI, 0.99–1.40) or change in mean SBP within 1 year after hospital discharge in those who received intensification vs those who did not (mean BP, 134.7 vs 134.4 mm Hg; difference-in-differences estimate = 0.2 mm Hg; 95% CI, −2.0 to 2.4 mm Hg).
WHAT’S NEW
First study on outcomes related to HTN med changes at hospital discharge
This well-designed, retrospective cohort study provides important clinical data to help guide inpatient blood pressure management decisions for patients with noncardiac conditions. No clinical trials up to that time had assessed patient-oriented outcomes when antihypertensive medication regimens were intensified at hospital discharge.
CAVEATS
Study population: Primarily older men with noncardiac conditions
Selected populations benefit from intensive blood pressure control based on specific risk factors and medical conditions. In patients at high risk for cardiovascular disease, without a history of stroke or diabetes, intensive blood pressure control (SBP < 120 mm Hg) improves cardiovascular outcomes and overall survival compared with standard therapy (SBP < 140 mm Hg).9 This retrospective cohort study involved mainly elderly male patients with noncardiac conditions. The study also excluded patients with a secondary diagnosis requiring modifications to an antihypertensive regimen, such as atrial fibrillation, acute coronary syndrome, or cerebrovascular accident. Thus, the findings may not be applicable to these patient populations.
CHALLENGES TO IMPLEMENTATION
Clinicians will need to address individual needs
Physicians have to balance various antihypertensive management strategies, as competing medical specialty society guidelines recommend differing targets for optimal blood pressure control. Given the concern for medicolegal liability and potential harms of therapeutic inertia, inpatient physicians must consider whether hospitalization is the best time to alter medications for long-term outpatient blood pressure control. Finally, the decision to leave blood pressure management to outpatient physicians assumes the patient has a continuity relationship with a primary care medical home.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536.
2. Harris CM, Sridharan A, Landis R, et al. What happens to the medication regimens of older adults during and after an acute hospitalization? J Patient Saf. 2013;9:150-153.
3. Aung WM, Menon SV, Materson BJ. Management of hypertension in hospitalized patients. Hosp Pract (1995). 2015;43:101-106.
4. Covinsky KE, Palmer RM, Fortinsky RH, et al. Loss of independence in activities of daily living in older adults hospitalized with medical illnesses: increased vulnerability with age. J Am Geriatr Soc. 2003;51:451-458.
5. Omer HMRB, Hodson J, Pontefract SK, et al. Inpatient falls in older adults: a cohort study of antihypertensive prescribing pre- and post-fall. BMC Geriatr. 2018;18:58.
6. Alhawassi TM, Krass I, Pont LG. Antihypertensive-related adverse drug reactions among older hospitalized adults. Int J Clin Pharm. 2018;40:428-435.
7. Passarelli MCG, Jacob-Filho W, Figueras A. Adverse drug reactions in an elderly hospitalised population: inappropriate prescription is a leading cause. Drugs Aging. 2005;22:767-777.
8. Beckett NS, Peters R, Fletcher AE, et al; HYVET Study Group. Treatment of hypertension in patients 80 years of age or older. N Engl J Med. 2008;358:1887-1898.
9. SPRINT Research Group; Wright JT Jr, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2116. Published correction appears in N Engl J Med. 2017;377:2506.
ILLUSTRATIVE CASE
A 67-year-old man with hypertension that is well controlled on hydrochlorothiazide 25 mg po daily was admitted to the family medicine inpatient service for community-acquired pneumonia requiring antibiotic therapy and oxygen support. Despite improvement in his overall condition, his blood pressure was consistently > 160/90 mm Hg during his hospitalization. He was treated with lisinopril 10 mg po daily in addition to his home medications, which helped achieve recommended blood pressure goals.
Prior to discharge, his blood pressure was noted to be 108/62 mm Hg. He asks if it is necessary to continue this new blood pressure medicine, as his home blood pressure readings had been within the goal set by his primary care physician. Should you continue this new antihypertensive agent at discharge?
Outpatient antihypertensive medication regimens are commonly intensified at hospital discharge in response to transient short-term elevations in blood pressure during inpatient encounters for noncardiac conditions.1,2 This is typically a reflexive response during a hospitalization, despite the unknown long-term, patient-oriented clinical outcomes. These short-term, in-hospital blood pressure elevations may be due to numerous temporary causes, such as stress/anxiety, a pain response, agitation, a medication adverse effect, or volume overload.3
The transition from inpatient to outpatient care is a high-risk period, especially for older adults, as functional status is generally worse at hospital discharge than prehospitalization baseline.4 To compound this problem, adverse drug reactions are a common cause of hospitalization for older adults. Changing blood pressure medications in response to acute physiologic changes during illness may contribute to patient harm. Although observational studies of adverse drug reactions related to blood pressure medications are numerous, researchers have only evaluated adverse drug reactions pertaining to hospital admissions.5-8 This study sought to evaluate the clinical outcomes associated with intensification of antihypertensive regimens at discharge among older adults.
STUDY SUMMARY
Increased risk of readmission, adverse events after intensification at discharge
This retrospective cohort study, which was conducted across multiple
Antihypertensive medication changes at discharge were evaluated using information pulled from VHA pharmacies, combined with clinical data merged from VHA and Medicare claims. Intensification was defined as either adding a new blood pressure medication or a dose increase of more than 20% on a previously prescribed antihypertensive medication. Patients were excluded if they were discharged with a secondary diagnosis that required modifications to a blood pressure medication (such as atrial fibrillation, acute coronary syndrome, or stroke), were hospitalized in the previous 30 days, were admitted from a skilled nursing facility, or received more than 20% of their care (including filling prescriptions) outside the VHA system.
Primary outcomes included hospital readmission or SAEs (falls, syncope, hypotension, serious electrolyte abnormalities, or acute kidney injury) within 30 days or having a cardiovascular event within 1 year of hospital discharge. Secondary outcomes included the change in systolic blood pressure (SBP) within 1 year after discharge. Propensity score matching was used as a balancing factor to create a matched-pairs cohort to compare those receiving blood pressure medication intensification at hospital discharge with those who did not.
Continue to: Intensification of the blood pressure...
Intensification of the blood pressure regimen at hospital discharge was associated with an increased risk in 30-day hospital readmission (hazard ratio [HR] = 1.23; 95% CI, 1.07–1.42; number needed to harm [NNH] = 27) and SAEs (HR = 1.41; 95% CI, 1.06–1.88; NNH = 63). There was no associated reduction in cardiovascular events (HR = 1.18; 95% CI, 0.99–1.40) or change in mean SBP within 1 year after hospital discharge in those who received intensification vs those who did not (mean BP, 134.7 vs 134.4 mm Hg; difference-in-differences estimate = 0.2 mm Hg; 95% CI, −2.0 to 2.4 mm Hg).
WHAT’S NEW
First study on outcomes related to HTN med changes at hospital discharge
This well-designed, retrospective cohort study provides important clinical data to help guide inpatient blood pressure management decisions for patients with noncardiac conditions. No clinical trials up to that time had assessed patient-oriented outcomes when antihypertensive medication regimens were intensified at hospital discharge.
CAVEATS
Study population: Primarily older men with noncardiac conditions
Selected populations benefit from intensive blood pressure control based on specific risk factors and medical conditions. In patients at high risk for cardiovascular disease, without a history of stroke or diabetes, intensive blood pressure control (SBP < 120 mm Hg) improves cardiovascular outcomes and overall survival compared with standard therapy (SBP < 140 mm Hg).9 This retrospective cohort study involved mainly elderly male patients with noncardiac conditions. The study also excluded patients with a secondary diagnosis requiring modifications to an antihypertensive regimen, such as atrial fibrillation, acute coronary syndrome, or cerebrovascular accident. Thus, the findings may not be applicable to these patient populations.
CHALLENGES TO IMPLEMENTATION
Clinicians will need to address individual needs
Physicians have to balance various antihypertensive management strategies, as competing medical specialty society guidelines recommend differing targets for optimal blood pressure control. Given the concern for medicolegal liability and potential harms of therapeutic inertia, inpatient physicians must consider whether hospitalization is the best time to alter medications for long-term outpatient blood pressure control. Finally, the decision to leave blood pressure management to outpatient physicians assumes the patient has a continuity relationship with a primary care medical home.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
ILLUSTRATIVE CASE
A 67-year-old man with hypertension that is well controlled on hydrochlorothiazide 25 mg po daily was admitted to the family medicine inpatient service for community-acquired pneumonia requiring antibiotic therapy and oxygen support. Despite improvement in his overall condition, his blood pressure was consistently > 160/90 mm Hg during his hospitalization. He was treated with lisinopril 10 mg po daily in addition to his home medications, which helped achieve recommended blood pressure goals.
Prior to discharge, his blood pressure was noted to be 108/62 mm Hg. He asks if it is necessary to continue this new blood pressure medicine, as his home blood pressure readings had been within the goal set by his primary care physician. Should you continue this new antihypertensive agent at discharge?
Outpatient antihypertensive medication regimens are commonly intensified at hospital discharge in response to transient short-term elevations in blood pressure during inpatient encounters for noncardiac conditions.1,2 This is typically a reflexive response during a hospitalization, despite the unknown long-term, patient-oriented clinical outcomes. These short-term, in-hospital blood pressure elevations may be due to numerous temporary causes, such as stress/anxiety, a pain response, agitation, a medication adverse effect, or volume overload.3
The transition from inpatient to outpatient care is a high-risk period, especially for older adults, as functional status is generally worse at hospital discharge than prehospitalization baseline.4 To compound this problem, adverse drug reactions are a common cause of hospitalization for older adults. Changing blood pressure medications in response to acute physiologic changes during illness may contribute to patient harm. Although observational studies of adverse drug reactions related to blood pressure medications are numerous, researchers have only evaluated adverse drug reactions pertaining to hospital admissions.5-8 This study sought to evaluate the clinical outcomes associated with intensification of antihypertensive regimens at discharge among older adults.
STUDY SUMMARY
Increased risk of readmission, adverse events after intensification at discharge
This retrospective cohort study, which was conducted across multiple
Antihypertensive medication changes at discharge were evaluated using information pulled from VHA pharmacies, combined with clinical data merged from VHA and Medicare claims. Intensification was defined as either adding a new blood pressure medication or a dose increase of more than 20% on a previously prescribed antihypertensive medication. Patients were excluded if they were discharged with a secondary diagnosis that required modifications to a blood pressure medication (such as atrial fibrillation, acute coronary syndrome, or stroke), were hospitalized in the previous 30 days, were admitted from a skilled nursing facility, or received more than 20% of their care (including filling prescriptions) outside the VHA system.
Primary outcomes included hospital readmission or SAEs (falls, syncope, hypotension, serious electrolyte abnormalities, or acute kidney injury) within 30 days or having a cardiovascular event within 1 year of hospital discharge. Secondary outcomes included the change in systolic blood pressure (SBP) within 1 year after discharge. Propensity score matching was used as a balancing factor to create a matched-pairs cohort to compare those receiving blood pressure medication intensification at hospital discharge with those who did not.
Continue to: Intensification of the blood pressure...
Intensification of the blood pressure regimen at hospital discharge was associated with an increased risk in 30-day hospital readmission (hazard ratio [HR] = 1.23; 95% CI, 1.07–1.42; number needed to harm [NNH] = 27) and SAEs (HR = 1.41; 95% CI, 1.06–1.88; NNH = 63). There was no associated reduction in cardiovascular events (HR = 1.18; 95% CI, 0.99–1.40) or change in mean SBP within 1 year after hospital discharge in those who received intensification vs those who did not (mean BP, 134.7 vs 134.4 mm Hg; difference-in-differences estimate = 0.2 mm Hg; 95% CI, −2.0 to 2.4 mm Hg).
WHAT’S NEW
First study on outcomes related to HTN med changes at hospital discharge
This well-designed, retrospective cohort study provides important clinical data to help guide inpatient blood pressure management decisions for patients with noncardiac conditions. No clinical trials up to that time had assessed patient-oriented outcomes when antihypertensive medication regimens were intensified at hospital discharge.
CAVEATS
Study population: Primarily older men with noncardiac conditions
Selected populations benefit from intensive blood pressure control based on specific risk factors and medical conditions. In patients at high risk for cardiovascular disease, without a history of stroke or diabetes, intensive blood pressure control (SBP < 120 mm Hg) improves cardiovascular outcomes and overall survival compared with standard therapy (SBP < 140 mm Hg).9 This retrospective cohort study involved mainly elderly male patients with noncardiac conditions. The study also excluded patients with a secondary diagnosis requiring modifications to an antihypertensive regimen, such as atrial fibrillation, acute coronary syndrome, or cerebrovascular accident. Thus, the findings may not be applicable to these patient populations.
CHALLENGES TO IMPLEMENTATION
Clinicians will need to address individual needs
Physicians have to balance various antihypertensive management strategies, as competing medical specialty society guidelines recommend differing targets for optimal blood pressure control. Given the concern for medicolegal liability and potential harms of therapeutic inertia, inpatient physicians must consider whether hospitalization is the best time to alter medications for long-term outpatient blood pressure control. Finally, the decision to leave blood pressure management to outpatient physicians assumes the patient has a continuity relationship with a primary care medical home.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536.
2. Harris CM, Sridharan A, Landis R, et al. What happens to the medication regimens of older adults during and after an acute hospitalization? J Patient Saf. 2013;9:150-153.
3. Aung WM, Menon SV, Materson BJ. Management of hypertension in hospitalized patients. Hosp Pract (1995). 2015;43:101-106.
4. Covinsky KE, Palmer RM, Fortinsky RH, et al. Loss of independence in activities of daily living in older adults hospitalized with medical illnesses: increased vulnerability with age. J Am Geriatr Soc. 2003;51:451-458.
5. Omer HMRB, Hodson J, Pontefract SK, et al. Inpatient falls in older adults: a cohort study of antihypertensive prescribing pre- and post-fall. BMC Geriatr. 2018;18:58.
6. Alhawassi TM, Krass I, Pont LG. Antihypertensive-related adverse drug reactions among older hospitalized adults. Int J Clin Pharm. 2018;40:428-435.
7. Passarelli MCG, Jacob-Filho W, Figueras A. Adverse drug reactions in an elderly hospitalised population: inappropriate prescription is a leading cause. Drugs Aging. 2005;22:767-777.
8. Beckett NS, Peters R, Fletcher AE, et al; HYVET Study Group. Treatment of hypertension in patients 80 years of age or older. N Engl J Med. 2008;358:1887-1898.
9. SPRINT Research Group; Wright JT Jr, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2116. Published correction appears in N Engl J Med. 2017;377:2506.
1. Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536.
2. Harris CM, Sridharan A, Landis R, et al. What happens to the medication regimens of older adults during and after an acute hospitalization? J Patient Saf. 2013;9:150-153.
3. Aung WM, Menon SV, Materson BJ. Management of hypertension in hospitalized patients. Hosp Pract (1995). 2015;43:101-106.
4. Covinsky KE, Palmer RM, Fortinsky RH, et al. Loss of independence in activities of daily living in older adults hospitalized with medical illnesses: increased vulnerability with age. J Am Geriatr Soc. 2003;51:451-458.
5. Omer HMRB, Hodson J, Pontefract SK, et al. Inpatient falls in older adults: a cohort study of antihypertensive prescribing pre- and post-fall. BMC Geriatr. 2018;18:58.
6. Alhawassi TM, Krass I, Pont LG. Antihypertensive-related adverse drug reactions among older hospitalized adults. Int J Clin Pharm. 2018;40:428-435.
7. Passarelli MCG, Jacob-Filho W, Figueras A. Adverse drug reactions in an elderly hospitalised population: inappropriate prescription is a leading cause. Drugs Aging. 2005;22:767-777.
8. Beckett NS, Peters R, Fletcher AE, et al; HYVET Study Group. Treatment of hypertension in patients 80 years of age or older. N Engl J Med. 2008;358:1887-1898.
9. SPRINT Research Group; Wright JT Jr, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103-2116. Published correction appears in N Engl J Med. 2017;377:2506.
PRACTICE CHANGER
Avoid intensifying antihypertensive medication regimens at hospital discharge in older adults; making such changes increases the risk of serious adverse events (SAEs) and hospital readmission within 30 days without reducing the risk of serious cardiovascular events at 1 year post discharge.
STRENGTH OF RECOMMENDATION
B: Based on a large retrospective cohort study evaluating patient-oriented outcomes.1
Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensifying antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528-1536.
Managing work disability to help patients return to the job
All clinicians who have patients who are employed play an essential role in work disability programs—whether or not those clinicians have received formal training in occupational health. A study found that primary care clinicians are asked to provide guidance about work activities in nearly 10% of their patient encounters; however, 25% of those clinicians thought they had little influence over work disability outcomes.1
In this article, we explain why it is important for family physicians to better manage work disability at the point of care, to help patients return to their pre-injury or pre-illness level of activity.
Why managing the duration of work disability matters
Each year, millions of American workers leave their jobs—temporarily or permanently—because of illness, injury, or the effects of a chronic condition.2 It is estimated that 893 million workdays are lost annually due to a new medical problem; an additional 527 million workdays are lost due to the impact of chronic health conditions on the ability to perform at work.3 The great majority of these lost workdays are the result of personal health conditions, not work-related problems; patients must therefore cope with the accompanying disruption of life and work.
Significant injury and illness can create a life crisis, especially when there is uncertainty about future livelihood, such as an income shortfall during a lengthy recovery. Only 40% of the US workforce is covered by a short-term disability insurance program; only 10% of low-wage and low-skill workers have this type of coverage.4 Benefits rarely replace loss of income entirely, and worker compensation insurance programs provide only partial wage replacement.
In short, work disability is destabilizing and can threaten overall well-being.5
Furthermore, the longer a person remains on temporary disability, the more likely that person is to move to a publicly funded disability program or leave the workforce entirely—thus, potentially losing future earnings and self-identity related to being a working member of society.6-8
Most of the annual cost of poor health for US employers derives from medical and wage benefits ($226 billion) and impaired or reduced employee performance ($223 billion).3 In addition, temporarily disabled workers likely account for a disproportionate share of health care costs: A study found that one-half of medical and pharmacy payments were paid out to the one-quarter of employees requiring disability benefits.9
Continue to: Benefits of staying on the job
Benefits of staying on the job. Research shows that there are physical and mental health benefits to remaining at, or returning to, work after an injury or illness.10,11 For example, in a longitudinal cohort of people with low back pain, immediate or early return to work (in 1-7 days) was associated with reduced pain and improved functioning at 3 months.12 Physicians who can guide patients safely back to normal activities, including work, minimize the physical and mental health impact of the injury or illness and avoid chronicity.13
Emphasizing the importance of health, not disease or injury
Health researchers have found that diagnosis, cause, and extent of morbidity do not adequately explain observed variability in the impact of health conditions, utilization of resources, or need for services. A wider view of the functional implications of an injury or illness is therefore required for physicians to effectively recommend disability duration.
The World Health Organization recommends a shift toward a more holistic view of health, impairment, and disability, including an emphasis on functional ability, intrinsic capacity, and environmental context.14 The American Medical Association, American College of Occupational and Environmental Medicine, and Canadian Medical Association emphasize that prolonged absence from one’s normal role can be detrimental to mental, physical, and social well-being.8 These advisory groups recommend that physicians encourage patients who are unable to work to (1) focus on restoring the rhythm of their everyday life in a stepwise fashion and (2) resume their usual responsibilities as soon as possible.
Advising a patient to focus on “what you can do,” not “what you can’t do,” might make all the difference in their return to productivity. Keeping the patient’s—as well as your own—attention focused on the positive process of recovery and documenting evidence of functional progress is an important addition to (or substitute for) detailed inquiries about pain and dysfunction.
Why does duration of disability vary so much from case to case?
Disability duration is influenced by the individual patient, employer, physician, jurisdiction, insurer or benefits structure, and access to care.15 For you to effectively manage a patient who is out of work for a medical reason, it is important to understand how nonmedical variables often influence the pace of recovery and the timing of return to work (FIGURE).
Continue to: Deficient communication
Deficient communication. Often, employers, insurers, third-party administrators, and clinicians—each a key stakeholder in disability care—are disconnected from one another, resulting in poor communication with the injured worker. Such fragmented communication can delay treatment and recovery.16 Data systems are not designed to measure the duration of disability or provide proactive notification for key stakeholders who might intervene to facilitate a patient’s recovery.
Alternatively, a collaborative approach to disability management has been shown to improve outcomes.17,18 Communication among the various professionals involved can be coordinated and expedited by a case manager or disability manager hired by the medical practice, the employer, or the insurance company.
Psychosocial and economic influences can radically affect the time it takes to return to pre-injury or pre-illness functional status. Demographic variables (age, sex, income, education, and support system) influence how a person responds to a debilitating injury or illness.19 Fear of re-injury, anxiety over the intensity of pain upon movement, worry over dependency on others, and resiliency play an important role when a patient is attempting to return to full activity.20,21
Job satisfaction has been identified as the most significant variable associated with prompt return to work.15 Work has many health-enhancing aspects, including socioeconomic status, psychosocial support, and self-identity22; however, not everyone wants, or feels ready, to go back to work even once they are physically able. Workplace variables, such as the patient–employee’s dislike of the position, coworkers, or manager, have been cited by physicians as leading barriers to returning to work at an appropriate time.23,24
Other external variables. Physicians should formulate activity prescriptions and medical restrictions based on the impact the medical condition has on the usual ability to function, as well as the anticipated impact of specific activities on the body’s natural healing process. However, Rainville and colleagues found that external variables—patient requests, employer characteristics, and jurisdiction issues—considerably influence physicians’ recommendations.20 For example, benefit structure might influence how long a patient wants to remain out of work—thus altering the requests they make to their physician. Jurisdictional characteristics, such as health care systems, state workers’ compensation departments, and payer systems, all influence a patient’s recovery timeline and time away from work.25
Continue to: What does your patient need so that they can recover?
What does your patient need so that they can recover? Individual and systemic factors must be appropriately addressed to minimize the impact that recovery from a disability has on a person’s life. Successful functional recovery enables the person to self-manage symptoms, reduce disruption-associated stress, preserve mental health, and maintain healthy relationships at home and work. An example is the patient who has successfully coped with the entire predicament that their medical condition posed and resumed their usual daily routine and responsibilities at home and at work—albeit sometimes with temporary or permanent modification necessitated by their specific condition.
Strategies that help patients stay at, or return to, their job
Physicians who anticipate, monitor, and actively manage the duration of a work disability can improve patient outcomes by minimizing life disruption, avoiding unnecessary medical care, and shortening the period of absence from work.
Key strategy: Set expectations for functional recovery early in the episode, including a forecast of how long it will take to get life and work back to normal.26,27 This is similar to discussing expectations about pain before surgery, which has been shown to decrease subsequent requests for opioids.28 It is crucial to educate the patient about timelines, define functional outcomes, and encourage them to set goals for recovery.29
Devise an evidence-based treatment plan. A fundamental way to reduce disability duration is to (1) devise a treatment plan that is evidence based and (2) take the most effective route to recovery. Given the pace with which medical research changes the understanding of diseases and treatments, it is essential to rely on up-to-date, comprehensive, independent, and authoritative resources to support your care decisions.
Aligning clinical practice with evidence-based medicine (EBM) is a good way to accomplish that goal. By definition, EBM practice guidelines recommend the safest and most effective treatments after unbiased assessment of the best available research. Increasingly, EBM is adopted to improve clinical and functional outcomes, establish national standards of care, and set criteria to evaluate clinical performance.30
Continue to: Utilize established guidelines
Utilize established guidelines. A tactic that can make it easier to discuss return to work with patients is to rely on an independent and authoritative reference set of codified disability duration guidelines, which, typically, can be searched by diagnosis, procedure, or presenting symptoms. Such guidelines provide a condition-specific expected duration of work disability in the form of number of days, with shortest, typical, and maximum durations for different levels of job demands. If necessary, you can then adjust the guideline’s estimated duration to account for the patient’s age, underlying state of health, comorbidities, and so forth.
The use of disability duration guidelines at the point of care can facilitate the process of setting early and appropriate expectations for a patient’s recovery. If a patient is confrontational in response to your recommendation on the duration of work disability, guidelines can be used to address specific objections and facilitate understanding of functional recovery.
Consider the employer’s needs. To support return-to-work efforts, your guidance about work should consider the employer’s business needs. Employers require that the patient’s abilities, restrictions, and limitations be described in concrete terms because they must decide which specific tasks are unsafe and which ones they can reasonably expect the recovering worker to perform. However, employers often fail to send information to the physician about the patient’s job tasks—such that the clinician must rely on patient self-reporting, which might be inaccurate, incomplete, or biased.15 When a patient needs protection against foreseeable harm, highlight specific activities that are currently unsafe on the recovery timeline.
Employers rely on the physician to (1) estimate what the patient can do and (2) describe work ability in clear, objective terms that both patient and employer can interpret (TABLE). For example, “no heavy lifting” might be hard for an employer to interpret; “may lift 10 pounds from the floor to the waist as many as 12 times an hour” might be applied in a more practical manner to help a patient return to work safely.31 Including specific numbers, rates, and metrics in activity restrictions can also help demonstrate improvement over the course of treatment.
Be clear and specific on work restrictions. During recovery, it is important to tell the patient which temporary work restrictions are intended to prevent further injury or recurrence (prophylactic work restrictions) and which are an estimate of what they are able to do safely at work (capacity-based restrictions). Your written work restrictions form should be kept separate from private medical information because those restrictions will be the basis of subsequent conversations between patient and employer, who should be invited to give feedback if the guidance needs revision or clarification.
Continue to: Employer programs
Employer programs, such as modified duty, transitional duty, or early return to work programs, have been found to resolve claims faster and improve recovery outcomes.10,12 Such programs might also reduce occupational stress and improve productivity when an employee realizes that their functional abilities are matched to realistic job expectations during recovery.16 You can play an important role in empowering your patients to seek out these support programs.
What’s ahead for managing disability durations?
Work disability duration is influenced by the complex mix of biological, psychosocial, and economic variables that we have touched on here. All stakeholders involved in the recovery process should support the patient’s ability to live life with as few restrictions as possible; you play a key role in their recovery by focusing on ability, highlighting remaining capabilities, emphasizing activities that are safe to perform, and encouraging acceptance of, and adaptation to, any irrevocable losses.
This is a holistic approach that might help patients overcome the stress and anxiety associated with major life events arising from illness or injury that trigger disability benefits. Open communication and establishing a shared goal, among all involved, of the best possible outcome increases the likelihood that working patients will return to their familiar life or find another positive path forward.
Using EBM and disability duration guidelines can help decrease the length of life–work disruption by ensuring that patients are given a diagnosis, treated, and managed appropriately.32,33 Although these practices have been adopted by some physicians, health care systems, and insurers, they are not being implemented systematically and are unlikely to become ubiquitous unless they are mandated by payers or by law.
Family physicians are front-line providers for America’s workforce. They are distinctly situated to help patients achieve their best life at home and work. Improving the timeliness and quality of work guidance provided by the physician is an important way to minimize the impact of health problems on working people’s lives and livelihoods—and to help them stay employed.
CORRESPONDENCE
Kerri Wizner, MPH, 10355 Westmoor Drive, Westminster, CO 80021; [email protected].
1. Pransky G, Katz JN, Benjamin K, et al. Improving the physician role in evaluating work ability and managing disability: A survey of primary care practitioners. Disabil Rehabil. 2002;24:867-874. doi: 10.1080/09638280210142176
2. Hollenbeck K. Promoting Retention or Reemployment of Workers After a Significant Injury or Illness. Mathematica Policy Research; October 22, 2015. Accessed June 1, 2021. https://mathematica.org/publications/promoting-retention-or-reemployment-of-workers-after-a-significant-injury-or-illness
3. Poor health costs us employers $530 billion and 1.4 billion work days of absence and impaired performance according to Integrated Benefits Institute. Press release. November 15, 2018. Accessed June 1, 2021. www.ibiweb.org/poor-health-costs-us-employers-530-billion-and-1-4-billion-work-days-of-absence-and-impaired-performance
4. US Bureau of Labor Statistics. Life and disability insurance benefits: How extensive is the employer-provided safety net? BLS looks at life and disability benefits. Program Perspectives. 2010;2:7:1-4. Accessed June 8, 2021. www.bls.gov/opub/btn/archive/program-perspectives-on-life-and-disability-insurance-benefits.pdf
5. Kettlewell N, Morris RW, Ho N, et al. The differential impact of major life events on cognitive and affective wellbeing. SSM Popul Health. 2019;10:100533. doi: 10.1016/j.ssmph.2019.100533
6. Contreary K, Ben-Shalom Y, Gifford B. Using predictive analytics for early identification of short-term disability claimants who exhaust their benefits. J Occup Rehabil. 2018;28:584-596. doi: 10.1007/s10926-018-9815-5
7. Hultin H, Lindholm C, Möller J. Is there an association between long-term sick leave and disability pension and unemployment beyond the effect of health status? – A cohort study. PLoS One. 2012;7:e35614. doi: 10.1371/journal.pone.0035614
8. Canadian Medical Association. CMA policy: The treating physician’s role in helping patients return to work after an illness or injury (update 2013); 2013:1-6. Accessed June 1, 2021. https://policybase.cma.ca/documents/policypdf/PD13-05.pdf
9. Gifford B. Temporarily disabled workers account for a disproportionate share of health care payments. Health Aff (Millwood). 2017;36:245-249. doi:10.1377/hlthaff.2016.1013
10. Rueda S, Chambers L, Wilson M, et al. Association of returning to work with better health in working-aged adults: a systematic review. Am J Public Health. 2012;102:541-556. doi: 10.2105/AJPH.2011.300401
11. Modini M, Joyce S, Mykletun A, et al. The mental health benefits of employment: results of a systematic meta-review. Australas Psychiatry. 2016;24:331-336. doi: 10.1177/1039856215618523
12. Shaw WS, Nelson CC, Woiszwillo MJ, et al. Early return to work has benefits for relief of back pain and functional recovery after controlling for multiple confounds. J Occup Environ Med. 2018;60:901-910. doi: 10.1097/JOM.0000000000001380
13. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59:e125-e131. doi: 10.1097/JOM.0000000000001055
14. World Health Organization. Towards a common language for functioning, disability and health. ICF: The International Classification of Functioning, Disability and Health. 2002. Accessed June 2, 2021. www.who.int/classifications/icf/icfbeginnersguide.pdf
15. Talmage JB, Melhorn JM, Hyman MH. AMA Guides to the Evaluation of Work Ability and Return to Work. 2nd ed. American Medical Association; 2011.
16. Harrell M. Psychological factors and workforce health. In: Lee LP, Martin DW, Kancelbaum B. Occupational Medicine: A Basic Guide. American College of Occupational and Environmental Medicine; 2019. Accessed June 1, 2021. https://ohguides.acoem.org/07-psychological-factors-and-workforce-health-stress-management
17. Wickizer TM, Franklin GM, Fulton-Kehoe D. Innovations in occupational health care delivery can prevent entry into permanent disability: 8-year follow-up of the Washington State Centers for Occupational Health and Education. Med Care. 2018;56:1018-1023. doi: 10.1097/MLR.0000000000000991
18. Christian J, Wickizer T, Burton K. Implementing a community-focused health & work service. SSDI Solution Initiative, Fiscal Institute of the Committee for a Responsible Federal Budget. May 2019. Accessed June 2, 2021. www.crfb.org/sites/default/files/Implementing_a_Community-Focused_HWS.pdf
19. Macpherson RA, Koehoorn M, Fan J, et al. Do differences in work disability duration between men and women vary by province in Canada? J Occup Rehabil. 2018;29:560-568. doi: 10.1007/s10926-018-9819-1
20. Rainville J, Pransky G, Indahl A, et al. The physician as disability advisor for patients with musculoskeletal complaints. Spine (Phila Pa 1976). 2005;30:2579-2584. doi: 10.1097/01.brs.0000186589.69382.1d
21. Jay K, Thorsen SV, Sundstrup E, et al. Fear avoidance beliefs and risk of long-term sickness absence: prospective cohort study among workers with musculoskeletal pain. Pain Res Treat. 2018;2018:8347120. doi: 10.1155/2018/8347120
22. Burgard S, Lin KY. Bad jobs, bad health? How work and working conditions contribute to health disparities. Am Behav Sci. 2013;57:10.1177/0002764213487347. doi: 10.1177/0002764213487347
23. Soklaridis S, Tang G, Cartmill C, et al. “Can you go back to work?” Family physicians’ experiences with assessing patients’ functional ability to return to work. Can Fam Physician. 2011;57:202-209.
