main topic: “glaucoma and concomitant eye diseases” · uveitis and scleritis are the main...

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LEARNING OBJECTIVES

• Special Focus

A comprehensive overview on glaucoma in thesetting of inflammatory diseases includingincidence and prevalence, pre-dispositions andunderlying diseases, pathophysiology andpathomechanisms.

• What’s New

A review of current principles of medical and non-medical management of glaucoma in dry eyepatients including a review of the newest clinicaldata.

• Clinical Issues

A summary on detecting and diagnosing pediatricuveitic glaucoma, current treatment approachesand management of complications such assecondary glaucoma.

• Practical Tips

A practical lesson to differential diagnosis andtreatment measures taken for specific entities suchas Sjogren's syndrome, Posner SchlossmannSyndrome and Fuchs Syndrome.

Inside thisissue:

TARGET AUDIENCE

This educational program is aimed at generalophthalmologists, ophthalmology residents andglaucoma specialists.

EDITORIAL BOARD

Ivan Goldberg AM, MBBS, FRANZCO, FRACS,Clinical Professor, Discipline of Ophthalmology,University of Sydney and Glaucoma Unit, SydneyEye Hospital

Remo Susanna MD, Professor and Head ofDepartment of Ophthalmology, University of SãoPaulo, Brazil.

Main topic:“GLAUCOMA ANDCONCOMITANT EYEDISEASES”

Glaucoma Now is a continuing medical education publication hosted byGlaucomaAustralia Inc. Distributed worldwide, our goal is to educate andupdate general ophthalmologists, glaucoma specialists and ophthalmologyresidents. International leaders are invited to contribute to the program,sharing the most recent insights.

Supported by an unrestricted educational grant, the publication is non-promotional and has a fully independent Editorial Board.

For each issue CME credits can be obtained by registering on ourwebsite https://www.glaucoma.org.au/glaucoma-now/ and completingthe eLearning Course.

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I S S U E 12 0 1 9

Special Focus:

Comprehensive overviewon glaucoma in the settingof inflammatory diseases

PAGE 2

What’s New:

Principles of medical andnon-medical managementof glaucoma in dry eyepatients: State of play andrecent advances

PAGE 7

Clinical Issues:

Pediatric Uveitic Glaucoma:A summary of underlyingdiseases, differentialdiagnosis, screening andtreatment, management ofcomplications

PAGE 10

Practical Tips:

An approach to differentialdiagnosis and measurestaken for concomitant eyedisease: Sjogren'ssyndrome, PosnerSchlossmann Syndrome,Fuchs Syndrome

PAGE 14

In the developed world, ocularinflammation is one of the commoncauses of preventable visual disability andblindness. Recent advances in the medicaltreatment of ocular inflammation hasdramatically improved the visual outcomefor an increasing number of patients.Glaucoma remains a major complication:visual prognosis depends more on thecontrol of ocular pressure (IOP) than onthe inflammation. The best way to avoiduncontrolled glaucoma is to prevent itsoccurrence, mainly by rapid andaggressive inflammation treatment and byminimizing the use of corticosteroids.

I- Incidence and prevalence

The epidemiology of inflammatoryglaucoma is limited to studies, many ofwhich are retrospective with missingdetails. Differences between transitoryocular hypertension (OHT) andglaucomatous optic neuropathy are rarelyhighlighted. Results from tertiary centersare biased by a higher proportion of moresevere cases than in those managed incommunity-based ophthalmologypractice.

Scleritis is a rare inflammatory eyedisease[1] associated with secondaryglaucoma. Heinz et al. have reported onthe incidence of OHT and glaucoma in

patients with scleritis.[2] 271 patients wereincluded in this single-center,retrospective study. Even though themedian follow-up was limited, IOPincreased in 56 patients with an openangle with angle-closure in 4 patients. Thenecrotizing form was the main type ofscleritis associated with high IOP, mainlyobserved during acute episodes ofinflammation. The diagnosis of OHT wasdocumented in 72% of patients at referralbut the rate decreased to 56% at the endof the follow-up. The presence of anterioruveitis, peripheral ulcerative keratitis,posterior synechiae, and previous cataractsurgery were the major risk factors forOHT and glaucoma in this cohort.

