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The Journal of Family Practice is a peer-reviewed and indexed journal that provides its 95,000 family physician readers with timely, practical, and evidence-based information that they can immediately put into practice. Research and applied evidence articles, plus patient-oriented departments like Practice Alert, PURLs, and Clinical Inquiries can be found in print and at jfponline.com. The Web site, which logs an average of 125,000 visitors every month, also offers audiocasts by physician specialists and interactive features like Instant Polls and Photo Rounds Friday—a weekly diagnostic puzzle.
gambling
compulsive behaviors
ammunition
assault rifle
black jack
Boko Haram
bondage
child abuse
cocaine
Daech
drug paraphernalia
explosion
gun
human trafficking
ISIL
ISIS
Islamic caliphate
Islamic state
mixed martial arts
MMA
molestation
national rifle association
NRA
nsfw
pedophile
pedophilia
poker
porn
pornography
psychedelic drug
recreational drug
sex slave rings
slot machine
terrorism
terrorist
Texas hold 'em
UFC
substance abuse
abuseed
abuseer
abusees
abuseing
abusely
abuses
aeolus
aeolused
aeoluser
aeoluses
aeolusing
aeolusly
aeoluss
ahole
aholeed
aholeer
aholees
aholeing
aholely
aholes
alcohol
alcoholed
alcoholer
alcoholes
alcoholing
alcoholly
alcohols
allman
allmaned
allmaner
allmanes
allmaning
allmanly
allmans
alted
altes
alting
altly
alts
analed
analer
anales
analing
anally
analprobe
analprobeed
analprobeer
analprobees
analprobeing
analprobely
analprobes
anals
anilingus
anilingused
anilinguser
anilinguses
anilingusing
anilingusly
anilinguss
anus
anused
anuser
anuses
anusing
anusly
anuss
areola
areolaed
areolaer
areolaes
areolaing
areolaly
areolas
areole
areoleed
areoleer
areolees
areoleing
areolely
areoles
arian
arianed
arianer
arianes
arianing
arianly
arians
aryan
aryaned
aryaner
aryanes
aryaning
aryanly
aryans
asiaed
asiaer
asiaes
asiaing
asialy
asias
ass
ass hole
ass lick
ass licked
ass licker
ass lickes
ass licking
ass lickly
ass licks
assbang
assbanged
assbangeded
assbangeder
assbangedes
assbangeding
assbangedly
assbangeds
assbanger
assbanges
assbanging
assbangly
assbangs
assbangsed
assbangser
assbangses
assbangsing
assbangsly
assbangss
assed
asser
asses
assesed
asseser
asseses
assesing
assesly
assess
assfuck
assfucked
assfucker
assfuckered
assfuckerer
assfuckeres
assfuckering
assfuckerly
assfuckers
assfuckes
assfucking
assfuckly
assfucks
asshat
asshated
asshater
asshates
asshating
asshatly
asshats
assholeed
assholeer
assholees
assholeing
assholely
assholes
assholesed
assholeser
assholeses
assholesing
assholesly
assholess
assing
assly
assmaster
assmastered
assmasterer
assmasteres
assmastering
assmasterly
assmasters
assmunch
assmunched
assmuncher
assmunches
assmunching
assmunchly
assmunchs
asss
asswipe
asswipeed
asswipeer
asswipees
asswipeing
asswipely
asswipes
asswipesed
asswipeser
asswipeses
asswipesing
asswipesly
asswipess
azz
azzed
azzer
azzes
azzing
azzly
azzs
babeed
babeer
babees
babeing
babely
babes
babesed
babeser
babeses
babesing
babesly
babess
ballsac
ballsaced
ballsacer
ballsaces
ballsacing
ballsack
ballsacked
ballsacker
ballsackes
ballsacking
ballsackly
ballsacks
ballsacly
ballsacs
ballsed
ballser
ballses
ballsing
ballsly
ballss
barf
barfed
barfer
barfes
barfing
barfly
barfs
bastard
bastarded
bastarder
bastardes
bastarding
bastardly
bastards
bastardsed
bastardser
bastardses
bastardsing
bastardsly
bastardss
bawdy
bawdyed
bawdyer
bawdyes
bawdying
bawdyly
bawdys
beaner
beanered
beanerer
beaneres
beanering
beanerly
beaners
beardedclam
beardedclamed
beardedclamer
beardedclames
beardedclaming
beardedclamly
beardedclams
beastiality
beastialityed
beastialityer
beastialityes
beastialitying
beastialityly
beastialitys
beatch
beatched
beatcher
beatches
beatching
beatchly
beatchs
beater
beatered
beaterer
beateres
beatering
beaterly
beaters
beered
beerer
beeres
beering
beerly
beeyotch
beeyotched
beeyotcher
beeyotches
beeyotching
beeyotchly
beeyotchs
beotch
beotched
beotcher
beotches
beotching
beotchly
beotchs
biatch
biatched
biatcher
biatches
biatching
biatchly
biatchs
big tits
big titsed
big titser
big titses
big titsing
big titsly
big titss
bigtits
bigtitsed
bigtitser
bigtitses
bigtitsing
bigtitsly
bigtitss
bimbo
bimboed
bimboer
bimboes
bimboing
bimboly
bimbos
bisexualed
bisexualer
bisexuales
bisexualing
bisexually
bisexuals
bitch
bitched
bitcheded
bitcheder
bitchedes
bitcheding
bitchedly
bitcheds
bitcher
bitches
bitchesed
bitcheser
bitcheses
bitchesing
bitchesly
bitchess
bitching
bitchly
bitchs
bitchy
bitchyed
bitchyer
bitchyes
bitchying
bitchyly
bitchys
bleached
bleacher
bleaches
bleaching
bleachly
bleachs
blow job
blow jobed
blow jober
blow jobes
blow jobing
blow jobly
blow jobs
blowed
blower
blowes
blowing
blowjob
blowjobed
blowjober
blowjobes
blowjobing
blowjobly
blowjobs
blowjobsed
blowjobser
blowjobses
blowjobsing
blowjobsly
blowjobss
blowly
blows
boink
boinked
boinker
boinkes
boinking
boinkly
boinks
bollock
bollocked
bollocker
bollockes
bollocking
bollockly
bollocks
bollocksed
bollockser
bollockses
bollocksing
bollocksly
bollockss
bollok
bolloked
bolloker
bollokes
bolloking
bollokly
bolloks
boner
bonered
bonerer
boneres
bonering
bonerly
boners
bonersed
bonerser
bonerses
bonersing
bonersly
bonerss
bong
bonged
bonger
bonges
bonging
bongly
bongs
boob
boobed
boober
boobes
boobies
boobiesed
boobieser
boobieses
boobiesing
boobiesly
boobiess
boobing
boobly
boobs
boobsed
boobser
boobses
boobsing
boobsly
boobss
booby
boobyed
boobyer
boobyes
boobying
boobyly
boobys
booger
boogered
boogerer
boogeres
boogering
boogerly
boogers
bookie
bookieed
bookieer
bookiees
bookieing
bookiely
bookies
bootee
booteeed
booteeer
booteees
booteeing
booteely
bootees
bootie
bootieed
bootieer
bootiees
bootieing
bootiely
booties
booty
bootyed
bootyer
bootyes
bootying
bootyly
bootys
boozeed
boozeer
boozees
boozeing
boozely
boozer
boozered
boozerer
boozeres
boozering
boozerly
boozers
boozes
boozy
boozyed
boozyer
boozyes
boozying
boozyly
boozys
bosomed
bosomer
bosomes
bosoming
bosomly
bosoms
bosomy
bosomyed
bosomyer
bosomyes
bosomying
bosomyly
bosomys
bugger
buggered
buggerer
buggeres
buggering
buggerly
buggers
bukkake
bukkakeed
bukkakeer
bukkakees
bukkakeing
bukkakely
bukkakes
bull shit
bull shited
bull shiter
bull shites
bull shiting
bull shitly
bull shits
bullshit
bullshited
bullshiter
bullshites
bullshiting
bullshitly
bullshits
bullshitsed
bullshitser
bullshitses
bullshitsing
bullshitsly
bullshitss
bullshitted
bullshitteded
bullshitteder
bullshittedes
bullshitteding
bullshittedly
bullshitteds
bullturds
bullturdsed
bullturdser
bullturdses
bullturdsing
bullturdsly
bullturdss
bung
bunged
bunger
bunges
bunging
bungly
bungs
busty
bustyed
bustyer
bustyes
bustying
bustyly
bustys
butt
butt fuck
butt fucked
butt fucker
butt fuckes
butt fucking
butt fuckly
butt fucks
butted
buttes
buttfuck
buttfucked
buttfucker
buttfuckered
buttfuckerer
buttfuckeres
buttfuckering
buttfuckerly
buttfuckers
buttfuckes
buttfucking
buttfuckly
buttfucks
butting
buttly
buttplug
buttpluged
buttpluger
buttpluges
buttpluging
buttplugly
buttplugs
butts
caca
cacaed
cacaer
cacaes
cacaing
cacaly
cacas
cahone
cahoneed
cahoneer
cahonees
cahoneing
cahonely
cahones
cameltoe
cameltoeed
cameltoeer
cameltoees
cameltoeing
cameltoely
cameltoes
carpetmuncher
carpetmunchered
carpetmuncherer
carpetmuncheres
carpetmunchering
carpetmuncherly
carpetmunchers
cawk
cawked
cawker
cawkes
cawking
cawkly
cawks
chinc
chinced
chincer
chinces
chincing
chincly
chincs
chincsed
chincser
chincses
chincsing
chincsly
chincss
chink
chinked
chinker
chinkes
chinking
chinkly
chinks
chode
chodeed
chodeer
chodees
chodeing
chodely
chodes
chodesed
chodeser
chodeses
chodesing
chodesly
chodess
clit
clited
cliter
clites
cliting
clitly
clitoris
clitorised
clitoriser
clitorises
clitorising
clitorisly
clitoriss
clitorus
clitorused
clitoruser
clitoruses
clitorusing
clitorusly
clitoruss
clits
clitsed
clitser
clitses
clitsing
clitsly
clitss
clitty
clittyed
clittyer
clittyes
clittying
clittyly
clittys
cocain
cocaine
cocained
cocaineed
cocaineer
cocainees
cocaineing
cocainely
cocainer
cocaines
cocaining
cocainly
cocains
cock
cock sucker
cock suckered
cock suckerer
cock suckeres
cock suckering
cock suckerly
cock suckers
cockblock
cockblocked
cockblocker
cockblockes
cockblocking
cockblockly
cockblocks
cocked
cocker
cockes
cockholster
cockholstered
cockholsterer
cockholsteres
cockholstering
cockholsterly
cockholsters
cocking
cockknocker
cockknockered
cockknockerer
cockknockeres
cockknockering
cockknockerly
cockknockers
cockly
cocks
cocksed
cockser
cockses
cocksing
cocksly
cocksmoker
cocksmokered
cocksmokerer
cocksmokeres
cocksmokering
cocksmokerly
cocksmokers
cockss
cocksucker
cocksuckered
cocksuckerer
cocksuckeres
cocksuckering
cocksuckerly
cocksuckers
coital
coitaled
coitaler
coitales
coitaling
coitally
coitals
commie
commieed
commieer
commiees
commieing
commiely
commies
condomed
condomer
condomes
condoming
condomly
condoms
coon
cooned
cooner
coones
cooning
coonly
coons
coonsed
coonser
coonses
coonsing
coonsly
coonss
corksucker
corksuckered
corksuckerer
corksuckeres
corksuckering
corksuckerly
corksuckers
cracked
crackwhore
crackwhoreed
crackwhoreer
crackwhorees
crackwhoreing
crackwhorely
crackwhores
crap
craped