24. Peters SE, Truong AP, Johnston V. Stakeholders identify similar barriers but different strategies to facilitate return-to-work: a vignette of a worker with an upper extremity condition. Work. 2018;59:401-412. doi: 10.3233/WOR-182692
25. Shraim M, Cifuentes M, Willetts JL, et al. Regional socioeconomic disparities in outcomes for workers with low back pain in the United States. Am J Ind Med. 2017;60:472-483. doi: 10.1002/ajim.22712
26. Hill JC, Fritz JM. Psychosocial influences on low back pain, disability, and response to treatment. Phys Ther. 2011;91:712-721. doi: 10.2522/ptj.20100280
27. Aasdahl L, Pape K, Jensen C, et al. Associations between the readiness for return to work scale and return to work: a prospective study. J Occup Rehabil. 2018;28:97-106. doi: 10.1007/s10926-017-9705-2
28. Pino C, Covington M. Prescription of opioids for acute pain in opioid naïve patients. UpToDate Web site. February 9, 2021. Accessed June 2, 2021. www.uptodate.com/contents/prescription-of-opioids-for-acute-pain-in-opioid-naive-patients
29. Cancelliere C, Donovan J, Stochkendahl MJ, et al. Factors affecting return to work after injury or illness: best evidence synthesis of systematic reviews. Chiropr Man Therap. 2016;24:32. doi: 10.1186/s12998-016-0113-z
30. Lewis SJ, Orland BI. The importance and impact of evidence-based medicine. J Manag Care Pharm. 2004;10(5 suppl A):S3-S5. doi: 10.18553/jmcp.2004.10.S5-A.S3
31. Rupe KL. Work restrictions: documenting a patient’s return to work. Nurse Pract. 2010;35:49-53. doi: 10.1097/01.NPR.0000388901.49604.a8
32. Owens JD, Hegmann KT, Thiese MS, et al. Impacts of adherence to evidence-based medicine guidelines for the management of acute low back pain on costs of worker's compensation claims. J Occup Environ Med. 2019;61:445-452. doi: 10.1097/JOM.0000000000001593
33. Gaspar FW, Kownacki R, Zaidel CS, et al. Reducing disability durations and medical costs for patients with a carpal tunnel release surgery through the use of opioid prescribing guidelines. J Occup Environ Med. 2017;59:1180-1187. doi: 10.1097/JOM.0000000000001168
All clinicians who have patients who are employed play an essential role in work disability programs—whether or not those clinicians have received formal training in occupational health. A study found that primary care clinicians are asked to provide guidance about work activities in nearly 10% of their patient encounters; however, 25% of those clinicians thought they had little influence over work disability outcomes.1
In this article, we explain why it is important for family physicians to better manage work disability at the point of care, to help patients return to their pre-injury or pre-illness level of activity.
Why managing the duration of work disability matters
Each year, millions of American workers leave their jobs—temporarily or permanently—because of illness, injury, or the effects of a chronic condition.2 It is estimated that 893 million workdays are lost annually due to a new medical problem; an additional 527 million workdays are lost due to the impact of chronic health conditions on the ability to perform at work.3 The great majority of these lost workdays are the result of personal health conditions, not work-related problems; patients must therefore cope with the accompanying disruption of life and work.
Significant injury and illness can create a life crisis, especially when there is uncertainty about future livelihood, such as an income shortfall during a lengthy recovery. Only 40% of the US workforce is covered by a short-term disability insurance program; only 10% of low-wage and low-skill workers have this type of coverage.4 Benefits rarely replace loss of income entirely, and worker compensation insurance programs provide only partial wage replacement.
In short, work disability is destabilizing and can threaten overall well-being.5
Furthermore, the longer a person remains on temporary disability, the more likely that person is to move to a publicly funded disability program or leave the workforce entirely—thus, potentially losing future earnings and self-identity related to being a working member of society.6-8
Most of the annual cost of poor health for US employers derives from medical and wage benefits ($226 billion) and impaired or reduced employee performance ($223 billion).3 In addition, temporarily disabled workers likely account for a disproportionate share of health care costs: A study found that one-half of medical and pharmacy payments were paid out to the one-quarter of employees requiring disability benefits.9
Continue to: Benefits of staying on the job
Benefits of staying on the job. Research shows that there are physical and mental health benefits to remaining at, or returning to, work after an injury or illness.10,11 For example, in a longitudinal cohort of people with low back pain, immediate or early return to work (in 1-7 days) was associated with reduced pain and improved functioning at 3 months.12 Physicians who can guide patients safely back to normal activities, including work, minimize the physical and mental health impact of the injury or illness and avoid chronicity.13
Emphasizing the importance of health, not disease or injury
Health researchers have found that diagnosis, cause, and extent of morbidity do not adequately explain observed variability in the impact of health conditions, utilization of resources, or need for services. A wider view of the functional implications of an injury or illness is therefore required for physicians to effectively recommend disability duration.
The World Health Organization recommends a shift toward a more holistic view of health, impairment, and disability, including an emphasis on functional ability, intrinsic capacity, and environmental context.14 The American Medical Association, American College of Occupational and Environmental Medicine, and Canadian Medical Association emphasize that prolonged absence from one’s normal role can be detrimental to mental, physical, and social well-being.8 These advisory groups recommend that physicians encourage patients who are unable to work to (1) focus on restoring the rhythm of their everyday life in a stepwise fashion and (2) resume their usual responsibilities as soon as possible.
Advising a patient to focus on “what you can do,” not “what you can’t do,” might make all the difference in their return to productivity. Keeping the patient’s—as well as your own—attention focused on the positive process of recovery and documenting evidence of functional progress is an important addition to (or substitute for) detailed inquiries about pain and dysfunction.
Why does duration of disability vary so much from case to case?
Disability duration is influenced by the individual patient, employer, physician, jurisdiction, insurer or benefits structure, and access to care.15 For you to effectively manage a patient who is out of work for a medical reason, it is important to understand how nonmedical variables often influence the pace of recovery and the timing of return to work (FIGURE).
Continue to: Deficient communication
Deficient communication. Often, employers, insurers, third-party administrators, and clinicians—each a key stakeholder in disability care—are disconnected from one another, resulting in poor communication with the injured worker. Such fragmented communication can delay treatment and recovery.16 Data systems are not designed to measure the duration of disability or provide proactive notification for key stakeholders who might intervene to facilitate a patient’s recovery.
Alternatively, a collaborative approach to disability management has been shown to improve outcomes.17,18 Communication among the various professionals involved can be coordinated and expedited by a case manager or disability manager hired by the medical practice, the employer, or the insurance company.
Psychosocial and economic influences can radically affect the time it takes to return to pre-injury or pre-illness functional status. Demographic variables (age, sex, income, education, and support system) influence how a person responds to a debilitating injury or illness.19 Fear of re-injury, anxiety over the intensity of pain upon movement, worry over dependency on others, and resiliency play an important role when a patient is attempting to return to full activity.20,21
Job satisfaction has been identified as the most significant variable associated with prompt return to work.15 Work has many health-enhancing aspects, including socioeconomic status, psychosocial support, and self-identity22; however, not everyone wants, or feels ready, to go back to work even once they are physically able. Workplace variables, such as the patient–employee’s dislike of the position, coworkers, or manager, have been cited by physicians as leading barriers to returning to work at an appropriate time.23,24
Other external variables. Physicians should formulate activity prescriptions and medical restrictions based on the impact the medical condition has on the usual ability to function, as well as the anticipated impact of specific activities on the body’s natural healing process. However, Rainville and colleagues found that external variables—patient requests, employer characteristics, and jurisdiction issues—considerably influence physicians’ recommendations.20 For example, benefit structure might influence how long a patient wants to remain out of work—thus altering the requests they make to their physician. Jurisdictional characteristics, such as health care systems, state workers’ compensation departments, and payer systems, all influence a patient’s recovery timeline and time away from work.25
Continue to: What does your patient need so that they can recover?
What does your patient need so that they can recover? Individual and systemic factors must be appropriately addressed to minimize the impact that recovery from a disability has on a person’s life. Successful functional recovery enables the person to self-manage symptoms, reduce disruption-associated stress, preserve mental health, and maintain healthy relationships at home and work. An example is the patient who has successfully coped with the entire predicament that their medical condition posed and resumed their usual daily routine and responsibilities at home and at work—albeit sometimes with temporary or permanent modification necessitated by their specific condition.
Strategies that help patients stay at, or return to, their job
Physicians who anticipate, monitor, and actively manage the duration of a work disability can improve patient outcomes by minimizing life disruption, avoiding unnecessary medical care, and shortening the period of absence from work.
Key strategy: Set expectations for functional recovery early in the episode, including a forecast of how long it will take to get life and work back to normal.26,27 This is similar to discussing expectations about pain before surgery, which has been shown to decrease subsequent requests for opioids.28 It is crucial to educate the patient about timelines, define functional outcomes, and encourage them to set goals for recovery.29
Devise an evidence-based treatment plan. A fundamental way to reduce disability duration is to (1) devise a treatment plan that is evidence based and (2) take the most effective route to recovery. Given the pace with which medical research changes the understanding of diseases and treatments, it is essential to rely on up-to-date, comprehensive, independent, and authoritative resources to support your care decisions.
Aligning clinical practice with evidence-based medicine (EBM) is a good way to accomplish that goal. By definition, EBM practice guidelines recommend the safest and most effective treatments after unbiased assessment of the best available research. Increasingly, EBM is adopted to improve clinical and functional outcomes, establish national standards of care, and set criteria to evaluate clinical performance.30
Continue to: Utilize established guidelines
Utilize established guidelines. A tactic that can make it easier to discuss return to work with patients is to rely on an independent and authoritative reference set of codified disability duration guidelines, which, typically, can be searched by diagnosis, procedure, or presenting symptoms. Such guidelines provide a condition-specific expected duration of work disability in the form of number of days, with shortest, typical, and maximum durations for different levels of job demands. If necessary, you can then adjust the guideline’s estimated duration to account for the patient’s age, underlying state of health, comorbidities, and so forth.
The use of disability duration guidelines at the point of care can facilitate the process of setting early and appropriate expectations for a patient’s recovery. If a patient is confrontational in response to your recommendation on the duration of work disability, guidelines can be used to address specific objections and facilitate understanding of functional recovery.
Consider the employer’s needs. To support return-to-work efforts, your guidance about work should consider the employer’s business needs. Employers require that the patient’s abilities, restrictions, and limitations be described in concrete terms because they must decide which specific tasks are unsafe and which ones they can reasonably expect the recovering worker to perform. However, employers often fail to send information to the physician about the patient’s job tasks—such that the clinician must rely on patient self-reporting, which might be inaccurate, incomplete, or biased.15 When a patient needs protection against foreseeable harm, highlight specific activities that are currently unsafe on the recovery timeline.
Employers rely on the physician to (1) estimate what the patient can do and (2) describe work ability in clear, objective terms that both patient and employer can interpret (TABLE). For example, “no heavy lifting” might be hard for an employer to interpret; “may lift 10 pounds from the floor to the waist as many as 12 times an hour” might be applied in a more practical manner to help a patient return to work safely.31 Including specific numbers, rates, and metrics in activity restrictions can also help demonstrate improvement over the course of treatment.
Be clear and specific on work restrictions. During recovery, it is important to tell the patient which temporary work restrictions are intended to prevent further injury or recurrence (prophylactic work restrictions) and which are an estimate of what they are able to do safely at work (capacity-based restrictions). Your written work restrictions form should be kept separate from private medical information because those restrictions will be the basis of subsequent conversations between patient and employer, who should be invited to give feedback if the guidance needs revision or clarification.
Continue to: Employer programs
Employer programs, such as modified duty, transitional duty, or early return to work programs, have been found to resolve claims faster and improve recovery outcomes.10,12 Such programs might also reduce occupational stress and improve productivity when an employee realizes that their functional abilities are matched to realistic job expectations during recovery.16 You can play an important role in empowering your patients to seek out these support programs.
What’s ahead for managing disability durations?
Work disability duration is influenced by the complex mix of biological, psychosocial, and economic variables that we have touched on here. All stakeholders involved in the recovery process should support the patient’s ability to live life with as few restrictions as possible; you play a key role in their recovery by focusing on ability, highlighting remaining capabilities, emphasizing activities that are safe to perform, and encouraging acceptance of, and adaptation to, any irrevocable losses.
This is a holistic approach that might help patients overcome the stress and anxiety associated with major life events arising from illness or injury that trigger disability benefits. Open communication and establishing a shared goal, among all involved, of the best possible outcome increases the likelihood that working patients will return to their familiar life or find another positive path forward.
Using EBM and disability duration guidelines can help decrease the length of life–work disruption by ensuring that patients are given a diagnosis, treated, and managed appropriately.32,33 Although these practices have been adopted by some physicians, health care systems, and insurers, they are not being implemented systematically and are unlikely to become ubiquitous unless they are mandated by payers or by law.
Family physicians are front-line providers for America’s workforce. They are distinctly situated to help patients achieve their best life at home and work. Improving the timeliness and quality of work guidance provided by the physician is an important way to minimize the impact of health problems on working people’s lives and livelihoods—and to help them stay employed.
CORRESPONDENCE
Kerri Wizner, MPH, 10355 Westmoor Drive, Westminster, CO 80021; [email protected].
All clinicians who have patients who are employed play an essential role in work disability programs—whether or not those clinicians have received formal training in occupational health. A study found that primary care clinicians are asked to provide guidance about work activities in nearly 10% of their patient encounters; however, 25% of those clinicians thought they had little influence over work disability outcomes.1
In this article, we explain why it is important for family physicians to better manage work disability at the point of care, to help patients return to their pre-injury or pre-illness level of activity.
Why managing the duration of work disability matters
Each year, millions of American workers leave their jobs—temporarily or permanently—because of illness, injury, or the effects of a chronic condition.2 It is estimated that 893 million workdays are lost annually due to a new medical problem; an additional 527 million workdays are lost due to the impact of chronic health conditions on the ability to perform at work.3 The great majority of these lost workdays are the result of personal health conditions, not work-related problems; patients must therefore cope with the accompanying disruption of life and work.
Significant injury and illness can create a life crisis, especially when there is uncertainty about future livelihood, such as an income shortfall during a lengthy recovery. Only 40% of the US workforce is covered by a short-term disability insurance program; only 10% of low-wage and low-skill workers have this type of coverage.4 Benefits rarely replace loss of income entirely, and worker compensation insurance programs provide only partial wage replacement.
In short, work disability is destabilizing and can threaten overall well-being.5
Furthermore, the longer a person remains on temporary disability, the more likely that person is to move to a publicly funded disability program or leave the workforce entirely—thus, potentially losing future earnings and self-identity related to being a working member of society.6-8
Most of the annual cost of poor health for US employers derives from medical and wage benefits ($226 billion) and impaired or reduced employee performance ($223 billion).3 In addition, temporarily disabled workers likely account for a disproportionate share of health care costs: A study found that one-half of medical and pharmacy payments were paid out to the one-quarter of employees requiring disability benefits.9
Continue to: Benefits of staying on the job
Benefits of staying on the job. Research shows that there are physical and mental health benefits to remaining at, or returning to, work after an injury or illness.10,11 For example, in a longitudinal cohort of people with low back pain, immediate or early return to work (in 1-7 days) was associated with reduced pain and improved functioning at 3 months.12 Physicians who can guide patients safely back to normal activities, including work, minimize the physical and mental health impact of the injury or illness and avoid chronicity.13
Emphasizing the importance of health, not disease or injury
Health researchers have found that diagnosis, cause, and extent of morbidity do not adequately explain observed variability in the impact of health conditions, utilization of resources, or need for services. A wider view of the functional implications of an injury or illness is therefore required for physicians to effectively recommend disability duration.
The World Health Organization recommends a shift toward a more holistic view of health, impairment, and disability, including an emphasis on functional ability, intrinsic capacity, and environmental context.14 The American Medical Association, American College of Occupational and Environmental Medicine, and Canadian Medical Association emphasize that prolonged absence from one’s normal role can be detrimental to mental, physical, and social well-being.8 These advisory groups recommend that physicians encourage patients who are unable to work to (1) focus on restoring the rhythm of their everyday life in a stepwise fashion and (2) resume their usual responsibilities as soon as possible.
Advising a patient to focus on “what you can do,” not “what you can’t do,” might make all the difference in their return to productivity. Keeping the patient’s—as well as your own—attention focused on the positive process of recovery and documenting evidence of functional progress is an important addition to (or substitute for) detailed inquiries about pain and dysfunction.
Why does duration of disability vary so much from case to case?
Disability duration is influenced by the individual patient, employer, physician, jurisdiction, insurer or benefits structure, and access to care.15 For you to effectively manage a patient who is out of work for a medical reason, it is important to understand how nonmedical variables often influence the pace of recovery and the timing of return to work (FIGURE).
Continue to: Deficient communication
Deficient communication. Often, employers, insurers, third-party administrators, and clinicians—each a key stakeholder in disability care—are disconnected from one another, resulting in poor communication with the injured worker. Such fragmented communication can delay treatment and recovery.16 Data systems are not designed to measure the duration of disability or provide proactive notification for key stakeholders who might intervene to facilitate a patient’s recovery.
Alternatively, a collaborative approach to disability management has been shown to improve outcomes.17,18 Communication among the various professionals involved can be coordinated and expedited by a case manager or disability manager hired by the medical practice, the employer, or the insurance company.
Psychosocial and economic influences can radically affect the time it takes to return to pre-injury or pre-illness functional status. Demographic variables (age, sex, income, education, and support system) influence how a person responds to a debilitating injury or illness.19 Fear of re-injury, anxiety over the intensity of pain upon movement, worry over dependency on others, and resiliency play an important role when a patient is attempting to return to full activity.20,21
Job satisfaction has been identified as the most significant variable associated with prompt return to work.15 Work has many health-enhancing aspects, including socioeconomic status, psychosocial support, and self-identity22; however, not everyone wants, or feels ready, to go back to work even once they are physically able. Workplace variables, such as the patient–employee’s dislike of the position, coworkers, or manager, have been cited by physicians as leading barriers to returning to work at an appropriate time.23,24
Other external variables. Physicians should formulate activity prescriptions and medical restrictions based on the impact the medical condition has on the usual ability to function, as well as the anticipated impact of specific activities on the body’s natural healing process. However, Rainville and colleagues found that external variables—patient requests, employer characteristics, and jurisdiction issues—considerably influence physicians’ recommendations.20 For example, benefit structure might influence how long a patient wants to remain out of work—thus altering the requests they make to their physician. Jurisdictional characteristics, such as health care systems, state workers’ compensation departments, and payer systems, all influence a patient’s recovery timeline and time away from work.25
Continue to: What does your patient need so that they can recover?
What does your patient need so that they can recover? Individual and systemic factors must be appropriately addressed to minimize the impact that recovery from a disability has on a person’s life. Successful functional recovery enables the person to self-manage symptoms, reduce disruption-associated stress, preserve mental health, and maintain healthy relationships at home and work. An example is the patient who has successfully coped with the entire predicament that their medical condition posed and resumed their usual daily routine and responsibilities at home and at work—albeit sometimes with temporary or permanent modification necessitated by their specific condition.
Strategies that help patients stay at, or return to, their job
Physicians who anticipate, monitor, and actively manage the duration of a work disability can improve patient outcomes by minimizing life disruption, avoiding unnecessary medical care, and shortening the period of absence from work.
Key strategy: Set expectations for functional recovery early in the episode, including a forecast of how long it will take to get life and work back to normal.26,27 This is similar to discussing expectations about pain before surgery, which has been shown to decrease subsequent requests for opioids.28 It is crucial to educate the patient about timelines, define functional outcomes, and encourage them to set goals for recovery.29
Devise an evidence-based treatment plan. A fundamental way to reduce disability duration is to (1) devise a treatment plan that is evidence based and (2) take the most effective route to recovery. Given the pace with which medical research changes the understanding of diseases and treatments, it is essential to rely on up-to-date, comprehensive, independent, and authoritative resources to support your care decisions.
Aligning clinical practice with evidence-based medicine (EBM) is a good way to accomplish that goal. By definition, EBM practice guidelines recommend the safest and most effective treatments after unbiased assessment of the best available research. Increasingly, EBM is adopted to improve clinical and functional outcomes, establish national standards of care, and set criteria to evaluate clinical performance.30
Continue to: Utilize established guidelines
Utilize established guidelines. A tactic that can make it easier to discuss return to work with patients is to rely on an independent and authoritative reference set of codified disability duration guidelines, which, typically, can be searched by diagnosis, procedure, or presenting symptoms. Such guidelines provide a condition-specific expected duration of work disability in the form of number of days, with shortest, typical, and maximum durations for different levels of job demands. If necessary, you can then adjust the guideline’s estimated duration to account for the patient’s age, underlying state of health, comorbidities, and so forth.
The use of disability duration guidelines at the point of care can facilitate the process of setting early and appropriate expectations for a patient’s recovery. If a patient is confrontational in response to your recommendation on the duration of work disability, guidelines can be used to address specific objections and facilitate understanding of functional recovery.
Consider the employer’s needs. To support return-to-work efforts, your guidance about work should consider the employer’s business needs. Employers require that the patient’s abilities, restrictions, and limitations be described in concrete terms because they must decide which specific tasks are unsafe and which ones they can reasonably expect the recovering worker to perform. However, employers often fail to send information to the physician about the patient’s job tasks—such that the clinician must rely on patient self-reporting, which might be inaccurate, incomplete, or biased.15 When a patient needs protection against foreseeable harm, highlight specific activities that are currently unsafe on the recovery timeline.
Employers rely on the physician to (1) estimate what the patient can do and (2) describe work ability in clear, objective terms that both patient and employer can interpret (TABLE). For example, “no heavy lifting” might be hard for an employer to interpret; “may lift 10 pounds from the floor to the waist as many as 12 times an hour” might be applied in a more practical manner to help a patient return to work safely.31 Including specific numbers, rates, and metrics in activity restrictions can also help demonstrate improvement over the course of treatment.
Be clear and specific on work restrictions. During recovery, it is important to tell the patient which temporary work restrictions are intended to prevent further injury or recurrence (prophylactic work restrictions) and which are an estimate of what they are able to do safely at work (capacity-based restrictions). Your written work restrictions form should be kept separate from private medical information because those restrictions will be the basis of subsequent conversations between patient and employer, who should be invited to give feedback if the guidance needs revision or clarification.
Continue to: Employer programs
Employer programs, such as modified duty, transitional duty, or early return to work programs, have been found to resolve claims faster and improve recovery outcomes.10,12 Such programs might also reduce occupational stress and improve productivity when an employee realizes that their functional abilities are matched to realistic job expectations during recovery.16 You can play an important role in empowering your patients to seek out these support programs.
What’s ahead for managing disability durations?
Work disability duration is influenced by the complex mix of biological, psychosocial, and economic variables that we have touched on here. All stakeholders involved in the recovery process should support the patient’s ability to live life with as few restrictions as possible; you play a key role in their recovery by focusing on ability, highlighting remaining capabilities, emphasizing activities that are safe to perform, and encouraging acceptance of, and adaptation to, any irrevocable losses.
This is a holistic approach that might help patients overcome the stress and anxiety associated with major life events arising from illness or injury that trigger disability benefits. Open communication and establishing a shared goal, among all involved, of the best possible outcome increases the likelihood that working patients will return to their familiar life or find another positive path forward.
Using EBM and disability duration guidelines can help decrease the length of life–work disruption by ensuring that patients are given a diagnosis, treated, and managed appropriately.32,33 Although these practices have been adopted by some physicians, health care systems, and insurers, they are not being implemented systematically and are unlikely to become ubiquitous unless they are mandated by payers or by law.
Family physicians are front-line providers for America’s workforce. They are distinctly situated to help patients achieve their best life at home and work. Improving the timeliness and quality of work guidance provided by the physician is an important way to minimize the impact of health problems on working people’s lives and livelihoods—and to help them stay employed.
CORRESPONDENCE
Kerri Wizner, MPH, 10355 Westmoor Drive, Westminster, CO 80021; [email protected].
1. Pransky G, Katz JN, Benjamin K, et al. Improving the physician role in evaluating work ability and managing disability: A survey of primary care practitioners. Disabil Rehabil. 2002;24:867-874. doi: 10.1080/09638280210142176
2. Hollenbeck K. Promoting Retention or Reemployment of Workers After a Significant Injury or Illness. Mathematica Policy Research; October 22, 2015. Accessed June 1, 2021. https://mathematica.org/publications/promoting-retention-or-reemployment-of-workers-after-a-significant-injury-or-illness
3. Poor health costs us employers $530 billion and 1.4 billion work days of absence and impaired performance according to Integrated Benefits Institute. Press release. November 15, 2018. Accessed June 1, 2021. www.ibiweb.org/poor-health-costs-us-employers-530-billion-and-1-4-billion-work-days-of-absence-and-impaired-performance
4. US Bureau of Labor Statistics. Life and disability insurance benefits: How extensive is the employer-provided safety net? BLS looks at life and disability benefits. Program Perspectives. 2010;2:7:1-4. Accessed June 8, 2021. www.bls.gov/opub/btn/archive/program-perspectives-on-life-and-disability-insurance-benefits.pdf
5. Kettlewell N, Morris RW, Ho N, et al. The differential impact of major life events on cognitive and affective wellbeing. SSM Popul Health. 2019;10:100533. doi: 10.1016/j.ssmph.2019.100533
6. Contreary K, Ben-Shalom Y, Gifford B. Using predictive analytics for early identification of short-term disability claimants who exhaust their benefits. J Occup Rehabil. 2018;28:584-596. doi: 10.1007/s10926-018-9815-5
7. Hultin H, Lindholm C, Möller J. Is there an association between long-term sick leave and disability pension and unemployment beyond the effect of health status? – A cohort study. PLoS One. 2012;7:e35614. doi: 10.1371/journal.pone.0035614
8. Canadian Medical Association. CMA policy: The treating physician’s role in helping patients return to work after an illness or injury (update 2013); 2013:1-6. Accessed June 1, 2021. https://policybase.cma.ca/documents/policypdf/PD13-05.pdf
9. Gifford B. Temporarily disabled workers account for a disproportionate share of health care payments. Health Aff (Millwood). 2017;36:245-249. doi:10.1377/hlthaff.2016.1013
10. Rueda S, Chambers L, Wilson M, et al. Association of returning to work with better health in working-aged adults: a systematic review. Am J Public Health. 2012;102:541-556. doi: 10.2105/AJPH.2011.300401
11. Modini M, Joyce S, Mykletun A, et al. The mental health benefits of employment: results of a systematic meta-review. Australas Psychiatry. 2016;24:331-336. doi: 10.1177/1039856215618523
12. Shaw WS, Nelson CC, Woiszwillo MJ, et al. Early return to work has benefits for relief of back pain and functional recovery after controlling for multiple confounds. J Occup Environ Med. 2018;60:901-910. doi: 10.1097/JOM.0000000000001380
13. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59:e125-e131. doi: 10.1097/JOM.0000000000001055
14. World Health Organization. Towards a common language for functioning, disability and health. ICF: The International Classification of Functioning, Disability and Health. 2002. Accessed June 2, 2021. www.who.int/classifications/icf/icfbeginnersguide.pdf
15. Talmage JB, Melhorn JM, Hyman MH. AMA Guides to the Evaluation of Work Ability and Return to Work. 2nd ed. American Medical Association; 2011.
16. Harrell M. Psychological factors and workforce health. In: Lee LP, Martin DW, Kancelbaum B. Occupational Medicine: A Basic Guide. American College of Occupational and Environmental Medicine; 2019. Accessed June 1, 2021. https://ohguides.acoem.org/07-psychological-factors-and-workforce-health-stress-management
17. Wickizer TM, Franklin GM, Fulton-Kehoe D. Innovations in occupational health care delivery can prevent entry into permanent disability: 8-year follow-up of the Washington State Centers for Occupational Health and Education. Med Care. 2018;56:1018-1023. doi: 10.1097/MLR.0000000000000991
18. Christian J, Wickizer T, Burton K. Implementing a community-focused health & work service. SSDI Solution Initiative, Fiscal Institute of the Committee for a Responsible Federal Budget. May 2019. Accessed June 2, 2021. www.crfb.org/sites/default/files/Implementing_a_Community-Focused_HWS.pdf
19. Macpherson RA, Koehoorn M, Fan J, et al. Do differences in work disability duration between men and women vary by province in Canada? J Occup Rehabil. 2018;29:560-568. doi: 10.1007/s10926-018-9819-1
20. Rainville J, Pransky G, Indahl A, et al. The physician as disability advisor for patients with musculoskeletal complaints. Spine (Phila Pa 1976). 2005;30:2579-2584. doi: 10.1097/01.brs.0000186589.69382.1d
21. Jay K, Thorsen SV, Sundstrup E, et al. Fear avoidance beliefs and risk of long-term sickness absence: prospective cohort study among workers with musculoskeletal pain. Pain Res Treat. 2018;2018:8347120. doi: 10.1155/2018/8347120
22. Burgard S, Lin KY. Bad jobs, bad health? How work and working conditions contribute to health disparities. Am Behav Sci. 2013;57:10.1177/0002764213487347. doi: 10.1177/0002764213487347
23. Soklaridis S, Tang G, Cartmill C, et al. “Can you go back to work?” Family physicians’ experiences with assessing patients’ functional ability to return to work. Can Fam Physician. 2011;57:202-209.
24. Peters SE, Truong AP, Johnston V. Stakeholders identify similar barriers but different strategies to facilitate return-to-work: a vignette of a worker with an upper extremity condition. Work. 2018;59:401-412. doi: 10.3233/WOR-182692
25. Shraim M, Cifuentes M, Willetts JL, et al. Regional socioeconomic disparities in outcomes for workers with low back pain in the United States. Am J Ind Med. 2017;60:472-483. doi: 10.1002/ajim.22712
26. Hill JC, Fritz JM. Psychosocial influences on low back pain, disability, and response to treatment. Phys Ther. 2011;91:712-721. doi: 10.2522/ptj.20100280
27. Aasdahl L, Pape K, Jensen C, et al. Associations between the readiness for return to work scale and return to work: a prospective study. J Occup Rehabil. 2018;28:97-106. doi: 10.1007/s10926-017-9705-2
28. Pino C, Covington M. Prescription of opioids for acute pain in opioid naïve patients. UpToDate Web site. February 9, 2021. Accessed June 2, 2021. www.uptodate.com/contents/prescription-of-opioids-for-acute-pain-in-opioid-naive-patients
29. Cancelliere C, Donovan J, Stochkendahl MJ, et al. Factors affecting return to work after injury or illness: best evidence synthesis of systematic reviews. Chiropr Man Therap. 2016;24:32. doi: 10.1186/s12998-016-0113-z
30. Lewis SJ, Orland BI. The importance and impact of evidence-based medicine. J Manag Care Pharm. 2004;10(5 suppl A):S3-S5. doi: 10.18553/jmcp.2004.10.S5-A.S3
31. Rupe KL. Work restrictions: documenting a patient’s return to work. Nurse Pract. 2010;35:49-53. doi: 10.1097/01.NPR.0000388901.49604.a8
32. Owens JD, Hegmann KT, Thiese MS, et al. Impacts of adherence to evidence-based medicine guidelines for the management of acute low back pain on costs of worker's compensation claims. J Occup Environ Med. 2019;61:445-452. doi: 10.1097/JOM.0000000000001593
33. Gaspar FW, Kownacki R, Zaidel CS, et al. Reducing disability durations and medical costs for patients with a carpal tunnel release surgery through the use of opioid prescribing guidelines. J Occup Environ Med. 2017;59:1180-1187. doi: 10.1097/JOM.0000000000001168
1. Pransky G, Katz JN, Benjamin K, et al. Improving the physician role in evaluating work ability and managing disability: A survey of primary care practitioners. Disabil Rehabil. 2002;24:867-874. doi: 10.1080/09638280210142176
2. Hollenbeck K. Promoting Retention or Reemployment of Workers After a Significant Injury or Illness. Mathematica Policy Research; October 22, 2015. Accessed June 1, 2021. https://mathematica.org/publications/promoting-retention-or-reemployment-of-workers-after-a-significant-injury-or-illness
3. Poor health costs us employers $530 billion and 1.4 billion work days of absence and impaired performance according to Integrated Benefits Institute. Press release. November 15, 2018. Accessed June 1, 2021. www.ibiweb.org/poor-health-costs-us-employers-530-billion-and-1-4-billion-work-days-of-absence-and-impaired-performance
4. US Bureau of Labor Statistics. Life and disability insurance benefits: How extensive is the employer-provided safety net? BLS looks at life and disability benefits. Program Perspectives. 2010;2:7:1-4. Accessed June 8, 2021. www.bls.gov/opub/btn/archive/program-perspectives-on-life-and-disability-insurance-benefits.pdf
5. Kettlewell N, Morris RW, Ho N, et al. The differential impact of major life events on cognitive and affective wellbeing. SSM Popul Health. 2019;10:100533. doi: 10.1016/j.ssmph.2019.100533
6. Contreary K, Ben-Shalom Y, Gifford B. Using predictive analytics for early identification of short-term disability claimants who exhaust their benefits. J Occup Rehabil. 2018;28:584-596. doi: 10.1007/s10926-018-9815-5
7. Hultin H, Lindholm C, Möller J. Is there an association between long-term sick leave and disability pension and unemployment beyond the effect of health status? – A cohort study. PLoS One. 2012;7:e35614. doi: 10.1371/journal.pone.0035614
8. Canadian Medical Association. CMA policy: The treating physician’s role in helping patients return to work after an illness or injury (update 2013); 2013:1-6. Accessed June 1, 2021. https://policybase.cma.ca/documents/policypdf/PD13-05.pdf
9. Gifford B. Temporarily disabled workers account for a disproportionate share of health care payments. Health Aff (Millwood). 2017;36:245-249. doi:10.1377/hlthaff.2016.1013
10. Rueda S, Chambers L, Wilson M, et al. Association of returning to work with better health in working-aged adults: a systematic review. Am J Public Health. 2012;102:541-556. doi: 10.2105/AJPH.2011.300401
11. Modini M, Joyce S, Mykletun A, et al. The mental health benefits of employment: results of a systematic meta-review. Australas Psychiatry. 2016;24:331-336. doi: 10.1177/1039856215618523
12. Shaw WS, Nelson CC, Woiszwillo MJ, et al. Early return to work has benefits for relief of back pain and functional recovery after controlling for multiple confounds. J Occup Environ Med. 2018;60:901-910. doi: 10.1097/JOM.0000000000001380
13. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59:e125-e131. doi: 10.1097/JOM.0000000000001055
14. World Health Organization. Towards a common language for functioning, disability and health. ICF: The International Classification of Functioning, Disability and Health. 2002. Accessed June 2, 2021. www.who.int/classifications/icf/icfbeginnersguide.pdf
15. Talmage JB, Melhorn JM, Hyman MH. AMA Guides to the Evaluation of Work Ability and Return to Work. 2nd ed. American Medical Association; 2011.
