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TABLE16.6
RecommendedOrderofTreatmentforDryEyeDisease
Order Agent Comments
First
line
MildDES:artificialtearsubstituteQID
or
ModeratetosevereDES:preservative-free
artificialtearsubstitute,administeredupto
IfthepatienthasunderlyingSjögrensyndrome,administer
pilocarpinetablets5mgQIDorcevimelinetablets30mg
TID.

hourly
Second
line
Cyclosporine0.05%ophthalmicemulsion
BID
or
Lifitegrast5%solutionq12h
Ophthalmiccorticosteroidtherapymaybeusefulforthe
short-term(2-wk)suppressionofirritationsecondaryto
inflammation.
DES,dryeyesyndrome.
Second-LineTherapy
Patients with moderate to severe DED who fail to experience any improvement in symptoms with
artificialtearsmaybenefitfromtherapywith0.05%cyclosporineophthalmicemulsion1dropineacheye
twicedailyorlifitegrast5%ophthalmicsolution1dropineacheyeevery12hours.Duetotheadverse
effect profile, corticosteroid therapy is limited to second-line therapy for short-term (2 weeks)
suppressionofirritationsecondarytoinflammation.
Third-LineTherapy
Patients with severe DED that fails to respond to drug therapy are candidates for permanent punctal
occlusionortarsorrhaphy.
MonitoringPatientResponse
The frequency and extent of follow-up will depend upon the severity of DED and the therapeutic
approachselected.PatientswithmildDEDcanbeseenonceortwiceperyearforfollow-upifsymptoms
arecontrolled bytherapy.PatientswithsterilecornealulcerationassociatedwithDEDrequirecareful,
sometimesdaily,monitoring(AAO,2018c).
PatientEducation
Patients with DED should be educated about the chronic nature of the disease and given specific
instructionsabouttheirtherapeutic regimens.PatientswithmoderatetosevereDEDareatanelevated
riskforcontactlensintolerance.
GLAUCOMA:PRIMARYOPEN-ANGLEGLAUCOMA
Glaucomaisagroupofeyediseasesinvolvingopticneuropathycharacterizedbyirreversibledamageto
theopticnerveandretinalganglioncells(Figure16.2).Overtime,thisdeteriorationresultsinthelossof
visual sensitivity and field, whichfrequently goes unnoticed until a significant amountofdamage has
occurred. Glaucomais the leading causeofirreversible blindness intheworld (Bourneet al.,2017).
Therearenumeroustypesofglaucoma,includingprimaryopen-angleglaucoma(POAG),acuteclosedangleglaucoma, andnarrow-angle glaucoma.POAG accounts for upto80%of glaucomacasesinthe
UnitedStatesandafflicts2.7millionAmericans(Liu&Tanna,2016;Weinrabetal.,2014);assuch,this
sectionwillspecificallyreviewPOAG.

FIGURE16-2Anatomyoftheeye.
Causes
SeveralstudieshaveshownthattheprevalenceofPOAGincreaseswithincreasingIOP(Gordonetal.,
2002;Leskeetal.,2003).ThemedianIOPinlargepopulationsis15.5±2.5mmHg.Previously,itwas
thought that increased IOPwas the sole cause ofPOAG, but it is now recognizedthat IOP is one of
severalfactorsassociatedwiththedevelopmentofPOAG,andanincreasedIOPisnotrequiredforthe
diagnosisofPOAG.
AdditionalriskfactorsforthedevelopmentofPOAGincludeincreasingage,blackrace(threetimes
greater thanwhites), a familyhistory of glaucoma,a thincentral cornea,andtype 2 diabetes mellitus
(AAO,2020;Kapetenakisetal.,2016).