craper
crapes
craping
craply
crappy
crappyed
crappyer
crappyes
crappying
crappyly
crappys
cum
cumed
cumer
cumes
cuming
cumly
cummin
cummined
cumminer
cummines
cumming
cumminged
cumminger
cumminges
cumminging
cummingly
cummings
cummining
cumminly
cummins
cums
cumshot
cumshoted
cumshoter
cumshotes
cumshoting
cumshotly
cumshots
cumshotsed
cumshotser
cumshotses
cumshotsing
cumshotsly
cumshotss
cumslut
cumsluted
cumsluter
cumslutes
cumsluting
cumslutly
cumsluts
cumstain
cumstained
cumstainer
cumstaines
cumstaining
cumstainly
cumstains
cunilingus
cunilingused
cunilinguser
cunilinguses
cunilingusing
cunilingusly
cunilinguss
cunnilingus
cunnilingused
cunnilinguser
cunnilinguses
cunnilingusing
cunnilingusly
cunnilinguss
cunny
cunnyed
cunnyer
cunnyes
cunnying
cunnyly
cunnys
cunt
cunted
cunter
cuntes
cuntface
cuntfaceed
cuntfaceer
cuntfacees
cuntfaceing
cuntfacely
cuntfaces
cunthunter
cunthuntered
cunthunterer
cunthunteres
cunthuntering
cunthunterly
cunthunters
cunting
cuntlick
cuntlicked
cuntlicker
cuntlickered
cuntlickerer
cuntlickeres
cuntlickering
cuntlickerly
cuntlickers
cuntlickes
cuntlicking
cuntlickly
cuntlicks
cuntly
cunts
cuntsed
cuntser
cuntses
cuntsing
cuntsly
cuntss
dago
dagoed
dagoer
dagoes
dagoing
dagoly
dagos
dagosed
dagoser
dagoses
dagosing
dagosly
dagoss
dammit
dammited
dammiter
dammites
dammiting
dammitly
dammits
damn
damned
damneded
damneder
damnedes
damneding
damnedly
damneds
damner
damnes
damning
damnit
damnited
damniter
damnites
damniting
damnitly
damnits
damnly
damns
dick
dickbag
dickbaged
dickbager
dickbages
dickbaging
dickbagly
dickbags
dickdipper
dickdippered
dickdipperer
dickdipperes
dickdippering
dickdipperly
dickdippers
dicked
dicker
dickes
dickface
dickfaceed
dickfaceer
dickfacees
dickfaceing
dickfacely
dickfaces
dickflipper
dickflippered
dickflipperer
dickflipperes
dickflippering
dickflipperly
dickflippers
dickhead
dickheaded
dickheader
dickheades
dickheading
dickheadly
dickheads
dickheadsed
dickheadser
dickheadses
dickheadsing
dickheadsly
dickheadss
dicking
dickish
dickished
dickisher
dickishes
dickishing
dickishly
dickishs
dickly
dickripper
dickrippered
dickripperer
dickripperes
dickrippering
dickripperly
dickrippers
dicks
dicksipper
dicksippered
dicksipperer
dicksipperes
dicksippering
dicksipperly
dicksippers
dickweed
dickweeded
dickweeder
dickweedes
dickweeding
dickweedly
dickweeds
dickwhipper
dickwhippered
dickwhipperer
dickwhipperes
dickwhippering
dickwhipperly
dickwhippers
dickzipper
dickzippered
dickzipperer
dickzipperes
dickzippering
dickzipperly
dickzippers
diddle
diddleed
diddleer
diddlees
diddleing
diddlely
diddles
dike
dikeed
dikeer
dikees
dikeing
dikely
dikes
dildo
dildoed
dildoer
dildoes
dildoing
dildoly
dildos
dildosed
dildoser
dildoses
dildosing
dildosly
dildoss
diligaf
diligafed
diligafer
diligafes
diligafing
diligafly
diligafs
dillweed
dillweeded
dillweeder
dillweedes
dillweeding
dillweedly
dillweeds
dimwit
dimwited
dimwiter
dimwites
dimwiting
dimwitly
dimwits
dingle
dingleed
dingleer
dinglees
dingleing
dinglely
dingles
dipship
dipshiped
dipshiper
dipshipes
dipshiping
dipshiply
dipships
dizzyed
dizzyer
dizzyes
dizzying
dizzyly
dizzys
doggiestyleed
doggiestyleer
doggiestylees
doggiestyleing
doggiestylely
doggiestyles
doggystyleed
doggystyleer
doggystylees
doggystyleing
doggystylely
doggystyles
dong
donged
donger
donges
donging
dongly
dongs
doofus
doofused
doofuser
doofuses
doofusing
doofusly
doofuss
doosh
dooshed
doosher
dooshes
dooshing
dooshly
dooshs
dopeyed
dopeyer
dopeyes
dopeying
dopeyly
dopeys
douchebag
douchebaged
douchebager
douchebages
douchebaging
douchebagly
douchebags
douchebagsed
douchebagser
douchebagses
douchebagsing
douchebagsly
douchebagss
doucheed
doucheer
douchees
doucheing
douchely
douches
douchey
doucheyed
doucheyer
doucheyes
doucheying
doucheyly
doucheys
drunk
drunked
drunker
drunkes
drunking
drunkly
drunks
dumass
dumassed
dumasser
dumasses
dumassing
dumassly
dumasss
dumbass
dumbassed
dumbasser
dumbasses
dumbassesed
dumbasseser
dumbasseses
dumbassesing
dumbassesly
dumbassess
dumbassing
dumbassly
dumbasss
dummy
dummyed
dummyer
dummyes
dummying
dummyly
dummys
dyke
dykeed
dykeer
dykees
dykeing
dykely
dykes
dykesed
dykeser
dykeses
dykesing
dykesly
dykess
erotic
eroticed
eroticer
erotices
eroticing
eroticly
erotics
extacy
extacyed
extacyer
extacyes
extacying
extacyly
extacys
extasy
extasyed
extasyer
extasyes
extasying
extasyly
extasys
fack
facked
facker
fackes
facking
fackly
facks
fag
faged
fager
fages
fagg
fagged
faggeded
faggeder
faggedes
faggeding
faggedly
faggeds
fagger
fagges
fagging
faggit
faggited
faggiter
faggites
faggiting
faggitly
faggits
faggly
faggot
faggoted
faggoter
faggotes
faggoting
faggotly
faggots
faggs
faging
fagly
fagot
fagoted
fagoter
fagotes
fagoting
fagotly
fagots
fags
fagsed
fagser
fagses
fagsing
fagsly
fagss
faig
faiged
faiger
faiges
faiging
faigly
faigs
faigt
faigted
faigter
faigtes
faigting
faigtly
faigts
fannybandit
fannybandited
fannybanditer
fannybandites
fannybanditing
fannybanditly
fannybandits
farted
farter
fartes
farting
fartknocker
fartknockered
fartknockerer
fartknockeres
fartknockering
fartknockerly
fartknockers
fartly
farts
felch
felched
felcher
felchered
felcherer
felcheres
felchering
felcherly
felchers
felches
felching
felchinged
felchinger
felchinges
felchinging
felchingly
felchings
felchly
felchs
fellate
fellateed
fellateer
fellatees
fellateing
fellately
fellates
fellatio
fellatioed
fellatioer
fellatioes
fellatioing
fellatioly
fellatios
feltch
feltched
feltcher
feltchered
feltcherer
feltcheres
feltchering
feltcherly
feltchers
feltches
feltching
feltchly
feltchs
feom
feomed
feomer
feomes
feoming
feomly
feoms
fisted
fisteded
fisteder
fistedes
fisteding
fistedly
fisteds
fisting
fistinged
fistinger
fistinges
fistinging
fistingly
fistings
fisty
fistyed
fistyer
fistyes
fistying
fistyly
fistys
floozy
floozyed
floozyer
floozyes
floozying
floozyly
floozys
foad
foaded
foader
foades
foading
foadly
foads
fondleed
fondleer
fondlees
fondleing
fondlely
fondles
foobar
foobared
foobarer
foobares
foobaring
foobarly
foobars
freex
freexed
freexer
freexes
freexing
freexly
freexs
frigg
frigga
friggaed
friggaer
friggaes
friggaing
friggaly
friggas
frigged
frigger
frigges
frigging
friggly
friggs
fubar
fubared
fubarer
fubares
fubaring
fubarly
fubars
fuck
fuckass
fuckassed
fuckasser
fuckasses
fuckassing
fuckassly
fuckasss
fucked
fuckeded
fuckeder
fuckedes
fuckeding
fuckedly
fuckeds
fucker
fuckered
fuckerer
fuckeres
fuckering
fuckerly
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rumper
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Itchy scalp with scale
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
A new model of care to return holism to family medicine
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; wayne@drwaynejonas.com.
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; wayne@drwaynejonas.com.
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; wayne@drwaynejonas.com.
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
PRACTICE RECOMMENDATIONS
❯ Build care teams into your practice so that you integrate “what matters” into the center of the clinical encounter. C
❯ Add practice approaches that help patients engage in healthy lifestyles and that remove social and economic barriers for improving health and well-being. 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
How to identify and treat common bites and stings
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; ejaqua@llu.edu.
1. Numbers of insects (species and individuals). Smithsonian BugInfo Web site. www.si.edu/spotlight/buginfo/bugnos. Accessed November 25, 2020.
2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
5. Goodnight ML. Arachnid. In: Encyclopædia Britannica. 2012. www.britannica.com/animal/arachnid. Accessed November 25, 2020.
6. Despommier DD, Gwadz RW, Hotez PJ. Arachnids. In: Despommier DD, Gwadz RW, Hotez PJ. Parasitic Diseases. 3rd ed. Springer-Verlag; 1995:268-283.
7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
9. Pucci S, Antonicelli L, Bilò MB, et al. Shortness of interval between two stings as risk factor for developing Hymenoptera venom allergy. Allergy.1994;49:894-896.
10. Müller UR. Bee venom allergy in beekeepers and their family members. Curr Opin Allergy Clin Immunol. 2005;5:343-347.
11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
14. Bilò BM, Rueff F, Mosbech H, et al; EAACI Interest Group on Insect Venom Hypersensitivity. Diagnosis of Hymenoptera venom allergy. Allergy. 2005;60:1339-1349.
15. Reisman RE. Insect stings. N Engl J Med. 1994;331:523-527.
16. Pucci S, D’Alò S, De Pasquale T, et al. Risk of anaphylaxis in patients with large local reactions to hymenoptera stings: a retrospective and prospective study. Clin Mol Allergy. 2015;13:21.
17. Golden DBK. Large local reactions to insect stings. J Allergy Clin Immunol Pract. 2015;3:331-334.
18. Clark S, Camargo CA Jr. Emergency treatment and prevention of insect-sting anaphylaxis. Curr Opin Allergy Clin Immunol. 2006;6:279-283.
19. Stinging insect allergy. In: Volcheck GW. Clinical Allergy: Diagnosis and Management. Humana Press; 2009:465-479.
20. Järvinen KM, Celestin J. Anaphylaxis avoidance and management: educating patients and their caregivers. J Asthma Allergy. 2014;7:95-104.