16. Harrell M. Psychological factors and workforce health. In: Lee LP, Martin DW, Kancelbaum B. Occupational Medicine: A Basic Guide. American College of Occupational and Environmental Medicine; 2019. Accessed June 1, 2021. https://ohguides.acoem.org/07-psychological-factors-and-workforce-health-stress-management
17. Wickizer TM, Franklin GM, Fulton-Kehoe D. Innovations in occupational health care delivery can prevent entry into permanent disability: 8-year follow-up of the Washington State Centers for Occupational Health and Education. Med Care. 2018;56:1018-1023. doi: 10.1097/MLR.0000000000000991
18. Christian J, Wickizer T, Burton K. Implementing a community-focused health & work service. SSDI Solution Initiative, Fiscal Institute of the Committee for a Responsible Federal Budget. May 2019. Accessed June 2, 2021. www.crfb.org/sites/default/files/Implementing_a_Community-Focused_HWS.pdf
19. Macpherson RA, Koehoorn M, Fan J, et al. Do differences in work disability duration between men and women vary by province in Canada? J Occup Rehabil. 2018;29:560-568. doi: 10.1007/s10926-018-9819-1
20. Rainville J, Pransky G, Indahl A, et al. The physician as disability advisor for patients with musculoskeletal complaints. Spine (Phila Pa 1976). 2005;30:2579-2584. doi: 10.1097/01.brs.0000186589.69382.1d
21. Jay K, Thorsen SV, Sundstrup E, et al. Fear avoidance beliefs and risk of long-term sickness absence: prospective cohort study among workers with musculoskeletal pain. Pain Res Treat. 2018;2018:8347120. doi: 10.1155/2018/8347120
22. Burgard S, Lin KY. Bad jobs, bad health? How work and working conditions contribute to health disparities. Am Behav Sci. 2013;57:10.1177/0002764213487347. doi: 10.1177/0002764213487347
23. Soklaridis S, Tang G, Cartmill C, et al. “Can you go back to work?” Family physicians’ experiences with assessing patients’ functional ability to return to work. Can Fam Physician. 2011;57:202-209.
24. Peters SE, Truong AP, Johnston V. Stakeholders identify similar barriers but different strategies to facilitate return-to-work: a vignette of a worker with an upper extremity condition. Work. 2018;59:401-412. doi: 10.3233/WOR-182692
25. Shraim M, Cifuentes M, Willetts JL, et al. Regional socioeconomic disparities in outcomes for workers with low back pain in the United States. Am J Ind Med. 2017;60:472-483. doi: 10.1002/ajim.22712
26. Hill JC, Fritz JM. Psychosocial influences on low back pain, disability, and response to treatment. Phys Ther. 2011;91:712-721. doi: 10.2522/ptj.20100280
27. Aasdahl L, Pape K, Jensen C, et al. Associations between the readiness for return to work scale and return to work: a prospective study. J Occup Rehabil. 2018;28:97-106. doi: 10.1007/s10926-017-9705-2
28. Pino C, Covington M. Prescription of opioids for acute pain in opioid naïve patients. UpToDate Web site. February 9, 2021. Accessed June 2, 2021. www.uptodate.com/contents/prescription-of-opioids-for-acute-pain-in-opioid-naive-patients
29. Cancelliere C, Donovan J, Stochkendahl MJ, et al. Factors affecting return to work after injury or illness: best evidence synthesis of systematic reviews. Chiropr Man Therap. 2016;24:32. doi: 10.1186/s12998-016-0113-z
30. Lewis SJ, Orland BI. The importance and impact of evidence-based medicine. J Manag Care Pharm. 2004;10(5 suppl A):S3-S5. doi: 10.18553/jmcp.2004.10.S5-A.S3
31. Rupe KL. Work restrictions: documenting a patient’s return to work. Nurse Pract. 2010;35:49-53. doi: 10.1097/01.NPR.0000388901.49604.a8
32. Owens JD, Hegmann KT, Thiese MS, et al. Impacts of adherence to evidence-based medicine guidelines for the management of acute low back pain on costs of worker's compensation claims. J Occup Environ Med. 2019;61:445-452. doi: 10.1097/JOM.0000000000001593
33. Gaspar FW, Kownacki R, Zaidel CS, et al. Reducing disability durations and medical costs for patients with a carpal tunnel release surgery through the use of opioid prescribing guidelines. J Occup Environ Med. 2017;59:1180-1187. doi: 10.1097/JOM.0000000000001168
PRACTICE RECOMMENDATIONS
› Set appropriate expectations for the patient at the start of any episode of work disability: Estimate the course of functional recovery over time and the total duration of life–work disruption. A
› Include detailed activity prescriptions in the treatment plan, with stepwise progression over time toward full recovery. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Can family physicians accurately screen for AAA with point-of-care ultrasound?
EVIDENCE SUMMARY
Meta-analysis demonstrates accuracy of nonradiologist providers with POCUS
A systematic review and meta-analysis (11 studies; 946 exams) compared nonradiologist-performed AAA screening with POCUS vs radiologist-performed aortic imaging as a gold standard. Eight trials involved emergency medicine physicians (718 exams); 1 trial, surgical residents (104 exams); 1 trial, primary care internal medicine physicians (79 exams); and 1 trial, rural family physicians (45 exams). The majority of studies were conducted in Ireland, the United Kingdom, Australia, and Canada, with 4 trials performed in the United States.1
Researchers compared all POCUS exam findings with radiologist-performed imaging (using ultrasound, computed tomography, magnetic resonance imaging, or angiography) and with operative findings or pathology where available. There were 193 true positives, 8 false-positives, 740 true negatives, and 5 false-negatives. Primary care physicians identified 6 patients with AAA, with no false-positives or false-negatives. Overall, POCUS demonstrated a sensitivity of 0.975 (95% CI, 0.942 to 0.992) and a specificity of 0.989 (95% CI, 0.979 to 0.995).1
Nonradiologist providers received POCUS training as follows: emergency medicine residents, 5 hours to 3 days; emergency medicine physicians, 4 to 24 hours of didactics, 50 AAA scans, or American College of Emergency Medicine certification; and primary care physicians, 2.3 hours or 50 AAA scans. Information on training for surgical residents was not supplied. The authors rated the studies for quality (10-14 points on the 14-point QUADA quality score) and heterogeneity (I2 = 0 for sensitivity and I2 = .38 for specificity).1
European studies support FPs’ ability to diagnose AAA with POCUS
Two subsequent prospective diagnostic accuracy studies both found that POCUS performed by family physicians had 100% concordance with radiologist overread. The first study (in Spain) included 106 men (ages 50 and older; mean, 69 years) with chronic hypertension or a history of tobacco use. One family physician underwent training (duration not reported) by a radiologist, including experience measuring standard cross-sections of the aorta. Radiologists reviewed all POCUS images, which identified 6 patients with AAA (confirmed by CT scan). The concordance between the family physician and the radiologists was absolute (kappa = 1.0; sensitivity and specificity, 100%; positive and negative predictive values, both 1.0).2
The second study (in Denmark) compared 29 POCUS screenings for AAA performed by 5 family physicians vs a gold standard of a radiologist-performed abdominal ultrasound blinded to previous ultrasound findings. Four of the family physicians were board certified and 1 was a final-year resident in training. They all underwent a 3-day ultrasonography course that included initial e-learning followed by 2 days of hands-on training; all passed a final certification exam. The family physicians identified 1 patient with AAA. Radiologists overread all the scans and found 100% agreement with the 1 positive AAA and the 28 negative scans.3
Recommendations from others
In 2019, the US Preventive Services Task Force (USPSTF) offered a Grade “B” (moderate net benefit) recommendation for screening with ultrasonography for AAA in men ages 65 to 75 years who have ever smoked, and a Grade “C” recommendation (small net benefit) for screening men ages 65 to 75 years who have never smoked.4 In 2017, the Canadian Task Force on Preventive Health Care recommended screening all men ages 65 to 80 years with 1 ultrasound exam for AAA (weak recommendation; moderate-quality evidence). The Canadian Task Force also noted that, with adequate training, AAA screening could be performed in a family practice setting.5
Editor’s takeaway
While these studies evaluating POCUS performed by nonradiologists included a small number of family physicians, their finding that all participants (attending physicians and residents) demonstrate high sensitivity and specificity for AAA detection with relatively limited training bodes well for more widespread use of the technology. Offering POCUS to detect AAAs in family physician offices has the potential to dramatically improve access to USPSTF-recommended screening.
1. Concannon E, McHugh S, Healy DA, et al. Diagnostic accuracy of non-radiologist performed ultrasound for abdominal aortic aneurysm: systematic review and meta-analysis. Int J Clin Pract. 2014;9:1122-1129. doi: 10.1111/ijcp.12453
2. Sisó-Almirall A, Gilabert Solé R, Bru Saumell C, et al. Feasibility of hand-held-ultrasonography in the screening of abdominal aortic aneurysms and abdominal aortic atherosclerosis [article in Spanish]. Med Clin (Barc). 2013;141:417-422. doi: 10.1016/j.medcli.2013.02.038
3. Lindgaard K, Riisgaard L. ‘Validation of ultrasound examinations performed by general practitioners’. Scand J Prim Health Care. 2017;3:256-261. doi: 10.1080/02813432.2017.1358437
4. US Preventive Task Force. Screening for abdominal aortic aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322:2211-2218. doi:10.1001/jama.2019.18928
5. Canadian Task Force on Preventive Health Care. Recommendations on screening for abdominal aortic aneurysm in primary care. CMAJ. 2017;189:E1137-E1145. doi: 10.1503/cmaj.170118
EVIDENCE SUMMARY
Meta-analysis demonstrates accuracy of nonradiologist providers with POCUS
A systematic review and meta-analysis (11 studies; 946 exams) compared nonradiologist-performed AAA screening with POCUS vs radiologist-performed aortic imaging as a gold standard. Eight trials involved emergency medicine physicians (718 exams); 1 trial, surgical residents (104 exams); 1 trial, primary care internal medicine physicians (79 exams); and 1 trial, rural family physicians (45 exams). The majority of studies were conducted in Ireland, the United Kingdom, Australia, and Canada, with 4 trials performed in the United States.1
Researchers compared all POCUS exam findings with radiologist-performed imaging (using ultrasound, computed tomography, magnetic resonance imaging, or angiography) and with operative findings or pathology where available. There were 193 true positives, 8 false-positives, 740 true negatives, and 5 false-negatives. Primary care physicians identified 6 patients with AAA, with no false-positives or false-negatives. Overall, POCUS demonstrated a sensitivity of 0.975 (95% CI, 0.942 to 0.992) and a specificity of 0.989 (95% CI, 0.979 to 0.995).1
Nonradiologist providers received POCUS training as follows: emergency medicine residents, 5 hours to 3 days; emergency medicine physicians, 4 to 24 hours of didactics, 50 AAA scans, or American College of Emergency Medicine certification; and primary care physicians, 2.3 hours or 50 AAA scans. Information on training for surgical residents was not supplied. The authors rated the studies for quality (10-14 points on the 14-point QUADA quality score) and heterogeneity (I2 = 0 for sensitivity and I2 = .38 for specificity).1
European studies support FPs’ ability to diagnose AAA with POCUS
Two subsequent prospective diagnostic accuracy studies both found that POCUS performed by family physicians had 100% concordance with radiologist overread. The first study (in Spain) included 106 men (ages 50 and older; mean, 69 years) with chronic hypertension or a history of tobacco use. One family physician underwent training (duration not reported) by a radiologist, including experience measuring standard cross-sections of the aorta. Radiologists reviewed all POCUS images, which identified 6 patients with AAA (confirmed by CT scan). The concordance between the family physician and the radiologists was absolute (kappa = 1.0; sensitivity and specificity, 100%; positive and negative predictive values, both 1.0).2
The second study (in Denmark) compared 29 POCUS screenings for AAA performed by 5 family physicians vs a gold standard of a radiologist-performed abdominal ultrasound blinded to previous ultrasound findings. Four of the family physicians were board certified and 1 was a final-year resident in training. They all underwent a 3-day ultrasonography course that included initial e-learning followed by 2 days of hands-on training; all passed a final certification exam. The family physicians identified 1 patient with AAA. Radiologists overread all the scans and found 100% agreement with the 1 positive AAA and the 28 negative scans.3
Recommendations from others
In 2019, the US Preventive Services Task Force (USPSTF) offered a Grade “B” (moderate net benefit) recommendation for screening with ultrasonography for AAA in men ages 65 to 75 years who have ever smoked, and a Grade “C” recommendation (small net benefit) for screening men ages 65 to 75 years who have never smoked.4 In 2017, the Canadian Task Force on Preventive Health Care recommended screening all men ages 65 to 80 years with 1 ultrasound exam for AAA (weak recommendation; moderate-quality evidence). The Canadian Task Force also noted that, with adequate training, AAA screening could be performed in a family practice setting.5
Editor’s takeaway
While these studies evaluating POCUS performed by nonradiologists included a small number of family physicians, their finding that all participants (attending physicians and residents) demonstrate high sensitivity and specificity for AAA detection with relatively limited training bodes well for more widespread use of the technology. Offering POCUS to detect AAAs in family physician offices has the potential to dramatically improve access to USPSTF-recommended screening.
EVIDENCE SUMMARY
Meta-analysis demonstrates accuracy of nonradiologist providers with POCUS
A systematic review and meta-analysis (11 studies; 946 exams) compared nonradiologist-performed AAA screening with POCUS vs radiologist-performed aortic imaging as a gold standard. Eight trials involved emergency medicine physicians (718 exams); 1 trial, surgical residents (104 exams); 1 trial, primary care internal medicine physicians (79 exams); and 1 trial, rural family physicians (45 exams). The majority of studies were conducted in Ireland, the United Kingdom, Australia, and Canada, with 4 trials performed in the United States.1
Researchers compared all POCUS exam findings with radiologist-performed imaging (using ultrasound, computed tomography, magnetic resonance imaging, or angiography) and with operative findings or pathology where available. There were 193 true positives, 8 false-positives, 740 true negatives, and 5 false-negatives. Primary care physicians identified 6 patients with AAA, with no false-positives or false-negatives. Overall, POCUS demonstrated a sensitivity of 0.975 (95% CI, 0.942 to 0.992) and a specificity of 0.989 (95% CI, 0.979 to 0.995).1
Nonradiologist providers received POCUS training as follows: emergency medicine residents, 5 hours to 3 days; emergency medicine physicians, 4 to 24 hours of didactics, 50 AAA scans, or American College of Emergency Medicine certification; and primary care physicians, 2.3 hours or 50 AAA scans. Information on training for surgical residents was not supplied. The authors rated the studies for quality (10-14 points on the 14-point QUADA quality score) and heterogeneity (I2 = 0 for sensitivity and I2 = .38 for specificity).1
European studies support FPs’ ability to diagnose AAA with POCUS
Two subsequent prospective diagnostic accuracy studies both found that POCUS performed by family physicians had 100% concordance with radiologist overread. The first study (in Spain) included 106 men (ages 50 and older; mean, 69 years) with chronic hypertension or a history of tobacco use. One family physician underwent training (duration not reported) by a radiologist, including experience measuring standard cross-sections of the aorta. Radiologists reviewed all POCUS images, which identified 6 patients with AAA (confirmed by CT scan). The concordance between the family physician and the radiologists was absolute (kappa = 1.0; sensitivity and specificity, 100%; positive and negative predictive values, both 1.0).2
The second study (in Denmark) compared 29 POCUS screenings for AAA performed by 5 family physicians vs a gold standard of a radiologist-performed abdominal ultrasound blinded to previous ultrasound findings. Four of the family physicians were board certified and 1 was a final-year resident in training. They all underwent a 3-day ultrasonography course that included initial e-learning followed by 2 days of hands-on training; all passed a final certification exam. The family physicians identified 1 patient with AAA. Radiologists overread all the scans and found 100% agreement with the 1 positive AAA and the 28 negative scans.3
Recommendations from others
In 2019, the US Preventive Services Task Force (USPSTF) offered a Grade “B” (moderate net benefit) recommendation for screening with ultrasonography for AAA in men ages 65 to 75 years who have ever smoked, and a Grade “C” recommendation (small net benefit) for screening men ages 65 to 75 years who have never smoked.4 In 2017, the Canadian Task Force on Preventive Health Care recommended screening all men ages 65 to 80 years with 1 ultrasound exam for AAA (weak recommendation; moderate-quality evidence). The Canadian Task Force also noted that, with adequate training, AAA screening could be performed in a family practice setting.5
Editor’s takeaway
While these studies evaluating POCUS performed by nonradiologists included a small number of family physicians, their finding that all participants (attending physicians and residents) demonstrate high sensitivity and specificity for AAA detection with relatively limited training bodes well for more widespread use of the technology. Offering POCUS to detect AAAs in family physician offices has the potential to dramatically improve access to USPSTF-recommended screening.
1. Concannon E, McHugh S, Healy DA, et al. Diagnostic accuracy of non-radiologist performed ultrasound for abdominal aortic aneurysm: systematic review and meta-analysis. Int J Clin Pract. 2014;9:1122-1129. doi: 10.1111/ijcp.12453
2. Sisó-Almirall A, Gilabert Solé R, Bru Saumell C, et al. Feasibility of hand-held-ultrasonography in the screening of abdominal aortic aneurysms and abdominal aortic atherosclerosis [article in Spanish]. Med Clin (Barc). 2013;141:417-422. doi: 10.1016/j.medcli.2013.02.038
3. Lindgaard K, Riisgaard L. ‘Validation of ultrasound examinations performed by general practitioners’. Scand J Prim Health Care. 2017;3:256-261. doi: 10.1080/02813432.2017.1358437
4. US Preventive Task Force. Screening for abdominal aortic aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322:2211-2218. doi:10.1001/jama.2019.18928
5. Canadian Task Force on Preventive Health Care. Recommendations on screening for abdominal aortic aneurysm in primary care. CMAJ. 2017;189:E1137-E1145. doi: 10.1503/cmaj.170118
1. Concannon E, McHugh S, Healy DA, et al. Diagnostic accuracy of non-radiologist performed ultrasound for abdominal aortic aneurysm: systematic review and meta-analysis. Int J Clin Pract. 2014;9:1122-1129. doi: 10.1111/ijcp.12453
2. Sisó-Almirall A, Gilabert Solé R, Bru Saumell C, et al. Feasibility of hand-held-ultrasonography in the screening of abdominal aortic aneurysms and abdominal aortic atherosclerosis [article in Spanish]. Med Clin (Barc). 2013;141:417-422. doi: 10.1016/j.medcli.2013.02.038
3. Lindgaard K, Riisgaard L. ‘Validation of ultrasound examinations performed by general practitioners’. Scand J Prim Health Care. 2017;3:256-261. doi: 10.1080/02813432.2017.1358437
4. US Preventive Task Force. Screening for abdominal aortic aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322:2211-2218. doi:10.1001/jama.2019.18928
5. Canadian Task Force on Preventive Health Care. Recommendations on screening for abdominal aortic aneurysm in primary care. CMAJ. 2017;189:E1137-E1145. doi: 10.1503/cmaj.170118
EVIDENCE-BASED ANSWER:
Likely yes. Point-of-care ultrasound (POCUS) screening for abdominal aortic aneurysm (AAA) by nonradiologist physicians is 98% sensitive and 99% specific, compared with imaging performed by radiologists (strength of recommendation [SOR]: B, meta-analysis of diagnostic accuracy studies mostly involving emergency medicine physicians). European family physicians demonstrated 100% concordance with radiologist readings (SOR: C, very small subsequent diagnostic accuracy studies).
Separation and discoloration of thumb nail
The color change in this case is subtle, but consistent with green nail syndrome also termed chloronychia.
Green nail syndrome is a form of chronic paronychia caused by Pseudomonas aeruginosa and is associated with frequent water exposure. Pseudomonas expresses pyocyanin and pyoverdine, leading to the characteristic blue or green coloration. A Woods lamp may reveal neon green fluorescence.
Risk factors include frequent water exposure, use of an instrument to relieve symptoms of an ingrown nail, and chronic immunosuppression. In this case, frequent hand washing being performed by this patient during the COVID-19 pandemic was the likely culprit.
The differential diagnosis includes simple structural onycholysis, onychomycosis, and nail psoriasis. Polymicrobial infection can occur. When in doubt, culture or pathologic examination of nail clippings with Grocott methenamine silver and periodic acid–Schiff can identify coincident fungal infection.1 While systemic pseudomonas infection could also occur with green nail syndrome, the latter is usually only a mild nuisance and not associated with severe disease.
Treatment consists of avoidance of water and instrumentation. Topical sodium hypochlorite 2% solution applied to the nail or acetic acid soaks for 2 to 3 weeks is often curative. Antibiotic therapy may also be used. Topical tobramycin or gentamicin are available as otic or ophthalmic drops and can be applied just under the nail.
The patient was advised to meticulously dry her hands after washing them and to apply 1 drop of topical gentamicin solution 0.3% tid for 3 weeks. The green discoloration cleared in 3 weeks and the onycholysis resolved within 4 months.
Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).
1. Ohn J, Yu D-A, Park H, et al. Green nail syndrome: analysis of the association with onychomycosis. J Am Acad Dermatol. 2020;83:940-942. doi: 10.1016/j.jaad.2020.01.040
The color change in this case is subtle, but consistent with green nail syndrome also termed chloronychia.
Green nail syndrome is a form of chronic paronychia caused by Pseudomonas aeruginosa and is associated with frequent water exposure. Pseudomonas expresses pyocyanin and pyoverdine, leading to the characteristic blue or green coloration. A Woods lamp may reveal neon green fluorescence.
Risk factors include frequent water exposure, use of an instrument to relieve symptoms of an ingrown nail, and chronic immunosuppression. In this case, frequent hand washing being performed by this patient during the COVID-19 pandemic was the likely culprit.
The differential diagnosis includes simple structural onycholysis, onychomycosis, and nail psoriasis. Polymicrobial infection can occur. When in doubt, culture or pathologic examination of nail clippings with Grocott methenamine silver and periodic acid–Schiff can identify coincident fungal infection.1 While systemic pseudomonas infection could also occur with green nail syndrome, the latter is usually only a mild nuisance and not associated with severe disease.
Treatment consists of avoidance of water and instrumentation. Topical sodium hypochlorite 2% solution applied to the nail or acetic acid soaks for 2 to 3 weeks is often curative. Antibiotic therapy may also be used. Topical tobramycin or gentamicin are available as otic or ophthalmic drops and can be applied just under the nail.
The patient was advised to meticulously dry her hands after washing them and to apply 1 drop of topical gentamicin solution 0.3% tid for 3 weeks. The green discoloration cleared in 3 weeks and the onycholysis resolved within 4 months.
Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).
The color change in this case is subtle, but consistent with green nail syndrome also termed chloronychia.
Green nail syndrome is a form of chronic paronychia caused by Pseudomonas aeruginosa and is associated with frequent water exposure. Pseudomonas expresses pyocyanin and pyoverdine, leading to the characteristic blue or green coloration. A Woods lamp may reveal neon green fluorescence.
Risk factors include frequent water exposure, use of an instrument to relieve symptoms of an ingrown nail, and chronic immunosuppression. In this case, frequent hand washing being performed by this patient during the COVID-19 pandemic was the likely culprit.
The differential diagnosis includes simple structural onycholysis, onychomycosis, and nail psoriasis. Polymicrobial infection can occur. When in doubt, culture or pathologic examination of nail clippings with Grocott methenamine silver and periodic acid–Schiff can identify coincident fungal infection.1 While systemic pseudomonas infection could also occur with green nail syndrome, the latter is usually only a mild nuisance and not associated with severe disease.
Treatment consists of avoidance of water and instrumentation. Topical sodium hypochlorite 2% solution applied to the nail or acetic acid soaks for 2 to 3 weeks is often curative. Antibiotic therapy may also be used. Topical tobramycin or gentamicin are available as otic or ophthalmic drops and can be applied just under the nail.
The patient was advised to meticulously dry her hands after washing them and to apply 1 drop of topical gentamicin solution 0.3% tid for 3 weeks. The green discoloration cleared in 3 weeks and the onycholysis resolved within 4 months.
Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).
1. Ohn J, Yu D-A, Park H, et al. Green nail syndrome: analysis of the association with onychomycosis. J Am Acad Dermatol. 2020;83:940-942. doi: 10.1016/j.jaad.2020.01.040
1. Ohn J, Yu D-A, Park H, et al. Green nail syndrome: analysis of the association with onychomycosis. J Am Acad Dermatol. 2020;83:940-942. doi: 10.1016/j.jaad.2020.01.040
Erythematous ear with drainage
A 6-year-old boy was seen in the hospital in consultation for a 3-week history of suspected cellulitis of the right ear. Drainage from the right ear was refractory to treatment with a 7-day course of cephalexin 15 mL po bid of 250 mg/5 mL solution and clindamycin 24.4 mL po tid of 75 mg/5 mL solution. Treatment was followed by admission to the hospital for treatment with intravenous (IV) cefazolin 1000 mg q6h and IV vancomycin 825 mg q6h for 1 week.
The patient had a significant past medical history for asthma, allergic rhinitis, and severe atopic dermatitis that had been treated with methotrexate 10 mg per week for 6 months beginning when the child was 5 years of age. When the methotrexate proved to be ineffective, the patient was started on Aquaphor and mometasone 0.1% ointment. A 6-month trial of these agents failed as well.
Physical examination revealed that the right ear and skin around it were edematous, erythematous, pruritic, and tender. There was also purulent drainage coming from the ear (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infectious eczematoid dermatitis
The patient was referred to a dermatologist after seeing an ear, nose, and throat (ENT) specialist who made the diagnosis of otitis externa when the rash failed to respond to topical and systemic antibiotics. The patient’s tender, pruritic, oozing, edematous eruption was recognized as an infectious eczematoid dermatitis (IED).
Although it is not an uncommon condition, IED may be underrecognized. It accounted for 2.9% of admissions to a dermatology-run inpatient service between 2000 and 2010.1 IED results from cutaneous sensitization to purulent drainage secondary to acute otitis externa or another primary infection.2 In fact, cultures from the purulent drainage in this patient grew methicillin-resistant Staphylococcus aureus. The patient’s right otitis externa drainage may have been associated with the previous history of atopic dermatitis. Atopic dermatitis is associated with an increased risk of skin infections due to decreased inflammatory mediators (defensins).
Cellulitis and herpes zoster oticus are part of the differential
The differential diagnosis in this case includes bacterial cellulitis, acute otitis media, and herpes zoster oticus.
Bacterial cellulitis manifests with erythema, edema, and tenderness with blistering when associated with bullous impetigo rather than pruritus. The clinical appearance of the patient’s diffuse, weeping, edematous external ear, the lack of response to guided antibiotic therapy, and the pruritus experienced by the patient argue against the diagnosis of bacterial cellulitis.
Acute otitis media, like otitis externa, produces ear discharge usually associated with significant pain. Thus, it is important when working through the differential to define the source of the ear discharge. In this case, a consultation with an ENT specialist confirmed that there was an intact tympanic membrane with no middle ear involvement, ruling out the diagnosis of acute otitis media.
Continue to: Herpes zoster oticus
Herpes zoster oticus. The absence of grouped vesicles at any point during the eruption, itching rather than pain, and negative viral culture and polymerase chain reaction studies for herpes simplex and varicella zoster virus excluded the diagnosis of herpes zoster oticus.
Diagnostic criteria were met
This case was compatible with the characterizations of IED as initially described by Engman3 in 1902 and further detailed by Sutton,4 who provided the following criteria for diagnosis:
- an initial eczematous or pustular lesion
- extension peripherally by autoinoculation
- an absence of central clearing
- Staphylococcus on culture of the initial lesion
- a history of infection.
Case reports have added to our understanding of the mechanism of autosensitization of surrounding skin.5 Yamany and Schwartz have proposed the diagnostic criteria summarized in the TABLE.2
Age factors into location. The ears, nose, and face are predominantly involved in cases of IED in the pediatric population, while the lower extremities are predominantly involved in adults.6 Laboratory tests and imaging may aid in excluding other potential diagnoses or complications, but the diagnosis remains clinical and requires the clinician to avoid jumping to the conclusion that every moist, erythematous crusting eruption is purely infectious in nature.
Tx and prevention hinge on a combination of antibiotics, steroids
The management of IED should be aimed at fighting the infection, eliminating the allergic contact dermatitis associated with infectious products, and improving barrier protection. Topical and/or systemic antibiotics guided by culture focus on killing bacteria. The allergic immune response is dampened by systemic steroids. Topical steroids, however, are difficult to utilize on moist, draining skin. In the case of otitis externa, a combination topical antibiotic and steroid otic drop can be utilized. As healing begins, emollients are applied to aid in skin repair.2 Topical antibiotics containing neomycin or polymyxin should be avoided to eliminate the possibility of developing contact sensitivity to these agents.
For our patient, inpatient wound cultures demonstrated methicillin-resistant S aureus, and empiric treatment with IV cefepime and vancomycin was transitioned to IV clindamycin based on sensitivities and then transitioned to a 12-day course of oral clindamycin 150 mg bid. In addition, the patient received ciprofloxacin/dexamethasone otic drops 3 times/d to treat his otitis externa. After initiating prednisone 30 mg (1 mg/kg/d) for 10 days to cover the allergic component, the patient showed prompt clinical improvement. Gentle cleansing of the right ear with hypoallergenic soap and water followed by application of petrolatum ointment 4 times/d was used to promote healing and improve barrier function (FIGURE 2). The patient’s mother indicated during a follow-up call that the affected area had dramatically improved.
1. Storan ER, McEvoy MT, Wetter DA, et al. Experience with the dermatology inpatient hospital service for adults: Mayo Clinic, 2000–2010. J Eur Acad Dermatol Venereol. 2013;27:1360-1365. doi: 10.1111/jdv.12010
2. Yamany T, Schwartz RA. Infectious eczematoid dermatitis: a comprehensive review. J Eur Acad Dermatol Venereol. 2015;29:203-208. doi: 10.1111/jdv.12715
An infectious form of an eczematoid dermatitis. St. Louis Courier of Med. 1902;27:401414.
.4Infectious eczematoid dermatitis. J Am Med Assoc. 1920;75:976-979.
.Autosensitization dermatitis: report of five cases and protocol of an experiment. Arch Derm Syphilol. 1949;59:68-77. doi: 10.1001/archderm.1949.01520260072010
, , .Autosensitization in infectious eczematoid dermatitis. AMA Arch Derm Syphilol. 1950;62:703-704. doi: 10.1001/archderm.1950.01530180092021
, .A 6-year-old boy was seen in the hospital in consultation for a 3-week history of suspected cellulitis of the right ear. Drainage from the right ear was refractory to treatment with a 7-day course of cephalexin 15 mL po bid of 250 mg/5 mL solution and clindamycin 24.4 mL po tid of 75 mg/5 mL solution. Treatment was followed by admission to the hospital for treatment with intravenous (IV) cefazolin 1000 mg q6h and IV vancomycin 825 mg q6h for 1 week.
The patient had a significant past medical history for asthma, allergic rhinitis, and severe atopic dermatitis that had been treated with methotrexate 10 mg per week for 6 months beginning when the child was 5 years of age. When the methotrexate proved to be ineffective, the patient was started on Aquaphor and mometasone 0.1% ointment. A 6-month trial of these agents failed as well.
Physical examination revealed that the right ear and skin around it were edematous, erythematous, pruritic, and tender. There was also purulent drainage coming from the ear (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infectious eczematoid dermatitis
The patient was referred to a dermatologist after seeing an ear, nose, and throat (ENT) specialist who made the diagnosis of otitis externa when the rash failed to respond to topical and systemic antibiotics. The patient’s tender, pruritic, oozing, edematous eruption was recognized as an infectious eczematoid dermatitis (IED).
Although it is not an uncommon condition, IED may be underrecognized. It accounted for 2.9% of admissions to a dermatology-run inpatient service between 2000 and 2010.1 IED results from cutaneous sensitization to purulent drainage secondary to acute otitis externa or another primary infection.2 In fact, cultures from the purulent drainage in this patient grew methicillin-resistant Staphylococcus aureus. The patient’s right otitis externa drainage may have been associated with the previous history of atopic dermatitis. Atopic dermatitis is associated with an increased risk of skin infections due to decreased inflammatory mediators (defensins).