Pathophysiology
The pathophysiology of glaucoma-induced vision loss is not well understood. Aqueous humor is
producedbytheciliarybodyandsecretedintotheposteriorchamberoftheeye.Apressuregradientinthe
posterior chamber forces theaqueous humor between the iris andlens and through the pupil into the
anteriorchamber.Aqueoushumorintheanteriorchamberleavestheeyethroughtwomethods:filtration
throughthetrabecularmeshworktoSchlemmcanal(80%-85%)ortraversaloftheanteriorfaceoftheiris
and absorption into iris blood vessels (uveoscleral outflow). In POAG, degenerative changes in the
trabecular meshwork and Schlemm canal result in a decrease in the outflow of the aqueous humor,
resultinginIOPelevationandcompressionoftheopticnerveresultingindamageandopticneuropathy
(Marshalletal.,

2018).
DiagnosticCriteria
SymptomsofPOAGdonotmanifestuntilsubstantialdamagehasalreadyoccurred.Thediagnosisofany
glaucomashouldbemadebyaneyecareprofessional.Anypatientsreportingvisualfieldlossshouldbe
referredtoaneyecareprofessionalforpromptevaluation.
During the physical examination, IOP is measured in each eye, preferably with a Goldmann-type
applanation tonometer, before gonioscopy or dilation of the pupil (AAO, 2020). Unfortunately, the
measurementofIOPisnotaneffectivemethodforscreeningpopulationsforglaucoma.AtanIOPcutoffof
21mmHg,thesensitivityforthediagnosisofPOAGbytonometrywas47.1%(Tielschetal.,1991),and
halfofallindividualswithPOAGaremeasuredwithanIOPoflessthan22mmHgatasinglescreening
(Leske et al., 2003). As such, the AAO recommends, in addition to the measurement of IOP, that a
physical examination include the followingelements: patient history, test of pupil reactivity, slit-lamp
biomicroscopyoftheanteriorsegment,determinationofcentralcornealthickness,gonioscopy,evaluation
oftheopticnerveheadandretinalnervefiberlayer,documentationoftheopticnerveheadappearance,
evaluationofthefundus,andevaluationofthevisualfield(AAO,2020).
InitiatingDrugTherapy
ThegoalsoftherapyforPOAGaretocontrol IOP, tostabilizethestatusoftheopticnerveandretinal
fiberlayer,andtostabilizethevisualfield(AAO,2020).Mostcasesofglaucomacanbecontrolledand
visionlosspreventedwithearlydetectionandtreatment.TreatmentofPOAGentailsdecreasingaqueous
humorproduction,increasingaqueousoutflow,oracombinationofboth.
Over the past 30 years, glaucoma management has changed significantly, primarily due to the
introductionofpharmaceuticalagentsthathaveshownclinicaleffectiveness(Table16.7).Theseagents
havebeenassociatedwithasignificantreductioninsurgeryratesamongglaucomapatients(Conlonetal.,
2017).
OnceatargetIOPhasbeendetermined,treatmentmayincludedrugtherapy,lasertherapy,orsurgery.
Topicalmedicationis,inmostcases,indicatedasfirst-linetherapy.Severaltrialshaveclearlyshownthat
reducing IOP by treatment with ocular hypotensive medication can prevent or reduce the risk of
progressionofglaucoma.Furthermore,themoreIOPisreduced,themoretheriskofglaucomatouseye
damagedecreases.
GoalsofDrugTherapy
The goals of drug therapy for POAG are to reduce IOP to a target level and to prevent or slow the
progressionofvisionloss.InpatientswithPOAG,theinitial IOP targetshouldbe 20% to30% lower
thanbaseline. Additional IOPlowering maybe justified, based uponthe severityof the existing optic
nerve damage,thespeedatwhichthedamageoccurred, andthepresence ofother riskfactors suchas
familyhistory,age, or disc hemorrhage. (AAO,2020). Visual fields andoptic nerve status should be
monitoredforsignsofchange;ifprogressionisdetected,theIOPtargetshouldbelowered.