21. Institute for Quality and Efficiency in Health Care (IQWiG). Insect venom allergies: overview. InformedHealth.org. Updated May 7, 2020. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0096282/. Accessed November 25, 2020.
22. Casale TB, Burks AW. Clinical practice. Hymenoptera-sting hypersensitivity. N Engl J Med. 2014;370:1432-1439.
23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
25. Cushing PE. Spiders (Arachnida: Araneae). In: Capinera JL, ed. Encyclopedia of Entomology. Springer, Dordrecht; 2008:226.
26. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; ejaqua@llu.edu.
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; ejaqua@llu.edu.
1. Numbers of insects (species and individuals). Smithsonian BugInfo Web site. www.si.edu/spotlight/buginfo/bugnos. Accessed November 25, 2020.
2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
5. Goodnight ML. Arachnid. In: Encyclopædia Britannica. 2012. www.britannica.com/animal/arachnid. Accessed November 25, 2020.
6. Despommier DD, Gwadz RW, Hotez PJ. Arachnids. In: Despommier DD, Gwadz RW, Hotez PJ. Parasitic Diseases. 3rd ed. Springer-Verlag; 1995:268-283.
7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
9. Pucci S, Antonicelli L, Bilò MB, et al. Shortness of interval between two stings as risk factor for developing Hymenoptera venom allergy. Allergy.1994;49:894-896.
10. Müller UR. Bee venom allergy in beekeepers and their family members. Curr Opin Allergy Clin Immunol. 2005;5:343-347.
11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
14. Bilò BM, Rueff F, Mosbech H, et al; EAACI Interest Group on Insect Venom Hypersensitivity. Diagnosis of Hymenoptera venom allergy. Allergy. 2005;60:1339-1349.
15. Reisman RE. Insect stings. N Engl J Med. 1994;331:523-527.
16. Pucci S, D’Alò S, De Pasquale T, et al. Risk of anaphylaxis in patients with large local reactions to hymenoptera stings: a retrospective and prospective study. Clin Mol Allergy. 2015;13:21.
17. Golden DBK. Large local reactions to insect stings. J Allergy Clin Immunol Pract. 2015;3:331-334.
18. Clark S, Camargo CA Jr. Emergency treatment and prevention of insect-sting anaphylaxis. Curr Opin Allergy Clin Immunol. 2006;6:279-283.
19. Stinging insect allergy. In: Volcheck GW. Clinical Allergy: Diagnosis and Management. Humana Press; 2009:465-479.
20. Järvinen KM, Celestin J. Anaphylaxis avoidance and management: educating patients and their caregivers. J Asthma Allergy. 2014;7:95-104.
21. Institute for Quality and Efficiency in Health Care (IQWiG). Insect venom allergies: overview. InformedHealth.org. Updated May 7, 2020. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0096282/. Accessed November 25, 2020.
22. Casale TB, Burks AW. Clinical practice. Hymenoptera-sting hypersensitivity. N Engl J Med. 2014;370:1432-1439.
23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
25. Cushing PE. Spiders (Arachnida: Araneae). In: Capinera JL, ed. Encyclopedia of Entomology. Springer, Dordrecht; 2008:226.
26. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
1. Numbers of insects (species and individuals). Smithsonian BugInfo Web site. www.si.edu/spotlight/buginfo/bugnos. Accessed November 25, 2020.
2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
5. Goodnight ML. Arachnid. In: Encyclopædia Britannica. 2012. www.britannica.com/animal/arachnid. Accessed November 25, 2020.
6. Despommier DD, Gwadz RW, Hotez PJ. Arachnids. In: Despommier DD, Gwadz RW, Hotez PJ. Parasitic Diseases. 3rd ed. Springer-Verlag; 1995:268-283.
7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
9. Pucci S, Antonicelli L, Bilò MB, et al. Shortness of interval between two stings as risk factor for developing Hymenoptera venom allergy. Allergy.1994;49:894-896.
10. Müller UR. Bee venom allergy in beekeepers and their family members. Curr Opin Allergy Clin Immunol. 2005;5:343-347.
11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
14. Bilò BM, Rueff F, Mosbech H, et al; EAACI Interest Group on Insect Venom Hypersensitivity. Diagnosis of Hymenoptera venom allergy. Allergy. 2005;60:1339-1349.
15. Reisman RE. Insect stings. N Engl J Med. 1994;331:523-527.
16. Pucci S, D’Alò S, De Pasquale T, et al. Risk of anaphylaxis in patients with large local reactions to hymenoptera stings: a retrospective and prospective study. Clin Mol Allergy. 2015;13:21.
17. Golden DBK. Large local reactions to insect stings. J Allergy Clin Immunol Pract. 2015;3:331-334.
18. Clark S, Camargo CA Jr. Emergency treatment and prevention of insect-sting anaphylaxis. Curr Opin Allergy Clin Immunol. 2006;6:279-283.
19. Stinging insect allergy. In: Volcheck GW. Clinical Allergy: Diagnosis and Management. Humana Press; 2009:465-479.
20. Järvinen KM, Celestin J. Anaphylaxis avoidance and management: educating patients and their caregivers. J Asthma Allergy. 2014;7:95-104.
21. Institute for Quality and Efficiency in Health Care (IQWiG). Insect venom allergies: overview. InformedHealth.org. Updated May 7, 2020. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0096282/. Accessed November 25, 2020.
22. Casale TB, Burks AW. Clinical practice. Hymenoptera-sting hypersensitivity. N Engl J Med. 2014;370:1432-1439.
23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
25. Cushing PE. Spiders (Arachnida: Araneae). In: Capinera JL, ed. Encyclopedia of Entomology. Springer, Dordrecht; 2008:226.
26. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
PRACTICE RECOMMENDATIONS
❯ Recommend that patients use an insect repellent, such as an over-the-counter formulation that contains DEET, picaridin, or PMD (a chemical constituent of Eucalyptus citriodora oil) to prevent flea bites. C
❯ Prescribe nonsedating oral antihistamines as first-line symptomatic treatment of mild-to-moderate pruritus secondary to an insect bite. C
❯ When indicated, refer patients for venom immunotherapy, which is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis and death. C
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
Home visits: A practical approach
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; curtis.elliott@uscmed.sc.edu.
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
29. Leff B, Burton L, Mader SL, et al. Hospital at home: feasibility and outcomes of a program to provide hospital-level care at home for acutely ill older patients. Ann Intern Med. 2005;143:798-808.
30. Shepperd S, Iliffe S, Doll HA, et al. Admission avoidance hospital at home. Cochrane Database Syst Rev. 2016;9:CD007491.
31. Levine DM, Ouchi K, Blanchfield B, et al. Hospital-level care at home for acutely ill adults: a randomized controlled trial. Ann Intern Med. 2020;172:77-85.
32. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p18.
33. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p19.
34. Accreditation Council for Graduate Medical Education. ACGME Program Requirements for Graduate Medical Education in Family Medicine. www.acgme.org/Portals/0/PFAssets/ProgramRequirements/120_FamilyMedicine_2020.pdf. (section IV.C.1.b). Accessed November 30, 2020.
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; curtis.elliott@uscmed.sc.edu.
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; curtis.elliott@uscmed.sc.edu.
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
29. Leff B, Burton L, Mader SL, et al. Hospital at home: feasibility and outcomes of a program to provide hospital-level care at home for acutely ill older patients. Ann Intern Med. 2005;143:798-808.
30. Shepperd S, Iliffe S, Doll HA, et al. Admission avoidance hospital at home. Cochrane Database Syst Rev. 2016;9:CD007491.
31. Levine DM, Ouchi K, Blanchfield B, et al. Hospital-level care at home for acutely ill adults: a randomized controlled trial. Ann Intern Med. 2020;172:77-85.
32. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p18.
33. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p19.
34. Accreditation Council for Graduate Medical Education. ACGME Program Requirements for Graduate Medical Education in Family Medicine. www.acgme.org/Portals/0/PFAssets/ProgramRequirements/120_FamilyMedicine_2020.pdf. (section IV.C.1.b). Accessed November 30, 2020.
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
29. Leff B, Burton L, Mader SL, et al. Hospital at home: feasibility and outcomes of a program to provide hospital-level care at home for acutely ill older patients. Ann Intern Med. 2005;143:798-808.
30. Shepperd S, Iliffe S, Doll HA, et al. Admission avoidance hospital at home. Cochrane Database Syst Rev. 2016;9:CD007491.
31. Levine DM, Ouchi K, Blanchfield B, et al. Hospital-level care at home for acutely ill adults: a randomized controlled trial. Ann Intern Med. 2020;172:77-85.
32. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p18.
33. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p19.
34. Accreditation Council for Graduate Medical Education. ACGME Program Requirements for Graduate Medical Education in Family Medicine. www.acgme.org/Portals/0/PFAssets/ProgramRequirements/120_FamilyMedicine_2020.pdf. (section IV.C.1.b). Accessed November 30, 2020.
PRACTICE RECOMMENDATIONS
❯ Consider incorporating home visits into the primary care of select vulnerable patients because doing so improves clinical outcomes, including mortality rates in neonates and elders. A
❯ Employ team-based home care and include community health workers, nurses, pharmacists, social workers, chaplains, and others. 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
Whole-person care: Our foundation, our future
In this issue of The Journal of Family Practice, Dr. Wayne Jonas explains his model for Advanced Primary Care (see page 493). The figure he uses to illustrate Advanced Primary Care is compelling, and the effectiveness of this model of health care is supported by a great deal of research and evaluation over the past 20 years. Let me provide some historical context.
The idea that healing requires more than curative, biology-based medical care dates back to Greek mythology. Asclepius, the god of medicine, had 5 daughters, Hygeia (the goddess of good health and hygiene), Iaso (cures and remedies), Aceso (healing wounds), Aegle (radiant good health), and Panacea (cures).1 Clearly, the Greeks believed that integrative care is essential for maintaining good health!
Modern, scientific medicine is a relatively recent development in human history. Other traditions of healing such as acupuncture and herbal medicines are actually much older than mainstream Western medicine. But they come together in family medicine—a specialty founded on the principles of whole person, whole family, and whole community care.
The first modern model of comprehensive care, the patient-centered medical home (PCMH), was introduced by the American Academy of Pediatrics in 1967. This idea caught on widely and was institutionalized by the National Committee for Quality Assurance in 2008 with PCMH certification.
Advanced Primary Care is the latest and best rendition of comprehensive primary health care. Funding this model through our current payment mechanisms, however, has been difficult because of the need to support social and behavioral interventions in addition to medical care—areas of care not traditionally paid for by medical premiums. In 2011, CMS collaborated with private insurers in a national demonstration project to test the financial feasibility of implementing Advanced Primary Care. Some organizations have been highly successful; others not as much.
We can no longer go “halfway” into whole-person care. The COVID-19 pandemic has put a spotlight on our need to transform payment models away from fee-for-service to reimbursement for whole person primary care. Our nation’s health and the viability of our health care system depend on it.
PS: I recommend reading Dr. Jonas’ book, How Healing Works, which provides a scientific rationale for the application of whole-person care to healing.
1. Theoi Greek Mythology Web site. https://www.theoi.com/Ouranios/Asklepios.html. Accessed November 30, 2020.
In this issue of The Journal of Family Practice, Dr. Wayne Jonas explains his model for Advanced Primary Care (see page 493). The figure he uses to illustrate Advanced Primary Care is compelling, and the effectiveness of this model of health care is supported by a great deal of research and evaluation over the past 20 years. Let me provide some historical context.