Cellulitis and herpes zoster oticus are part of the differential
The differential diagnosis in this case includes bacterial cellulitis, acute otitis media, and herpes zoster oticus.
Bacterial cellulitis manifests with erythema, edema, and tenderness with blistering when associated with bullous impetigo rather than pruritus. The clinical appearance of the patient’s diffuse, weeping, edematous external ear, the lack of response to guided antibiotic therapy, and the pruritus experienced by the patient argue against the diagnosis of bacterial cellulitis.
Acute otitis media, like otitis externa, produces ear discharge usually associated with significant pain. Thus, it is important when working through the differential to define the source of the ear discharge. In this case, a consultation with an ENT specialist confirmed that there was an intact tympanic membrane with no middle ear involvement, ruling out the diagnosis of acute otitis media.
Continue to: Herpes zoster oticus
Herpes zoster oticus. The absence of grouped vesicles at any point during the eruption, itching rather than pain, and negative viral culture and polymerase chain reaction studies for herpes simplex and varicella zoster virus excluded the diagnosis of herpes zoster oticus.
Diagnostic criteria were met
This case was compatible with the characterizations of IED as initially described by Engman3 in 1902 and further detailed by Sutton,4 who provided the following criteria for diagnosis:
- an initial eczematous or pustular lesion
- extension peripherally by autoinoculation
- an absence of central clearing
- Staphylococcus on culture of the initial lesion
- a history of infection.
Case reports have added to our understanding of the mechanism of autosensitization of surrounding skin.5 Yamany and Schwartz have proposed the diagnostic criteria summarized in the TABLE.2
Age factors into location. The ears, nose, and face are predominantly involved in cases of IED in the pediatric population, while the lower extremities are predominantly involved in adults.6 Laboratory tests and imaging may aid in excluding other potential diagnoses or complications, but the diagnosis remains clinical and requires the clinician to avoid jumping to the conclusion that every moist, erythematous crusting eruption is purely infectious in nature.
Tx and prevention hinge on a combination of antibiotics, steroids
The management of IED should be aimed at fighting the infection, eliminating the allergic contact dermatitis associated with infectious products, and improving barrier protection. Topical and/or systemic antibiotics guided by culture focus on killing bacteria. The allergic immune response is dampened by systemic steroids. Topical steroids, however, are difficult to utilize on moist, draining skin. In the case of otitis externa, a combination topical antibiotic and steroid otic drop can be utilized. As healing begins, emollients are applied to aid in skin repair.2 Topical antibiotics containing neomycin or polymyxin should be avoided to eliminate the possibility of developing contact sensitivity to these agents.
For our patient, inpatient wound cultures demonstrated methicillin-resistant S aureus, and empiric treatment with IV cefepime and vancomycin was transitioned to IV clindamycin based on sensitivities and then transitioned to a 12-day course of oral clindamycin 150 mg bid. In addition, the patient received ciprofloxacin/dexamethasone otic drops 3 times/d to treat his otitis externa. After initiating prednisone 30 mg (1 mg/kg/d) for 10 days to cover the allergic component, the patient showed prompt clinical improvement. Gentle cleansing of the right ear with hypoallergenic soap and water followed by application of petrolatum ointment 4 times/d was used to promote healing and improve barrier function (FIGURE 2). The patient’s mother indicated during a follow-up call that the affected area had dramatically improved.
A 6-year-old boy was seen in the hospital in consultation for a 3-week history of suspected cellulitis of the right ear. Drainage from the right ear was refractory to treatment with a 7-day course of cephalexin 15 mL po bid of 250 mg/5 mL solution and clindamycin 24.4 mL po tid of 75 mg/5 mL solution. Treatment was followed by admission to the hospital for treatment with intravenous (IV) cefazolin 1000 mg q6h and IV vancomycin 825 mg q6h for 1 week.
The patient had a significant past medical history for asthma, allergic rhinitis, and severe atopic dermatitis that had been treated with methotrexate 10 mg per week for 6 months beginning when the child was 5 years of age. When the methotrexate proved to be ineffective, the patient was started on Aquaphor and mometasone 0.1% ointment. A 6-month trial of these agents failed as well.
Physical examination revealed that the right ear and skin around it were edematous, erythematous, pruritic, and tender. There was also purulent drainage coming from the ear (FIGURE 1).
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Infectious eczematoid dermatitis
The patient was referred to a dermatologist after seeing an ear, nose, and throat (ENT) specialist who made the diagnosis of otitis externa when the rash failed to respond to topical and systemic antibiotics. The patient’s tender, pruritic, oozing, edematous eruption was recognized as an infectious eczematoid dermatitis (IED).
Although it is not an uncommon condition, IED may be underrecognized. It accounted for 2.9% of admissions to a dermatology-run inpatient service between 2000 and 2010.1 IED results from cutaneous sensitization to purulent drainage secondary to acute otitis externa or another primary infection.2 In fact, cultures from the purulent drainage in this patient grew methicillin-resistant Staphylococcus aureus. The patient’s right otitis externa drainage may have been associated with the previous history of atopic dermatitis. Atopic dermatitis is associated with an increased risk of skin infections due to decreased inflammatory mediators (defensins).
Cellulitis and herpes zoster oticus are part of the differential
The differential diagnosis in this case includes bacterial cellulitis, acute otitis media, and herpes zoster oticus.
Bacterial cellulitis manifests with erythema, edema, and tenderness with blistering when associated with bullous impetigo rather than pruritus. The clinical appearance of the patient’s diffuse, weeping, edematous external ear, the lack of response to guided antibiotic therapy, and the pruritus experienced by the patient argue against the diagnosis of bacterial cellulitis.
Acute otitis media, like otitis externa, produces ear discharge usually associated with significant pain. Thus, it is important when working through the differential to define the source of the ear discharge. In this case, a consultation with an ENT specialist confirmed that there was an intact tympanic membrane with no middle ear involvement, ruling out the diagnosis of acute otitis media.
Continue to: Herpes zoster oticus
Herpes zoster oticus. The absence of grouped vesicles at any point during the eruption, itching rather than pain, and negative viral culture and polymerase chain reaction studies for herpes simplex and varicella zoster virus excluded the diagnosis of herpes zoster oticus.
Diagnostic criteria were met
This case was compatible with the characterizations of IED as initially described by Engman3 in 1902 and further detailed by Sutton,4 who provided the following criteria for diagnosis:
- an initial eczematous or pustular lesion
- extension peripherally by autoinoculation
- an absence of central clearing
- Staphylococcus on culture of the initial lesion
- a history of infection.
Case reports have added to our understanding of the mechanism of autosensitization of surrounding skin.5 Yamany and Schwartz have proposed the diagnostic criteria summarized in the TABLE.2
Age factors into location. The ears, nose, and face are predominantly involved in cases of IED in the pediatric population, while the lower extremities are predominantly involved in adults.6 Laboratory tests and imaging may aid in excluding other potential diagnoses or complications, but the diagnosis remains clinical and requires the clinician to avoid jumping to the conclusion that every moist, erythematous crusting eruption is purely infectious in nature.
Tx and prevention hinge on a combination of antibiotics, steroids
The management of IED should be aimed at fighting the infection, eliminating the allergic contact dermatitis associated with infectious products, and improving barrier protection. Topical and/or systemic antibiotics guided by culture focus on killing bacteria. The allergic immune response is dampened by systemic steroids. Topical steroids, however, are difficult to utilize on moist, draining skin. In the case of otitis externa, a combination topical antibiotic and steroid otic drop can be utilized. As healing begins, emollients are applied to aid in skin repair.2 Topical antibiotics containing neomycin or polymyxin should be avoided to eliminate the possibility of developing contact sensitivity to these agents.
For our patient, inpatient wound cultures demonstrated methicillin-resistant S aureus, and empiric treatment with IV cefepime and vancomycin was transitioned to IV clindamycin based on sensitivities and then transitioned to a 12-day course of oral clindamycin 150 mg bid. In addition, the patient received ciprofloxacin/dexamethasone otic drops 3 times/d to treat his otitis externa. After initiating prednisone 30 mg (1 mg/kg/d) for 10 days to cover the allergic component, the patient showed prompt clinical improvement. Gentle cleansing of the right ear with hypoallergenic soap and water followed by application of petrolatum ointment 4 times/d was used to promote healing and improve barrier function (FIGURE 2). The patient’s mother indicated during a follow-up call that the affected area had dramatically improved.
1. Storan ER, McEvoy MT, Wetter DA, et al. Experience with the dermatology inpatient hospital service for adults: Mayo Clinic, 2000–2010. J Eur Acad Dermatol Venereol. 2013;27:1360-1365. doi: 10.1111/jdv.12010
2. Yamany T, Schwartz RA. Infectious eczematoid dermatitis: a comprehensive review. J Eur Acad Dermatol Venereol. 2015;29:203-208. doi: 10.1111/jdv.12715
An infectious form of an eczematoid dermatitis. St. Louis Courier of Med. 1902;27:401414.
.4Infectious eczematoid dermatitis. J Am Med Assoc. 1920;75:976-979.
.Autosensitization dermatitis: report of five cases and protocol of an experiment. Arch Derm Syphilol. 1949;59:68-77. doi: 10.1001/archderm.1949.01520260072010
, , .Autosensitization in infectious eczematoid dermatitis. AMA Arch Derm Syphilol. 1950;62:703-704. doi: 10.1001/archderm.1950.01530180092021
, .1. Storan ER, McEvoy MT, Wetter DA, et al. Experience with the dermatology inpatient hospital service for adults: Mayo Clinic, 2000–2010. J Eur Acad Dermatol Venereol. 2013;27:1360-1365. doi: 10.1111/jdv.12010
2. Yamany T, Schwartz RA. Infectious eczematoid dermatitis: a comprehensive review. J Eur Acad Dermatol Venereol. 2015;29:203-208. doi: 10.1111/jdv.12715
An infectious form of an eczematoid dermatitis. St. Louis Courier of Med. 1902;27:401414.
.4Infectious eczematoid dermatitis. J Am Med Assoc. 1920;75:976-979.
.Autosensitization dermatitis: report of five cases and protocol of an experiment. Arch Derm Syphilol. 1949;59:68-77. doi: 10.1001/archderm.1949.01520260072010
, , .Autosensitization in infectious eczematoid dermatitis. AMA Arch Derm Syphilol. 1950;62:703-704. doi: 10.1001/archderm.1950.01530180092021
, .27-year-old woman • postpartum seizures • PTSD • history of depression • Dx?
THE CASE
A 27-year-old woman presented to the family medicine clinic to establish care for a recent onset of seizures, for which she had previously been admitted, 4 months after delivering her first child. Her pregnancy was complicated by type 1 diabetes and poor glycemic control. Labor was induced at 37 weeks; however, vaginal delivery was impeded by arrest of dilation. An emergency cesarean section was performed under general anesthesia, resulting in a healthy newborn male.
Six weeks after giving birth, the patient was started on sertraline 50 mg/d for postpartum depression. Her history was significant for depression 8 years prior that was controlled with psychotherapy, and treated prior to coming to our clinic. She had not experienced any depressive symptoms during pregnancy.
Three months postpartum, she was hospitalized for recurrent syncopal episodes. They lasted about 2 minutes, with prodromal generalized weakness followed by loss of consciousness. There was no post-event confusion, tongue-biting, or incontinence. Physical exam, electroencephalogram (EEG), echocardiogram, and magnetic resonance imaging of the head and neck demonstrated no acute findings.
These episodes escalated in frequency weeks after they began, involving as many as 40 daily attacks, some of which lasted up to 45 minutes. During these events, the patient was nonresponsive but reported reliving the delivery of her child. Upon initial consultation with Neurology, no cause was found, and she was advised to wear a helmet, stop driving, and refrain from carrying her son. No antiepileptic medications were initiated because there were no EEG findings that supported seizure, and her mood had not improved, despite an increase in sertraline dosage, a switch to citalopram, and the addition of bupropion. She described anxiety, nightmares, and intrusive thoughts during psychotherapy sessions. Her psychiatrist gave her an additional diagnosis of posttraumatic stress disorder (PTSD) secondary to her delivery. The family medicine clinic assisted the patient and her family throughout her care by functioning as a home base for her.
Eight months following initial symptoms, repeat evaluation with a video-EEG revealed no evidence of EEG changes during seizure-like activity.
THE DIAGNOSIS
The patient was given a diagnosis of
DISCUSSION
With a prevalence of 5% to 10% and 20% to 40% in outpatient and inpatient epilepsy clinics respectively, PNES events have become of increasing interest to physicians.2 There are few cases of PNES in women during pregnancy reported in the literature.3,4 This is the first case report of PNES with postpartum onset.
Continue to: Epilepsy vs psychogenic nonepileptic seizures
Epilepsy vs psychogenic nonepileptic seizures
PNES episodes appear similar to epileptic seizures, but without a definitive neurobiologic source.2,3 However, recent literature suggests the root cause may be found in abnormalities in neurologic networks, such as dysfunction of frontal and parietal lobe connectivity and increased communication from emotional centers of the brain.2,5 There are no typical pathognomonic symptoms of PNES, leading to diagnostic difficulty.2 A definitive diagnosis may be made when a patient experiences seizures without EEG abnormalities.2 Further diagnostic brain imaging is unnecessary.
Trauma may be the underlying cause
A predominance of PNES in both women and young adults, with no definitive associated factors, has been reported in the literature.2 Studies suggest childhood sexual abuse, physical abuse, traumatic brain injury, and health-related trauma, such as distressing medical experiences and surgeries, may be risk factors, while depression, misdiagnosis, and mistreatment can heighten seizure activity.2,3
Treatment requires a multidisciplinary team
Effective management of PNES requires collaboration between the primary care physician, neurologist, psychiatrist, and psychotherapist, with an emphasis on evaluation and control of the underlying trigger(s).3 Randomized controlled trials have demonstrated the efficacy of cognitive behavioral therapy (CBT), supportive care, and patient education in reducing seizure frequency at the 6-month follow-up.3,6 Additional studies have reported the best prognostic factor in PNES management is patient employment of an internal locus of control—the patient’s belief that they control life events.7,8 Case series suggest electroconvulsive therapy (ECT) is an effective alternative mood stabilization and seizure reduction therapy when tolerated.9
Our patient tried several combinations of treatment to manage PNES and comorbid psychiatric conditions, including CBT, antidepressants, and anxiolytics. After about 5 treatment failures, she pursued ECT for treatment-resistant depression and PNES frequency reduction but failed to tolerate therapy. Currently, her PNES has been reduced to 1 to 2 weekly episodes with a 200 mg/d dose of lamotrigine as a mood stabilizer combined with CBT.
THE TAKEAWAY
Providers should investigate a patient’s history and psychologic disposition when the patient presents with seizure-like behavior without a neurobiologic source or with a negative video-EEG study. A history of depression, traumatic experience, PTSD, or other psychosocial triggers must be noted early to prevent a delay in treatment when PNES is part of the differential. Due to a delayed diagnosis of PNES in our patient, she went without full treatment for almost 12 months and experienced worsening episodes. The primary care physician plays an integral role in early identification and intervention through anticipatory guidance, initial work-up, and support for patients with suspected PNES (TABLE).
CORRESPONDENCE
Karim Hanna, MD, 13330 USF Laurel Drive, Tampa, FL; [email protected]
1. LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. Epilepsia. 2013;54:2005-2018. doi: 10.1111/epi.12356
2. Asadi-Pooya AA, Sperling MR. Epidemiology of psychogenic nonepileptic seizures. Epilepsy Behav. 2015;46:60-65. doi: 10.1016/j.yebeh.2015.03.015
3. Devireddy VK, Sharma A. A case of psychogenic non-epileptic seizures, unresponsive type, in pregnancy. Prim Care Companion CNS Disord. 2014;16:PCC.13l01574. doi: 10.4088/PCC.13l01574
4. DeToledo JC, Lowe MR, Puig A. Nonepileptic seizures in pregnancy. Neurology. 2000;55:120-121. doi: 10.1212/wnl.55.1.120
5. Ding J-R, An D, Liao W, et al. Altered functional and structural connectivity networks in psychogenic non-epileptic seizures. PLoS One. 2013;8:e63850. doi: 10.1371/journal.pone.0063850
6. Goldstein LH, Chalder T, Chigwedere C, et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: a pilot RCT. Neurology. 2010;74:1986-1994. doi: 0.1212/WNL.0b013e3181e39658
7. McLaughlin DP, Pachana NA, McFarland K. The impact of depression, seizure variables and locus of control on health related quality of life in a community dwelling sample of older adults. Seizure. 2010;19:232-236. doi: 10.1016/j.seizure.2010.02.008
8. Duncan R, Anderson J, Cullen B, et al. Predictors of 6-month and 3-year outcomes after psychological intervention for psychogenic non epileptic seizures. Seizure. 2016;36:22-26. doi: 10.1016/j.seizure.2015.12.016
9. Blumer D, Rice S, Adamolekun B. Electroconvulsive treatment for nonepileptic seizure disorders. Epilepsy Behav. 2009;15:382-387. doi: 10.1016/j.yebeh.2009.05.004
THE CASE
A 27-year-old woman presented to the family medicine clinic to establish care for a recent onset of seizures, for which she had previously been admitted, 4 months after delivering her first child. Her pregnancy was complicated by type 1 diabetes and poor glycemic control. Labor was induced at 37 weeks; however, vaginal delivery was impeded by arrest of dilation. An emergency cesarean section was performed under general anesthesia, resulting in a healthy newborn male.
Six weeks after giving birth, the patient was started on sertraline 50 mg/d for postpartum depression. Her history was significant for depression 8 years prior that was controlled with psychotherapy, and treated prior to coming to our clinic. She had not experienced any depressive symptoms during pregnancy.
Three months postpartum, she was hospitalized for recurrent syncopal episodes. They lasted about 2 minutes, with prodromal generalized weakness followed by loss of consciousness. There was no post-event confusion, tongue-biting, or incontinence. Physical exam, electroencephalogram (EEG), echocardiogram, and magnetic resonance imaging of the head and neck demonstrated no acute findings.
These episodes escalated in frequency weeks after they began, involving as many as 40 daily attacks, some of which lasted up to 45 minutes. During these events, the patient was nonresponsive but reported reliving the delivery of her child. Upon initial consultation with Neurology, no cause was found, and she was advised to wear a helmet, stop driving, and refrain from carrying her son. No antiepileptic medications were initiated because there were no EEG findings that supported seizure, and her mood had not improved, despite an increase in sertraline dosage, a switch to citalopram, and the addition of bupropion. She described anxiety, nightmares, and intrusive thoughts during psychotherapy sessions. Her psychiatrist gave her an additional diagnosis of posttraumatic stress disorder (PTSD) secondary to her delivery. The family medicine clinic assisted the patient and her family throughout her care by functioning as a home base for her.
Eight months following initial symptoms, repeat evaluation with a video-EEG revealed no evidence of EEG changes during seizure-like activity.
THE DIAGNOSIS
The patient was given a diagnosis of
DISCUSSION
With a prevalence of 5% to 10% and 20% to 40% in outpatient and inpatient epilepsy clinics respectively, PNES events have become of increasing interest to physicians.2 There are few cases of PNES in women during pregnancy reported in the literature.3,4 This is the first case report of PNES with postpartum onset.
Continue to: Epilepsy vs psychogenic nonepileptic seizures
Epilepsy vs psychogenic nonepileptic seizures
PNES episodes appear similar to epileptic seizures, but without a definitive neurobiologic source.2,3 However, recent literature suggests the root cause may be found in abnormalities in neurologic networks, such as dysfunction of frontal and parietal lobe connectivity and increased communication from emotional centers of the brain.2,5 There are no typical pathognomonic symptoms of PNES, leading to diagnostic difficulty.2 A definitive diagnosis may be made when a patient experiences seizures without EEG abnormalities.2 Further diagnostic brain imaging is unnecessary.
Trauma may be the underlying cause
A predominance of PNES in both women and young adults, with no definitive associated factors, has been reported in the literature.2 Studies suggest childhood sexual abuse, physical abuse, traumatic brain injury, and health-related trauma, such as distressing medical experiences and surgeries, may be risk factors, while depression, misdiagnosis, and mistreatment can heighten seizure activity.2,3
Treatment requires a multidisciplinary team
Effective management of PNES requires collaboration between the primary care physician, neurologist, psychiatrist, and psychotherapist, with an emphasis on evaluation and control of the underlying trigger(s).3 Randomized controlled trials have demonstrated the efficacy of cognitive behavioral therapy (CBT), supportive care, and patient education in reducing seizure frequency at the 6-month follow-up.3,6 Additional studies have reported the best prognostic factor in PNES management is patient employment of an internal locus of control—the patient’s belief that they control life events.7,8 Case series suggest electroconvulsive therapy (ECT) is an effective alternative mood stabilization and seizure reduction therapy when tolerated.9
Our patient tried several combinations of treatment to manage PNES and comorbid psychiatric conditions, including CBT, antidepressants, and anxiolytics. After about 5 treatment failures, she pursued ECT for treatment-resistant depression and PNES frequency reduction but failed to tolerate therapy. Currently, her PNES has been reduced to 1 to 2 weekly episodes with a 200 mg/d dose of lamotrigine as a mood stabilizer combined with CBT.
THE TAKEAWAY
Providers should investigate a patient’s history and psychologic disposition when the patient presents with seizure-like behavior without a neurobiologic source or with a negative video-EEG study. A history of depression, traumatic experience, PTSD, or other psychosocial triggers must be noted early to prevent a delay in treatment when PNES is part of the differential. Due to a delayed diagnosis of PNES in our patient, she went without full treatment for almost 12 months and experienced worsening episodes. The primary care physician plays an integral role in early identification and intervention through anticipatory guidance, initial work-up, and support for patients with suspected PNES (TABLE).
CORRESPONDENCE
Karim Hanna, MD, 13330 USF Laurel Drive, Tampa, FL; [email protected]
THE CASE
A 27-year-old woman presented to the family medicine clinic to establish care for a recent onset of seizures, for which she had previously been admitted, 4 months after delivering her first child. Her pregnancy was complicated by type 1 diabetes and poor glycemic control. Labor was induced at 37 weeks; however, vaginal delivery was impeded by arrest of dilation. An emergency cesarean section was performed under general anesthesia, resulting in a healthy newborn male.
Six weeks after giving birth, the patient was started on sertraline 50 mg/d for postpartum depression. Her history was significant for depression 8 years prior that was controlled with psychotherapy, and treated prior to coming to our clinic. She had not experienced any depressive symptoms during pregnancy.
Three months postpartum, she was hospitalized for recurrent syncopal episodes. They lasted about 2 minutes, with prodromal generalized weakness followed by loss of consciousness. There was no post-event confusion, tongue-biting, or incontinence. Physical exam, electroencephalogram (EEG), echocardiogram, and magnetic resonance imaging of the head and neck demonstrated no acute findings.
These episodes escalated in frequency weeks after they began, involving as many as 40 daily attacks, some of which lasted up to 45 minutes. During these events, the patient was nonresponsive but reported reliving the delivery of her child. Upon initial consultation with Neurology, no cause was found, and she was advised to wear a helmet, stop driving, and refrain from carrying her son. No antiepileptic medications were initiated because there were no EEG findings that supported seizure, and her mood had not improved, despite an increase in sertraline dosage, a switch to citalopram, and the addition of bupropion. She described anxiety, nightmares, and intrusive thoughts during psychotherapy sessions. Her psychiatrist gave her an additional diagnosis of posttraumatic stress disorder (PTSD) secondary to her delivery. The family medicine clinic assisted the patient and her family throughout her care by functioning as a home base for her.
Eight months following initial symptoms, repeat evaluation with a video-EEG revealed no evidence of EEG changes during seizure-like activity.
THE DIAGNOSIS
The patient was given a diagnosis of
DISCUSSION
With a prevalence of 5% to 10% and 20% to 40% in outpatient and inpatient epilepsy clinics respectively, PNES events have become of increasing interest to physicians.2 There are few cases of PNES in women during pregnancy reported in the literature.3,4 This is the first case report of PNES with postpartum onset.
Continue to: Epilepsy vs psychogenic nonepileptic seizures
Epilepsy vs psychogenic nonepileptic seizures
PNES episodes appear similar to epileptic seizures, but without a definitive neurobiologic source.2,3 However, recent literature suggests the root cause may be found in abnormalities in neurologic networks, such as dysfunction of frontal and parietal lobe connectivity and increased communication from emotional centers of the brain.2,5 There are no typical pathognomonic symptoms of PNES, leading to diagnostic difficulty.2 A definitive diagnosis may be made when a patient experiences seizures without EEG abnormalities.2 Further diagnostic brain imaging is unnecessary.
Trauma may be the underlying cause
A predominance of PNES in both women and young adults, with no definitive associated factors, has been reported in the literature.2 Studies suggest childhood sexual abuse, physical abuse, traumatic brain injury, and health-related trauma, such as distressing medical experiences and surgeries, may be risk factors, while depression, misdiagnosis, and mistreatment can heighten seizure activity.2,3
Treatment requires a multidisciplinary team
Effective management of PNES requires collaboration between the primary care physician, neurologist, psychiatrist, and psychotherapist, with an emphasis on evaluation and control of the underlying trigger(s).3 Randomized controlled trials have demonstrated the efficacy of cognitive behavioral therapy (CBT), supportive care, and patient education in reducing seizure frequency at the 6-month follow-up.3,6 Additional studies have reported the best prognostic factor in PNES management is patient employment of an internal locus of control—the patient’s belief that they control life events.7,8 Case series suggest electroconvulsive therapy (ECT) is an effective alternative mood stabilization and seizure reduction therapy when tolerated.9
Our patient tried several combinations of treatment to manage PNES and comorbid psychiatric conditions, including CBT, antidepressants, and anxiolytics. After about 5 treatment failures, she pursued ECT for treatment-resistant depression and PNES frequency reduction but failed to tolerate therapy. Currently, her PNES has been reduced to 1 to 2 weekly episodes with a 200 mg/d dose of lamotrigine as a mood stabilizer combined with CBT.
THE TAKEAWAY
Providers should investigate a patient’s history and psychologic disposition when the patient presents with seizure-like behavior without a neurobiologic source or with a negative video-EEG study. A history of depression, traumatic experience, PTSD, or other psychosocial triggers must be noted early to prevent a delay in treatment when PNES is part of the differential. Due to a delayed diagnosis of PNES in our patient, she went without full treatment for almost 12 months and experienced worsening episodes. The primary care physician plays an integral role in early identification and intervention through anticipatory guidance, initial work-up, and support for patients with suspected PNES (TABLE).
CORRESPONDENCE
Karim Hanna, MD, 13330 USF Laurel Drive, Tampa, FL; [email protected]
1. LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. Epilepsia. 2013;54:2005-2018. doi: 10.1111/epi.12356
2. Asadi-Pooya AA, Sperling MR. Epidemiology of psychogenic nonepileptic seizures. Epilepsy Behav. 2015;46:60-65. doi: 10.1016/j.yebeh.2015.03.015
3. Devireddy VK, Sharma A. A case of psychogenic non-epileptic seizures, unresponsive type, in pregnancy. Prim Care Companion CNS Disord. 2014;16:PCC.13l01574. doi: 10.4088/PCC.13l01574
4. DeToledo JC, Lowe MR, Puig A. Nonepileptic seizures in pregnancy. Neurology. 2000;55:120-121. doi: 10.1212/wnl.55.1.120
5. Ding J-R, An D, Liao W, et al. Altered functional and structural connectivity networks in psychogenic non-epileptic seizures. PLoS One. 2013;8:e63850. doi: 10.1371/journal.pone.0063850
6. Goldstein LH, Chalder T, Chigwedere C, et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: a pilot RCT. Neurology. 2010;74:1986-1994. doi: 0.1212/WNL.0b013e3181e39658
7. McLaughlin DP, Pachana NA, McFarland K. The impact of depression, seizure variables and locus of control on health related quality of life in a community dwelling sample of older adults. Seizure. 2010;19:232-236. doi: 10.1016/j.seizure.2010.02.008
8. Duncan R, Anderson J, Cullen B, et al. Predictors of 6-month and 3-year outcomes after psychological intervention for psychogenic non epileptic seizures. Seizure. 2016;36:22-26. doi: 10.1016/j.seizure.2015.12.016
9. Blumer D, Rice S, Adamolekun B. Electroconvulsive treatment for nonepileptic seizure disorders. Epilepsy Behav. 2009;15:382-387. doi: 10.1016/j.yebeh.2009.05.004
1. LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. Epilepsia. 2013;54:2005-2018. doi: 10.1111/epi.12356
2. Asadi-Pooya AA, Sperling MR. Epidemiology of psychogenic nonepileptic seizures. Epilepsy Behav. 2015;46:60-65. doi: 10.1016/j.yebeh.2015.03.015
3. Devireddy VK, Sharma A. A case of psychogenic non-epileptic seizures, unresponsive type, in pregnancy. Prim Care Companion CNS Disord. 2014;16:PCC.13l01574. doi: 10.4088/PCC.13l01574
4. DeToledo JC, Lowe MR, Puig A. Nonepileptic seizures in pregnancy. Neurology. 2000;55:120-121. doi: 10.1212/wnl.55.1.120
5. Ding J-R, An D, Liao W, et al. Altered functional and structural connectivity networks in psychogenic non-epileptic seizures. PLoS One. 2013;8:e63850. doi: 10.1371/journal.pone.0063850
6. Goldstein LH, Chalder T, Chigwedere C, et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: a pilot RCT. Neurology. 2010;74:1986-1994. doi: 0.1212/WNL.0b013e3181e39658
7. McLaughlin DP, Pachana NA, McFarland K. The impact of depression, seizure variables and locus of control on health related quality of life in a community dwelling sample of older adults. Seizure. 2010;19:232-236. doi: 10.1016/j.seizure.2010.02.008
8. Duncan R, Anderson J, Cullen B, et al. Predictors of 6-month and 3-year outcomes after psychological intervention for psychogenic non epileptic seizures. Seizure. 2016;36:22-26. doi: 10.1016/j.seizure.2015.12.016
9. Blumer D, Rice S, Adamolekun B. Electroconvulsive treatment for nonepileptic seizure disorders. Epilepsy Behav. 2009;15:382-387. doi: 10.1016/j.yebeh.2009.05.004
How to proceed when it comes to vitamin D
In April 2021, the US Preventive Services Task Force (USPSTF) published an updated recommendation on screening for vitamin D deficiency in adults. It reaffirmed an “I” statement first made in 2014: evidence is insufficient to balance the benefits and harms of screening.1 This recommendation applies to asymptomatic, community-dwelling, nonpregnant adults without conditions treatable with vitamin D. It’s important to remember that screening refers to testing asymptomatic individuals to detect a condition early before it causes illness. Testing performed to determine whether symptoms are evidence of an underlying condition is not screening but diagnostic testing.
The Task Force statement explains the problems they found with the current level of knowledge about screening for vitamin D deficiency. First, while 25-hydroxyvitamin D [25(OH)D] is considered the best test for vitamin D levels, it is hard to measure accurately and test results vary by the method used and laboratories doing the testing. There also is uncertainty about how best to measure vitamin D status in different racial and ethnic groups, especially those with dark skin pigmentation. In addition, 25(OH)D in the blood is predominantly the bound form, with only 10% to 15% being unbound and bioavailable. Current tests do not determine the amount of bound vs unbound 25(OH)D.1-3
There is no consensus about the optimal blood level of vitamin D or the level that defines deficiency. The Institute of Medicine (now the National Academy of Medicine—NAM) stated that serum 25(OH)D levels ≥ 20 ng/mL are adequate to meet the metabolic needs of 97.5% of people, and that levels of 12 to 20 ng/mL pose a risk of deficiency, with levels < 12 considered to be very low.4 The Endocrine Society defines deficiency as < 20 ng/mL and insufficiency as 21 to 29 ng/mL.5
The rate of testing for vitamin D deficiency in primary care in unknown, but there is evidence that since 2000, it has increased 80 fold at least among those with Medicare.6 Data from the 2011-2014 National Health and Nutrition Examination Survey showed that 5% of the population had 25(OH)D levels < 12 ng/mL and 18% had levels between 12 and 19 ng/mL.7 Some have estimated that as many as half of all adults would be considered vitamin D deficient or insufficient using current less conservative definitions, with higher rates in racial/ethnic minorities.2,8
There are no firm data on the frequency, or benefits, of screening for vitamin D levels in asymptomatic adults (and treating those found to have vitamin D deficiency). The Task Force looked for indirect evidence by examining the effect of treating vitamin D deficiency in a number of conditions and found that for some, there was adequate evidence of no benefit and for others there was inadequate evidence for possible benefits.9 No benefit was found for incidence of fractures, type 2 diabetes, and overall mortality.9 Inadequate evidence was found for incidence of cancer, cardiovascular disease, scores on measures of depression and physical functioning, and urinary tract infections in those with impaired fasting glucose.9
Known risk factors for low vitamin D levels include low vitamin D intake, older age, obesity, low UVB exposure or absorption due to long winter seasons in northern latitudes, sun avoidance, and dark skin pigmentation.1 In addition, certain medical conditions contribute to, or are caused by, low vitamin D levels—eg, osteoporosis, chronic kidney disease, malabsorption syndromes, and medication use (ie, glucocorticoids).1-3
The Task Force recommendation on screening for vitamin D deficiency differs from those of some other organizations. However, none recommend universal population-based screening. The Endocrine Society and the American Association of Clinical Endocrinologists recommend screening but only in those at risk for vitamin D deficiency.5,10 The American Academy of Family Physicians endorses the USPSTF recommendation.11
Continue to: Specific USPSTF topics related to vitamin D
Specific USPSTF topics related to vitamin D
The Task Force has specifically addressed 3 topics pertaining to vitamin D.