BetaBlockers

Beta blockers are the benchmark against which other IOP-lowering medications are measured. Beta
blockersreduceade-nylylcyclaseactivity,whichinturnreducestheproductionofaqueoushumorinthe
ciliarybody.Beta blockers lower IOPbyanaverage of20%to 25%. There are fiveophthalmic beta
blockersavailableintheUnitedStates:timolol,levobunolol,carteolol,andmetipranololarenonselective
betablockers,while betaxolol isabeta1-selectiveagent.Althoughnonselec-tive betablockersmaybe
more efficacious in lowering IOP, selective beta blockers appear to be better tolerated systemi-cally,
particularlyinpatientswithchronicobstructivepulmonarydisease.
TABLE16.7
OverviewofGlaucomaAgents
Generic(Trade)
NameandDosage
SelectedAdverseEvents Contraindications SpecialConsiderations
BetaBlockers
Betaxolol0.5%
solutionor0.25%
suspension(Betoptic
S)
Dosing:1-2dropsin
theaffectedeye(s)
BID
Discomfortoninstillation,
tearing,decreasedcorneal
sensitivity,edema,bradycardia,
hypotension,dizziness,
photophobia
Cardiogenicshock
Second-orthird-degree
AVblock
Sinusbradycardia
Overtcardiacfailure
Acardioselective(beta-1)
blocker;ithasfewereffectson
pulmonaryandcardiovascular
parameters.
Carteolol1%solution
Dosing:1dropinthe
affectedeye(s)BID
Transienteyeirritation,burning,
tearing,conjunctivalhyper-emia,
edema,bradycardia,
hypotension,arrhythmia,
palpitations,photophopia
Bronchialasthmaor
severeCOPDSinus
bradycardiaSecond-or
third-degreeAVblock
Overtcardiacfailure
Cardiogenicshock
Maybeabsorbedsystemically;
thesameadversereactions
seenwithoralbetablockers
mayoccur.
Maymaskthesymptomsof
acutehypoglycemiaor
hyperthyroidism
Levobunolol0.5%
solution(Betagan)
Dosing:1-2dropsin
theaffectedeye(s)
oncedaily;dosecan
beincreasedto1drop
BIDinsevere
glaucoma.
Burningandstinging,
blepharoconjunctivitis,urticaria,
ataxia,bradycardia,arrhythmia,
hypotension,syncope,heart
block,bronchospasm
Bronchialasthmaor
severeCOPDSinus
bradycardiaSecond-or
third-degreeAVblock
Overtcardiacfailure
Cardiogenicshock
Maybeabsorbedsystemically;
thesameadversereactions
seenwithoralbetablockers
mayoccur.
Maymaskthesymptomsof
acutehypoglycemiaor
hyperthyroidism
Metipranolol0.3%
solutionDosing:1
dropintheaffected
eye(s)BID
Transientlocaldiscomfort,
conjunctivitis,eyeliddermatitis,
blepharitis,blurredvision,
photophobia,headache,asthenia,
angina,palpitation,bradycardia
Bronchialasthmaor
severeCOPD
Symptomaticsinus
bradycardiaSecond-or
third-degreeAVblock
Overtcardiacfailure
Cardiogenicshock
Maybeabsorbedsystemically;
thesameadversereactions
seenwithoralbetablockers
mayoccur.
Maymaskthesymptomsof
acutehypoglycemiaor
hyperthyroidism
Timolol0.25%or
0.5%solution
(Timoptic,Timoptic
Ocudose,Betimol,
Istalol)orgel-forming
Ocularirritation,decreased
cornealsensitivity,visual
disturbances,conjunctivitis,
tearing,headache,dizziness,
bradycardia,arrhythmia,angina,
Bronchialasthmaor
severeCOPDSinus
bradycardiaSecond-or
third-degreeAVblock
Overtcardiacfailure
Maybeabsorbedsystemically;
thesameadversereactions
seenwithoralbetablockers
mayoccur.
Maymaskthesymptomsof

solution(TimopticXE)
Dosing:
Solution:1dropinthe
affectedeye(s)BID;
Islatol:1dropinthe
affectedeye(s)once
dailyAM
Gel-formingsolution:
1dropintheaffected
eye(s)oncedaily
bronchospasm Cardiogenicshock acutehypoglycemiaor
hyperthyroidism.Other
ophthalmicmedicationsshould
beadministered10minbefore
thegel-formingsolution.