The idea that healing requires more than curative, biology-based medical care dates back to Greek mythology. Asclepius, the god of medicine, had 5 daughters, Hygeia (the goddess of good health and hygiene), Iaso (cures and remedies), Aceso (healing wounds), Aegle (radiant good health), and Panacea (cures).1 Clearly, the Greeks believed that integrative care is essential for maintaining good health!
Modern, scientific medicine is a relatively recent development in human history. Other traditions of healing such as acupuncture and herbal medicines are actually much older than mainstream Western medicine. But they come together in family medicine—a specialty founded on the principles of whole person, whole family, and whole community care.
The first modern model of comprehensive care, the patient-centered medical home (PCMH), was introduced by the American Academy of Pediatrics in 1967. This idea caught on widely and was institutionalized by the National Committee for Quality Assurance in 2008 with PCMH certification.
Advanced Primary Care is the latest and best rendition of comprehensive primary health care. Funding this model through our current payment mechanisms, however, has been difficult because of the need to support social and behavioral interventions in addition to medical care—areas of care not traditionally paid for by medical premiums. In 2011, CMS collaborated with private insurers in a national demonstration project to test the financial feasibility of implementing Advanced Primary Care. Some organizations have been highly successful; others not as much.
We can no longer go “halfway” into whole-person care. The COVID-19 pandemic has put a spotlight on our need to transform payment models away from fee-for-service to reimbursement for whole person primary care. Our nation’s health and the viability of our health care system depend on it.
PS: I recommend reading Dr. Jonas’ book, How Healing Works, which provides a scientific rationale for the application of whole-person care to healing.
In this issue of The Journal of Family Practice, Dr. Wayne Jonas explains his model for Advanced Primary Care (see page 493). The figure he uses to illustrate Advanced Primary Care is compelling, and the effectiveness of this model of health care is supported by a great deal of research and evaluation over the past 20 years. Let me provide some historical context.
The idea that healing requires more than curative, biology-based medical care dates back to Greek mythology. Asclepius, the god of medicine, had 5 daughters, Hygeia (the goddess of good health and hygiene), Iaso (cures and remedies), Aceso (healing wounds), Aegle (radiant good health), and Panacea (cures).1 Clearly, the Greeks believed that integrative care is essential for maintaining good health!
Modern, scientific medicine is a relatively recent development in human history. Other traditions of healing such as acupuncture and herbal medicines are actually much older than mainstream Western medicine. But they come together in family medicine—a specialty founded on the principles of whole person, whole family, and whole community care.
The first modern model of comprehensive care, the patient-centered medical home (PCMH), was introduced by the American Academy of Pediatrics in 1967. This idea caught on widely and was institutionalized by the National Committee for Quality Assurance in 2008 with PCMH certification.
Advanced Primary Care is the latest and best rendition of comprehensive primary health care. Funding this model through our current payment mechanisms, however, has been difficult because of the need to support social and behavioral interventions in addition to medical care—areas of care not traditionally paid for by medical premiums. In 2011, CMS collaborated with private insurers in a national demonstration project to test the financial feasibility of implementing Advanced Primary Care. Some organizations have been highly successful; others not as much.
We can no longer go “halfway” into whole-person care. The COVID-19 pandemic has put a spotlight on our need to transform payment models away from fee-for-service to reimbursement for whole person primary care. Our nation’s health and the viability of our health care system depend on it.
PS: I recommend reading Dr. Jonas’ book, How Healing Works, which provides a scientific rationale for the application of whole-person care to healing.
1. Theoi Greek Mythology Web site. https://www.theoi.com/Ouranios/Asklepios.html. Accessed November 30, 2020.
1. Theoi Greek Mythology Web site. https://www.theoi.com/Ouranios/Asklepios.html. Accessed November 30, 2020.
17-year-old girl • abdominal pain • lower-leg itching • dark urine and yellow eyes • Dx?
THE CASE
A 17-year-old White girl with no known past medical history presented to the emergency department (ED) with complaints of abdominal pain and pruritus. The abdominal pain had started 9 days prior and lasted for 3 days. One day after resolution, she developed bilateral lower extremity itching, which was not relieved with loratadine.
Review of systems included dark urine and yellow eyes noted for several days. The patient denied nausea, vomiting, diarrhea, constipation, fevers, chills, arthralgias, recent illness, travel, or sick contacts. Immunizations were up to date. The patient had no history of surgery or liver disease and no pertinent family history. Her current medications included ethinyl estradiol/norethindrone acetate for birth control and minocycline for acne vulgaris. She had been taking the latter medication for 2 years. No additional medications were noted, including vitamins, over-the-counter medications, or supplements. She denied smoking and alcohol or recreational drug use.
In the ED, the patient had normal vital signs. Physical exam findings included bilateral scleral icterus and scattered skin excoriations on the hands, arms, back of the neck, and feet. At the time of hospital admission, the patient’s minocycline and birth control were held under the initial presumption that one or both might be contributing to her presentation.
Pertinent laboratory findings included aspartate transaminase (AST), 828 U/L (normal range, 2-40 U/L); alanine aminotransferase (ALT), 784 U/L (normal range, 3-30 U/L); lactic acid dehydrogenase, 520 U/L (normal range, 140-280 U/L); alkaline phosphatase, 119 U/L (normal range, 44-147 U/L); total bilirubin, 1.9 µmol/L (normal range, 2-18 µmol/L); and direct bilirubin, 1.3 µmol/L (normal range, 0-4 µmol/L). Baseline liver function test results (prior to admission) were unknown. Results of a coagulation panel, complete blood count, basic metabolic panel, amylase, lipase, urine toxicology, and urinalysis all were within normal limits.
Ultrasound of the abdomen revealed a normal abdomen, liver, pancreas, gallbladder, and common bile duct. This imaging study was negative for other obstructive pathologies.
THE DIAGNOSIS
During hospital admission, a noninvasive liver work-up was pursued by Gastroenterology. A hepatitis panel, Epstein-Barr virus testing, and levels of ceruloplasmin and acetaminophen were all found to be within normal limits, excluding additional causes of liver disease. Serum antinuclear antibody (ANA) testing was significantly positive, with a titer of 1:640 (range, < 1:20) and, as noted above, liver transaminases were severely elevated, leading to a presumptive diagnosis of drug-induced liver pathology.
Continue to: During outpatient follow-up...
During outpatient follow-up with Gastroenterology 2 days after discharge, the patient’s liver transaminases and bilirubin continued to trend upward (to a maximum ALT of 871 U/L; AST, 1097 U/L; alkaline phosphatase, 122 U/L; and bilirubin, 2.9 µmol/L). Immunoglobulin G was 1342 mg/mL (normal range, 694-1618 mg/mL).
An ultrasound-guided liver biopsy was performed; it demonstrated lobular, portal, and periportal hepatitis with focal bridging necrosis, consistent with a diagnosis of autoimmune hepatitis. Mild-to-moderate focal cholestasis was demonstrated, consistent with cholestatic hepatitis.
DISCUSSION
Autoimmune hepatitis is characterized by inflammation of the liver, secondary to the presence of circulating antibodies or hypergammaglobulinemia. The pathogenesis is thought to involve a T-cell–mediated immune attack on the liver. Based on case reports,the use of minocycline is associated with risk for liver injury, although the incidence is rare.1-4 Use of this medication may be associated with autoimmune disease in patients who are predisposed to autoimmune tendencies or who have genetic predeterminants.
Diagnosis is typically made based on abnormalities in aminotransferases (AST, ALT), elevation in serum immunoglobulins, and positive auto-antibody titers including ANA, smooth muscle antibodies, and anti-liver kidney microsomal type 1 antibodies. Although clinical presentations tend to differ, the confirmatory diagnosis is typically made histologically, with the presence of lobular and perivenular necro-inflammatory changes and plasma cell infiltration.5
Other infectious and metabolic causes of hepatitis should be excluded. Many medications and herbal agents have been noted to cause autoimmune hepatitis or similar syndromes that mimic the condition.
Medication history. Review of the case patient’s medication list identified ethinyl estradiol/norethindrone acetate and minocycline as potential culprits. Ethinyl estradiol/norethindrone acetate is a low-dose combination oral contraceptive pill (OCP). Although earlier formulations of OCPs were associated with hepatobiliary complications, these adverse effects are noted to be rare in the absence of predisposing conditions.6 In some cases, OCPs have been linked to cholestasis, chronic hepatocellular carcinoma, or hepatic adenomas, but studies have shown that these medications do not affect the course of acute liver failure.7
Continue to: Minocycline...
Minocycline is a second-generation tetracycline commonly used to treat acne vulgaris. Long-term treatment with minocycline has been associated with severe adverse effects, including autoimmune and hypersensitivity reactions.8 Minocycline-associated hepatotoxicity can be due to a systemic hypersensitivity reaction, occurring within a few weeks of therapy initiation, whereas autoimmune hepatitis manifests after a year or more of exposure to the medication (as in this case). Patients may present acutely several months after starting the medication, with symptoms of jaundice, fatigue, and/or joint aches. The acute liver injury is typically self-limited and often resolves with cessation of the drug. However, patients may require corticosteroids and immunosuppressive therapy.
Which is it? Histologically, drug-induced autoimmune hepatitis is indistinguishable from idiopathic autoimmune hepatitis.3 The estimated incidence of idiopathic autoimmune liver disease ranges from 0.7 to 2 out of 100,000 population.9 A systematic review of the literature identified 65 reported cases of liver damage associated with minocycline specifically.1
In this case, given the patient’s 2-year history of minocycline use, it is possible that she developed an acute presentation of autoimmune hepatitis. With drug-induced autoimmune liver injury, complete resolution occurs after withdrawal of the offending medication, and a response to corticosteroid therapy supports the diagnosis. Recurrence of signs or symptoms following corticosteroid cessation may indicate idiopathic autoimmune hepatitis as opposed to a drug-induced form.2
Our patient was started on steroid and immunomodulator therapy, with prednisone 40 mg/d and mycophenolate 250 mg bid. At follow-up with Gastroenterology, the patient’s symptoms and liver function test results had improved significantly (AST, 27 U/L; ALT, 14 U/L; alkaline phosphatase, 51 U/L; and total bilirubin, 0.4 µmol/L). The patient was continued on a prednisone taper while simultaneously titrating mycophenolate. The ultimate plan of care included continuing mycophenolate for a total of 4 to 5 years.
THE TAKEAWAY
During evaluation of a patient with new-onset liver disease, it is important to inquire about prescription medications, drugs, vitamins, and herbal supplements as possible contributors to the disease process. This case highlights the importance of monitoring patients while on minocycline and of weighing the risks vs benefits of long-term therapy. It has been suggested that liver enzymes be tested before therapy initiation and about every 3 months during long-term antibiotic treatment.4 Careful consideration and caution should be taken prior to the initiation of medications that have been linked to rare, but important, adverse reactions.
ACKNOWLEDGEMENT
The authors would like to thank Frank Bauer, MD, and Eva Sotil, MD, for their contributions to this case presentation.
CORRESPONDENCE
Andrea Gillis, DO, Asylum Hill Family Medicine Center, 99 Woodland Street, Hartford, CT 06105; andrea.gillis@ trinityhealthofne.org
1. Lawrenson RA, Seaman HE, Sundström A, et al. Liver damage associated with minocycline use in acne: a systematic review of the published literature and pharmacovigilance data. Drug Saf. 2000;23:333-349.