Prevention of falls in the elderly. In 2018 the Task Force recommended against the use of vitamin D to prevent falls in community-dwelling adults ≥ 65 years.12 This reversed its 2012 recommendation advising vitamin D supplementation to prevent falls. The Task Force re-examined the old evidence and looked at newer studies and concluded that their previous conclusion was wrong and that the evidence showed no benefit from vitamin D in preventing falls in the elderly. The reversal of a prior recommendation is rare for the USPSTF because of the rigor of its evidence reviews and its policy of not making a recommendation unless solid evidence for or against exists.
Prevention of cardiovascular disease and cancer. The Task Force concludes that current evidence is insufficient to assess the balance of benefits and harms in the use of single- or paired-nutrient supplements to prevent cardiovascular disease or cancer.13 (The exceptions are beta-carotene and vitamin E, which the Task Force recommends against.) This statement is consistent with the lack of evidence the Task Force found regarding prevention of these conditions by vitamin D supplementation in those who are vitamin D deficient.
Prevention of fractures in men and in premenopausal and postmenopausal women. For men and premenopausal women, the Task Force concludes that evidence is insufficient to assess the benefits and harms of vitamin D and calcium supplementation, alone or in combination, to prevent fractures.14 For prevention of fractures in postmenopausal women, there are 2 recommendations. The first one advises against the use of ≤ 400 IU of vitamin D and ≤ 1000 mg of calcium because the evidence indicates ineffectiveness. The second one is another “I” statement for the use of doses > 400 IU of vitamin D and > 1000 mg of calcium. These 3 recommendations apply to adults who live in the community and not in nursing homes or other institutional care facilities; they do not apply to those who have osteoporosis.
What should the family physician do?
Encourage all patients to take the recommended dietary allowances (RDA) of vitamin D. The RDA is the average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%-98%) healthy individuals. Most professional organizations recommend that adults ≥ 50 years consume 800 to 1000 IU of vitamin D daily. TABLE 2 lists the RDA for vitamin D by age and sex.15 The amount of vitamin D in selected food products is listed in TABLE 3.15 Some increase in levels of vitamin D can occur as a result of sun exposure, but current practices of sun avoidance make it difficult to achieve a significant contribution to vitamin D requirements.15
Continue to: Alternatives to universal screening
Alternatives to universal screening. Screening for vitamin D deficiency might benefit some patients, although there is no evidence to support it. Universal screening will likely lead to overdiagnosis and overtreatment based on what is essentially a poorly understood blood test. This was the concern expressed by the NAM.4,16 An editorial accompanying publication of the recent USPSTF recommendation suggested not measuring vitamin D levels but instead advising patients to consume the age-based RDA of vitamin D.3 For those at increased risk for vitamin D deficiency, advise a higher dose of vitamin D (eg, 2000 IU/d, which is still lower than the upper daily limit).3
Other options are to screen for vitamin D deficiency only in those at high risk for low vitamin D levels, and to test for vitamin D deficiency in those with symptoms associated with deficiency such as bone pain and muscle weakness. These options would be consistent with recommendations from the Endocrine Society.5 Some have recommended that if testing is ordered, it should be performed by a laboratory that uses liquid chromatography-mass spectrometry because it is the criterion standard.2
Treatment options. Vitamin D deficiency can be treated with either ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). These treatments can also be recommended for those whose diets may not provide the RDA for vitamin D. Both are readily available over the counter and by prescription. The Task Force found that the harms of treating vitamin D deficiency with vitamin D at recommended doses are small to none.1 There is possibly a small increase in kidney stones with the combined use of 1000 mg/d calcium and 10 mcg (400 IU)/d vitamin D.17 Large doses of vitamin D can cause toxicity including marked hypercalcemia, nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.15A cautious evidence-based approach would be to selectively screen for vitamin D deficiency, conduct diagnostic testing when indicated, and advise vitamin D supplementation as needed.
1. USPSTF. Screening for vitamin D deficiency in adults: US Preventive Services Task Force recommendation statement. JAMA. 2021;325:1436-1442.
2. Michos ED, Kalyani RR, Segal JB. Why USPSTF still finds insufficient evidence to support screening for vitamin D deficiency. JAMA Netw Open. 2021;4:e213627.
3. Burnett-Bowie AAM, Cappola AR. The USPSTF 2021 recommendations on screening for asymptomatic vitamin D deficiency in adults: the challenge for clinicians continues. JAMA. 2021;325:1401-1402.
4. Institute of Medicine. Dietary reference intakes for calcium and vitamin D. National Academies Press; 2011. Accessed May 22, 2021. https://pubmed.ncbi.nlm.nih.gov/21796828/
5. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinolgy Metab. 2011;96:1911-1930.
6. Shahangian S, Alspach TD, Astles JR, et al. Trends in laboratory test volumes for Medicare part B reimbursements, 2000-2010. Arch Pathol Lab Med. 2014;138:189-203.
7. Herrick KA, Storandt RJ, Afful J, et al. Vitamin D status in the United States, 2011-2014. Am J Clin Nutr. 2019;110:150-157.
8. Forrest KYZ, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31:48-54.
9. Kahwati LC, LeBlanc E, Weber RP, et al. Screening for vitamin D deficiency in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2021;325:1443-1463.
10. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis-2016. Endocr Pract. 2016;22(supp 4):1-42.
11. AAFP. Clinical preventive services. Accessed May 22, 2021. www.aafp.org/family-physician/patient-care/clinical-recommendations/aafp-cps.html
12. USPSTF. Falls prevention in community-dwelling older adults: interventions. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/falls-prevention-in-older-adults-interventions
13. USPSTF. Vitamin supplementation to prevent cancer and CVD: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-supplementation-to-prevent-cancer-and-cvd-counseling
14. USPSTF. Vitamin D, calcium, or combined supplementation for the primary prevention of fractures in community-dwelling adults: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-d-calcium-or-combined-supplementation-for-the-primary-prevention-of-fractures-in-adults-preventive-medication
15. NIH. Vitamin D. Accessed May 22, 2021. https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
16. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96:53-58.
17. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354:669-683.
In April 2021, the US Preventive Services Task Force (USPSTF) published an updated recommendation on screening for vitamin D deficiency in adults. It reaffirmed an “I” statement first made in 2014: evidence is insufficient to balance the benefits and harms of screening.1 This recommendation applies to asymptomatic, community-dwelling, nonpregnant adults without conditions treatable with vitamin D. It’s important to remember that screening refers to testing asymptomatic individuals to detect a condition early before it causes illness. Testing performed to determine whether symptoms are evidence of an underlying condition is not screening but diagnostic testing.
The Task Force statement explains the problems they found with the current level of knowledge about screening for vitamin D deficiency. First, while 25-hydroxyvitamin D [25(OH)D] is considered the best test for vitamin D levels, it is hard to measure accurately and test results vary by the method used and laboratories doing the testing. There also is uncertainty about how best to measure vitamin D status in different racial and ethnic groups, especially those with dark skin pigmentation. In addition, 25(OH)D in the blood is predominantly the bound form, with only 10% to 15% being unbound and bioavailable. Current tests do not determine the amount of bound vs unbound 25(OH)D.1-3
There is no consensus about the optimal blood level of vitamin D or the level that defines deficiency. The Institute of Medicine (now the National Academy of Medicine—NAM) stated that serum 25(OH)D levels ≥ 20 ng/mL are adequate to meet the metabolic needs of 97.5% of people, and that levels of 12 to 20 ng/mL pose a risk of deficiency, with levels < 12 considered to be very low.4 The Endocrine Society defines deficiency as < 20 ng/mL and insufficiency as 21 to 29 ng/mL.5
The rate of testing for vitamin D deficiency in primary care in unknown, but there is evidence that since 2000, it has increased 80 fold at least among those with Medicare.6 Data from the 2011-2014 National Health and Nutrition Examination Survey showed that 5% of the population had 25(OH)D levels < 12 ng/mL and 18% had levels between 12 and 19 ng/mL.7 Some have estimated that as many as half of all adults would be considered vitamin D deficient or insufficient using current less conservative definitions, with higher rates in racial/ethnic minorities.2,8
There are no firm data on the frequency, or benefits, of screening for vitamin D levels in asymptomatic adults (and treating those found to have vitamin D deficiency). The Task Force looked for indirect evidence by examining the effect of treating vitamin D deficiency in a number of conditions and found that for some, there was adequate evidence of no benefit and for others there was inadequate evidence for possible benefits.9 No benefit was found for incidence of fractures, type 2 diabetes, and overall mortality.9 Inadequate evidence was found for incidence of cancer, cardiovascular disease, scores on measures of depression and physical functioning, and urinary tract infections in those with impaired fasting glucose.9
Known risk factors for low vitamin D levels include low vitamin D intake, older age, obesity, low UVB exposure or absorption due to long winter seasons in northern latitudes, sun avoidance, and dark skin pigmentation.1 In addition, certain medical conditions contribute to, or are caused by, low vitamin D levels—eg, osteoporosis, chronic kidney disease, malabsorption syndromes, and medication use (ie, glucocorticoids).1-3
The Task Force recommendation on screening for vitamin D deficiency differs from those of some other organizations. However, none recommend universal population-based screening. The Endocrine Society and the American Association of Clinical Endocrinologists recommend screening but only in those at risk for vitamin D deficiency.5,10 The American Academy of Family Physicians endorses the USPSTF recommendation.11
Continue to: Specific USPSTF topics related to vitamin D
Specific USPSTF topics related to vitamin D
The Task Force has specifically addressed 3 topics pertaining to vitamin D.
Prevention of falls in the elderly. In 2018 the Task Force recommended against the use of vitamin D to prevent falls in community-dwelling adults ≥ 65 years.12 This reversed its 2012 recommendation advising vitamin D supplementation to prevent falls. The Task Force re-examined the old evidence and looked at newer studies and concluded that their previous conclusion was wrong and that the evidence showed no benefit from vitamin D in preventing falls in the elderly. The reversal of a prior recommendation is rare for the USPSTF because of the rigor of its evidence reviews and its policy of not making a recommendation unless solid evidence for or against exists.
Prevention of cardiovascular disease and cancer. The Task Force concludes that current evidence is insufficient to assess the balance of benefits and harms in the use of single- or paired-nutrient supplements to prevent cardiovascular disease or cancer.13 (The exceptions are beta-carotene and vitamin E, which the Task Force recommends against.) This statement is consistent with the lack of evidence the Task Force found regarding prevention of these conditions by vitamin D supplementation in those who are vitamin D deficient.
Prevention of fractures in men and in premenopausal and postmenopausal women. For men and premenopausal women, the Task Force concludes that evidence is insufficient to assess the benefits and harms of vitamin D and calcium supplementation, alone or in combination, to prevent fractures.14 For prevention of fractures in postmenopausal women, there are 2 recommendations. The first one advises against the use of ≤ 400 IU of vitamin D and ≤ 1000 mg of calcium because the evidence indicates ineffectiveness. The second one is another “I” statement for the use of doses > 400 IU of vitamin D and > 1000 mg of calcium. These 3 recommendations apply to adults who live in the community and not in nursing homes or other institutional care facilities; they do not apply to those who have osteoporosis.
What should the family physician do?
Encourage all patients to take the recommended dietary allowances (RDA) of vitamin D. The RDA is the average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%-98%) healthy individuals. Most professional organizations recommend that adults ≥ 50 years consume 800 to 1000 IU of vitamin D daily. TABLE 2 lists the RDA for vitamin D by age and sex.15 The amount of vitamin D in selected food products is listed in TABLE 3.15 Some increase in levels of vitamin D can occur as a result of sun exposure, but current practices of sun avoidance make it difficult to achieve a significant contribution to vitamin D requirements.15
Continue to: Alternatives to universal screening
Alternatives to universal screening. Screening for vitamin D deficiency might benefit some patients, although there is no evidence to support it. Universal screening will likely lead to overdiagnosis and overtreatment based on what is essentially a poorly understood blood test. This was the concern expressed by the NAM.4,16 An editorial accompanying publication of the recent USPSTF recommendation suggested not measuring vitamin D levels but instead advising patients to consume the age-based RDA of vitamin D.3 For those at increased risk for vitamin D deficiency, advise a higher dose of vitamin D (eg, 2000 IU/d, which is still lower than the upper daily limit).3
Other options are to screen for vitamin D deficiency only in those at high risk for low vitamin D levels, and to test for vitamin D deficiency in those with symptoms associated with deficiency such as bone pain and muscle weakness. These options would be consistent with recommendations from the Endocrine Society.5 Some have recommended that if testing is ordered, it should be performed by a laboratory that uses liquid chromatography-mass spectrometry because it is the criterion standard.2
Treatment options. Vitamin D deficiency can be treated with either ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). These treatments can also be recommended for those whose diets may not provide the RDA for vitamin D. Both are readily available over the counter and by prescription. The Task Force found that the harms of treating vitamin D deficiency with vitamin D at recommended doses are small to none.1 There is possibly a small increase in kidney stones with the combined use of 1000 mg/d calcium and 10 mcg (400 IU)/d vitamin D.17 Large doses of vitamin D can cause toxicity including marked hypercalcemia, nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.15A cautious evidence-based approach would be to selectively screen for vitamin D deficiency, conduct diagnostic testing when indicated, and advise vitamin D supplementation as needed.
In April 2021, the US Preventive Services Task Force (USPSTF) published an updated recommendation on screening for vitamin D deficiency in adults. It reaffirmed an “I” statement first made in 2014: evidence is insufficient to balance the benefits and harms of screening.1 This recommendation applies to asymptomatic, community-dwelling, nonpregnant adults without conditions treatable with vitamin D. It’s important to remember that screening refers to testing asymptomatic individuals to detect a condition early before it causes illness. Testing performed to determine whether symptoms are evidence of an underlying condition is not screening but diagnostic testing.
The Task Force statement explains the problems they found with the current level of knowledge about screening for vitamin D deficiency. First, while 25-hydroxyvitamin D [25(OH)D] is considered the best test for vitamin D levels, it is hard to measure accurately and test results vary by the method used and laboratories doing the testing. There also is uncertainty about how best to measure vitamin D status in different racial and ethnic groups, especially those with dark skin pigmentation. In addition, 25(OH)D in the blood is predominantly the bound form, with only 10% to 15% being unbound and bioavailable. Current tests do not determine the amount of bound vs unbound 25(OH)D.1-3
There is no consensus about the optimal blood level of vitamin D or the level that defines deficiency. The Institute of Medicine (now the National Academy of Medicine—NAM) stated that serum 25(OH)D levels ≥ 20 ng/mL are adequate to meet the metabolic needs of 97.5% of people, and that levels of 12 to 20 ng/mL pose a risk of deficiency, with levels < 12 considered to be very low.4 The Endocrine Society defines deficiency as < 20 ng/mL and insufficiency as 21 to 29 ng/mL.5
The rate of testing for vitamin D deficiency in primary care in unknown, but there is evidence that since 2000, it has increased 80 fold at least among those with Medicare.6 Data from the 2011-2014 National Health and Nutrition Examination Survey showed that 5% of the population had 25(OH)D levels < 12 ng/mL and 18% had levels between 12 and 19 ng/mL.7 Some have estimated that as many as half of all adults would be considered vitamin D deficient or insufficient using current less conservative definitions, with higher rates in racial/ethnic minorities.2,8
There are no firm data on the frequency, or benefits, of screening for vitamin D levels in asymptomatic adults (and treating those found to have vitamin D deficiency). The Task Force looked for indirect evidence by examining the effect of treating vitamin D deficiency in a number of conditions and found that for some, there was adequate evidence of no benefit and for others there was inadequate evidence for possible benefits.9 No benefit was found for incidence of fractures, type 2 diabetes, and overall mortality.9 Inadequate evidence was found for incidence of cancer, cardiovascular disease, scores on measures of depression and physical functioning, and urinary tract infections in those with impaired fasting glucose.9
Known risk factors for low vitamin D levels include low vitamin D intake, older age, obesity, low UVB exposure or absorption due to long winter seasons in northern latitudes, sun avoidance, and dark skin pigmentation.1 In addition, certain medical conditions contribute to, or are caused by, low vitamin D levels—eg, osteoporosis, chronic kidney disease, malabsorption syndromes, and medication use (ie, glucocorticoids).1-3
The Task Force recommendation on screening for vitamin D deficiency differs from those of some other organizations. However, none recommend universal population-based screening. The Endocrine Society and the American Association of Clinical Endocrinologists recommend screening but only in those at risk for vitamin D deficiency.5,10 The American Academy of Family Physicians endorses the USPSTF recommendation.11
Continue to: Specific USPSTF topics related to vitamin D
Specific USPSTF topics related to vitamin D
The Task Force has specifically addressed 3 topics pertaining to vitamin D.
Prevention of falls in the elderly. In 2018 the Task Force recommended against the use of vitamin D to prevent falls in community-dwelling adults ≥ 65 years.12 This reversed its 2012 recommendation advising vitamin D supplementation to prevent falls. The Task Force re-examined the old evidence and looked at newer studies and concluded that their previous conclusion was wrong and that the evidence showed no benefit from vitamin D in preventing falls in the elderly. The reversal of a prior recommendation is rare for the USPSTF because of the rigor of its evidence reviews and its policy of not making a recommendation unless solid evidence for or against exists.
Prevention of cardiovascular disease and cancer. The Task Force concludes that current evidence is insufficient to assess the balance of benefits and harms in the use of single- or paired-nutrient supplements to prevent cardiovascular disease or cancer.13 (The exceptions are beta-carotene and vitamin E, which the Task Force recommends against.) This statement is consistent with the lack of evidence the Task Force found regarding prevention of these conditions by vitamin D supplementation in those who are vitamin D deficient.
Prevention of fractures in men and in premenopausal and postmenopausal women. For men and premenopausal women, the Task Force concludes that evidence is insufficient to assess the benefits and harms of vitamin D and calcium supplementation, alone or in combination, to prevent fractures.14 For prevention of fractures in postmenopausal women, there are 2 recommendations. The first one advises against the use of ≤ 400 IU of vitamin D and ≤ 1000 mg of calcium because the evidence indicates ineffectiveness. The second one is another “I” statement for the use of doses > 400 IU of vitamin D and > 1000 mg of calcium. These 3 recommendations apply to adults who live in the community and not in nursing homes or other institutional care facilities; they do not apply to those who have osteoporosis.
What should the family physician do?
Encourage all patients to take the recommended dietary allowances (RDA) of vitamin D. The RDA is the average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%-98%) healthy individuals. Most professional organizations recommend that adults ≥ 50 years consume 800 to 1000 IU of vitamin D daily. TABLE 2 lists the RDA for vitamin D by age and sex.15 The amount of vitamin D in selected food products is listed in TABLE 3.15 Some increase in levels of vitamin D can occur as a result of sun exposure, but current practices of sun avoidance make it difficult to achieve a significant contribution to vitamin D requirements.15
Continue to: Alternatives to universal screening
Alternatives to universal screening. Screening for vitamin D deficiency might benefit some patients, although there is no evidence to support it. Universal screening will likely lead to overdiagnosis and overtreatment based on what is essentially a poorly understood blood test. This was the concern expressed by the NAM.4,16 An editorial accompanying publication of the recent USPSTF recommendation suggested not measuring vitamin D levels but instead advising patients to consume the age-based RDA of vitamin D.3 For those at increased risk for vitamin D deficiency, advise a higher dose of vitamin D (eg, 2000 IU/d, which is still lower than the upper daily limit).3
Other options are to screen for vitamin D deficiency only in those at high risk for low vitamin D levels, and to test for vitamin D deficiency in those with symptoms associated with deficiency such as bone pain and muscle weakness. These options would be consistent with recommendations from the Endocrine Society.5 Some have recommended that if testing is ordered, it should be performed by a laboratory that uses liquid chromatography-mass spectrometry because it is the criterion standard.2
Treatment options. Vitamin D deficiency can be treated with either ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). These treatments can also be recommended for those whose diets may not provide the RDA for vitamin D. Both are readily available over the counter and by prescription. The Task Force found that the harms of treating vitamin D deficiency with vitamin D at recommended doses are small to none.1 There is possibly a small increase in kidney stones with the combined use of 1000 mg/d calcium and 10 mcg (400 IU)/d vitamin D.17 Large doses of vitamin D can cause toxicity including marked hypercalcemia, nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.15A cautious evidence-based approach would be to selectively screen for vitamin D deficiency, conduct diagnostic testing when indicated, and advise vitamin D supplementation as needed.
1. USPSTF. Screening for vitamin D deficiency in adults: US Preventive Services Task Force recommendation statement. JAMA. 2021;325:1436-1442.
2. Michos ED, Kalyani RR, Segal JB. Why USPSTF still finds insufficient evidence to support screening for vitamin D deficiency. JAMA Netw Open. 2021;4:e213627.
3. Burnett-Bowie AAM, Cappola AR. The USPSTF 2021 recommendations on screening for asymptomatic vitamin D deficiency in adults: the challenge for clinicians continues. JAMA. 2021;325:1401-1402.
4. Institute of Medicine. Dietary reference intakes for calcium and vitamin D. National Academies Press; 2011. Accessed May 22, 2021. https://pubmed.ncbi.nlm.nih.gov/21796828/
5. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinolgy Metab. 2011;96:1911-1930.
6. Shahangian S, Alspach TD, Astles JR, et al. Trends in laboratory test volumes for Medicare part B reimbursements, 2000-2010. Arch Pathol Lab Med. 2014;138:189-203.
7. Herrick KA, Storandt RJ, Afful J, et al. Vitamin D status in the United States, 2011-2014. Am J Clin Nutr. 2019;110:150-157.
8. Forrest KYZ, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31:48-54.
9. Kahwati LC, LeBlanc E, Weber RP, et al. Screening for vitamin D deficiency in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2021;325:1443-1463.
10. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis-2016. Endocr Pract. 2016;22(supp 4):1-42.
11. AAFP. Clinical preventive services. Accessed May 22, 2021. www.aafp.org/family-physician/patient-care/clinical-recommendations/aafp-cps.html
12. USPSTF. Falls prevention in community-dwelling older adults: interventions. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/falls-prevention-in-older-adults-interventions
13. USPSTF. Vitamin supplementation to prevent cancer and CVD: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-supplementation-to-prevent-cancer-and-cvd-counseling
14. USPSTF. Vitamin D, calcium, or combined supplementation for the primary prevention of fractures in community-dwelling adults: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-d-calcium-or-combined-supplementation-for-the-primary-prevention-of-fractures-in-adults-preventive-medication
15. NIH. Vitamin D. Accessed May 22, 2021. https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
16. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96:53-58.
17. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354:669-683.
1. USPSTF. Screening for vitamin D deficiency in adults: US Preventive Services Task Force recommendation statement. JAMA. 2021;325:1436-1442.
2. Michos ED, Kalyani RR, Segal JB. Why USPSTF still finds insufficient evidence to support screening for vitamin D deficiency. JAMA Netw Open. 2021;4:e213627.
3. Burnett-Bowie AAM, Cappola AR. The USPSTF 2021 recommendations on screening for asymptomatic vitamin D deficiency in adults: the challenge for clinicians continues. JAMA. 2021;325:1401-1402.
4. Institute of Medicine. Dietary reference intakes for calcium and vitamin D. National Academies Press; 2011. Accessed May 22, 2021. https://pubmed.ncbi.nlm.nih.gov/21796828/
5. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinolgy Metab. 2011;96:1911-1930.
6. Shahangian S, Alspach TD, Astles JR, et al. Trends in laboratory test volumes for Medicare part B reimbursements, 2000-2010. Arch Pathol Lab Med. 2014;138:189-203.
7. Herrick KA, Storandt RJ, Afful J, et al. Vitamin D status in the United States, 2011-2014. Am J Clin Nutr. 2019;110:150-157.
8. Forrest KYZ, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31:48-54.
9. Kahwati LC, LeBlanc E, Weber RP, et al. Screening for vitamin D deficiency in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2021;325:1443-1463.
10. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis-2016. Endocr Pract. 2016;22(supp 4):1-42.
11. AAFP. Clinical preventive services. Accessed May 22, 2021. www.aafp.org/family-physician/patient-care/clinical-recommendations/aafp-cps.html
12. USPSTF. Falls prevention in community-dwelling older adults: interventions. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/falls-prevention-in-older-adults-interventions
13. USPSTF. Vitamin supplementation to prevent cancer and CVD: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-supplementation-to-prevent-cancer-and-cvd-counseling
14. USPSTF. Vitamin D, calcium, or combined supplementation for the primary prevention of fractures in community-dwelling adults: preventive medication. Accessed May 22, 2021. https://uspreventiveservicestaskforce.org/uspstf/recommendation/vitamin-d-calcium-or-combined-supplementation-for-the-primary-prevention-of-fractures-in-adults-preventive-medication
15. NIH. Vitamin D. Accessed May 22, 2021. https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
16. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96:53-58.
17. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354:669-683.
Melanoma: An FP’s guide to diagnosis and management
CASE
A 48-year-old man comes to your clinic with a dark nevus on his right upper arm that appeared 2 months earlier. He says that the lesion has continued to grow and has bled (he thought because he initially picked at it). On exam, there is a 7-mm brown papule with 2 black dots and slightly asymmetric borders.
How would you proceed with this patient?
Melanoma is the fifth leading cause of new cancer cases annually, with > 96,000 new cases in 2019.1 Overall, melanoma is more common in men and in Whites, with 48% diagnosed in people ages 55 to 74.1 The past 2 decades have seen numerous developments in the diagnosis, treatment, and surveillance of melanoma. This article covers recommendations, controversies, and issues that require future study. It does not cover uveal or mucosal melanoma.
Evaluating a patient with a new or changing nevus
Known risk factors for melanoma include a changing nevus, indoor tanning, older age, many melanocytic nevi, history of a dysplastic nevus or of blistering sunburns during teen years, red or blonde hair, large congenital nevus, Fitzpatrick skin type I or II, high socioeconomic status, personal or family history of melanoma, and intermittent high-intensity sun exposure.2-3 Presence of 1 or more of these risk factors should lower the threshold for biopsy.
Worrisome physical exam features (FIGURE) are nevus asymmetry, irregular borders, variegated color, and a diameter > 6 mm (the size of a pencil eraser). Inquire as to whether the nevus’ appearance has evolved and if it has bled without trauma. In a patient with multiple nevi, 1 nevus that looks different than the rest (the so-called “ugly duckling”) is concerning. Accuracy of diagnosis is enhanced with dermoscopy. A Cochrane review showed that skilled use of dermoscopy, in addition to inspection with the naked eye, considerably increases the sensitivity and specificity of diagnosing melanoma.4 Yet a 2017 study of 705 US primary care practitioners showed that only 8.3% of them used dermoscopy to evaluate pigmented lesions.5
Several published algorithms and checklists can aid clinicians in identifying lesions suggestive of melanoma—eg, ABCDE, CASH, Menzies method, “chaos and clues,” and 2-step and 3- and 7-point checklists.6-10 A simple 3-step algorithm, the TADA (triage amalgamated dermoscopic algorithm) method is available to novice dermoscopy users.11 Experts in pigmented lesions prefer to use pattern analysis, which requires simultaneously assessing multiple lesion patterns that vary according to body site.12,13
Dermoscopic features suggesting melanoma are atypical pigment networks, pseudopods, radial streaking, irregular dots or globules, blue-whitish veil, and granularity or peppering.14 Appropriate and effective use of dermoscopy requires training.15,16 Available methods for learning dermoscopy include online and in-person courses, mentoring by experienced dermoscopists, books and articles, and free apps and online resources.17
Continue to: Perform a skin biopsy, but do this first
Perform a skin biopsy, but do this first
Skin biopsy is the definitive way to diagnose melanoma. Prior to biopsy, take photographs to document the exact location of the lesion and to ensure that the correct area is removed in wide excision (WE). A complete biopsy should include the full depth and breadth of the lesion to ensure there are clinically negative margins. This can be achieved with an elliptical excision (for larger lesions), punch excision (for small lesions), or saucerization (deep shave with 1- to 2-mm peripheral margins, used for intermediate-size lesions).18 Saucerization is distinctly different from a superficial shave biopsy, which is not recommended for lesions with features of melanoma.19
A decision to perform a biopsy on a part of the lesion (partial biopsy) depends on the size of the lesion and its anatomic location, and is best made in agreement with the patient.
If you are untrained or uncomfortable performing the biopsy, contact a dermatologist immediately. In many communities, such referrals are subject to long delays, which further supports the advisability of family physicians doing their own biopsies after photographing the suspicious lesion. Many resources are available to help family physicians learn to do biopsies proficiently (www.mdedge.com/familymedicine/article/164358/oncology/biopsies-skin-cancer-detection-dispelling-myths).19
What to communicate to the pathologist. At a minimum, the biopsy request form should include patient age, sex, biopsy type (punch, excisional, or scoop shave), intention (complete or partial sample), exact site of the biopsy with laterality, and clinical details. These details should include the lesion size and clinical description, the suspected diagnosis, and clinical information, such as whether there is a history of bleeding or changing color, size, or symmetry. In standard biopsy specimens, the pathologist is only examining a portion of the lesion. Communicating clearly to the pathologist may lead to a request for deeper or additional sections or special stains.
If the biopsy results do not match the clinical impression, a phone call to the pathologist is warranted. In addition, evaluation by a dermatopathologist may be merited as pathologic diagnosis of melanoma can be quite challenging. Newer molecular tests, such as fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH), can assist in the histologic evaluation of complex pigmented lesions.
Continue to: CASE
CASE
You perform an elliptical excisional biopsy on your patient. The biopsy report comes back as a nodular malignant melanoma, Breslow depth 2.5 mm without ulceration, and no evidence of lymphovascular invasion or microsatellitosis. The report states that the biopsy margins appear clear of tumor involvement.
Further evaluation when the biopsy result is positive
Key steps in initial patient care include relaying pathology results to the patient, conducting (as needed) a more extensive evaluation, and obtaining appropriate consultation.
Clearly explain the diagnosis and convey an accurate reading of the pathology report. The vital pieces of information in the biopsy report are the Breslow depth and presence of ulceration, as evidence shows these 2 factors to be important independent predictors of outcome.22,23 Also important are the presence of microsatellitosis (essential for staging purposes), pathologic stage, and the status of the peripheral and deep biopsy margins. Review Breslow depth with the patient as this largely dictates treatment options and prognosis.
Evaluate for possible metastatic disease. Obtain a complete history from every patient with cutaneous melanoma, looking for any positive review of systems as a harbinger of metastatic disease. A full-body skin and lymph node exam is vital, given that melanoma can arise anywhere including on the scalp, in the gluteal cleft, and beneath nails. If the lymph node exam is worrisome, conduct an ultrasound exam, even while referring to specialty care. Treating a patient with melanoma requires a multidisciplinary approach that may include dermatologists, surgeons, and oncologists based on the stage of disease. A challenge for family physicians is knowing which consultation to prioritize and how to counsel the patient to schedule these for the most cost-effective and timely evaluation.
Expedite a dermatology consultation. If the melanoma is deep or appears advanced based on size or palpable lymph nodes, contact the dermatologist immediately by phone to set up a rapid referral. Delays in the definitive management of thick melanomas can negatively affect outcome. Paper, facsimile, or electronic referrals can get lost in the system and are not reliable methods for referring patients for a melanoma consultation. One benefit of the family physician performing the initial biopsy is that a confirmed melanoma diagnosis will almost certainly get an expedited dermatology appointment.
Continue to: Wide excision and sentinel node biopsy
Wide excision and sentinel node biopsy
Wide excision of a primary melanoma is standard practice, with evidence favoring the following surgical margins: 0.5 to 1 cm for melanoma in situ, 1 cm for tumors up to 1 mm in thickness, 1 to 2 cm for tumors > 1 to 2 mm thick, and 2 cm for tumors > 2 mm thick.18 WE is often performed by dermatologists for nonulcerated tumors < 0.8 mm thick (T1a) without adverse features. If trained in cutaneous surgery, you can also choose to excise these thin melanomas in your office. Otherwise refer all patients with biopsy-proven melanoma to dermatologists to perform an adequate WE.
Refer patients who have tumors ≥ 0.8 mm thick to the appropriate surgical specialty (surgical oncology, if available) for consultation on sentinel lymph node biopsy. SLNB, when indicated, should be performed prior to WE of the primary tumor, and whenever possible in the same surgical setting, to maximize lymphatic drainage mapping techniques.18 Medical oncology referral, if needed, is usually made after WE.