CarbonicAnhydraseInhibitors
Brinzolamide1%
suspension(Azopt)
Dosing:1dropinthe
affectedeye(s)TID
Blurredvision,bittertaste,
blepharitis,dermatitis,dryeye,
headache,hyperemiaocularpain,
pruritus
Usewithcautioninpatients
withrenalimpairment,hepatic
impairment,orsulfonamides
hypersensitivity.
Dorzolamide2%
solution(Trusopt)
Dosing:1dropinthe
affected
eye(s)TID
Ocularburningandstinging,
bittertaste,keratitis,ocular
allergy,blurredvision,tearing,
photophobia
Sulfaallergy Usewithcautioninpatients
withrenalimpairment,hepatic
impairment,orsulfonamides
hypersensitivity.
ProstaglandinAnalogs
Bimatoprost0.03%
solution(Lumigan)
Dosing:1dropinthe
affectedeye(s)once
dailyPM
Conjunctivalhyperemia,growth
ofeyelashes,ocularpruritus,dry
eye,irisdiscoloration,visual
disturbance,eyepain,
pigmentationoftheperiocular
skin,foreignbodysensation
Irisdiscolorationisirreversible;
incidencelessthanwith
latanoprost
Latanoprost0.005%
solution(Xalatan)
Dosing:1dropinthe
affectedeye(s)once
dailyPM
Irisdiscoloration,blurredvision,
burningandstinging,conjunctival
hyperemia,itching,eyelash
changes,eyelidskindarkening
Irisdiscolorationisirreversible.
Requiresrefrigerationuntil
dispensed
Tafluprost0.0015%
solution(Zioptan)
Dosing:1dropinthe
affectedeye(s)once
dailyPM
Conjunctivalhyperemia,ocular
stinging,headache,ocular
pruritus,dryeye,growthof
eyelashes,irisdiscoloration,
pigmentationoftheperiocular
skin
Irisdiscolorationisirreversible.
Travoprost0.004%
solution(TravatanZ)
Dosing:1dropinthe
affectedeye(s)once
dailyPM
Ocularhyperemia,decreased
visualacuity,eyediscomfort,
foreignbodysensation,eyepain,
pruritus
Irisdiscolorationisirreversible.
Mayinterfereinpregnancy;
shouldnotbeusedduring
pregnancyorbythose
attemptingtobecomepregnant
NitricOxideDonatingProstaglandinAnalogs
Latanoprostenebunod
0.024%solution
(Vyzulta)
Dosing:1dropinthe
Sameaslatanoprost Sameaslatanoprost

affectedeye(s)once
dailyPM
AdrenergicAgonists
Apraclonidine0.5%
solution(Iopidine)
Dosing:1-2dropsin
theaffectedeye(s)
TID
Hyperemia,tearing,pruritus,lid
edema,drymouth,foreignbody
sensation,eyelidretraction
Hypersensitivityto
clonidinePatients
receivingMAOinhibitors
Forshort-termuseonlyasan
adjuncttherapyA1%solution
isavailableforpreventionof
postsurgicalelevationsinIOP.
Brimonidine0.1%,
0.15%,or0.2%
solution(AlphaganP)
Dosing:1dropinthe
affectedeye(s)TID,
approximately8h
apart
Ocularhyperemia,ocular
pruritus,visualdisturbance,
allergicconjunctivitis
somnolence,headache,
hypertension,fatigue,
drowsiness,drymouth
PatientsreceivingMAO
inhibitors
Notrecommendedinchildren
lessthanage2
CholinergicAgonists
Pilocarpine1%,2%,
or4%solution(Isopto
Carpine)
Dosing:1-2drops
TIDorQID
Stingingandburning,tearing,
ciliaryspasm,blurredvision,
browache,hypertension,
tachycardia,bronchospasm,
Acuteiritisorother
conditionswherepapillary
constrictionisundesirable
RhoKinaseInhibitors
Netarsudil0.02%
solution(Rhopressa)
Dosing:1dropinthe
affectedeye(s)once
daily
Conjunctivalhyperemia,corneal
verticillata,stingingandburning,
conjunctivalhemorrhage,blurred
vision,decreasedvisualacuity
Labeling:wait15min
followingadministrationbefore
insertingcontactlenses.