2. Teitelbaum JE, Perez-Atayde AR, Cohen M, et al. Minocycline-related autoimmune hepatitis case series and literature review. Arch Pediatr Adolesc Med. 1998;152:1132-1136.
3. Goldstein NS, Bayati N, Silverman AL, et al. Minocycline as a cause of drug induced autoimmune hepatitis: report of four cases and comparison with autoimmune hepatitis. Am J Clinic Pathol. 2000;114:591-598.
4. Ramakrishna J, Johnson AR, Banner BF. Long-term minocycline use for acne in healthy adolescents can cause severe autoimmune hepatitis. J Clin Gastroenterol. 2009;43:787-790.
5. Nguyen Canh H, Harada K, Ouchi H, et al. Acute presentation of autoimmune hepatitis: a multicentre study with detailed histological evaluation in a large cohort of patients. J Clin Pathol. 2017;70:961-969.
6. Lindberg MC. Hepatobiliary complications of oral contraceptives. J Gen Intern Med. 1992; 7:199-209.
7. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive use among women with viral hepatitis or cirrhosis of the liver: a systematic review. Contraception. 2009;80:381-386.
8. DeLemos AS, Foureau DM, Jacobs C, et al. Drug-induced liver injury with autoimmune features. Semin Liver Dis. 2014;34:194-204.
9. Jepsen P, Gronbaek L, Vilstrup H. Worldwide incidence of autoimmune liver disease. Dig Dis. 2015;33(suppl 2):2-12.
THE CASE
A 17-year-old White girl with no known past medical history presented to the emergency department (ED) with complaints of abdominal pain and pruritus. The abdominal pain had started 9 days prior and lasted for 3 days. One day after resolution, she developed bilateral lower extremity itching, which was not relieved with loratadine.
Review of systems included dark urine and yellow eyes noted for several days. The patient denied nausea, vomiting, diarrhea, constipation, fevers, chills, arthralgias, recent illness, travel, or sick contacts. Immunizations were up to date. The patient had no history of surgery or liver disease and no pertinent family history. Her current medications included ethinyl estradiol/norethindrone acetate for birth control and minocycline for acne vulgaris. She had been taking the latter medication for 2 years. No additional medications were noted, including vitamins, over-the-counter medications, or supplements. She denied smoking and alcohol or recreational drug use.
In the ED, the patient had normal vital signs. Physical exam findings included bilateral scleral icterus and scattered skin excoriations on the hands, arms, back of the neck, and feet. At the time of hospital admission, the patient’s minocycline and birth control were held under the initial presumption that one or both might be contributing to her presentation.
Pertinent laboratory findings included aspartate transaminase (AST), 828 U/L (normal range, 2-40 U/L); alanine aminotransferase (ALT), 784 U/L (normal range, 3-30 U/L); lactic acid dehydrogenase, 520 U/L (normal range, 140-280 U/L); alkaline phosphatase, 119 U/L (normal range, 44-147 U/L); total bilirubin, 1.9 µmol/L (normal range, 2-18 µmol/L); and direct bilirubin, 1.3 µmol/L (normal range, 0-4 µmol/L). Baseline liver function test results (prior to admission) were unknown. Results of a coagulation panel, complete blood count, basic metabolic panel, amylase, lipase, urine toxicology, and urinalysis all were within normal limits.
Ultrasound of the abdomen revealed a normal abdomen, liver, pancreas, gallbladder, and common bile duct. This imaging study was negative for other obstructive pathologies.
THE DIAGNOSIS
During hospital admission, a noninvasive liver work-up was pursued by Gastroenterology. A hepatitis panel, Epstein-Barr virus testing, and levels of ceruloplasmin and acetaminophen were all found to be within normal limits, excluding additional causes of liver disease. Serum antinuclear antibody (ANA) testing was significantly positive, with a titer of 1:640 (range, < 1:20) and, as noted above, liver transaminases were severely elevated, leading to a presumptive diagnosis of drug-induced liver pathology.
Continue to: During outpatient follow-up...
During outpatient follow-up with Gastroenterology 2 days after discharge, the patient’s liver transaminases and bilirubin continued to trend upward (to a maximum ALT of 871 U/L; AST, 1097 U/L; alkaline phosphatase, 122 U/L; and bilirubin, 2.9 µmol/L). Immunoglobulin G was 1342 mg/mL (normal range, 694-1618 mg/mL).
An ultrasound-guided liver biopsy was performed; it demonstrated lobular, portal, and periportal hepatitis with focal bridging necrosis, consistent with a diagnosis of autoimmune hepatitis. Mild-to-moderate focal cholestasis was demonstrated, consistent with cholestatic hepatitis.
DISCUSSION
Autoimmune hepatitis is characterized by inflammation of the liver, secondary to the presence of circulating antibodies or hypergammaglobulinemia. The pathogenesis is thought to involve a T-cell–mediated immune attack on the liver. Based on case reports,the use of minocycline is associated with risk for liver injury, although the incidence is rare.1-4 Use of this medication may be associated with autoimmune disease in patients who are predisposed to autoimmune tendencies or who have genetic predeterminants.
Diagnosis is typically made based on abnormalities in aminotransferases (AST, ALT), elevation in serum immunoglobulins, and positive auto-antibody titers including ANA, smooth muscle antibodies, and anti-liver kidney microsomal type 1 antibodies. Although clinical presentations tend to differ, the confirmatory diagnosis is typically made histologically, with the presence of lobular and perivenular necro-inflammatory changes and plasma cell infiltration.5
Other infectious and metabolic causes of hepatitis should be excluded. Many medications and herbal agents have been noted to cause autoimmune hepatitis or similar syndromes that mimic the condition.
Medication history. Review of the case patient’s medication list identified ethinyl estradiol/norethindrone acetate and minocycline as potential culprits. Ethinyl estradiol/norethindrone acetate is a low-dose combination oral contraceptive pill (OCP). Although earlier formulations of OCPs were associated with hepatobiliary complications, these adverse effects are noted to be rare in the absence of predisposing conditions.6 In some cases, OCPs have been linked to cholestasis, chronic hepatocellular carcinoma, or hepatic adenomas, but studies have shown that these medications do not affect the course of acute liver failure.7
Continue to: Minocycline...
Minocycline is a second-generation tetracycline commonly used to treat acne vulgaris. Long-term treatment with minocycline has been associated with severe adverse effects, including autoimmune and hypersensitivity reactions.8 Minocycline-associated hepatotoxicity can be due to a systemic hypersensitivity reaction, occurring within a few weeks of therapy initiation, whereas autoimmune hepatitis manifests after a year or more of exposure to the medication (as in this case). Patients may present acutely several months after starting the medication, with symptoms of jaundice, fatigue, and/or joint aches. The acute liver injury is typically self-limited and often resolves with cessation of the drug. However, patients may require corticosteroids and immunosuppressive therapy.
Which is it? Histologically, drug-induced autoimmune hepatitis is indistinguishable from idiopathic autoimmune hepatitis.3 The estimated incidence of idiopathic autoimmune liver disease ranges from 0.7 to 2 out of 100,000 population.9 A systematic review of the literature identified 65 reported cases of liver damage associated with minocycline specifically.1
In this case, given the patient’s 2-year history of minocycline use, it is possible that she developed an acute presentation of autoimmune hepatitis. With drug-induced autoimmune liver injury, complete resolution occurs after withdrawal of the offending medication, and a response to corticosteroid therapy supports the diagnosis. Recurrence of signs or symptoms following corticosteroid cessation may indicate idiopathic autoimmune hepatitis as opposed to a drug-induced form.2
Our patient was started on steroid and immunomodulator therapy, with prednisone 40 mg/d and mycophenolate 250 mg bid. At follow-up with Gastroenterology, the patient’s symptoms and liver function test results had improved significantly (AST, 27 U/L; ALT, 14 U/L; alkaline phosphatase, 51 U/L; and total bilirubin, 0.4 µmol/L). The patient was continued on a prednisone taper while simultaneously titrating mycophenolate. The ultimate plan of care included continuing mycophenolate for a total of 4 to 5 years.
THE TAKEAWAY
During evaluation of a patient with new-onset liver disease, it is important to inquire about prescription medications, drugs, vitamins, and herbal supplements as possible contributors to the disease process. This case highlights the importance of monitoring patients while on minocycline and of weighing the risks vs benefits of long-term therapy. It has been suggested that liver enzymes be tested before therapy initiation and about every 3 months during long-term antibiotic treatment.4 Careful consideration and caution should be taken prior to the initiation of medications that have been linked to rare, but important, adverse reactions.
ACKNOWLEDGEMENT
The authors would like to thank Frank Bauer, MD, and Eva Sotil, MD, for their contributions to this case presentation.
CORRESPONDENCE
Andrea Gillis, DO, Asylum Hill Family Medicine Center, 99 Woodland Street, Hartford, CT 06105; andrea.gillis@ trinityhealthofne.org
THE CASE
A 17-year-old White girl with no known past medical history presented to the emergency department (ED) with complaints of abdominal pain and pruritus. The abdominal pain had started 9 days prior and lasted for 3 days. One day after resolution, she developed bilateral lower extremity itching, which was not relieved with loratadine.
Review of systems included dark urine and yellow eyes noted for several days. The patient denied nausea, vomiting, diarrhea, constipation, fevers, chills, arthralgias, recent illness, travel, or sick contacts. Immunizations were up to date. The patient had no history of surgery or liver disease and no pertinent family history. Her current medications included ethinyl estradiol/norethindrone acetate for birth control and minocycline for acne vulgaris. She had been taking the latter medication for 2 years. No additional medications were noted, including vitamins, over-the-counter medications, or supplements. She denied smoking and alcohol or recreational drug use.
In the ED, the patient had normal vital signs. Physical exam findings included bilateral scleral icterus and scattered skin excoriations on the hands, arms, back of the neck, and feet. At the time of hospital admission, the patient’s minocycline and birth control were held under the initial presumption that one or both might be contributing to her presentation.
Pertinent laboratory findings included aspartate transaminase (AST), 828 U/L (normal range, 2-40 U/L); alanine aminotransferase (ALT), 784 U/L (normal range, 3-30 U/L); lactic acid dehydrogenase, 520 U/L (normal range, 140-280 U/L); alkaline phosphatase, 119 U/L (normal range, 44-147 U/L); total bilirubin, 1.9 µmol/L (normal range, 2-18 µmol/L); and direct bilirubin, 1.3 µmol/L (normal range, 0-4 µmol/L). Baseline liver function test results (prior to admission) were unknown. Results of a coagulation panel, complete blood count, basic metabolic panel, amylase, lipase, urine toxicology, and urinalysis all were within normal limits.
Ultrasound of the abdomen revealed a normal abdomen, liver, pancreas, gallbladder, and common bile duct. This imaging study was negative for other obstructive pathologies.
THE DIAGNOSIS
During hospital admission, a noninvasive liver work-up was pursued by Gastroenterology. A hepatitis panel, Epstein-Barr virus testing, and levels of ceruloplasmin and acetaminophen were all found to be within normal limits, excluding additional causes of liver disease. Serum antinuclear antibody (ANA) testing was significantly positive, with a titer of 1:640 (range, < 1:20) and, as noted above, liver transaminases were severely elevated, leading to a presumptive diagnosis of drug-induced liver pathology.
Continue to: During outpatient follow-up...