SLNB remains the standard for lymph node staging. It is controversial mainly in its use for very thin or very thick lesions. Randomized controlled trials, including the Multicenter Selective Lymphadenectomy Trial,24 have shown no difference in melanoma-specific survival for patients with intermediate-thickness melanomas who had undergone SLNB.24
Many professional organizations consider SLNB to be the most significant prognostic indicator of disease recurrence. With a negative SLNB result, the risk of regional node recurrence is 5% or lower.18,25 In addition, sentinel lymph node status is a critical determinant for systemic adjuvant therapy consideration and clinical trial eligibility. For patients who have primary cutaneous melanoma without clinical lymphadenopathy, an online tool is available for patients to use with their physician in predicting the likelihood of SLNB positivity.26
Recommendations for SLNB, supported by multidisciplinary consensus:18
- Do not pursue SLNB for melanoma in situ or most cutaneous melanomas < 0.8 mm without ulceration (T1a). (See TABLE 127)
- Discuss SLNB with patients who have T1a melanoma and additional adverse features: young age, high mitotic rate, lymphovascular invasion, and nevus depth close to 0.8 mm with positive deep biopsy margins.
- Discuss SLNB with patients who have T1b disease (< 0.8 mm with ulceration, or 0.8-1 mm), although rates of SLNB positivity are low.
- Offer SLNB to patients with T2a and higher disease (> 1 mm).18
Continue to: Patients who have...
Patients who have clinical Stage I or II disease (TABLE 127)
Melanoma in women: Considerations to keep in mind
Hormonal influences of pregnancy, lactation, contraception, and menopause introduce special considerations regarding melanoma, which is the most common cancer occurring during pregnancy, accounting for 31% of new malignancies.33 Risk of melanoma lessens, however, for women who first give birth at a younger age or who have had > 5 live births.18,34,35 There is no evidence that nevi darken during pregnancy, although nevi on the breast and abdomen may seem to enlarge due to skin stretching.18 All changing nevi in pregnancy warrant an examination, preferably with dermoscopy, and patients should be offered biopsy if there are any nevus characteristics associated with melanoma.18
The effect of pregnancy on an existing melanoma is not fully understood, but evidence from controlled studies shows no negative effect. Recent working group guidelines advise WE with local anesthesia without delay in pregnant patients.18 Definitive treatment after melanoma diagnosis should take a multidisciplinary approach involving obstetric care coordinated with Dermatology, Surgery, and Medical Oncology.18
Most recommendations on the timing of pregnancy following a melanoma diagnosis have limited evidence. One meta-analysis concluded that pregnancy occurring after successful treatment of melanoma did not change a woman’s prognosis.36 Current guidelines do not recommend delaying future pregnancy if a woman had an early-stage melanoma. For melanomas deemed higher risk, a woman could consider a 2- to 3-year delay in the next planned pregnancy, owing to current data on recurrence rates.18
A systematic review of women who used hormonal contraception or postmenopausal hormone replacement therapy (HRT) showed no associated increased risk of melanoma.35 An additional randomized trial showed no effect of HRT on melanoma risk.37
Continue to: Systemic melanoma treatment and common adverse effects
Systemic melanoma treatment and common adverse effects
Multiple systemic therapies have been approved for the treatment of advanced or unresectable cutaneous melanomas. While these treatments are managed primarily by Oncology in concert with Dermatology, an awareness of the medications’ common dermatologic toxicities is important for the primary care provider. The 2 broad categories of FDA-approved systemic medications for advanced melanoma are mitogen-activated protein kinase (MAPK) inhibitors and immune checkpoint inhibitors, each having its own set of adverse cutaneous effects.
MAPK pathway–targeting drugs include the B-Raf proto-oncogene serine/threonine-kinase inhibitors (BRAFIs) vemurafenib and dabrafenib, and the MAPK inhibitors (MEKIs) trametinib and cobimetinib. The most common adverse skin effects in MAPK pathway–targeting drugs are severe ultraviolet photosensitivity, cutaneous epidermal neoplasms (particularly squamous cell carcinoma, keratoacanthoma-type), thick actinic keratosis, wart-like keratosis, painful palmoplantar keratosis, and dry skin.38 These effects are most commonly seen with BRAFI monotherapy and can be abated with the addition of a MEKI. MEKI therapy can cause acneiform eruptions and paronychia.39 Additional adverse effects include diarrhea, pyrexia, arthralgias, and fatigue for BRAFIs and diarrhea, fatigue, and peripheral edema for MEKIs.40
Immune checkpoint inhibitors include anti-CTLA-4 (ipilimumab), anti-PD-1 (pembrolizumab and nivolumab), and anti-PDL-1 (atezolizumab). Adverse skin effects include morbilliform rash with or without an associated itch, itch with or without an associated rash, vitiligo, and lichenoid skin rashes. PD-1 and PDL-1 inhibitors have been associated with flares or unmasking of atopic dermatitis, psoriasis, sarcoidosis, and autoimmune bullous disease.18 Diarrhea, colitis, hepatitis, elevated liver enzymes, hypophysitis, and thyroiditis are some of the more common noncutaneous adverse effects reported with CTLA-4 inhibitors, while fatigue, diarrhea, nausea, pneumonitis, and thyroid disease are seen with anti-PD-1/PDL-1 therapy.3
A look at the prognosis
For patients diagnosed with primary cutaneous melanoma between 2011 and 2017, the 5-year survival rate for localized disease (Stages I-II) was 99%.1 For regional (Stage III) and distant (Stage IV) disease, the 5-year survival rates were 68% and 30%, respectively.1 With the advent of adjuvant systemic therapy, 5-year overall survival rates for metastatic melanoma have markedly improved from < 10% to up to 40% to 50%.41 The 3-year survival rate for patients with high tumor burden, brain metastasis, and elevated lactate dehydrogenase remains at < 10%.42 Relative survival decreases with increased age, although survival is higher in women than in men.43 Risk of melanoma recurrence after surgical excision is high in patients with stage IIB, IIC, III and IV (resectable) disease. The most important risk factor for recurrence is primary tumor thickness.44 The most common site of first recurrence in stage I-II disease is regional lymph node metastasis (42.8%), closely followed by distant metastasis (37.6%).44
Long-term follow-up and surveillance
Recommendations for long-term care of patients with melanoma have evolved with advances in treatment, prognostication, and imaging. Caring for these patients requires a multidisciplinary approach wherein the family physician provides frontline care and team coordination. Since most recurrences are discovered by the patient or the patient’s family, patient education and self-examination are the cost-effective foundation for recurrence screening. In a trial of patients and partners, a 30-minute structured session on skin examination followed by physician reminders every 4 months increased the detection of melanoma recurrence without significant increases in patient visits.45
Continue to: Patient education should include sun safety...
Patient education should include sun safety (wearing sun-protective clothing, using broad-spectrum sunscreen, and avoiding sun exposure during peak times of the day). The US Preventive Services Task Force (USPSTF) says the level of evidence is insufficient to support routine skin cancer screening in adults.46 However, the USPSTF recommends discussing efforts to minimize UV radiation exposure to prevent skin cancer in fair-skinned individuals 10 to 24 years of age.
Current National Comprehensive Cancer Network (NCCN) guidelines have outlined the follow-up frequency for all melanoma patients. TABLE 232 outlines those recommendations in addition to self-examination and patient education.
Melanoma epidemic or overdiagnosis?
Over the past 2 decades, a marked rise in the incidence of melanoma has been reported in developed countries worldwide, although melanoma mortality rates have not increased as rapidly, with melanoma-specific survival stable in most groups.47-50 Due to conflicting evidence, significant disagreement exists as to whether this is an actual epidemic caused by a true rise in disease burden or is merely an artifact stemming from overdiagnosis.47
Evidence supporting a true melanoma epidemic includes population-based studies demonstrating greater UV radiation–induced carcinogenesis (from the sun and tanning bed use), a larger aging population, and increased incidence regardless of socioeconomic status.47 Those challenging the validity of an epidemic instead attribute the rising incidence to early-detection public awareness campaigns, expanded screenings, improved diagnostic modalities, and increased biopsies. They also credit lower pathologic thresholds that help identify thinner tumors with little to no metastatic potential.48 Additionally, multiple studies report an increased incidence in melanomas of all histologic subtypes and thicknesses, not just thinner, more curable tumors.49,51,52 Although increased screening and biopsies are effective, they alone cannot account for the sharp rise in melanoma cases.47 This “melanoma paradox” of increasing incidence without a parallel increase in mortality remains unsettled.47
CASE
Your patient had Stage IIA disease and a WE was performed with 1-cm margins. Ultrasound of the axilla identified an enlarged node, which was removed and found not to be diseased. He has now returned to have you look at another lesion identified by his spouse. His review of symptoms is negative. His initial melanoma was removed 2 years earlier, and his last dermatology skin exam was 5 months prior. You look at the lesion using a dermatoscope and do not note any worrisome features. You recommend that the patient photograph the area for reexamination and follow-up with his dermatologist next month for a 6-month follow-up.
CORRESPONDENCE
Jessica Servey, MD, 4301 Jones Bridge Road, Bethesda, MD 20814; [email protected]
1. NIH. Cancer stat facts: melanoma of the skin. 2018. Accessed May 13, 2021. https://seer.cancer.gov/statfacts/html/melan.html
2. Watts CG, Dieng M, Morton RL, et al. Clinical practice guidelines for identification, screening and follow-up of individuals at high risk of primary cutaneous melanoma: a systematic review. Br J Dermatol. 2015;172:33-47.
3. Schadendorf D, van Akkooi ACJ, Berking C, et al. Melanoma. Lancet. 2018;392:971-984.
4. Dinnes J, Deeks JJ, Chuchu N, et al. Dermoscopy, with and without visual inspection, for diagnosing melanoma in adults. Cochrane Database Syst Rev. 2018(12):CD011902.
5. Morris JB, Alfonso SV, Hernandez N, et al. Examining the factors associated with past and present dermoscopy use among family physicians. Dermatol Pract Concept. 2017;7:63-70.
6. Henning JS, Dusza SW, Wang SQ, et al. The CASH (color, architecture, symmetry, and homogeneity) algorithm for dermoscopy. J Am Acad Dermatol. 2007;56:45-52.
7. Rosendahl C, Cameron A, McColl I, et al. Dermatoscopy in routine practice — “chaos and clues”. Aust Fam Physician. 2012;41:482-487.
8. Soyer HP, Argenziano G, Zalaudek I, et al. Three-point checklist of dermoscopy: a new screening method for early detection of melanoma. Dermatology. 2004;208:27-31.
9. Argenziano G, Fabbrocini G, Carli P, et al. Epiluminescence microscopy for the diagnosis of doubtful melanocytic skin lesions. Comparison of the ABCD rule of dermatoscopy and a new 7-point checklist based on pattern analysis. Arch Dermatol. 1998;134:1563-1570.
10. Marghoob AA, Usatine RP, Jaimes N. Dermoscopy for the family physician. Am Fam Physician. 2013;88:441-450.
11. Rogers T, Marino ML, Dusza SW, et al. A clinical aid for detecting skin cancer: the Triage Amalgamated Dermoscopic Algorithm (TADA). J Am Board Fam Med. 2016;29:694-701.
12. Argenziano G, Soyer HP, Chimenti S, et al. Dermoscopy of pigmented skin lesions: results of a consensus meeting via the Internet. J Am Acad Dermatol. 2003;48:679-93.
13. Carli P, Quercioli E, Sestini S, et al. Pattern analysis, not simplified algorithms, is the most reliable method for teaching dermoscopy for melanoma diagnosis to residents in dermatology. Br J Dermatol. 2003;148:981-984.
14. Yélamos O, Braun RP, Liopyris K, et al. Usefulness of dermoscopy to improve the clinical and histopathologic diagnosis of skin cancers. J Am Acad Dermatol. 2019;80:365-377.
15. Westerhoff K, McCarthy WH, Menzies SW. Increase in the sensitivity for melanoma diagnosis by primary care physicians using skin surface microscopy. Br J Dermatol. 2000;143:1016-1020.
16. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
17. Usatine RP, Shama LK, Marghoob AA, et al. Dermoscopy in family medicine: a primer. J Fam Pract. 2018;67:E1-E11.
18. Swetter SM, Tsao H, Bichakjian CK, et al. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2019;80:208-250.
19. Seiverling EV, Ahrns HT, Bacik LC, et al. Biopsies for skin cancer detection: dispelling the myths. J Fam Pract. 2018;67:270-274.
20. Martin RCG, Scoggins CR, Ross MI, et al. Is incisional biopsy of melanoma harmful? Am J Surg. 2005;190:913-917.
21. Mir M, Chan CS, Khan F, et al. The rate of melanoma transection with various biopsy techniques and the influence of tumor transection on patient survival. J Am Acad Dermatol. 2013;68:452-458.
22. Breslow A. Thickness, cross-sectional areas and depth of invasion in the prognosis of cutaneous melanoma. Ann Surg. 1970;172:902-908
23. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma staging: evidence-based changes in the American Joint Committee on Cancer 8th ed cancer staging manual. CA Cancer J Clin. 2017;67:472-492.
24. Morton DL, Thompson JF, Cochran AJ, et al. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. N Engl J Med. 2014;370:599-609.
25. Valsecchi ME, Silbermins D, de Rosa N, et al. Lymphatic mapping and sentinel lymph node biopsy in patients with melanoma: a meta-analysis. J Clin Oncol. 2011;29:1479-1487.
26. Memorial Sloan Kettering Cancer Center. Risk of sentinel lymph node metastasis nomogram. Accessed May 13, 2021. www.mskcc.org/nomograms/melanoma/sentinel_lymph_node_metastasis
27. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge SB, Greene FL, eds. AJCC Cancer Staging Manual. 8th ed. Springer International Publishing; 2017:563-581.
28. Xing Y, Bronstein Y, Ross MI, et al. Contemporary diagnostic imaging modalities for the staging and surveillance of melanoma patients: a meta-analysis. J Natl Cancer Inst. 2011;103:129-142.
29. Tsao H, Feldman M, Fullerton JE, et al. Early detection of asymptomatic pulmonary melanoma metastases by routine chest radiographs is not associated with improved survival. Arch Dermatol. 2004;140:67-70.
30. Wang TS, Johnson TM, Cascade PN, et al. Evaluation of staging chest radiographs and serum lactate dehydrogenase for localized melanoma. J Am Acad Dermatol. 2004;51:399-405.
31. Yancovitz M, Finelt N, Warycha MA, et al. Role of radiologic imaging at the time of initial diagnosis of stage T1b-T3b melanoma. Cancer. 2007; 110:1107-1114.
32. Swetter SM, Thompson JA, Albertini MR, et al. NCCN Guidelines: cutaneous melanoma, version 4.2020. Accessed June 7, 2021. http://medi-guide.meditool.cn/ymtpdf/ACC90A18-6CDF-9443-BF3F-E29394D495E8.pdf
33. Stensheim H, Møller B, van Dijk T, et al. Cause-specific survival for women diagnosed with cancer during pregnancy or lactation: a registry-based cohort study. J Clin Oncol. 2009;27:45-51.
34. Lens MB, Rosdahl I, Ahlbom A, et al. Effect of pregnancy on survival in women with cutaneous malignant melanoma. J Clin Oncol. 2004;22:4369-4375.
35. Gandini S, Iodice S, Koomen E, et al. Hormonal and reproductive factors in relation to melanoma in women: current review and meta-analysis. Eur J Cancer. 2011;47:2607-2617.
36. Byrom L, Olsen CM, Knight L, et al. Does pregnancy after a diagnosis of melanoma affect prognosis? Systematic review and meta-analysis. Dermatol Surg. 2015;41:875-882.
37. Tang JY, Spaunhurst KM, Chlebowski RT, et al. Menopausal hormone therapy and risks of melanoma and nonmelanoma skin cancers: women’s health initiative randomized trials. J Natl Cancer Inst. 2011;103:1469-1475.
38. Carlos G, Anforth R, Clements A, et al. Cutaneous toxic effects of BRAF inhibitors alone and in combination with MEK inhibitors for metastatic melanoma. JAMA Dermatol. 2015;151:1103-1109.
39. Macdonald JB, Macdonald B, Golitz LE, et al. Cutaneous adverse effects of targeted therapies: part I: inhibitors of the cellular membrane. J Am Acad Dermatol. 2015;72:203-218.
40. Welsh SJ, Corrie PG. Management of BRAF and MEK inhibitor toxicities in patients with metastatic melanoma. Ther Adv Med Oncol. 2015;7:122-136.
41. Kandolf Sekulovic L, Peris K, Hauschild A, et al. More than 5000 patients with metastatic melanoma in Europe per year do not have access to recommended first-line innovative treatments. Eur J Cancer. 2017;75:313-322.
42. Long GV, Grob JJ, Nathan P, et al. Factors predictive of response, disease progression, and overall survival after dabrafenib and trametinib combination treatment: a pooled analysis of individual patient data from randomised trials. Lancet Oncol. 2016;17:1743-1754.
43. Am J Cancer Res. 2019;9:1396-1414.
Trends in incidence and survival in patients with melanoma, 1974-2013.44. Lyth J, Falk M, Maroti M, et al. Prognostic risk factors of first recurrence in patients with primary stages I–II cutaneous malignant melanoma – from the population‐based Swedish melanoma register. J Eur Acad Dermatol Venereol. 2017;31:1468-1474.
45. Robinson JK, Wayne JD, Martini MC, et al. Early detection of new melanomas by patients with melanoma and their partners using a structured skin self-examination skills training intervention: a randomized clinical trial. JAMA Dermatol. 2016;152:979-985.
JAMA. 2016;316:429-435.
Screening for skin cancer: US Preventive Services Task Force recommendation statement.47. Gardner LJ, Strunck JL, Wu YP, et al. Current controversies in early-stage melanoma: questions on incidence, screening, and histologic regression. J Am Acad Dermatol. 2019;80:1-12.
48. Wei EX, Qureshi AA, Han J, et al. Trends in the diagnosis and clinical features of melanoma in situ (MIS) in US men and women: a prospective, observational study. J Am Acad Dermatol. 2016;75:698-705.
49. Linos E, Swetter SM, Cockburn MG, et al. Increasing burden of melanoma in the United States. J Invest Dermatol. 2009;129:1666-1674.
50. Curchin DJ, Forward E, Dickison P, et al. The acceleration of melanoma in situ: a population-based study of melanoma incidence trends from Victoria, Australia, 1985-2015. J Am Acad Dermatol. 2019;80:1791-1793.
51. Dennis LK. Analysis of the melanoma epidemic, both apparent and real: data from the 1973 through 1994 surveillance, epidemiology, and end results program registry. Arch Dermatol. 1999;135:275-280.
52. Jemal A, Saraiya M, Patel P, et al. Recent trends in cutaneous melanoma incidence and death rates in the United States, 1992-2006. J Am Acad Dermatol. 2011;65:S17-S25.
CASE
A 48-year-old man comes to your clinic with a dark nevus on his right upper arm that appeared 2 months earlier. He says that the lesion has continued to grow and has bled (he thought because he initially picked at it). On exam, there is a 7-mm brown papule with 2 black dots and slightly asymmetric borders.
How would you proceed with this patient?
Melanoma is the fifth leading cause of new cancer cases annually, with > 96,000 new cases in 2019.1 Overall, melanoma is more common in men and in Whites, with 48% diagnosed in people ages 55 to 74.1 The past 2 decades have seen numerous developments in the diagnosis, treatment, and surveillance of melanoma. This article covers recommendations, controversies, and issues that require future study. It does not cover uveal or mucosal melanoma.
Evaluating a patient with a new or changing nevus
Known risk factors for melanoma include a changing nevus, indoor tanning, older age, many melanocytic nevi, history of a dysplastic nevus or of blistering sunburns during teen years, red or blonde hair, large congenital nevus, Fitzpatrick skin type I or II, high socioeconomic status, personal or family history of melanoma, and intermittent high-intensity sun exposure.2-3 Presence of 1 or more of these risk factors should lower the threshold for biopsy.
Worrisome physical exam features (FIGURE) are nevus asymmetry, irregular borders, variegated color, and a diameter > 6 mm (the size of a pencil eraser). Inquire as to whether the nevus’ appearance has evolved and if it has bled without trauma. In a patient with multiple nevi, 1 nevus that looks different than the rest (the so-called “ugly duckling”) is concerning. Accuracy of diagnosis is enhanced with dermoscopy. A Cochrane review showed that skilled use of dermoscopy, in addition to inspection with the naked eye, considerably increases the sensitivity and specificity of diagnosing melanoma.4 Yet a 2017 study of 705 US primary care practitioners showed that only 8.3% of them used dermoscopy to evaluate pigmented lesions.5
Several published algorithms and checklists can aid clinicians in identifying lesions suggestive of melanoma—eg, ABCDE, CASH, Menzies method, “chaos and clues,” and 2-step and 3- and 7-point checklists.6-10 A simple 3-step algorithm, the TADA (triage amalgamated dermoscopic algorithm) method is available to novice dermoscopy users.11 Experts in pigmented lesions prefer to use pattern analysis, which requires simultaneously assessing multiple lesion patterns that vary according to body site.12,13
Dermoscopic features suggesting melanoma are atypical pigment networks, pseudopods, radial streaking, irregular dots or globules, blue-whitish veil, and granularity or peppering.14 Appropriate and effective use of dermoscopy requires training.15,16 Available methods for learning dermoscopy include online and in-person courses, mentoring by experienced dermoscopists, books and articles, and free apps and online resources.17
Continue to: Perform a skin biopsy, but do this first
Perform a skin biopsy, but do this first
Skin biopsy is the definitive way to diagnose melanoma. Prior to biopsy, take photographs to document the exact location of the lesion and to ensure that the correct area is removed in wide excision (WE). A complete biopsy should include the full depth and breadth of the lesion to ensure there are clinically negative margins. This can be achieved with an elliptical excision (for larger lesions), punch excision (for small lesions), or saucerization (deep shave with 1- to 2-mm peripheral margins, used for intermediate-size lesions).18 Saucerization is distinctly different from a superficial shave biopsy, which is not recommended for lesions with features of melanoma.19
A decision to perform a biopsy on a part of the lesion (partial biopsy) depends on the size of the lesion and its anatomic location, and is best made in agreement with the patient.
If you are untrained or uncomfortable performing the biopsy, contact a dermatologist immediately. In many communities, such referrals are subject to long delays, which further supports the advisability of family physicians doing their own biopsies after photographing the suspicious lesion. Many resources are available to help family physicians learn to do biopsies proficiently (www.mdedge.com/familymedicine/article/164358/oncology/biopsies-skin-cancer-detection-dispelling-myths).19
What to communicate to the pathologist. At a minimum, the biopsy request form should include patient age, sex, biopsy type (punch, excisional, or scoop shave), intention (complete or partial sample), exact site of the biopsy with laterality, and clinical details. These details should include the lesion size and clinical description, the suspected diagnosis, and clinical information, such as whether there is a history of bleeding or changing color, size, or symmetry. In standard biopsy specimens, the pathologist is only examining a portion of the lesion. Communicating clearly to the pathologist may lead to a request for deeper or additional sections or special stains.
If the biopsy results do not match the clinical impression, a phone call to the pathologist is warranted. In addition, evaluation by a dermatopathologist may be merited as pathologic diagnosis of melanoma can be quite challenging. Newer molecular tests, such as fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH), can assist in the histologic evaluation of complex pigmented lesions.
Continue to: CASE
CASE
You perform an elliptical excisional biopsy on your patient. The biopsy report comes back as a nodular malignant melanoma, Breslow depth 2.5 mm without ulceration, and no evidence of lymphovascular invasion or microsatellitosis. The report states that the biopsy margins appear clear of tumor involvement.
Further evaluation when the biopsy result is positive
Key steps in initial patient care include relaying pathology results to the patient, conducting (as needed) a more extensive evaluation, and obtaining appropriate consultation.
Clearly explain the diagnosis and convey an accurate reading of the pathology report. The vital pieces of information in the biopsy report are the Breslow depth and presence of ulceration, as evidence shows these 2 factors to be important independent predictors of outcome.22,23 Also important are the presence of microsatellitosis (essential for staging purposes), pathologic stage, and the status of the peripheral and deep biopsy margins. Review Breslow depth with the patient as this largely dictates treatment options and prognosis.
Evaluate for possible metastatic disease. Obtain a complete history from every patient with cutaneous melanoma, looking for any positive review of systems as a harbinger of metastatic disease. A full-body skin and lymph node exam is vital, given that melanoma can arise anywhere including on the scalp, in the gluteal cleft, and beneath nails. If the lymph node exam is worrisome, conduct an ultrasound exam, even while referring to specialty care. Treating a patient with melanoma requires a multidisciplinary approach that may include dermatologists, surgeons, and oncologists based on the stage of disease. A challenge for family physicians is knowing which consultation to prioritize and how to counsel the patient to schedule these for the most cost-effective and timely evaluation.
Expedite a dermatology consultation. If the melanoma is deep or appears advanced based on size or palpable lymph nodes, contact the dermatologist immediately by phone to set up a rapid referral. Delays in the definitive management of thick melanomas can negatively affect outcome. Paper, facsimile, or electronic referrals can get lost in the system and are not reliable methods for referring patients for a melanoma consultation. One benefit of the family physician performing the initial biopsy is that a confirmed melanoma diagnosis will almost certainly get an expedited dermatology appointment.
Continue to: Wide excision and sentinel node biopsy
Wide excision and sentinel node biopsy
Wide excision of a primary melanoma is standard practice, with evidence favoring the following surgical margins: 0.5 to 1 cm for melanoma in situ, 1 cm for tumors up to 1 mm in thickness, 1 to 2 cm for tumors > 1 to 2 mm thick, and 2 cm for tumors > 2 mm thick.18 WE is often performed by dermatologists for nonulcerated tumors < 0.8 mm thick (T1a) without adverse features. If trained in cutaneous surgery, you can also choose to excise these thin melanomas in your office. Otherwise refer all patients with biopsy-proven melanoma to dermatologists to perform an adequate WE.
Refer patients who have tumors ≥ 0.8 mm thick to the appropriate surgical specialty (surgical oncology, if available) for consultation on sentinel lymph node biopsy. SLNB, when indicated, should be performed prior to WE of the primary tumor, and whenever possible in the same surgical setting, to maximize lymphatic drainage mapping techniques.18 Medical oncology referral, if needed, is usually made after WE.
SLNB remains the standard for lymph node staging. It is controversial mainly in its use for very thin or very thick lesions. Randomized controlled trials, including the Multicenter Selective Lymphadenectomy Trial,24 have shown no difference in melanoma-specific survival for patients with intermediate-thickness melanomas who had undergone SLNB.24
Many professional organizations consider SLNB to be the most significant prognostic indicator of disease recurrence. With a negative SLNB result, the risk of regional node recurrence is 5% or lower.18,25 In addition, sentinel lymph node status is a critical determinant for systemic adjuvant therapy consideration and clinical trial eligibility. For patients who have primary cutaneous melanoma without clinical lymphadenopathy, an online tool is available for patients to use with their physician in predicting the likelihood of SLNB positivity.26
Recommendations for SLNB, supported by multidisciplinary consensus:18
- Do not pursue SLNB for melanoma in situ or most cutaneous melanomas < 0.8 mm without ulceration (T1a). (See TABLE 127)
- Discuss SLNB with patients who have T1a melanoma and additional adverse features: young age, high mitotic rate, lymphovascular invasion, and nevus depth close to 0.8 mm with positive deep biopsy margins.
- Discuss SLNB with patients who have T1b disease (< 0.8 mm with ulceration, or 0.8-1 mm), although rates of SLNB positivity are low.
- Offer SLNB to patients with T2a and higher disease (> 1 mm).18
Continue to: Patients who have...
Patients who have clinical Stage I or II disease (TABLE 127)
Melanoma in women: Considerations to keep in mind
Hormonal influences of pregnancy, lactation, contraception, and menopause introduce special considerations regarding melanoma, which is the most common cancer occurring during pregnancy, accounting for 31% of new malignancies.33 Risk of melanoma lessens, however, for women who first give birth at a younger age or who have had > 5 live births.18,34,35 There is no evidence that nevi darken during pregnancy, although nevi on the breast and abdomen may seem to enlarge due to skin stretching.18 All changing nevi in pregnancy warrant an examination, preferably with dermoscopy, and patients should be offered biopsy if there are any nevus characteristics associated with melanoma.18
The effect of pregnancy on an existing melanoma is not fully understood, but evidence from controlled studies shows no negative effect. Recent working group guidelines advise WE with local anesthesia without delay in pregnant patients.18 Definitive treatment after melanoma diagnosis should take a multidisciplinary approach involving obstetric care coordinated with Dermatology, Surgery, and Medical Oncology.18
Most recommendations on the timing of pregnancy following a melanoma diagnosis have limited evidence. One meta-analysis concluded that pregnancy occurring after successful treatment of melanoma did not change a woman’s prognosis.36 Current guidelines do not recommend delaying future pregnancy if a woman had an early-stage melanoma. For melanomas deemed higher risk, a woman could consider a 2- to 3-year delay in the next planned pregnancy, owing to current data on recurrence rates.18
A systematic review of women who used hormonal contraception or postmenopausal hormone replacement therapy (HRT) showed no associated increased risk of melanoma.35 An additional randomized trial showed no effect of HRT on melanoma risk.37
Continue to: Systemic melanoma treatment and common adverse effects
Systemic melanoma treatment and common adverse effects
Multiple systemic therapies have been approved for the treatment of advanced or unresectable cutaneous melanomas. While these treatments are managed primarily by Oncology in concert with Dermatology, an awareness of the medications’ common dermatologic toxicities is important for the primary care provider. The 2 broad categories of FDA-approved systemic medications for advanced melanoma are mitogen-activated protein kinase (MAPK) inhibitors and immune checkpoint inhibitors, each having its own set of adverse cutaneous effects.
MAPK pathway–targeting drugs include the B-Raf proto-oncogene serine/threonine-kinase inhibitors (BRAFIs) vemurafenib and dabrafenib, and the MAPK inhibitors (MEKIs) trametinib and cobimetinib. The most common adverse skin effects in MAPK pathway–targeting drugs are severe ultraviolet photosensitivity, cutaneous epidermal neoplasms (particularly squamous cell carcinoma, keratoacanthoma-type), thick actinic keratosis, wart-like keratosis, painful palmoplantar keratosis, and dry skin.38 These effects are most commonly seen with BRAFI monotherapy and can be abated with the addition of a MEKI. MEKI therapy can cause acneiform eruptions and paronychia.39 Additional adverse effects include diarrhea, pyrexia, arthralgias, and fatigue for BRAFIs and diarrhea, fatigue, and peripheral edema for MEKIs.40
Immune checkpoint inhibitors include anti-CTLA-4 (ipilimumab), anti-PD-1 (pembrolizumab and nivolumab), and anti-PDL-1 (atezolizumab). Adverse skin effects include morbilliform rash with or without an associated itch, itch with or without an associated rash, vitiligo, and lichenoid skin rashes. PD-1 and PDL-1 inhibitors have been associated with flares or unmasking of atopic dermatitis, psoriasis, sarcoidosis, and autoimmune bullous disease.18 Diarrhea, colitis, hepatitis, elevated liver enzymes, hypophysitis, and thyroiditis are some of the more common noncutaneous adverse effects reported with CTLA-4 inhibitors, while fatigue, diarrhea, nausea, pneumonitis, and thyroid disease are seen with anti-PD-1/PDL-1 therapy.3
A look at the prognosis
For patients diagnosed with primary cutaneous melanoma between 2011 and 2017, the 5-year survival rate for localized disease (Stages I-II) was 99%.1 For regional (Stage III) and distant (Stage IV) disease, the 5-year survival rates were 68% and 30%, respectively.1 With the advent of adjuvant systemic therapy, 5-year overall survival rates for metastatic melanoma have markedly improved from < 10% to up to 40% to 50%.41 The 3-year survival rate for patients with high tumor burden, brain metastasis, and elevated lactate dehydrogenase remains at < 10%.42 Relative survival decreases with increased age, although survival is higher in women than in men.43 Risk of melanoma recurrence after surgical excision is high in patients with stage IIB, IIC, III and IV (resectable) disease. The most important risk factor for recurrence is primary tumor thickness.44 The most common site of first recurrence in stage I-II disease is regional lymph node metastasis (42.8%), closely followed by distant metastasis (37.6%).44
Long-term follow-up and surveillance
Recommendations for long-term care of patients with melanoma have evolved with advances in treatment, prognostication, and imaging. Caring for these patients requires a multidisciplinary approach wherein the family physician provides frontline care and team coordination. Since most recurrences are discovered by the patient or the patient’s family, patient education and self-examination are the cost-effective foundation for recurrence screening. In a trial of patients and partners, a 30-minute structured session on skin examination followed by physician reminders every 4 months increased the detection of melanoma recurrence without significant increases in patient visits.45
Continue to: Patient education should include sun safety...
Patient education should include sun safety (wearing sun-protective clothing, using broad-spectrum sunscreen, and avoiding sun exposure during peak times of the day). The US Preventive Services Task Force (USPSTF) says the level of evidence is insufficient to support routine skin cancer screening in adults.46 However, the USPSTF recommends discussing efforts to minimize UV radiation exposure to prevent skin cancer in fair-skinned individuals 10 to 24 years of age.