CombinationProducts
Brimonidineand
timolol0.2%-0.5%
solution(Combigan)
Dosing:1dropinthe
affectedeye(s)q12h
Seeindividualcomponents. Seeindividual
components.
Combinedeffectresultsin
greaterIOPloweringthan
eitheragentalone,butnotas
greatasbrimonidineTIDand
timololBIDadministered
concomitantly.
Dorzolamideand
timolol2%-0.5%
solution(Cosopt)
Dosing:1dropinto
theaffectedeye(s)
BID
Seeindividualcomponents. Seeindividual
components.
Combinedeffectresultsin
greaterIOPloweringthan
eitheragentalone,butnotas
greatasdorzolamideTIDand
timololBIDadministered
concomitantly.
Brinzolamideand
brimoni-dine
1%-0.2%solution
(Simbrinza)
Dosing:1dropinto
theaffectedeye(s)
TID
Seeindividualcomponents. Seeindividual
components.
Netarsudiland
latanoprost
Seeindividualcomponents Seeindividualcomponents

0.02%-0.005%
solution
(Rocklatan)Dosing:1
dropintotheaffected
eye(s)oncedailyPM
AV,atrioventricularmode;COPD,chronicobstructivepulmonarydisease;IOP,increasedintraocularpressure;MAO,monoamineoxidase
Theophthalmicbetablockersaretypicallyappliedtwicedaily.Timololisavailableinasolutionthat
formsageluponapplication,allowingonce-dailydosing.Adverseeffectsincludestinging,burning,dry
eye,andblurredvision.Topicalbetablockerscanbeabsorbedsystemicallyandmaycausebradycardia,
reduced blood pressure, aggravationofcongestive heartfailure, heart block, bronchospasm in asthma
patients,andcentralnervoussystem(CNS)sideeffectssuchashallucinationsanddepression.Betaxolol
islesslikelytocausethesesystemicsideeffects,butariskremains.Alloftheophthalmicbetablockers
are contraindicated in patients with sinus bradycardia, second- or third-degree atrioventricular node
block, overt cardiac failure, and cardiogenic shock, and all except betaxolol are contraindicated in
patientswithbronchialasthmaorseverechronicobstructivepulmonarydisease.
ProstaglandinAnalogs
The prostaglandin analogs such as bimatoprost, latanoprost, tafluprost, and travoprost reduce IOP by
improvingthe uveoscleraloutflow ofaqueous humor.Givenoncedaily, theprostaglandinF2a analogs
reduce IOP by 25% to 33%. Studies of bimatoprost, latanoprost, and travoprost found no statistical
differenceinIOPloweringamongagents(Lietal.,2006).
Theseagentsaremoreeffectivewhengivenatbedtimeratherthaninthemorning.Latanoprostrequires
refrigerationuntildispensed;latanoprostandtravoprostshouldbediscardedwithin6weeksofthetime
the package is opened. Tafluprost is supplied in single-use containers packaged within a foil pouch;
unusedsingle-usecontainersshouldbediscarded28daysafteropeningthepouch.Adverseeffectsofthe
prostaglandinsincludeocularhyperemia,blurredvision,pruritus,dryeye,lengtheningandthickeningof
the eyelashes, and conjunctival hyperemia. These agents are also associated with irreversible iris
discoloration,mostoftenaffectingpatientswithmixed-coloririses.Irisdiscolorationisreportedby7%
to12%oflatanoprostusers,withdiscolorationstartingbetween18and26weeksaftercommencementof
therapy. Compared to latanoprost, the incidence of iris discoloration is lower for bimatoprost and
travoprost.Inaddition,darkeningoftheeyelidskin(periocularhyperpigmentation)canoccurwiththese
agents;therapydiscontinuationoftenresultsinreversalof periocular hyperpigmentation 3 to 6 months
aftertherapydiscontinuation.