During outpatient follow-up with Gastroenterology 2 days after discharge, the patient’s liver transaminases and bilirubin continued to trend upward (to a maximum ALT of 871 U/L; AST, 1097 U/L; alkaline phosphatase, 122 U/L; and bilirubin, 2.9 µmol/L). Immunoglobulin G was 1342 mg/mL (normal range, 694-1618 mg/mL).
An ultrasound-guided liver biopsy was performed; it demonstrated lobular, portal, and periportal hepatitis with focal bridging necrosis, consistent with a diagnosis of autoimmune hepatitis. Mild-to-moderate focal cholestasis was demonstrated, consistent with cholestatic hepatitis.
DISCUSSION
Autoimmune hepatitis is characterized by inflammation of the liver, secondary to the presence of circulating antibodies or hypergammaglobulinemia. The pathogenesis is thought to involve a T-cell–mediated immune attack on the liver. Based on case reports,the use of minocycline is associated with risk for liver injury, although the incidence is rare.1-4 Use of this medication may be associated with autoimmune disease in patients who are predisposed to autoimmune tendencies or who have genetic predeterminants.
Diagnosis is typically made based on abnormalities in aminotransferases (AST, ALT), elevation in serum immunoglobulins, and positive auto-antibody titers including ANA, smooth muscle antibodies, and anti-liver kidney microsomal type 1 antibodies. Although clinical presentations tend to differ, the confirmatory diagnosis is typically made histologically, with the presence of lobular and perivenular necro-inflammatory changes and plasma cell infiltration.5
Other infectious and metabolic causes of hepatitis should be excluded. Many medications and herbal agents have been noted to cause autoimmune hepatitis or similar syndromes that mimic the condition.
Medication history. Review of the case patient’s medication list identified ethinyl estradiol/norethindrone acetate and minocycline as potential culprits. Ethinyl estradiol/norethindrone acetate is a low-dose combination oral contraceptive pill (OCP). Although earlier formulations of OCPs were associated with hepatobiliary complications, these adverse effects are noted to be rare in the absence of predisposing conditions.6 In some cases, OCPs have been linked to cholestasis, chronic hepatocellular carcinoma, or hepatic adenomas, but studies have shown that these medications do not affect the course of acute liver failure.7
Continue to: Minocycline...
Minocycline is a second-generation tetracycline commonly used to treat acne vulgaris. Long-term treatment with minocycline has been associated with severe adverse effects, including autoimmune and hypersensitivity reactions.8 Minocycline-associated hepatotoxicity can be due to a systemic hypersensitivity reaction, occurring within a few weeks of therapy initiation, whereas autoimmune hepatitis manifests after a year or more of exposure to the medication (as in this case). Patients may present acutely several months after starting the medication, with symptoms of jaundice, fatigue, and/or joint aches. The acute liver injury is typically self-limited and often resolves with cessation of the drug. However, patients may require corticosteroids and immunosuppressive therapy.
Which is it? Histologically, drug-induced autoimmune hepatitis is indistinguishable from idiopathic autoimmune hepatitis.3 The estimated incidence of idiopathic autoimmune liver disease ranges from 0.7 to 2 out of 100,000 population.9 A systematic review of the literature identified 65 reported cases of liver damage associated with minocycline specifically.1
In this case, given the patient’s 2-year history of minocycline use, it is possible that she developed an acute presentation of autoimmune hepatitis. With drug-induced autoimmune liver injury, complete resolution occurs after withdrawal of the offending medication, and a response to corticosteroid therapy supports the diagnosis. Recurrence of signs or symptoms following corticosteroid cessation may indicate idiopathic autoimmune hepatitis as opposed to a drug-induced form.2
Our patient was started on steroid and immunomodulator therapy, with prednisone 40 mg/d and mycophenolate 250 mg bid. At follow-up with Gastroenterology, the patient’s symptoms and liver function test results had improved significantly (AST, 27 U/L; ALT, 14 U/L; alkaline phosphatase, 51 U/L; and total bilirubin, 0.4 µmol/L). The patient was continued on a prednisone taper while simultaneously titrating mycophenolate. The ultimate plan of care included continuing mycophenolate for a total of 4 to 5 years.
THE TAKEAWAY
During evaluation of a patient with new-onset liver disease, it is important to inquire about prescription medications, drugs, vitamins, and herbal supplements as possible contributors to the disease process. This case highlights the importance of monitoring patients while on minocycline and of weighing the risks vs benefits of long-term therapy. It has been suggested that liver enzymes be tested before therapy initiation and about every 3 months during long-term antibiotic treatment.4 Careful consideration and caution should be taken prior to the initiation of medications that have been linked to rare, but important, adverse reactions.
ACKNOWLEDGEMENT
The authors would like to thank Frank Bauer, MD, and Eva Sotil, MD, for their contributions to this case presentation.
CORRESPONDENCE
Andrea Gillis, DO, Asylum Hill Family Medicine Center, 99 Woodland Street, Hartford, CT 06105; andrea.gillis@ trinityhealthofne.org
1. Lawrenson RA, Seaman HE, Sundström A, et al. Liver damage associated with minocycline use in acne: a systematic review of the published literature and pharmacovigilance data. Drug Saf. 2000;23:333-349.
2. Teitelbaum JE, Perez-Atayde AR, Cohen M, et al. Minocycline-related autoimmune hepatitis case series and literature review. Arch Pediatr Adolesc Med. 1998;152:1132-1136.
3. Goldstein NS, Bayati N, Silverman AL, et al. Minocycline as a cause of drug induced autoimmune hepatitis: report of four cases and comparison with autoimmune hepatitis. Am J Clinic Pathol. 2000;114:591-598.
4. Ramakrishna J, Johnson AR, Banner BF. Long-term minocycline use for acne in healthy adolescents can cause severe autoimmune hepatitis. J Clin Gastroenterol. 2009;43:787-790.
5. Nguyen Canh H, Harada K, Ouchi H, et al. Acute presentation of autoimmune hepatitis: a multicentre study with detailed histological evaluation in a large cohort of patients. J Clin Pathol. 2017;70:961-969.
6. Lindberg MC. Hepatobiliary complications of oral contraceptives. J Gen Intern Med. 1992; 7:199-209.
7. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive use among women with viral hepatitis or cirrhosis of the liver: a systematic review. Contraception. 2009;80:381-386.
8. DeLemos AS, Foureau DM, Jacobs C, et al. Drug-induced liver injury with autoimmune features. Semin Liver Dis. 2014;34:194-204.
9. Jepsen P, Gronbaek L, Vilstrup H. Worldwide incidence of autoimmune liver disease. Dig Dis. 2015;33(suppl 2):2-12.
1. Lawrenson RA, Seaman HE, Sundström A, et al. Liver damage associated with minocycline use in acne: a systematic review of the published literature and pharmacovigilance data. Drug Saf. 2000;23:333-349.
2. Teitelbaum JE, Perez-Atayde AR, Cohen M, et al. Minocycline-related autoimmune hepatitis case series and literature review. Arch Pediatr Adolesc Med. 1998;152:1132-1136.
3. Goldstein NS, Bayati N, Silverman AL, et al. Minocycline as a cause of drug induced autoimmune hepatitis: report of four cases and comparison with autoimmune hepatitis. Am J Clinic Pathol. 2000;114:591-598.
4. Ramakrishna J, Johnson AR, Banner BF. Long-term minocycline use for acne in healthy adolescents can cause severe autoimmune hepatitis. J Clin Gastroenterol. 2009;43:787-790.
5. Nguyen Canh H, Harada K, Ouchi H, et al. Acute presentation of autoimmune hepatitis: a multicentre study with detailed histological evaluation in a large cohort of patients. J Clin Pathol. 2017;70:961-969.
6. Lindberg MC. Hepatobiliary complications of oral contraceptives. J Gen Intern Med. 1992; 7:199-209.
7. Kapp N, Tilley IB, Curtis KM. The effects of hormonal contraceptive use among women with viral hepatitis or cirrhosis of the liver: a systematic review. Contraception. 2009;80:381-386.
8. DeLemos AS, Foureau DM, Jacobs C, et al. Drug-induced liver injury with autoimmune features. Semin Liver Dis. 2014;34:194-204.
9. Jepsen P, Gronbaek L, Vilstrup H. Worldwide incidence of autoimmune liver disease. Dig Dis. 2015;33(suppl 2):2-12.
Does XR injectable naltrexone prevent relapse as effectively as daily sublingual buprenorphine-naloxone?
EVIDENCE SUMMARY
Two recent multicenter, open-label RCTs, 1 in the United States and 1 in Norway, compared monthly XR-NTX with daily BUP-NX.1,2 Both studies evaluated effectiveness (defined by either the number of people who relapsed or self-reported opioid use), cravings, and safety (defined as the absence of serious adverse events such as medically complex withdrawal or fatal overdose).
The participant populations were similar in both mean age and mean age of onset of opioid use. Duration of opioid use was reported differently (total duration or years of heavy heroin or other opioid use) and couldn’t be compared directly.
Naltrexone and buprenorphine-naloxone are similarly effective
The US study enrolled 570 opioid-dependent participants in a 24-week comparative effectiveness trial.1 The 8 study sites were community treatment programs, and the participants were recruited during voluntary inpatient detoxification admissions. Some participants were randomized while on methadone or buprenorphine tapers and some after complete detoxification.
The intention-to-treat analysis included 283 patients in the XR-NTX group and 287 in the BUP-NX group. At 24 weeks, the number of participants who’d had a relapse event (self-reported use or positive urine drug test for nonstudy opioids or refusal to provide a urine sample) was 185 (65%) for XR-NTX compared with 163 (57%) for BUP-NX (odds ratio [OR] = 1.44, 95% confidence interval [CI], 1.02 to 2.01; P = .036).
The 12-week Norwegian noninferiority trial enrolled 159 participants.2 In contrast to the US study, all participants were required to complete inpatient detoxification before randomization and induction onto the study medication.
Patients on BUP-NX reported 3.6 more days of heroin use within the previous 28 days than patients in the XR-NTX group (95% CI, 1.2 to 6; P = .003). For other illicit opioids, self-reported use was 2.4 days greater in the BUP-NX group (95% CI, −0.1 to 4.9; P = .06). Retention with XR-NTX was noninferior to BUP-NX (mean days in therapy [standard deviation], 69.3 [25.9] and 63.7 [29.9]; P = .33).
Randomizing after complete detox reduces induction failures
Naltrexone, a full opioid antagonist, precipitates withdrawal when a full or partial opioid agonist is engaging the opioid receptor. For this reason, an opioid-free interval of 7 to 10 days is generally recommended before initiating naltrexone, raising the risk for relapse during the induction process.
Continue to: The Norwegian trial...
The Norwegian trial randomized participants after detoxification. The US trial, in which some participants were randomized before completing detoxification, reported 79 (28%) induction failures for XR-NTX and 17 (6%) for BUP-NX.1 As a result, a per protocol analysis was completed with the 204 patients on XR-NTX and 270 patients on BUP-NX who were successfully inducted onto a study medication. The 24-week relapse rate was 52% (106) for XR-NTX and 56% (150) for BUP-NX (OR = 0.87; 95% CI, 0.60 to 1.25; P = .44).