Current National Comprehensive Cancer Network (NCCN) guidelines have outlined the follow-up frequency for all melanoma patients. TABLE 232 outlines those recommendations in addition to self-examination and patient education.
Melanoma epidemic or overdiagnosis?
Over the past 2 decades, a marked rise in the incidence of melanoma has been reported in developed countries worldwide, although melanoma mortality rates have not increased as rapidly, with melanoma-specific survival stable in most groups.47-50 Due to conflicting evidence, significant disagreement exists as to whether this is an actual epidemic caused by a true rise in disease burden or is merely an artifact stemming from overdiagnosis.47
Evidence supporting a true melanoma epidemic includes population-based studies demonstrating greater UV radiation–induced carcinogenesis (from the sun and tanning bed use), a larger aging population, and increased incidence regardless of socioeconomic status.47 Those challenging the validity of an epidemic instead attribute the rising incidence to early-detection public awareness campaigns, expanded screenings, improved diagnostic modalities, and increased biopsies. They also credit lower pathologic thresholds that help identify thinner tumors with little to no metastatic potential.48 Additionally, multiple studies report an increased incidence in melanomas of all histologic subtypes and thicknesses, not just thinner, more curable tumors.49,51,52 Although increased screening and biopsies are effective, they alone cannot account for the sharp rise in melanoma cases.47 This “melanoma paradox” of increasing incidence without a parallel increase in mortality remains unsettled.47
CASE
Your patient had Stage IIA disease and a WE was performed with 1-cm margins. Ultrasound of the axilla identified an enlarged node, which was removed and found not to be diseased. He has now returned to have you look at another lesion identified by his spouse. His review of symptoms is negative. His initial melanoma was removed 2 years earlier, and his last dermatology skin exam was 5 months prior. You look at the lesion using a dermatoscope and do not note any worrisome features. You recommend that the patient photograph the area for reexamination and follow-up with his dermatologist next month for a 6-month follow-up.
CORRESPONDENCE
Jessica Servey, MD, 4301 Jones Bridge Road, Bethesda, MD 20814; [email protected]
CASE
A 48-year-old man comes to your clinic with a dark nevus on his right upper arm that appeared 2 months earlier. He says that the lesion has continued to grow and has bled (he thought because he initially picked at it). On exam, there is a 7-mm brown papule with 2 black dots and slightly asymmetric borders.
How would you proceed with this patient?
Melanoma is the fifth leading cause of new cancer cases annually, with > 96,000 new cases in 2019.1 Overall, melanoma is more common in men and in Whites, with 48% diagnosed in people ages 55 to 74.1 The past 2 decades have seen numerous developments in the diagnosis, treatment, and surveillance of melanoma. This article covers recommendations, controversies, and issues that require future study. It does not cover uveal or mucosal melanoma.
Evaluating a patient with a new or changing nevus
Known risk factors for melanoma include a changing nevus, indoor tanning, older age, many melanocytic nevi, history of a dysplastic nevus or of blistering sunburns during teen years, red or blonde hair, large congenital nevus, Fitzpatrick skin type I or II, high socioeconomic status, personal or family history of melanoma, and intermittent high-intensity sun exposure.2-3 Presence of 1 or more of these risk factors should lower the threshold for biopsy.
Worrisome physical exam features (FIGURE) are nevus asymmetry, irregular borders, variegated color, and a diameter > 6 mm (the size of a pencil eraser). Inquire as to whether the nevus’ appearance has evolved and if it has bled without trauma. In a patient with multiple nevi, 1 nevus that looks different than the rest (the so-called “ugly duckling”) is concerning. Accuracy of diagnosis is enhanced with dermoscopy. A Cochrane review showed that skilled use of dermoscopy, in addition to inspection with the naked eye, considerably increases the sensitivity and specificity of diagnosing melanoma.4 Yet a 2017 study of 705 US primary care practitioners showed that only 8.3% of them used dermoscopy to evaluate pigmented lesions.5
Several published algorithms and checklists can aid clinicians in identifying lesions suggestive of melanoma—eg, ABCDE, CASH, Menzies method, “chaos and clues,” and 2-step and 3- and 7-point checklists.6-10 A simple 3-step algorithm, the TADA (triage amalgamated dermoscopic algorithm) method is available to novice dermoscopy users.11 Experts in pigmented lesions prefer to use pattern analysis, which requires simultaneously assessing multiple lesion patterns that vary according to body site.12,13
Dermoscopic features suggesting melanoma are atypical pigment networks, pseudopods, radial streaking, irregular dots or globules, blue-whitish veil, and granularity or peppering.14 Appropriate and effective use of dermoscopy requires training.15,16 Available methods for learning dermoscopy include online and in-person courses, mentoring by experienced dermoscopists, books and articles, and free apps and online resources.17
Continue to: Perform a skin biopsy, but do this first
Perform a skin biopsy, but do this first
Skin biopsy is the definitive way to diagnose melanoma. Prior to biopsy, take photographs to document the exact location of the lesion and to ensure that the correct area is removed in wide excision (WE). A complete biopsy should include the full depth and breadth of the lesion to ensure there are clinically negative margins. This can be achieved with an elliptical excision (for larger lesions), punch excision (for small lesions), or saucerization (deep shave with 1- to 2-mm peripheral margins, used for intermediate-size lesions).18 Saucerization is distinctly different from a superficial shave biopsy, which is not recommended for lesions with features of melanoma.19
A decision to perform a biopsy on a part of the lesion (partial biopsy) depends on the size of the lesion and its anatomic location, and is best made in agreement with the patient.
If you are untrained or uncomfortable performing the biopsy, contact a dermatologist immediately. In many communities, such referrals are subject to long delays, which further supports the advisability of family physicians doing their own biopsies after photographing the suspicious lesion. Many resources are available to help family physicians learn to do biopsies proficiently (www.mdedge.com/familymedicine/article/164358/oncology/biopsies-skin-cancer-detection-dispelling-myths).19
What to communicate to the pathologist. At a minimum, the biopsy request form should include patient age, sex, biopsy type (punch, excisional, or scoop shave), intention (complete or partial sample), exact site of the biopsy with laterality, and clinical details. These details should include the lesion size and clinical description, the suspected diagnosis, and clinical information, such as whether there is a history of bleeding or changing color, size, or symmetry. In standard biopsy specimens, the pathologist is only examining a portion of the lesion. Communicating clearly to the pathologist may lead to a request for deeper or additional sections or special stains.
If the biopsy results do not match the clinical impression, a phone call to the pathologist is warranted. In addition, evaluation by a dermatopathologist may be merited as pathologic diagnosis of melanoma can be quite challenging. Newer molecular tests, such as fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH), can assist in the histologic evaluation of complex pigmented lesions.
Continue to: CASE
CASE
You perform an elliptical excisional biopsy on your patient. The biopsy report comes back as a nodular malignant melanoma, Breslow depth 2.5 mm without ulceration, and no evidence of lymphovascular invasion or microsatellitosis. The report states that the biopsy margins appear clear of tumor involvement.
Further evaluation when the biopsy result is positive
Key steps in initial patient care include relaying pathology results to the patient, conducting (as needed) a more extensive evaluation, and obtaining appropriate consultation.
Clearly explain the diagnosis and convey an accurate reading of the pathology report. The vital pieces of information in the biopsy report are the Breslow depth and presence of ulceration, as evidence shows these 2 factors to be important independent predictors of outcome.22,23 Also important are the presence of microsatellitosis (essential for staging purposes), pathologic stage, and the status of the peripheral and deep biopsy margins. Review Breslow depth with the patient as this largely dictates treatment options and prognosis.
Evaluate for possible metastatic disease. Obtain a complete history from every patient with cutaneous melanoma, looking for any positive review of systems as a harbinger of metastatic disease. A full-body skin and lymph node exam is vital, given that melanoma can arise anywhere including on the scalp, in the gluteal cleft, and beneath nails. If the lymph node exam is worrisome, conduct an ultrasound exam, even while referring to specialty care. Treating a patient with melanoma requires a multidisciplinary approach that may include dermatologists, surgeons, and oncologists based on the stage of disease. A challenge for family physicians is knowing which consultation to prioritize and how to counsel the patient to schedule these for the most cost-effective and timely evaluation.
Expedite a dermatology consultation. If the melanoma is deep or appears advanced based on size or palpable lymph nodes, contact the dermatologist immediately by phone to set up a rapid referral. Delays in the definitive management of thick melanomas can negatively affect outcome. Paper, facsimile, or electronic referrals can get lost in the system and are not reliable methods for referring patients for a melanoma consultation. One benefit of the family physician performing the initial biopsy is that a confirmed melanoma diagnosis will almost certainly get an expedited dermatology appointment.
Continue to: Wide excision and sentinel node biopsy
Wide excision and sentinel node biopsy
Wide excision of a primary melanoma is standard practice, with evidence favoring the following surgical margins: 0.5 to 1 cm for melanoma in situ, 1 cm for tumors up to 1 mm in thickness, 1 to 2 cm for tumors > 1 to 2 mm thick, and 2 cm for tumors > 2 mm thick.18 WE is often performed by dermatologists for nonulcerated tumors < 0.8 mm thick (T1a) without adverse features. If trained in cutaneous surgery, you can also choose to excise these thin melanomas in your office. Otherwise refer all patients with biopsy-proven melanoma to dermatologists to perform an adequate WE.
Refer patients who have tumors ≥ 0.8 mm thick to the appropriate surgical specialty (surgical oncology, if available) for consultation on sentinel lymph node biopsy. SLNB, when indicated, should be performed prior to WE of the primary tumor, and whenever possible in the same surgical setting, to maximize lymphatic drainage mapping techniques.18 Medical oncology referral, if needed, is usually made after WE.
SLNB remains the standard for lymph node staging. It is controversial mainly in its use for very thin or very thick lesions. Randomized controlled trials, including the Multicenter Selective Lymphadenectomy Trial,24 have shown no difference in melanoma-specific survival for patients with intermediate-thickness melanomas who had undergone SLNB.24
Many professional organizations consider SLNB to be the most significant prognostic indicator of disease recurrence. With a negative SLNB result, the risk of regional node recurrence is 5% or lower.18,25 In addition, sentinel lymph node status is a critical determinant for systemic adjuvant therapy consideration and clinical trial eligibility. For patients who have primary cutaneous melanoma without clinical lymphadenopathy, an online tool is available for patients to use with their physician in predicting the likelihood of SLNB positivity.26
Recommendations for SLNB, supported by multidisciplinary consensus:18
- Do not pursue SLNB for melanoma in situ or most cutaneous melanomas < 0.8 mm without ulceration (T1a). (See TABLE 127)
- Discuss SLNB with patients who have T1a melanoma and additional adverse features: young age, high mitotic rate, lymphovascular invasion, and nevus depth close to 0.8 mm with positive deep biopsy margins.
- Discuss SLNB with patients who have T1b disease (< 0.8 mm with ulceration, or 0.8-1 mm), although rates of SLNB positivity are low.
- Offer SLNB to patients with T2a and higher disease (> 1 mm).18
Continue to: Patients who have...
Patients who have clinical Stage I or II disease (TABLE 127)
Melanoma in women: Considerations to keep in mind
Hormonal influences of pregnancy, lactation, contraception, and menopause introduce special considerations regarding melanoma, which is the most common cancer occurring during pregnancy, accounting for 31% of new malignancies.33 Risk of melanoma lessens, however, for women who first give birth at a younger age or who have had > 5 live births.18,34,35 There is no evidence that nevi darken during pregnancy, although nevi on the breast and abdomen may seem to enlarge due to skin stretching.18 All changing nevi in pregnancy warrant an examination, preferably with dermoscopy, and patients should be offered biopsy if there are any nevus characteristics associated with melanoma.18
The effect of pregnancy on an existing melanoma is not fully understood, but evidence from controlled studies shows no negative effect. Recent working group guidelines advise WE with local anesthesia without delay in pregnant patients.18 Definitive treatment after melanoma diagnosis should take a multidisciplinary approach involving obstetric care coordinated with Dermatology, Surgery, and Medical Oncology.18
Most recommendations on the timing of pregnancy following a melanoma diagnosis have limited evidence. One meta-analysis concluded that pregnancy occurring after successful treatment of melanoma did not change a woman’s prognosis.36 Current guidelines do not recommend delaying future pregnancy if a woman had an early-stage melanoma. For melanomas deemed higher risk, a woman could consider a 2- to 3-year delay in the next planned pregnancy, owing to current data on recurrence rates.18
A systematic review of women who used hormonal contraception or postmenopausal hormone replacement therapy (HRT) showed no associated increased risk of melanoma.35 An additional randomized trial showed no effect of HRT on melanoma risk.37
Continue to: Systemic melanoma treatment and common adverse effects
Systemic melanoma treatment and common adverse effects
Multiple systemic therapies have been approved for the treatment of advanced or unresectable cutaneous melanomas. While these treatments are managed primarily by Oncology in concert with Dermatology, an awareness of the medications’ common dermatologic toxicities is important for the primary care provider. The 2 broad categories of FDA-approved systemic medications for advanced melanoma are mitogen-activated protein kinase (MAPK) inhibitors and immune checkpoint inhibitors, each having its own set of adverse cutaneous effects.
MAPK pathway–targeting drugs include the B-Raf proto-oncogene serine/threonine-kinase inhibitors (BRAFIs) vemurafenib and dabrafenib, and the MAPK inhibitors (MEKIs) trametinib and cobimetinib. The most common adverse skin effects in MAPK pathway–targeting drugs are severe ultraviolet photosensitivity, cutaneous epidermal neoplasms (particularly squamous cell carcinoma, keratoacanthoma-type), thick actinic keratosis, wart-like keratosis, painful palmoplantar keratosis, and dry skin.38 These effects are most commonly seen with BRAFI monotherapy and can be abated with the addition of a MEKI. MEKI therapy can cause acneiform eruptions and paronychia.39 Additional adverse effects include diarrhea, pyrexia, arthralgias, and fatigue for BRAFIs and diarrhea, fatigue, and peripheral edema for MEKIs.40
Immune checkpoint inhibitors include anti-CTLA-4 (ipilimumab), anti-PD-1 (pembrolizumab and nivolumab), and anti-PDL-1 (atezolizumab). Adverse skin effects include morbilliform rash with or without an associated itch, itch with or without an associated rash, vitiligo, and lichenoid skin rashes. PD-1 and PDL-1 inhibitors have been associated with flares or unmasking of atopic dermatitis, psoriasis, sarcoidosis, and autoimmune bullous disease.18 Diarrhea, colitis, hepatitis, elevated liver enzymes, hypophysitis, and thyroiditis are some of the more common noncutaneous adverse effects reported with CTLA-4 inhibitors, while fatigue, diarrhea, nausea, pneumonitis, and thyroid disease are seen with anti-PD-1/PDL-1 therapy.3
A look at the prognosis
For patients diagnosed with primary cutaneous melanoma between 2011 and 2017, the 5-year survival rate for localized disease (Stages I-II) was 99%.1 For regional (Stage III) and distant (Stage IV) disease, the 5-year survival rates were 68% and 30%, respectively.1 With the advent of adjuvant systemic therapy, 5-year overall survival rates for metastatic melanoma have markedly improved from < 10% to up to 40% to 50%.41 The 3-year survival rate for patients with high tumor burden, brain metastasis, and elevated lactate dehydrogenase remains at < 10%.42 Relative survival decreases with increased age, although survival is higher in women than in men.43 Risk of melanoma recurrence after surgical excision is high in patients with stage IIB, IIC, III and IV (resectable) disease. The most important risk factor for recurrence is primary tumor thickness.44 The most common site of first recurrence in stage I-II disease is regional lymph node metastasis (42.8%), closely followed by distant metastasis (37.6%).44
Long-term follow-up and surveillance
Recommendations for long-term care of patients with melanoma have evolved with advances in treatment, prognostication, and imaging. Caring for these patients requires a multidisciplinary approach wherein the family physician provides frontline care and team coordination. Since most recurrences are discovered by the patient or the patient’s family, patient education and self-examination are the cost-effective foundation for recurrence screening. In a trial of patients and partners, a 30-minute structured session on skin examination followed by physician reminders every 4 months increased the detection of melanoma recurrence without significant increases in patient visits.45
Continue to: Patient education should include sun safety...
Patient education should include sun safety (wearing sun-protective clothing, using broad-spectrum sunscreen, and avoiding sun exposure during peak times of the day). The US Preventive Services Task Force (USPSTF) says the level of evidence is insufficient to support routine skin cancer screening in adults.46 However, the USPSTF recommends discussing efforts to minimize UV radiation exposure to prevent skin cancer in fair-skinned individuals 10 to 24 years of age.
Current National Comprehensive Cancer Network (NCCN) guidelines have outlined the follow-up frequency for all melanoma patients. TABLE 232 outlines those recommendations in addition to self-examination and patient education.
Melanoma epidemic or overdiagnosis?
Over the past 2 decades, a marked rise in the incidence of melanoma has been reported in developed countries worldwide, although melanoma mortality rates have not increased as rapidly, with melanoma-specific survival stable in most groups.47-50 Due to conflicting evidence, significant disagreement exists as to whether this is an actual epidemic caused by a true rise in disease burden or is merely an artifact stemming from overdiagnosis.47
Evidence supporting a true melanoma epidemic includes population-based studies demonstrating greater UV radiation–induced carcinogenesis (from the sun and tanning bed use), a larger aging population, and increased incidence regardless of socioeconomic status.47 Those challenging the validity of an epidemic instead attribute the rising incidence to early-detection public awareness campaigns, expanded screenings, improved diagnostic modalities, and increased biopsies. They also credit lower pathologic thresholds that help identify thinner tumors with little to no metastatic potential.48 Additionally, multiple studies report an increased incidence in melanomas of all histologic subtypes and thicknesses, not just thinner, more curable tumors.49,51,52 Although increased screening and biopsies are effective, they alone cannot account for the sharp rise in melanoma cases.47 This “melanoma paradox” of increasing incidence without a parallel increase in mortality remains unsettled.47
CASE
Your patient had Stage IIA disease and a WE was performed with 1-cm margins. Ultrasound of the axilla identified an enlarged node, which was removed and found not to be diseased. He has now returned to have you look at another lesion identified by his spouse. His review of symptoms is negative. His initial melanoma was removed 2 years earlier, and his last dermatology skin exam was 5 months prior. You look at the lesion using a dermatoscope and do not note any worrisome features. You recommend that the patient photograph the area for reexamination and follow-up with his dermatologist next month for a 6-month follow-up.
CORRESPONDENCE
Jessica Servey, MD, 4301 Jones Bridge Road, Bethesda, MD 20814; [email protected]
1. NIH. Cancer stat facts: melanoma of the skin. 2018. Accessed May 13, 2021. https://seer.cancer.gov/statfacts/html/melan.html
2. Watts CG, Dieng M, Morton RL, et al. Clinical practice guidelines for identification, screening and follow-up of individuals at high risk of primary cutaneous melanoma: a systematic review. Br J Dermatol. 2015;172:33-47.
3. Schadendorf D, van Akkooi ACJ, Berking C, et al. Melanoma. Lancet. 2018;392:971-984.
4. Dinnes J, Deeks JJ, Chuchu N, et al. Dermoscopy, with and without visual inspection, for diagnosing melanoma in adults. Cochrane Database Syst Rev. 2018(12):CD011902.
5. Morris JB, Alfonso SV, Hernandez N, et al. Examining the factors associated with past and present dermoscopy use among family physicians. Dermatol Pract Concept. 2017;7:63-70.
6. Henning JS, Dusza SW, Wang SQ, et al. The CASH (color, architecture, symmetry, and homogeneity) algorithm for dermoscopy. J Am Acad Dermatol. 2007;56:45-52.
7. Rosendahl C, Cameron A, McColl I, et al. Dermatoscopy in routine practice — “chaos and clues”. Aust Fam Physician. 2012;41:482-487.
8. Soyer HP, Argenziano G, Zalaudek I, et al. Three-point checklist of dermoscopy: a new screening method for early detection of melanoma. Dermatology. 2004;208:27-31.
9. Argenziano G, Fabbrocini G, Carli P, et al. Epiluminescence microscopy for the diagnosis of doubtful melanocytic skin lesions. Comparison of the ABCD rule of dermatoscopy and a new 7-point checklist based on pattern analysis. Arch Dermatol. 1998;134:1563-1570.
10. Marghoob AA, Usatine RP, Jaimes N. Dermoscopy for the family physician. Am Fam Physician. 2013;88:441-450.
11. Rogers T, Marino ML, Dusza SW, et al. A clinical aid for detecting skin cancer: the Triage Amalgamated Dermoscopic Algorithm (TADA). J Am Board Fam Med. 2016;29:694-701.
12. Argenziano G, Soyer HP, Chimenti S, et al. Dermoscopy of pigmented skin lesions: results of a consensus meeting via the Internet. J Am Acad Dermatol. 2003;48:679-93.
13. Carli P, Quercioli E, Sestini S, et al. Pattern analysis, not simplified algorithms, is the most reliable method for teaching dermoscopy for melanoma diagnosis to residents in dermatology. Br J Dermatol. 2003;148:981-984.
14. Yélamos O, Braun RP, Liopyris K, et al. Usefulness of dermoscopy to improve the clinical and histopathologic diagnosis of skin cancers. J Am Acad Dermatol. 2019;80:365-377.
15. Westerhoff K, McCarthy WH, Menzies SW. Increase in the sensitivity for melanoma diagnosis by primary care physicians using skin surface microscopy. Br J Dermatol. 2000;143:1016-1020.
16. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
17. Usatine RP, Shama LK, Marghoob AA, et al. Dermoscopy in family medicine: a primer. J Fam Pract. 2018;67:E1-E11.
18. Swetter SM, Tsao H, Bichakjian CK, et al. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2019;80:208-250.
19. Seiverling EV, Ahrns HT, Bacik LC, et al. Biopsies for skin cancer detection: dispelling the myths. J Fam Pract. 2018;67:270-274.
20. Martin RCG, Scoggins CR, Ross MI, et al. Is incisional biopsy of melanoma harmful? Am J Surg. 2005;190:913-917.
21. Mir M, Chan CS, Khan F, et al. The rate of melanoma transection with various biopsy techniques and the influence of tumor transection on patient survival. J Am Acad Dermatol. 2013;68:452-458.
22. Breslow A. Thickness, cross-sectional areas and depth of invasion in the prognosis of cutaneous melanoma. Ann Surg. 1970;172:902-908
23. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma staging: evidence-based changes in the American Joint Committee on Cancer 8th ed cancer staging manual. CA Cancer J Clin. 2017;67:472-492.
24. Morton DL, Thompson JF, Cochran AJ, et al. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. N Engl J Med. 2014;370:599-609.
25. Valsecchi ME, Silbermins D, de Rosa N, et al. Lymphatic mapping and sentinel lymph node biopsy in patients with melanoma: a meta-analysis. J Clin Oncol. 2011;29:1479-1487.
26. Memorial Sloan Kettering Cancer Center. Risk of sentinel lymph node metastasis nomogram. Accessed May 13, 2021. www.mskcc.org/nomograms/melanoma/sentinel_lymph_node_metastasis
27. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge SB, Greene FL, eds. AJCC Cancer Staging Manual. 8th ed. Springer International Publishing; 2017:563-581.
28. Xing Y, Bronstein Y, Ross MI, et al. Contemporary diagnostic imaging modalities for the staging and surveillance of melanoma patients: a meta-analysis. J Natl Cancer Inst. 2011;103:129-142.
29. Tsao H, Feldman M, Fullerton JE, et al. Early detection of asymptomatic pulmonary melanoma metastases by routine chest radiographs is not associated with improved survival. Arch Dermatol. 2004;140:67-70.
30. Wang TS, Johnson TM, Cascade PN, et al. Evaluation of staging chest radiographs and serum lactate dehydrogenase for localized melanoma. J Am Acad Dermatol. 2004;51:399-405.
31. Yancovitz M, Finelt N, Warycha MA, et al. Role of radiologic imaging at the time of initial diagnosis of stage T1b-T3b melanoma. Cancer. 2007; 110:1107-1114.
32. Swetter SM, Thompson JA, Albertini MR, et al. NCCN Guidelines: cutaneous melanoma, version 4.2020. Accessed June 7, 2021. http://medi-guide.meditool.cn/ymtpdf/ACC90A18-6CDF-9443-BF3F-E29394D495E8.pdf
33. Stensheim H, Møller B, van Dijk T, et al. Cause-specific survival for women diagnosed with cancer during pregnancy or lactation: a registry-based cohort study. J Clin Oncol. 2009;27:45-51.
34. Lens MB, Rosdahl I, Ahlbom A, et al. Effect of pregnancy on survival in women with cutaneous malignant melanoma. J Clin Oncol. 2004;22:4369-4375.
35. Gandini S, Iodice S, Koomen E, et al. Hormonal and reproductive factors in relation to melanoma in women: current review and meta-analysis. Eur J Cancer. 2011;47:2607-2617.
36. Byrom L, Olsen CM, Knight L, et al. Does pregnancy after a diagnosis of melanoma affect prognosis? Systematic review and meta-analysis. Dermatol Surg. 2015;41:875-882.
37. Tang JY, Spaunhurst KM, Chlebowski RT, et al. Menopausal hormone therapy and risks of melanoma and nonmelanoma skin cancers: women’s health initiative randomized trials. J Natl Cancer Inst. 2011;103:1469-1475.
38. Carlos G, Anforth R, Clements A, et al. Cutaneous toxic effects of BRAF inhibitors alone and in combination with MEK inhibitors for metastatic melanoma. JAMA Dermatol. 2015;151:1103-1109.
39. Macdonald JB, Macdonald B, Golitz LE, et al. Cutaneous adverse effects of targeted therapies: part I: inhibitors of the cellular membrane. J Am Acad Dermatol. 2015;72:203-218.
40. Welsh SJ, Corrie PG. Management of BRAF and MEK inhibitor toxicities in patients with metastatic melanoma. Ther Adv Med Oncol. 2015;7:122-136.
41. Kandolf Sekulovic L, Peris K, Hauschild A, et al. More than 5000 patients with metastatic melanoma in Europe per year do not have access to recommended first-line innovative treatments. Eur J Cancer. 2017;75:313-322.
42. Long GV, Grob JJ, Nathan P, et al. Factors predictive of response, disease progression, and overall survival after dabrafenib and trametinib combination treatment: a pooled analysis of individual patient data from randomised trials. Lancet Oncol. 2016;17:1743-1754.
43. Am J Cancer Res. 2019;9:1396-1414.
Trends in incidence and survival in patients with melanoma, 1974-2013.44. Lyth J, Falk M, Maroti M, et al. Prognostic risk factors of first recurrence in patients with primary stages I–II cutaneous malignant melanoma – from the population‐based Swedish melanoma register. J Eur Acad Dermatol Venereol. 2017;31:1468-1474.
45. Robinson JK, Wayne JD, Martini MC, et al. Early detection of new melanomas by patients with melanoma and their partners using a structured skin self-examination skills training intervention: a randomized clinical trial. JAMA Dermatol. 2016;152:979-985.
JAMA. 2016;316:429-435.
Screening for skin cancer: US Preventive Services Task Force recommendation statement.47. Gardner LJ, Strunck JL, Wu YP, et al. Current controversies in early-stage melanoma: questions on incidence, screening, and histologic regression. J Am Acad Dermatol. 2019;80:1-12.
48. Wei EX, Qureshi AA, Han J, et al. Trends in the diagnosis and clinical features of melanoma in situ (MIS) in US men and women: a prospective, observational study. J Am Acad Dermatol. 2016;75:698-705.
49. Linos E, Swetter SM, Cockburn MG, et al. Increasing burden of melanoma in the United States. J Invest Dermatol. 2009;129:1666-1674.
50. Curchin DJ, Forward E, Dickison P, et al. The acceleration of melanoma in situ: a population-based study of melanoma incidence trends from Victoria, Australia, 1985-2015. J Am Acad Dermatol. 2019;80:1791-1793.
51. Dennis LK. Analysis of the melanoma epidemic, both apparent and real: data from the 1973 through 1994 surveillance, epidemiology, and end results program registry. Arch Dermatol. 1999;135:275-280.
52. Jemal A, Saraiya M, Patel P, et al. Recent trends in cutaneous melanoma incidence and death rates in the United States, 1992-2006. J Am Acad Dermatol. 2011;65:S17-S25.
1. NIH. Cancer stat facts: melanoma of the skin. 2018. Accessed May 13, 2021. https://seer.cancer.gov/statfacts/html/melan.html
2. Watts CG, Dieng M, Morton RL, et al. Clinical practice guidelines for identification, screening and follow-up of individuals at high risk of primary cutaneous melanoma: a systematic review. Br J Dermatol. 2015;172:33-47.
3. Schadendorf D, van Akkooi ACJ, Berking C, et al. Melanoma. Lancet. 2018;392:971-984.
4. Dinnes J, Deeks JJ, Chuchu N, et al. Dermoscopy, with and without visual inspection, for diagnosing melanoma in adults. Cochrane Database Syst Rev. 2018(12):CD011902.
5. Morris JB, Alfonso SV, Hernandez N, et al. Examining the factors associated with past and present dermoscopy use among family physicians. Dermatol Pract Concept. 2017;7:63-70.
6. Henning JS, Dusza SW, Wang SQ, et al. The CASH (color, architecture, symmetry, and homogeneity) algorithm for dermoscopy. J Am Acad Dermatol. 2007;56:45-52.
7. Rosendahl C, Cameron A, McColl I, et al. Dermatoscopy in routine practice — “chaos and clues”. Aust Fam Physician. 2012;41:482-487.
8. Soyer HP, Argenziano G, Zalaudek I, et al. Three-point checklist of dermoscopy: a new screening method for early detection of melanoma. Dermatology. 2004;208:27-31.
9. Argenziano G, Fabbrocini G, Carli P, et al. Epiluminescence microscopy for the diagnosis of doubtful melanocytic skin lesions. Comparison of the ABCD rule of dermatoscopy and a new 7-point checklist based on pattern analysis. Arch Dermatol. 1998;134:1563-1570.
10. Marghoob AA, Usatine RP, Jaimes N. Dermoscopy for the family physician. Am Fam Physician. 2013;88:441-450.
11. Rogers T, Marino ML, Dusza SW, et al. A clinical aid for detecting skin cancer: the Triage Amalgamated Dermoscopic Algorithm (TADA). J Am Board Fam Med. 2016;29:694-701.
12. Argenziano G, Soyer HP, Chimenti S, et al. Dermoscopy of pigmented skin lesions: results of a consensus meeting via the Internet. J Am Acad Dermatol. 2003;48:679-93.
13. Carli P, Quercioli E, Sestini S, et al. Pattern analysis, not simplified algorithms, is the most reliable method for teaching dermoscopy for melanoma diagnosis to residents in dermatology. Br J Dermatol. 2003;148:981-984.
14. Yélamos O, Braun RP, Liopyris K, et al. Usefulness of dermoscopy to improve the clinical and histopathologic diagnosis of skin cancers. J Am Acad Dermatol. 2019;80:365-377.
15. Westerhoff K, McCarthy WH, Menzies SW. Increase in the sensitivity for melanoma diagnosis by primary care physicians using skin surface microscopy. Br J Dermatol. 2000;143:1016-1020.
16. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676.
17. Usatine RP, Shama LK, Marghoob AA, et al. Dermoscopy in family medicine: a primer. J Fam Pract. 2018;67:E1-E11.
18. Swetter SM, Tsao H, Bichakjian CK, et al. Guidelines of care for the management of primary cutaneous melanoma. J Am Acad Dermatol. 2019;80:208-250.
19. Seiverling EV, Ahrns HT, Bacik LC, et al. Biopsies for skin cancer detection: dispelling the myths. J Fam Pract. 2018;67:270-274.
20. Martin RCG, Scoggins CR, Ross MI, et al. Is incisional biopsy of melanoma harmful? Am J Surg. 2005;190:913-917.
21. Mir M, Chan CS, Khan F, et al. The rate of melanoma transection with various biopsy techniques and the influence of tumor transection on patient survival. J Am Acad Dermatol. 2013;68:452-458.
22. Breslow A. Thickness, cross-sectional areas and depth of invasion in the prognosis of cutaneous melanoma. Ann Surg. 1970;172:902-908
23. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma staging: evidence-based changes in the American Joint Committee on Cancer 8th ed cancer staging manual. CA Cancer J Clin. 2017;67:472-492.
24. Morton DL, Thompson JF, Cochran AJ, et al. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. N Engl J Med. 2014;370:599-609.
25. Valsecchi ME, Silbermins D, de Rosa N, et al. Lymphatic mapping and sentinel lymph node biopsy in patients with melanoma: a meta-analysis. J Clin Oncol. 2011;29:1479-1487.
26. Memorial Sloan Kettering Cancer Center. Risk of sentinel lymph node metastasis nomogram. Accessed May 13, 2021. www.mskcc.org/nomograms/melanoma/sentinel_lymph_node_metastasis
27. Gershenwald JE, Scolyer RA, Hess KR, et al. Melanoma of the skin. In: Amin MB, Edge SB, Greene FL, eds. AJCC Cancer Staging Manual. 8th ed. Springer International Publishing; 2017:563-581.