NitricOxideDonatingProstaglandinAnalogs
Latanoprostenebunodisamolecule thatismetabolizedontheocularsurfacetolatanoprosticacid(the
activeformoflatanoprost)andbutanediolmonohydrate,whichitselfisfurthermetabolizedtoformnitric
oxideandaninactivemetabolite.Inadditiontotheroleoflatanoprostinimprovinguveoscleraloutflow
ofaqueoushumor(describedpreviously),thenitricoxideactstoreducecellularcontractilityandvolume,
whichfacilitatesoutflowofaqueoushumorthroughthetrabecularmeshworkandSchlemm’scanal(Hoy,
2018;Marshalletal.,2018).LatanoprostenebunodreducesIOPby26%to34%andprovidesagreater
degreeof IOP loweringthan latanoprostor timolol monotherapy. Theadverse effectprofile oflatano-

prostenebunodissimilartolatanoprost.
CarbonicAnhydraseInhibitors
The topical carbonic anhydrase inhibitors (CAIs) brinzol-amide and dorzolamide work through the
reversibleandcompetitivebindingofcarbonicanhydrase.Carbonicanhydraseactsasacatalystforthe
reversible hydrationofcarbonicacid,whichplaysaroleinfluidtransportinvariouscellsystems. By
decreasing bicarbonate formation, the movement of bicarbonate, sodium, and fluid into the posterior
chamberoftheeyedeclines,andlessaqueousfluidisgenerated,reducingIOP(Abel&Sorensen,2018).
WhilethetopicalCAIsreduceIOPtoalesserextent(15%–26%)thanbetablockers,prostaglandins,or
systemicCAIs,theyarerarelyassociatedwithsystemicadverseeffects.
ThetopicalCAIsaregiventhreetimesdaily.Adverseeffectsincludeocularburningandstinging,bitter
taste,blurred vision, itching, tearing, and keratitis. Thetopical CAIs are not recommended for use in
patientswithsevererenalimpairment,respiratoryacidosis,andelectrolytedisordersandshouldbeused
withcautioninpatientswithhypersensitivitytosulfonamides.
ThesystemicCAIs(acetazolamide,methazolamide,anddichlorphenamide)arethemostpotentagents
for reducing IOP, producing a 25% to 40% decrease in IOP. However, these agents produce severe
adverse effects suchas paresthesias, gastrointestinal disturbances (anorexia,nausea,andweightloss),
metallictaste,CNSeffects(lethargy,malaise,anddepression),electrolytedisturbances,andrenalcalculi,
whichlimittheiruseintheolderpopulation(Swenson,2014).
AdrenergicAgonists
The adrenergic agonists apraclonidine and brimonidine activate the presynaptic alpha-2 receptors,
inhibitingthereleaseofnorepinephrine.Aslessnorepinephrineisavailableforactivationofpostsynaptic
betareceptorsontheciliaryepithelium,theformationofaqueoushumorisreduced.
ApraclonidineandbrimonidinereduceIOPby18%to27%.Brimonidineisahighlyselectivealpha-2
agonist, causing little or no alpha-1 activity. In addition to decreasing aqueous humor, it increases
uveoscleral outflow. Adverse effects include dry mouth, fatigue, ocular hyperemia, somnolence, and
headache. Apraclonidine is a relatively selective alpha-2 agonist; it is associated with some alpha-1
activity, which can lead to mydriasis, conjunctival bleeding, and eyelid retraction. Apraclonidine is
primarilyindicated for short-term adjunctivetherapy,as theefficacyofapraclonidinediminishes over
time;thebenefitformostpatientslastslessthan1to2months.Bothagentsarecontraindicatedinpatients
takingmonoamineoxidaseinhibitors.Inaddition,brimonidinehasbeenassociatedwithrespiratoryand
cardiacdepressionininfantsandshouldbeusedwithcautioninchildrenunder
age2.