Cravings, adverse events, and cost considerations
Patients reported cravings using a visual analog scale. At 12 weeks in both studies, the XR-NTX groups reported fewer cravings than the BUP-NX groups, although by the end of the 24-week US trial, no statistically significant difference in cravings was found between the 2 groups.1,2
The Norwegian trial found a difference between the XR-NTX and the BUP-NX groups in the percentage of nonserious adverse events such as nausea or chills (60.6% in the XR-NTX group vs 30.6% in the BUP-NX group; P < .001), and the US trial found a difference in total number of overdoses (64% of the total overdoses were in the XR-NTX group). Neither trial, however, reported a statistically significant difference in serious adverse events or fatal overdoses between the 2 groups.1,2
The price for naltrexone is $1665.06 per monthly injection.3 The price for buprenorphine-naloxone varies depending on dose and formulation, with a general range of $527 to $600 per month at 16 mg/d.4
Editor’s takeaway
Two higher-quality RCTs show similar but imperfect effectiveness for both XR-NTX and daily sublingual BUP-NX. Injectable naltrexone’s higher cost may influence medication choice.
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391:309-318.
2. Tanum L, Solli KK, Latif ZE, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence: a randomized clinical noninferiority trial. JAMA Psychiatry. 2017;74:1197-1205.
3. Naltrexone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
4. Buprenorphine and naloxone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
EVIDENCE SUMMARY
Two recent multicenter, open-label RCTs, 1 in the United States and 1 in Norway, compared monthly XR-NTX with daily BUP-NX.1,2 Both studies evaluated effectiveness (defined by either the number of people who relapsed or self-reported opioid use), cravings, and safety (defined as the absence of serious adverse events such as medically complex withdrawal or fatal overdose).
The participant populations were similar in both mean age and mean age of onset of opioid use. Duration of opioid use was reported differently (total duration or years of heavy heroin or other opioid use) and couldn’t be compared directly.
Naltrexone and buprenorphine-naloxone are similarly effective
The US study enrolled 570 opioid-dependent participants in a 24-week comparative effectiveness trial.1 The 8 study sites were community treatment programs, and the participants were recruited during voluntary inpatient detoxification admissions. Some participants were randomized while on methadone or buprenorphine tapers and some after complete detoxification.
The intention-to-treat analysis included 283 patients in the XR-NTX group and 287 in the BUP-NX group. At 24 weeks, the number of participants who’d had a relapse event (self-reported use or positive urine drug test for nonstudy opioids or refusal to provide a urine sample) was 185 (65%) for XR-NTX compared with 163 (57%) for BUP-NX (odds ratio [OR] = 1.44, 95% confidence interval [CI], 1.02 to 2.01; P = .036).
The 12-week Norwegian noninferiority trial enrolled 159 participants.2 In contrast to the US study, all participants were required to complete inpatient detoxification before randomization and induction onto the study medication.
Patients on BUP-NX reported 3.6 more days of heroin use within the previous 28 days than patients in the XR-NTX group (95% CI, 1.2 to 6; P = .003). For other illicit opioids, self-reported use was 2.4 days greater in the BUP-NX group (95% CI, −0.1 to 4.9; P = .06). Retention with XR-NTX was noninferior to BUP-NX (mean days in therapy [standard deviation], 69.3 [25.9] and 63.7 [29.9]; P = .33).
Randomizing after complete detox reduces induction failures
Naltrexone, a full opioid antagonist, precipitates withdrawal when a full or partial opioid agonist is engaging the opioid receptor. For this reason, an opioid-free interval of 7 to 10 days is generally recommended before initiating naltrexone, raising the risk for relapse during the induction process.
Continue to: The Norwegian trial...
The Norwegian trial randomized participants after detoxification. The US trial, in which some participants were randomized before completing detoxification, reported 79 (28%) induction failures for XR-NTX and 17 (6%) for BUP-NX.1 As a result, a per protocol analysis was completed with the 204 patients on XR-NTX and 270 patients on BUP-NX who were successfully inducted onto a study medication. The 24-week relapse rate was 52% (106) for XR-NTX and 56% (150) for BUP-NX (OR = 0.87; 95% CI, 0.60 to 1.25; P = .44).
Cravings, adverse events, and cost considerations
Patients reported cravings using a visual analog scale. At 12 weeks in both studies, the XR-NTX groups reported fewer cravings than the BUP-NX groups, although by the end of the 24-week US trial, no statistically significant difference in cravings was found between the 2 groups.1,2
The Norwegian trial found a difference between the XR-NTX and the BUP-NX groups in the percentage of nonserious adverse events such as nausea or chills (60.6% in the XR-NTX group vs 30.6% in the BUP-NX group; P < .001), and the US trial found a difference in total number of overdoses (64% of the total overdoses were in the XR-NTX group). Neither trial, however, reported a statistically significant difference in serious adverse events or fatal overdoses between the 2 groups.1,2
The price for naltrexone is $1665.06 per monthly injection.3 The price for buprenorphine-naloxone varies depending on dose and formulation, with a general range of $527 to $600 per month at 16 mg/d.4
Editor’s takeaway
Two higher-quality RCTs show similar but imperfect effectiveness for both XR-NTX and daily sublingual BUP-NX. Injectable naltrexone’s higher cost may influence medication choice.
EVIDENCE SUMMARY
Two recent multicenter, open-label RCTs, 1 in the United States and 1 in Norway, compared monthly XR-NTX with daily BUP-NX.1,2 Both studies evaluated effectiveness (defined by either the number of people who relapsed or self-reported opioid use), cravings, and safety (defined as the absence of serious adverse events such as medically complex withdrawal or fatal overdose).
The participant populations were similar in both mean age and mean age of onset of opioid use. Duration of opioid use was reported differently (total duration or years of heavy heroin or other opioid use) and couldn’t be compared directly.
Naltrexone and buprenorphine-naloxone are similarly effective
The US study enrolled 570 opioid-dependent participants in a 24-week comparative effectiveness trial.1 The 8 study sites were community treatment programs, and the participants were recruited during voluntary inpatient detoxification admissions. Some participants were randomized while on methadone or buprenorphine tapers and some after complete detoxification.
The intention-to-treat analysis included 283 patients in the XR-NTX group and 287 in the BUP-NX group. At 24 weeks, the number of participants who’d had a relapse event (self-reported use or positive urine drug test for nonstudy opioids or refusal to provide a urine sample) was 185 (65%) for XR-NTX compared with 163 (57%) for BUP-NX (odds ratio [OR] = 1.44, 95% confidence interval [CI], 1.02 to 2.01; P = .036).
The 12-week Norwegian noninferiority trial enrolled 159 participants.2 In contrast to the US study, all participants were required to complete inpatient detoxification before randomization and induction onto the study medication.
Patients on BUP-NX reported 3.6 more days of heroin use within the previous 28 days than patients in the XR-NTX group (95% CI, 1.2 to 6; P = .003). For other illicit opioids, self-reported use was 2.4 days greater in the BUP-NX group (95% CI, −0.1 to 4.9; P = .06). Retention with XR-NTX was noninferior to BUP-NX (mean days in therapy [standard deviation], 69.3 [25.9] and 63.7 [29.9]; P = .33).
Randomizing after complete detox reduces induction failures
Naltrexone, a full opioid antagonist, precipitates withdrawal when a full or partial opioid agonist is engaging the opioid receptor. For this reason, an opioid-free interval of 7 to 10 days is generally recommended before initiating naltrexone, raising the risk for relapse during the induction process.
Continue to: The Norwegian trial...
The Norwegian trial randomized participants after detoxification. The US trial, in which some participants were randomized before completing detoxification, reported 79 (28%) induction failures for XR-NTX and 17 (6%) for BUP-NX.1 As a result, a per protocol analysis was completed with the 204 patients on XR-NTX and 270 patients on BUP-NX who were successfully inducted onto a study medication. The 24-week relapse rate was 52% (106) for XR-NTX and 56% (150) for BUP-NX (OR = 0.87; 95% CI, 0.60 to 1.25; P = .44).
Cravings, adverse events, and cost considerations
Patients reported cravings using a visual analog scale. At 12 weeks in both studies, the XR-NTX groups reported fewer cravings than the BUP-NX groups, although by the end of the 24-week US trial, no statistically significant difference in cravings was found between the 2 groups.1,2
The Norwegian trial found a difference between the XR-NTX and the BUP-NX groups in the percentage of nonserious adverse events such as nausea or chills (60.6% in the XR-NTX group vs 30.6% in the BUP-NX group; P < .001), and the US trial found a difference in total number of overdoses (64% of the total overdoses were in the XR-NTX group). Neither trial, however, reported a statistically significant difference in serious adverse events or fatal overdoses between the 2 groups.1,2
The price for naltrexone is $1665.06 per monthly injection.3 The price for buprenorphine-naloxone varies depending on dose and formulation, with a general range of $527 to $600 per month at 16 mg/d.4
Editor’s takeaway
Two higher-quality RCTs show similar but imperfect effectiveness for both XR-NTX and daily sublingual BUP-NX. Injectable naltrexone’s higher cost may influence medication choice.
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391:309-318.
2. Tanum L, Solli KK, Latif ZE, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence: a randomized clinical noninferiority trial. JAMA Psychiatry. 2017;74:1197-1205.
3. Naltrexone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
4. Buprenorphine and naloxone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391:309-318.
2. Tanum L, Solli KK, Latif ZE, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence: a randomized clinical noninferiority trial. JAMA Psychiatry. 2017;74:1197-1205.
3. Naltrexone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
4. Buprenorphine and naloxone: drug information. Lexi-Comp, Inc (Lexi-Drugs). Wolters Kluwer Health, Inc. Riverwoods, IL. http://online.lexi.com. Accessed November 20, 2020.
EVIDENCE-BASED ANSWER:
Yes. Monthly extended-release injectable naltrexone (XR-NTX) treats opioid use disorder as effectively as daily sublingual buprenorphine-naloxone (BUP-NX) without causing any increase in serious adverse events or fatal overdoses. (strength of recommendation: A, 2 good-quality RCTs).
Painful, lower extremity rash
This woman’s palpable purpura with edema in her lower extremities was consistent with cutaneous leukocytoclastic vasculitis (LCV).
LCV is characterized by the circulation of immune complexes that promote activation of complement, leading to endothelial injury and palpable purpura. Pain, arthralgia, cutaneous ulceration, and constitutional symptoms may be observed. About 50% of LCV cases are idiopathic. Identified causes include infection (including syphilis infection), drugs, malignancy, and connective tissue disease.
Systemic involvement must be ruled out in any patient with cutaneous LCV. The work-up is based on the individual patient assessment and may include a complete blood count with differential, complete metabolic panel, inflammatory markers, urinalysis, hepatitis panel, anti-nuclear antibody, rheumatoid factor, anti-neutrophil cytoplasmic antibodies, cryoglobulins, serum protein electrophoresis, and serum complement. A cutaneous punch biopsy for both hematoxylin and eosin (H&E) and direct immunofluorescence (DIF) confirms the diagnosis of LCV.
For uncomplicated LCV cases without systemic involvement, treatment is generally supportive. Any identified underlying cause should be addressed. Analgesics may be considered for pain. Systemic therapy is indicated for patients with cutaneous ulceration, systemic vasculitis, or recurrent cases; this therapy may include colchicine, dapsone, corticosteroids, mycophenolate mofetil, and methotrexate.
In this patient’s case, a punch biopsy of the left lower extremity showed findings consistent with cutaneous LCV. She denied a history of intravenous drug use or initiation of new medications. Labs were notable for an elevated erythrocyte sedimentation rate, c-reactive protein, and elevated creatinine.
Incidentally, she was found to be 32-weeks pregnant, went into pre-term labor while admitted, and delivered her baby without complication.