28. Xing Y, Bronstein Y, Ross MI, et al. Contemporary diagnostic imaging modalities for the staging and surveillance of melanoma patients: a meta-analysis. J Natl Cancer Inst. 2011;103:129-142.
29. Tsao H, Feldman M, Fullerton JE, et al. Early detection of asymptomatic pulmonary melanoma metastases by routine chest radiographs is not associated with improved survival. Arch Dermatol. 2004;140:67-70.
30. Wang TS, Johnson TM, Cascade PN, et al. Evaluation of staging chest radiographs and serum lactate dehydrogenase for localized melanoma. J Am Acad Dermatol. 2004;51:399-405.
31. Yancovitz M, Finelt N, Warycha MA, et al. Role of radiologic imaging at the time of initial diagnosis of stage T1b-T3b melanoma. Cancer. 2007; 110:1107-1114.
32. Swetter SM, Thompson JA, Albertini MR, et al. NCCN Guidelines: cutaneous melanoma, version 4.2020. Accessed June 7, 2021. http://medi-guide.meditool.cn/ymtpdf/ACC90A18-6CDF-9443-BF3F-E29394D495E8.pdf
33. Stensheim H, Møller B, van Dijk T, et al. Cause-specific survival for women diagnosed with cancer during pregnancy or lactation: a registry-based cohort study. J Clin Oncol. 2009;27:45-51.
34. Lens MB, Rosdahl I, Ahlbom A, et al. Effect of pregnancy on survival in women with cutaneous malignant melanoma. J Clin Oncol. 2004;22:4369-4375.
35. Gandini S, Iodice S, Koomen E, et al. Hormonal and reproductive factors in relation to melanoma in women: current review and meta-analysis. Eur J Cancer. 2011;47:2607-2617.
36. Byrom L, Olsen CM, Knight L, et al. Does pregnancy after a diagnosis of melanoma affect prognosis? Systematic review and meta-analysis. Dermatol Surg. 2015;41:875-882.
37. Tang JY, Spaunhurst KM, Chlebowski RT, et al. Menopausal hormone therapy and risks of melanoma and nonmelanoma skin cancers: women’s health initiative randomized trials. J Natl Cancer Inst. 2011;103:1469-1475.
38. Carlos G, Anforth R, Clements A, et al. Cutaneous toxic effects of BRAF inhibitors alone and in combination with MEK inhibitors for metastatic melanoma. JAMA Dermatol. 2015;151:1103-1109.
39. Macdonald JB, Macdonald B, Golitz LE, et al. Cutaneous adverse effects of targeted therapies: part I: inhibitors of the cellular membrane. J Am Acad Dermatol. 2015;72:203-218.
40. Welsh SJ, Corrie PG. Management of BRAF and MEK inhibitor toxicities in patients with metastatic melanoma. Ther Adv Med Oncol. 2015;7:122-136.
41. Kandolf Sekulovic L, Peris K, Hauschild A, et al. More than 5000 patients with metastatic melanoma in Europe per year do not have access to recommended first-line innovative treatments. Eur J Cancer. 2017;75:313-322.
42. Long GV, Grob JJ, Nathan P, et al. Factors predictive of response, disease progression, and overall survival after dabrafenib and trametinib combination treatment: a pooled analysis of individual patient data from randomised trials. Lancet Oncol. 2016;17:1743-1754.
43. Am J Cancer Res. 2019;9:1396-1414.
Trends in incidence and survival in patients with melanoma, 1974-2013.44. Lyth J, Falk M, Maroti M, et al. Prognostic risk factors of first recurrence in patients with primary stages I–II cutaneous malignant melanoma – from the population‐based Swedish melanoma register. J Eur Acad Dermatol Venereol. 2017;31:1468-1474.
45. Robinson JK, Wayne JD, Martini MC, et al. Early detection of new melanomas by patients with melanoma and their partners using a structured skin self-examination skills training intervention: a randomized clinical trial. JAMA Dermatol. 2016;152:979-985.
JAMA. 2016;316:429-435.
Screening for skin cancer: US Preventive Services Task Force recommendation statement.47. Gardner LJ, Strunck JL, Wu YP, et al. Current controversies in early-stage melanoma: questions on incidence, screening, and histologic regression. J Am Acad Dermatol. 2019;80:1-12.
48. Wei EX, Qureshi AA, Han J, et al. Trends in the diagnosis and clinical features of melanoma in situ (MIS) in US men and women: a prospective, observational study. J Am Acad Dermatol. 2016;75:698-705.
49. Linos E, Swetter SM, Cockburn MG, et al. Increasing burden of melanoma in the United States. J Invest Dermatol. 2009;129:1666-1674.
50. Curchin DJ, Forward E, Dickison P, et al. The acceleration of melanoma in situ: a population-based study of melanoma incidence trends from Victoria, Australia, 1985-2015. J Am Acad Dermatol. 2019;80:1791-1793.
51. Dennis LK. Analysis of the melanoma epidemic, both apparent and real: data from the 1973 through 1994 surveillance, epidemiology, and end results program registry. Arch Dermatol. 1999;135:275-280.
52. Jemal A, Saraiya M, Patel P, et al. Recent trends in cutaneous melanoma incidence and death rates in the United States, 1992-2006. J Am Acad Dermatol. 2011;65:S17-S25.
PRACTICE RECOMMENDATIONS
› Consider adding dermoscopy to the physical exam to increase sensitivity and specificity in diagnosing melanoma. A
› Perform wide local excision for invasive cutaneous melanoma: 1-cm margin for tumors up to 1 mm thick; 1 to 2 cm for tumors > 1 mm to 2 mm thick; and 2 cm for tumors > 2 mm thick. A
› Do not hesitate to consider, as needed, hormone replacement therapy or hormonal contraception for women with a prior diagnosis of melanoma, as this form of contraception does not confer an increased risk of melanoma. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Prescribe an SGLT2 inhibitor for heart failure in the absence of diabetes?
ILLUSTRATIVE CASE
A 64-year-old overweight White man with a history of hypertension, hyperlipidemia, and HF with an ejection fraction (EF) of 40% presents for primary care follow-up after a recent inpatient admission for worsened HF symptoms. At baseline, he is comfortable at rest but becomes dyspneic upon walking to another room within his home. He is already taking a mineralocorticoid receptor antagonist, a high-intensity statin, a beta-blocker, and an angiotensin-converting enzyme (ACE) inhibitor. What other medication should be considered to minimize his cardiovascular (CV)risk?
An estimated 1% to 2% of the world’s adult population has HF.2 Although the exact prevalence is difficult to quantify due to variations in definitions and diagnostic methods, the American Heart Association (AHA) estimated that 6.2 million Americans had HF between 2013 and 2016.3 Prevalence increases with age, with an annual incidence of approximately 35 per 1000 by age 85.4 Due to the significant morbidity and mortality associated with HF, advancements in treatment are needed.
SGLT2 inhibitors work within the proximal tubule of the kidneys, resulting in increased glucose and sodium excretion with secondary osmotic diuresis and therefore a modest reduction in serum glucose.1,2,5,6 SGLT2 inhibitors are classically prescribed for hyperglycemia treatment in type 2 diabetes. However, preliminary data suggest that this class of medication also positively impacts cardiac function. The diuresis and natriuresis effects of SGLT2 inhibitors appear to optimize cardiac output and subsequent oxygen consumption through a reduction of afterload and preload.1,2,5,6 Further, SGLT2 inhibitors may decrease inflammatory pathways and lead to a secondary reduction of cardiac remodeling via a reduction and modulation of inflammatory pathways. This reduction and modulation may also be associated with a reduction in development, and possibly a reversal, of hypertrophic cardiomyopathy, cardiac fibrosis, and atherosclerosis.5,6 Some of the previously reported adverse effects of SGLT2 inhibitors include urinary tract infection, acute kidney injury, lower extremity amputation, bone fracture, and diabetic ketoacidosis.2
In several studies of patients with type 2 diabetes, SGLT2 inhibitors have shown benefit in reducing CV disease–related death and hospitalization for HF.1,2,5,6 A recent expert consensus from the American College of Cardiology (ACC) states that SGLT2 therapy should be considered for any patient with type 2 diabetes who also has established atherosclerotic CV disease, HF (a clinical syndrome as defined in ACC/AHA guidelines), or diabetic kidney disease, or who is at a high risk for atherosclerotic CV disease (ie, has signs of end-organ damage, such as left ventricular hypertrophy or retinopathy, or multiple risk factors such as advanced age, smoking, hypertension, and family history).7,8
Additionally, a 2019 randomized controlled trial (RCT) by Nassif et al showed that, compared to placebo, dapagliflozin significantly improved both patient-reported HF symptoms and cardiac natriuretic peptide levels over 12 weeks in patients with and without diabetes.9 In September 2020, UpToDate added SGLT2 inhibitors as an option for patients with continued symptoms of HF despite use of appropriate primary agents and mineralocorticoid receptor antagonists, whether or not they have type 2 diabetes; this update was based on 2 studies, 1 of which is reviewed here.10
STUDY SUMMARY
Dapagliflozin demonstrated better CV outcomes than placebo
The Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF) study is an RCT that compared dapagliflozin to placebo among 4744 patients ages 18 years and older who had HF with an EF ≤ 40% and NYHA class II, III, or IV symptoms. The study included patients with (41.8%) and without diabetes. Most patients were male (76.2%-77%), White (70%), and European (44.7%-46.1%).
Patients were randomized to receive either dapagliflozin 10 mg/d or a matching placebo in addition to standard HF therapy (including an ACE inhibitor, angiotensin receptor blocker, or sacubitril-valsartan plus a beta-blocker unless contraindicated; mineralocorticoid antagonist use was encouraged). Follow-up occurred at 14 days, 60 days, 4 months, and then every 4 months, for an average of about 18 months. Patients with diabetes continued to use their glucose-lowering therapies, with dose adjustments, as needed.
Continue to: The primary outcome...
The primary outcome was a composite of worsening HF (hospitalization or urgent visit requiring intravenous HF therapy) or death from a CV cause. Secondary outcomes included a composite of hospitalization for HF or CV death; total number of hospitalizations for HF (including repeat admissions) and CV death; a change in Kansas City Cardiomyopathy Questionnaire symptom score; a composite of worsening renal function including a sustained (≥ 28 d) decline in the estimated glomerular filtration rate (eGFR) of ≥ 50%, end-stage renal disease (defined as sustained eGFR of < 15 mL/min/1.73 m2, sustained dialysis, or renal transplantation), or renal death; and death from any cause.
The primary outcome of worsening HF or death from CV causes occurred in 386 of 2373 patients (16.3%) in the dapagliflozin group and in 502 of 2371 patients (21.2%) in the placebo group (hazard ratio [HR] = 0.74; 95% CI, 0.65-0.85; P < .001). The composite score of hospitalizations for HF plus death from a CV cause was lower in the dapagliflozin group compared to the placebo group (HR = 0.75; 95% CI, 0.65-0.85; P < .001).
A total of 276 patients (11.6%) in the dapagliflozin group and 329 patients (13.9%) in the placebo group died from any cause (HR = 0.83; 95% CI, 0.71-0.97). More patients in the dapagliflozin group than in the placebo group had an improvement in symptom score (58.3% vs 50.9%; odds ratio = 1.15; 95% CI, 1.08-1.23; P < .001). Renal composite outcome did not differ between the 2 treatment groups. Potential adverse effects included volume depletion, renal adverse event, and major hypoglycemia, which occurred at the same rate in the treatment and placebo groups. There was no difference in outcomes or adverse effects between patients with and without diabetes.1
WHAT'S NEW
Evidence supports dapagliflozin use in a new patient population
The DAPA-HF study compared dapagliflozin to placebo in HF patients both with and without diabetes and demonstrated decreased HF exacerbations and CV deaths, improved patient-reported HF symptoms, and lower all-cause mortality in the treatment group. This study supports use of dapagliflozin in a new patient population—those with HF—rather than solely in patients with diabetes, as the drug was originally marketed.
CAVEATS
Specific study population may limit generalizability
The DAPA-HF study included mostly male, White, European patients followed for an average of 18.2 months as part of initial Phase III studies funded by AstraZeneca (the pharmaceutical company that developed dapagliflozin). Given the potential conflict due to funding, all statistical results were verified by an independent academic group, and analyses were completed with an intention-to-treat model. The outlined benefits described here were only studied in a population of patients with reduced EF (≤ 40%), so the impact remains unclear for patients with preserved EF. Safety and benefits beyond 24 months were not studied in this RCT; therefore long-term data are still unknown.
Continue to: CHALLENGES TO IMPLEMENTATION
CHALLENGES TO IMPLEMENTATION
Adding an SGLT2 inhibitor may be cost prohibitive for some patients
An SGLT2 inhibitor costs, on average, $500 to $600 for a 30-day supply, which may be prohibitive for some patients.11 Integration of SGLT2 inhibitors into a patient’s medication regimen may require dose adjustments of other medications, particularly glucose-lowering therapies, and the optimal prioritization of medications is not yet known.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381:1995-2008. doi: 10.1056/NEJMoa1911303
2. Lytvyn Y, Bjornstad P, Udell JA, et al. Sodium glucose cotransporter-2 inhibition in heart failure: potential mechanisms, clinical applications, and summary of clinical trials. Circulation. 2017;136:1643-1658. doi: 10.1161/CIRCULATIONAHA.117.030012
3. Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141:e139-e596. doi: 10.1161/CIR.0000000000000757
4. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002;106:3068-3072. doi: 10.1161/01.cir.0000039105.49749.6f
5. Ghosh RK, Ghosh GC, Gupta M, et al. Sodium glucose co-transporter 2 inhibitors and heart failure. Am J Cardiol. 2019;124:1790-1796. doi: 10.1016/j.amjcard.2019.08.038
6. Verma S, McMurray JJV. SGLT2 inhibitors and mechanisms of cardiovascular benefit: a state-of-the-art review. Diabetologia. 2018;61:2108-2117. doi: 10.1007/s00125-018-4670-7
7. Das SR, Everett BM, Birtcher KK, et al. 2020 expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients with type 2 diabetes: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2020;76:1117-1145. doi: 10.1016/j.jacc.2020.05.037
8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240-e327. doi: 10.1161/CIR.0b013e31829e8776
9. Nassif ME, Windsor SL, Tang F, et al. Dapagliflozin effects on biomarkers, symptoms, and functional status in patients with heart failure with reduced ejection fraction: The DEFINE-HF Trial. Circulation. 2019;140:1463-1476. doi: 10.1161/CIRCULATIONAHA.119.042929
10. Colucci WS. Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults. UpToDate. Published October 9, 2020. Accessed June 23, 2021. www.uptodate.com/contents/secondary-pharmacologic-therapy-in-heart-failure-with-reduced-ejection-fraction-hfref-in-adults
11. Dapagliflozin. GoodRx. Accessed June 23, 2021. www.goodrx.com/dapagliflozin
ILLUSTRATIVE CASE
A 64-year-old overweight White man with a history of hypertension, hyperlipidemia, and HF with an ejection fraction (EF) of 40% presents for primary care follow-up after a recent inpatient admission for worsened HF symptoms. At baseline, he is comfortable at rest but becomes dyspneic upon walking to another room within his home. He is already taking a mineralocorticoid receptor antagonist, a high-intensity statin, a beta-blocker, and an angiotensin-converting enzyme (ACE) inhibitor. What other medication should be considered to minimize his cardiovascular (CV)risk?
An estimated 1% to 2% of the world’s adult population has HF.2 Although the exact prevalence is difficult to quantify due to variations in definitions and diagnostic methods, the American Heart Association (AHA) estimated that 6.2 million Americans had HF between 2013 and 2016.3 Prevalence increases with age, with an annual incidence of approximately 35 per 1000 by age 85.4 Due to the significant morbidity and mortality associated with HF, advancements in treatment are needed.
SGLT2 inhibitors work within the proximal tubule of the kidneys, resulting in increased glucose and sodium excretion with secondary osmotic diuresis and therefore a modest reduction in serum glucose.1,2,5,6 SGLT2 inhibitors are classically prescribed for hyperglycemia treatment in type 2 diabetes. However, preliminary data suggest that this class of medication also positively impacts cardiac function. The diuresis and natriuresis effects of SGLT2 inhibitors appear to optimize cardiac output and subsequent oxygen consumption through a reduction of afterload and preload.1,2,5,6 Further, SGLT2 inhibitors may decrease inflammatory pathways and lead to a secondary reduction of cardiac remodeling via a reduction and modulation of inflammatory pathways. This reduction and modulation may also be associated with a reduction in development, and possibly a reversal, of hypertrophic cardiomyopathy, cardiac fibrosis, and atherosclerosis.5,6 Some of the previously reported adverse effects of SGLT2 inhibitors include urinary tract infection, acute kidney injury, lower extremity amputation, bone fracture, and diabetic ketoacidosis.2
In several studies of patients with type 2 diabetes, SGLT2 inhibitors have shown benefit in reducing CV disease–related death and hospitalization for HF.1,2,5,6 A recent expert consensus from the American College of Cardiology (ACC) states that SGLT2 therapy should be considered for any patient with type 2 diabetes who also has established atherosclerotic CV disease, HF (a clinical syndrome as defined in ACC/AHA guidelines), or diabetic kidney disease, or who is at a high risk for atherosclerotic CV disease (ie, has signs of end-organ damage, such as left ventricular hypertrophy or retinopathy, or multiple risk factors such as advanced age, smoking, hypertension, and family history).7,8
Additionally, a 2019 randomized controlled trial (RCT) by Nassif et al showed that, compared to placebo, dapagliflozin significantly improved both patient-reported HF symptoms and cardiac natriuretic peptide levels over 12 weeks in patients with and without diabetes.9 In September 2020, UpToDate added SGLT2 inhibitors as an option for patients with continued symptoms of HF despite use of appropriate primary agents and mineralocorticoid receptor antagonists, whether or not they have type 2 diabetes; this update was based on 2 studies, 1 of which is reviewed here.10
STUDY SUMMARY
Dapagliflozin demonstrated better CV outcomes than placebo
The Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF) study is an RCT that compared dapagliflozin to placebo among 4744 patients ages 18 years and older who had HF with an EF ≤ 40% and NYHA class II, III, or IV symptoms. The study included patients with (41.8%) and without diabetes. Most patients were male (76.2%-77%), White (70%), and European (44.7%-46.1%).
Patients were randomized to receive either dapagliflozin 10 mg/d or a matching placebo in addition to standard HF therapy (including an ACE inhibitor, angiotensin receptor blocker, or sacubitril-valsartan plus a beta-blocker unless contraindicated; mineralocorticoid antagonist use was encouraged). Follow-up occurred at 14 days, 60 days, 4 months, and then every 4 months, for an average of about 18 months. Patients with diabetes continued to use their glucose-lowering therapies, with dose adjustments, as needed.
Continue to: The primary outcome...
The primary outcome was a composite of worsening HF (hospitalization or urgent visit requiring intravenous HF therapy) or death from a CV cause. Secondary outcomes included a composite of hospitalization for HF or CV death; total number of hospitalizations for HF (including repeat admissions) and CV death; a change in Kansas City Cardiomyopathy Questionnaire symptom score; a composite of worsening renal function including a sustained (≥ 28 d) decline in the estimated glomerular filtration rate (eGFR) of ≥ 50%, end-stage renal disease (defined as sustained eGFR of < 15 mL/min/1.73 m2, sustained dialysis, or renal transplantation), or renal death; and death from any cause.
The primary outcome of worsening HF or death from CV causes occurred in 386 of 2373 patients (16.3%) in the dapagliflozin group and in 502 of 2371 patients (21.2%) in the placebo group (hazard ratio [HR] = 0.74; 95% CI, 0.65-0.85; P < .001). The composite score of hospitalizations for HF plus death from a CV cause was lower in the dapagliflozin group compared to the placebo group (HR = 0.75; 95% CI, 0.65-0.85; P < .001).
A total of 276 patients (11.6%) in the dapagliflozin group and 329 patients (13.9%) in the placebo group died from any cause (HR = 0.83; 95% CI, 0.71-0.97). More patients in the dapagliflozin group than in the placebo group had an improvement in symptom score (58.3% vs 50.9%; odds ratio = 1.15; 95% CI, 1.08-1.23; P < .001). Renal composite outcome did not differ between the 2 treatment groups. Potential adverse effects included volume depletion, renal adverse event, and major hypoglycemia, which occurred at the same rate in the treatment and placebo groups. There was no difference in outcomes or adverse effects between patients with and without diabetes.1
WHAT'S NEW
Evidence supports dapagliflozin use in a new patient population
The DAPA-HF study compared dapagliflozin to placebo in HF patients both with and without diabetes and demonstrated decreased HF exacerbations and CV deaths, improved patient-reported HF symptoms, and lower all-cause mortality in the treatment group. This study supports use of dapagliflozin in a new patient population—those with HF—rather than solely in patients with diabetes, as the drug was originally marketed.
CAVEATS
Specific study population may limit generalizability
The DAPA-HF study included mostly male, White, European patients followed for an average of 18.2 months as part of initial Phase III studies funded by AstraZeneca (the pharmaceutical company that developed dapagliflozin). Given the potential conflict due to funding, all statistical results were verified by an independent academic group, and analyses were completed with an intention-to-treat model. The outlined benefits described here were only studied in a population of patients with reduced EF (≤ 40%), so the impact remains unclear for patients with preserved EF. Safety and benefits beyond 24 months were not studied in this RCT; therefore long-term data are still unknown.
Continue to: CHALLENGES TO IMPLEMENTATION
CHALLENGES TO IMPLEMENTATION
Adding an SGLT2 inhibitor may be cost prohibitive for some patients
An SGLT2 inhibitor costs, on average, $500 to $600 for a 30-day supply, which may be prohibitive for some patients.11 Integration of SGLT2 inhibitors into a patient’s medication regimen may require dose adjustments of other medications, particularly glucose-lowering therapies, and the optimal prioritization of medications is not yet known.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
ILLUSTRATIVE CASE
A 64-year-old overweight White man with a history of hypertension, hyperlipidemia, and HF with an ejection fraction (EF) of 40% presents for primary care follow-up after a recent inpatient admission for worsened HF symptoms. At baseline, he is comfortable at rest but becomes dyspneic upon walking to another room within his home. He is already taking a mineralocorticoid receptor antagonist, a high-intensity statin, a beta-blocker, and an angiotensin-converting enzyme (ACE) inhibitor. What other medication should be considered to minimize his cardiovascular (CV)risk?
An estimated 1% to 2% of the world’s adult population has HF.2 Although the exact prevalence is difficult to quantify due to variations in definitions and diagnostic methods, the American Heart Association (AHA) estimated that 6.2 million Americans had HF between 2013 and 2016.3 Prevalence increases with age, with an annual incidence of approximately 35 per 1000 by age 85.4 Due to the significant morbidity and mortality associated with HF, advancements in treatment are needed.
SGLT2 inhibitors work within the proximal tubule of the kidneys, resulting in increased glucose and sodium excretion with secondary osmotic diuresis and therefore a modest reduction in serum glucose.1,2,5,6 SGLT2 inhibitors are classically prescribed for hyperglycemia treatment in type 2 diabetes. However, preliminary data suggest that this class of medication also positively impacts cardiac function. The diuresis and natriuresis effects of SGLT2 inhibitors appear to optimize cardiac output and subsequent oxygen consumption through a reduction of afterload and preload.1,2,5,6 Further, SGLT2 inhibitors may decrease inflammatory pathways and lead to a secondary reduction of cardiac remodeling via a reduction and modulation of inflammatory pathways. This reduction and modulation may also be associated with a reduction in development, and possibly a reversal, of hypertrophic cardiomyopathy, cardiac fibrosis, and atherosclerosis.5,6 Some of the previously reported adverse effects of SGLT2 inhibitors include urinary tract infection, acute kidney injury, lower extremity amputation, bone fracture, and diabetic ketoacidosis.2
In several studies of patients with type 2 diabetes, SGLT2 inhibitors have shown benefit in reducing CV disease–related death and hospitalization for HF.1,2,5,6 A recent expert consensus from the American College of Cardiology (ACC) states that SGLT2 therapy should be considered for any patient with type 2 diabetes who also has established atherosclerotic CV disease, HF (a clinical syndrome as defined in ACC/AHA guidelines), or diabetic kidney disease, or who is at a high risk for atherosclerotic CV disease (ie, has signs of end-organ damage, such as left ventricular hypertrophy or retinopathy, or multiple risk factors such as advanced age, smoking, hypertension, and family history).7,8
Additionally, a 2019 randomized controlled trial (RCT) by Nassif et al showed that, compared to placebo, dapagliflozin significantly improved both patient-reported HF symptoms and cardiac natriuretic peptide levels over 12 weeks in patients with and without diabetes.9 In September 2020, UpToDate added SGLT2 inhibitors as an option for patients with continued symptoms of HF despite use of appropriate primary agents and mineralocorticoid receptor antagonists, whether or not they have type 2 diabetes; this update was based on 2 studies, 1 of which is reviewed here.10
STUDY SUMMARY
Dapagliflozin demonstrated better CV outcomes than placebo
The Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure (DAPA-HF) study is an RCT that compared dapagliflozin to placebo among 4744 patients ages 18 years and older who had HF with an EF ≤ 40% and NYHA class II, III, or IV symptoms. The study included patients with (41.8%) and without diabetes. Most patients were male (76.2%-77%), White (70%), and European (44.7%-46.1%).
Patients were randomized to receive either dapagliflozin 10 mg/d or a matching placebo in addition to standard HF therapy (including an ACE inhibitor, angiotensin receptor blocker, or sacubitril-valsartan plus a beta-blocker unless contraindicated; mineralocorticoid antagonist use was encouraged). Follow-up occurred at 14 days, 60 days, 4 months, and then every 4 months, for an average of about 18 months. Patients with diabetes continued to use their glucose-lowering therapies, with dose adjustments, as needed.
Continue to: The primary outcome...
The primary outcome was a composite of worsening HF (hospitalization or urgent visit requiring intravenous HF therapy) or death from a CV cause. Secondary outcomes included a composite of hospitalization for HF or CV death; total number of hospitalizations for HF (including repeat admissions) and CV death; a change in Kansas City Cardiomyopathy Questionnaire symptom score; a composite of worsening renal function including a sustained (≥ 28 d) decline in the estimated glomerular filtration rate (eGFR) of ≥ 50%, end-stage renal disease (defined as sustained eGFR of < 15 mL/min/1.73 m2, sustained dialysis, or renal transplantation), or renal death; and death from any cause.
The primary outcome of worsening HF or death from CV causes occurred in 386 of 2373 patients (16.3%) in the dapagliflozin group and in 502 of 2371 patients (21.2%) in the placebo group (hazard ratio [HR] = 0.74; 95% CI, 0.65-0.85; P < .001). The composite score of hospitalizations for HF plus death from a CV cause was lower in the dapagliflozin group compared to the placebo group (HR = 0.75; 95% CI, 0.65-0.85; P < .001).
A total of 276 patients (11.6%) in the dapagliflozin group and 329 patients (13.9%) in the placebo group died from any cause (HR = 0.83; 95% CI, 0.71-0.97). More patients in the dapagliflozin group than in the placebo group had an improvement in symptom score (58.3% vs 50.9%; odds ratio = 1.15; 95% CI, 1.08-1.23; P < .001). Renal composite outcome did not differ between the 2 treatment groups. Potential adverse effects included volume depletion, renal adverse event, and major hypoglycemia, which occurred at the same rate in the treatment and placebo groups. There was no difference in outcomes or adverse effects between patients with and without diabetes.1
WHAT'S NEW
Evidence supports dapagliflozin use in a new patient population
The DAPA-HF study compared dapagliflozin to placebo in HF patients both with and without diabetes and demonstrated decreased HF exacerbations and CV deaths, improved patient-reported HF symptoms, and lower all-cause mortality in the treatment group. This study supports use of dapagliflozin in a new patient population—those with HF—rather than solely in patients with diabetes, as the drug was originally marketed.
CAVEATS
Specific study population may limit generalizability
The DAPA-HF study included mostly male, White, European patients followed for an average of 18.2 months as part of initial Phase III studies funded by AstraZeneca (the pharmaceutical company that developed dapagliflozin). Given the potential conflict due to funding, all statistical results were verified by an independent academic group, and analyses were completed with an intention-to-treat model. The outlined benefits described here were only studied in a population of patients with reduced EF (≤ 40%), so the impact remains unclear for patients with preserved EF. Safety and benefits beyond 24 months were not studied in this RCT; therefore long-term data are still unknown.
Continue to: CHALLENGES TO IMPLEMENTATION
CHALLENGES TO IMPLEMENTATION
Adding an SGLT2 inhibitor may be cost prohibitive for some patients
An SGLT2 inhibitor costs, on average, $500 to $600 for a 30-day supply, which may be prohibitive for some patients.11 Integration of SGLT2 inhibitors into a patient’s medication regimen may require dose adjustments of other medications, particularly glucose-lowering therapies, and the optimal prioritization of medications is not yet known.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.
1. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381:1995-2008. doi: 10.1056/NEJMoa1911303
2. Lytvyn Y, Bjornstad P, Udell JA, et al. Sodium glucose cotransporter-2 inhibition in heart failure: potential mechanisms, clinical applications, and summary of clinical trials. Circulation. 2017;136:1643-1658. doi: 10.1161/CIRCULATIONAHA.117.030012
3. Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141:e139-e596. doi: 10.1161/CIR.0000000000000757
4. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002;106:3068-3072. doi: 10.1161/01.cir.0000039105.49749.6f
5. Ghosh RK, Ghosh GC, Gupta M, et al. Sodium glucose co-transporter 2 inhibitors and heart failure. Am J Cardiol. 2019;124:1790-1796. doi: 10.1016/j.amjcard.2019.08.038
6. Verma S, McMurray JJV. SGLT2 inhibitors and mechanisms of cardiovascular benefit: a state-of-the-art review. Diabetologia. 2018;61:2108-2117. doi: 10.1007/s00125-018-4670-7
7. Das SR, Everett BM, Birtcher KK, et al. 2020 expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients with type 2 diabetes: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2020;76:1117-1145. doi: 10.1016/j.jacc.2020.05.037
8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240-e327. doi: 10.1161/CIR.0b013e31829e8776
9. Nassif ME, Windsor SL, Tang F, et al. Dapagliflozin effects on biomarkers, symptoms, and functional status in patients with heart failure with reduced ejection fraction: The DEFINE-HF Trial. Circulation. 2019;140:1463-1476. doi: 10.1161/CIRCULATIONAHA.119.042929
10. Colucci WS. Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults. UpToDate. Published October 9, 2020. Accessed June 23, 2021. www.uptodate.com/contents/secondary-pharmacologic-therapy-in-heart-failure-with-reduced-ejection-fraction-hfref-in-adults
11. Dapagliflozin. GoodRx. Accessed June 23, 2021. www.goodrx.com/dapagliflozin
1. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381:1995-2008. doi: 10.1056/NEJMoa1911303
2. Lytvyn Y, Bjornstad P, Udell JA, et al. Sodium glucose cotransporter-2 inhibition in heart failure: potential mechanisms, clinical applications, and summary of clinical trials. Circulation. 2017;136:1643-1658. doi: 10.1161/CIRCULATIONAHA.117.030012
3. Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141:e139-e596. doi: 10.1161/CIR.0000000000000757
4. Lloyd-Jones DM, Larson MG, Leip EP, et al. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002;106:3068-3072. doi: 10.1161/01.cir.0000039105.49749.6f
5. Ghosh RK, Ghosh GC, Gupta M, et al. Sodium glucose co-transporter 2 inhibitors and heart failure. Am J Cardiol. 2019;124:1790-1796. doi: 10.1016/j.amjcard.2019.08.038
6. Verma S, McMurray JJV. SGLT2 inhibitors and mechanisms of cardiovascular benefit: a state-of-the-art review. Diabetologia. 2018;61:2108-2117. doi: 10.1007/s00125-018-4670-7
7. Das SR, Everett BM, Birtcher KK, et al. 2020 expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients with type 2 diabetes: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2020;76:1117-1145. doi: 10.1016/j.jacc.2020.05.037
8. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240-e327. doi: 10.1161/CIR.0b013e31829e8776
9. Nassif ME, Windsor SL, Tang F, et al. Dapagliflozin effects on biomarkers, symptoms, and functional status in patients with heart failure with reduced ejection fraction: The DEFINE-HF Trial. Circulation. 2019;140:1463-1476. doi: 10.1161/CIRCULATIONAHA.119.042929
10. Colucci WS. Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults. UpToDate. Published October 9, 2020. Accessed June 23, 2021. www.uptodate.com/contents/secondary-pharmacologic-therapy-in-heart-failure-with-reduced-ejection-fraction-hfref-in-adults
11. Dapagliflozin. GoodRx. Accessed June 23, 2021. www.goodrx.com/dapagliflozin
PRACTICE CHANGER
Prescribe dapagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, 10 mg/d in addition to standard therapies for adult patients with heart failure (HF) with a reduced ejection fraction (≤ 40%) and New York Heart Association (NYHA) class II or greater, regardless of type 2 diabetes history, due to improved heart failure and cardiovascular outcomes.1
STRENGTH OF RECOMMENDATION
B: Based on a single randomized controlled trial.1
McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381:1995‐2008.