Thenonselectiveophthalmicadrenergicagonistsepinephrineanddipivefrin(epinephrineprodrug)are
no longer available in the United States. These agents provided lackluster IOP control and were
associatedwithadverse reactionssuchasstingingandtearing,browache,andtheformationof black
conjunctivalspotsandconjunctivaldeposits.
CholinergicAgonists
Pilocarpineisadirect-actingcholinergicagonist.Pilocarpinestimulatestheparasympatheticmuscarinic
receptorsitetoincreaseaqueousoutflowthroughthetrabecularmeshwork.Whileeffectiveinlowering

IOPby20%to30%,pilocarpineusuallyneedstobegivenfourtimesaday.Adverseeffectsincludeeye
pain,browache,blurredvision,andaccommodativespasms.Itcanalsoprovokemioticresponsessuch
aspapillaryconstriction,whichcandecreasenightvision.Theintensedosingregimenandtheadverse
effectprofilemakeadherencedifficult.
RhoKinaseInhibitors
The rho kinase inhibitor netarsudil increases aqueous humor outflow by relaxing the cells that line
Schlemm’s canal, reducing the resistance to the flow of aqueous humor (Tanna & Johnson, 2018).
NetarsudilreducesIOPby14%to22%;head-to-headclinicaltrialsfoundthatnetarsudilproducedlesser
IOPloweringcomparedtolatanoprostandtimolol.Netarsudilislikelymosteffectivewhenusedasan
adjunctivetherapyforpatientsutilizingotherclassesofIOP-loweringagents(Schehlein&Robin,2019).
Netarsudil is dosed once daily. Adverse effects associated with netarsudil include conjunctival
hyperemia, stinging andburning,blurred vision,anddecreasedvisual acuity. Conjunctival hemorrhage
and corneal verticillata (corneal deposits that form a faint brown whorl pattern) were observed in
approximately20%ofpatientsreceivingnetarsudilinclinicaltrials;theverticillatadidnotaltervisual
function,andmostdissipatedupondiscontinuationoftreatment.
CombinationProducts
Combinationproductssimplifyadministrationandcanpromoteadherencetotherapy.Solutionsoftimolol
0.5%incombinationwithdorzolamide2%or brimonidine0.2%areavailable, as arecombinationsof
brimonidine 0.2% and brinzolamide 1% as well as netarsudil 0.02% and latanoprost 0.005%. The
combinedeffectresultsinadditionalIOPreductioncomparedtoeitheragentalone,buttheresultisoften
lessthaneachagentadministeredseparately.
SelectingtheMostAppropriateAgent
TheAAOdoesnotrecommendaspecificagentasfirst-linetherapy.Whenthefirst-lineagentdrugfailsto
reduceIOP,theAAOrecommendsthatitbediscontinuedinfavorofanothertherapybeforetheoriginal
agentissupplantedbyothermedications.Ifa first-lineagentlowersIOPbutfails tolower IOPtothe
targetlevel,combinationtherapyanddiscontinuationoftherapyinfavorofanotheragentareappropriate
options.Whenselectingthefirst-linetherapyforglaucoma,factorssuchasefficacy,adverseeffects,cost,
anddosingfrequencyshouldallbeconsidered.Table16.8liststherecommendedorderoftreatmentfor
theseagents.
First-LineTherapy
Theprostaglandinsareoftenutilizedasfirst-linetherapyforPOAGbecausetheypossessthebestbalance
amongefficacy,safety,cost,andeaseofdosingregimen.
Second-LineTherapy
If the prostaglandin fails to decrease IOP to a significant extent, the patient should be switched to a
differentclassofmedicine.Betablockersare recommendedbecauseoftheir efficacy, tolerability,and
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