She had a reactive treponemal antibody, with rapid plasma reagin titer of 1:128, which confirmed a diagnosis of syphilis. She was treated with 1 dose of intra-muscular penicillin G while an inpatient. Her arthralgias improved during her hospitalization without initiation of steroids or other immunomodulatory therapy. Outpatient follow-up was expected to consist of completion of 3 total doses of IM penicillin, as well as renal studies, given her elevated creatinine.
Photo courtesy of Cyrelle R. Fermin, MD, and text courtesy of Cyrelle R. Fermin, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306.
This woman’s palpable purpura with edema in her lower extremities was consistent with cutaneous leukocytoclastic vasculitis (LCV).
LCV is characterized by the circulation of immune complexes that promote activation of complement, leading to endothelial injury and palpable purpura. Pain, arthralgia, cutaneous ulceration, and constitutional symptoms may be observed. About 50% of LCV cases are idiopathic. Identified causes include infection (including syphilis infection), drugs, malignancy, and connective tissue disease.
Systemic involvement must be ruled out in any patient with cutaneous LCV. The work-up is based on the individual patient assessment and may include a complete blood count with differential, complete metabolic panel, inflammatory markers, urinalysis, hepatitis panel, anti-nuclear antibody, rheumatoid factor, anti-neutrophil cytoplasmic antibodies, cryoglobulins, serum protein electrophoresis, and serum complement. A cutaneous punch biopsy for both hematoxylin and eosin (H&E) and direct immunofluorescence (DIF) confirms the diagnosis of LCV.
For uncomplicated LCV cases without systemic involvement, treatment is generally supportive. Any identified underlying cause should be addressed. Analgesics may be considered for pain. Systemic therapy is indicated for patients with cutaneous ulceration, systemic vasculitis, or recurrent cases; this therapy may include colchicine, dapsone, corticosteroids, mycophenolate mofetil, and methotrexate.
In this patient’s case, a punch biopsy of the left lower extremity showed findings consistent with cutaneous LCV. She denied a history of intravenous drug use or initiation of new medications. Labs were notable for an elevated erythrocyte sedimentation rate, c-reactive protein, and elevated creatinine.
Incidentally, she was found to be 32-weeks pregnant, went into pre-term labor while admitted, and delivered her baby without complication.
She had a reactive treponemal antibody, with rapid plasma reagin titer of 1:128, which confirmed a diagnosis of syphilis. She was treated with 1 dose of intra-muscular penicillin G while an inpatient. Her arthralgias improved during her hospitalization without initiation of steroids or other immunomodulatory therapy. Outpatient follow-up was expected to consist of completion of 3 total doses of IM penicillin, as well as renal studies, given her elevated creatinine.
Photo courtesy of Cyrelle R. Fermin, MD, and text courtesy of Cyrelle R. Fermin, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
This woman’s palpable purpura with edema in her lower extremities was consistent with cutaneous leukocytoclastic vasculitis (LCV).
LCV is characterized by the circulation of immune complexes that promote activation of complement, leading to endothelial injury and palpable purpura. Pain, arthralgia, cutaneous ulceration, and constitutional symptoms may be observed. About 50% of LCV cases are idiopathic. Identified causes include infection (including syphilis infection), drugs, malignancy, and connective tissue disease.
Systemic involvement must be ruled out in any patient with cutaneous LCV. The work-up is based on the individual patient assessment and may include a complete blood count with differential, complete metabolic panel, inflammatory markers, urinalysis, hepatitis panel, anti-nuclear antibody, rheumatoid factor, anti-neutrophil cytoplasmic antibodies, cryoglobulins, serum protein electrophoresis, and serum complement. A cutaneous punch biopsy for both hematoxylin and eosin (H&E) and direct immunofluorescence (DIF) confirms the diagnosis of LCV.
For uncomplicated LCV cases without systemic involvement, treatment is generally supportive. Any identified underlying cause should be addressed. Analgesics may be considered for pain. Systemic therapy is indicated for patients with cutaneous ulceration, systemic vasculitis, or recurrent cases; this therapy may include colchicine, dapsone, corticosteroids, mycophenolate mofetil, and methotrexate.
In this patient’s case, a punch biopsy of the left lower extremity showed findings consistent with cutaneous LCV. She denied a history of intravenous drug use or initiation of new medications. Labs were notable for an elevated erythrocyte sedimentation rate, c-reactive protein, and elevated creatinine.
Incidentally, she was found to be 32-weeks pregnant, went into pre-term labor while admitted, and delivered her baby without complication.
She had a reactive treponemal antibody, with rapid plasma reagin titer of 1:128, which confirmed a diagnosis of syphilis. She was treated with 1 dose of intra-muscular penicillin G while an inpatient. Her arthralgias improved during her hospitalization without initiation of steroids or other immunomodulatory therapy. Outpatient follow-up was expected to consist of completion of 3 total doses of IM penicillin, as well as renal studies, given her elevated creatinine.
Photo courtesy of Cyrelle R. Fermin, MD, and text courtesy of Cyrelle R. Fermin, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306.
Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306.
“Polka-dotted” feet
This man has pitted keratolysis (PK), characterized by multiple small pits on the soles of the feet. PK is often associated with hyperhidrosis and significant odor. The lesions usually have a punched-out appearance and are flesh-colored. The dark color of these lesions was due to the patient’s footwear.
PK is caused by bacterial overgrowth in the stratum corneum. Corynebacterium is the most common bacterial culprit, but Kytococcus, Actinomyces, and Dermatophilus have also been implicated. The bacterial infection is thought to be secondary to hyperhidrosis or as a result of hygiene, footwear, or other conditions that retain moisture and promote maceration of the soles of the feet. Therefore, treatment includes a 2-pronged approach: Resolve the bacterial infection and reduce excess moisture. Effective antibacterials include topical clindamycin, erythromycin, fusidic acid, and benzoyl peroxide. Oral antibiotics are not often required.
Hyperhidrosis can be treated with prescription strength 20% aluminum chloride antiperspirant applied to the feet in a tapering schedule, first daily and then 2 or 3 times weekly. Aluminum chloride is frequently not covered by insurance companies, but over-the-counter (OTC) 12% formulations (Certain DRI) usually suffice. Additionally, changing socks and using moisture-wicking shoes or socks are helpful measures to keep feet dry.
One study treated PK with topical erythromycin 3% gel twice daily, without the use of aluminum chloride antiperspirants, and found that the hyperhidrosis greatly improved. The authors theorized that the gram-positive bacterial infection upregulated eccrine sweat glands causing hyperhidrosis as a secondary, rather than the primary, cause of PK.
This patient was prescribed topical erythromycin gel twice daily for the soles of his feet. For his hyperhidrosis, he was advised to purchase OTC aluminum chloride antiperspirants to apply to his feet daily for the first week and to then decrease to 2 or 3 times per week. He was counseled to take an extra pair of socks for changing midway through his workday and to return for reevaluation if his skin did not improve.
Image courtesy of Sarah Friedberg, MD, and text courtesy of Daniel Stulberg, MD, FAAFP, and Sarah Friedberg, MD, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Pranteda G, Carlesimo M, Pranteda G, et al. Pitted keratolysis, erythromycin, and hyperhidrosis. Dermatol Ther. 2014;27:101-104.
This man has pitted keratolysis (PK), characterized by multiple small pits on the soles of the feet. PK is often associated with hyperhidrosis and significant odor. The lesions usually have a punched-out appearance and are flesh-colored. The dark color of these lesions was due to the patient’s footwear.
PK is caused by bacterial overgrowth in the stratum corneum. Corynebacterium is the most common bacterial culprit, but Kytococcus, Actinomyces, and Dermatophilus have also been implicated. The bacterial infection is thought to be secondary to hyperhidrosis or as a result of hygiene, footwear, or other conditions that retain moisture and promote maceration of the soles of the feet. Therefore, treatment includes a 2-pronged approach: Resolve the bacterial infection and reduce excess moisture. Effective antibacterials include topical clindamycin, erythromycin, fusidic acid, and benzoyl peroxide. Oral antibiotics are not often required.
Hyperhidrosis can be treated with prescription strength 20% aluminum chloride antiperspirant applied to the feet in a tapering schedule, first daily and then 2 or 3 times weekly. Aluminum chloride is frequently not covered by insurance companies, but over-the-counter (OTC) 12% formulations (Certain DRI) usually suffice. Additionally, changing socks and using moisture-wicking shoes or socks are helpful measures to keep feet dry.
One study treated PK with topical erythromycin 3% gel twice daily, without the use of aluminum chloride antiperspirants, and found that the hyperhidrosis greatly improved. The authors theorized that the gram-positive bacterial infection upregulated eccrine sweat glands causing hyperhidrosis as a secondary, rather than the primary, cause of PK.
This patient was prescribed topical erythromycin gel twice daily for the soles of his feet. For his hyperhidrosis, he was advised to purchase OTC aluminum chloride antiperspirants to apply to his feet daily for the first week and to then decrease to 2 or 3 times per week. He was counseled to take an extra pair of socks for changing midway through his workday and to return for reevaluation if his skin did not improve.
Image courtesy of Sarah Friedberg, MD, and text courtesy of Daniel Stulberg, MD, FAAFP, and Sarah Friedberg, MD, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
This man has pitted keratolysis (PK), characterized by multiple small pits on the soles of the feet. PK is often associated with hyperhidrosis and significant odor. The lesions usually have a punched-out appearance and are flesh-colored. The dark color of these lesions was due to the patient’s footwear.
PK is caused by bacterial overgrowth in the stratum corneum. Corynebacterium is the most common bacterial culprit, but Kytococcus, Actinomyces, and Dermatophilus have also been implicated. The bacterial infection is thought to be secondary to hyperhidrosis or as a result of hygiene, footwear, or other conditions that retain moisture and promote maceration of the soles of the feet. Therefore, treatment includes a 2-pronged approach: Resolve the bacterial infection and reduce excess moisture. Effective antibacterials include topical clindamycin, erythromycin, fusidic acid, and benzoyl peroxide. Oral antibiotics are not often required.
Hyperhidrosis can be treated with prescription strength 20% aluminum chloride antiperspirant applied to the feet in a tapering schedule, first daily and then 2 or 3 times weekly. Aluminum chloride is frequently not covered by insurance companies, but over-the-counter (OTC) 12% formulations (Certain DRI) usually suffice. Additionally, changing socks and using moisture-wicking shoes or socks are helpful measures to keep feet dry.
One study treated PK with topical erythromycin 3% gel twice daily, without the use of aluminum chloride antiperspirants, and found that the hyperhidrosis greatly improved. The authors theorized that the gram-positive bacterial infection upregulated eccrine sweat glands causing hyperhidrosis as a secondary, rather than the primary, cause of PK.
This patient was prescribed topical erythromycin gel twice daily for the soles of his feet. For his hyperhidrosis, he was advised to purchase OTC aluminum chloride antiperspirants to apply to his feet daily for the first week and to then decrease to 2 or 3 times per week. He was counseled to take an extra pair of socks for changing midway through his workday and to return for reevaluation if his skin did not improve.
Image courtesy of Sarah Friedberg, MD, and text courtesy of Daniel Stulberg, MD, FAAFP, and Sarah Friedberg, MD, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.
Pranteda G, Carlesimo M, Pranteda G, et al. Pitted keratolysis, erythromycin, and hyperhidrosis. Dermatol Ther. 2014;27:101-104.
Pranteda G, Carlesimo M, Pranteda G, et al. Pitted keratolysis, erythromycin, and hyperhidrosis. Dermatol Ther. 2014;27:101-104.