Uveitis is more common than scleritis.Macular alterations and glaucoma are twoirreversible sight-threateningcomplications that appropriatemanagement could prevent.[3] Before theera of biologic agents, approximately10%-20% of uveitis patients used todevelop glaucoma in Western countries.

In a series of 927 patients, we haveidentified a higher risk of OHT orsecondary glaucoma in the subgroups ofanterior or panuveitis.[4] A more recentstudy from Thailand has shown asecondary glaucoma prevalence of 29%.[5]

Age at onset of uveitis above 60 years andlonger duration of ocular inflammationwere two risk factors. The prevalence ofpatients with at least 1 blind eye wassignificantly higher in those whodeveloped secondary glaucoma than inuveitis patients without glaucoma(P=0.001).

Other ocular inflammatory conditionshave a lower prevalence of OHT. Topicalcyclosporine significantly lowers the riskof steroid induced glaucoma in patientswith ocular surface inflammation.

II- Pre-dispositions and underlying

diseases (e.g. glaucoma as

immunogenetic inflammatory

component)

Glaucoma Now - Issue No 1, 2019. www.glaucoma.org.au2

Special Focus:

Glaucoma in the setting of inflammatory diseasesBahram Bodaghi MD, PhDDepartment of Ophthalmology, Sorbonne University, DHU ViewRestore,Pitié-Salpêtrière Hospital, Paris, France

Core Concepts

• Glaucoma is one of the worst sight-threatening complications of ocularinflammatory diseases

• Most etiologies are infectious with ahigh prevalence of classical or viraldisorders

• Clear diagnosis requires detailedclinical examination

• Optimal management requires bothuveitis and glaucoma expertise

Fig 1. Granulomatous anterior uveitis with inferior keratic precipitates in a patient with HSV1 uveitis

Uveitis and scleritis are the main entitiesto consider. B27-association is the mostfrequent etiology for anterior uveitis.Interestingly, in patients with unilateralacute anterior uveitis, IOP is usually lowerthan the fellow eye, perhaps related to atransient paralysis of the ciliary body.Many glaucoma-related uveitides arecaused by infection. Their prevalenceremains underestimated. Analysis ofocular fluids after anterior chamber tap orvitrectomy has dramatically modified thediagnostic and therapeutic management ofpatients with unilateral inflammatoryOHT or secondary glaucoma.[6]

A- Infectious uveitis

1- Viral infections

Uveitis is unilateral in most of cases, eventhough 10% may affect both eyes.Anterior uveitis or keratouveitis are theprincipal presentations, but rarelypanuveitis may also be associated with anacute retinal necrosis and OHT.

a- Herpetic anterior uveitis includingPosner Schlossman syndrome

Viral anterior uveitis is the second mostcommon etiology (Table 1). Secondaryglaucoma occurs in up to 54% of thesepatients.[7] Herpes simplex virus (HSV),varicella zoster virus (VZV) andcytomegaly virus (CMV) based anterioruveitides are usually acute, unilateral andgranulomatous. Keratic precipitates (KP)may guide the diagnosis but they are non-specific (Figure 1). Sectoral iris atrophy(Figure 3) is classically found in all 3entities even though early antiviraltreatment may avoid its occurrence orextension. Posterior synechiae are absentin CMV anterior uveitis. Chronic anterioruveitis and Posner Schlossman syndromeare the two main presentations of CMVuveitis in immunocompetent patients(Figure 2).[8] More information on PosnerSchlossman can be found in the PracticalTips Section. We have recently reportedon the clinical characteristics and long-term outcome of CMV anterior uveitis.[9]

In this series of 35 patients, keratic

precipitates and iris atrophy were seen in91.4% and 25.7% of cases, respectively.At baseline, mean IOP was 29 mmHg.Recurrences were reported in 73.5% ofcases and glaucoma surgery wasnecessary in one out of four cases. Earlyinitiation of antiviral therapy (≤700 days)seemed to decrease the risk of glaucomasurgery. Viral scleritis is less frequentlyassociated with OHT than uveitis. HSVand VZV are the main causative agents.

b- Rubella virus infection

Fuchs’ uveitis, first described in 1906represents 10 - 15% of all anterior uveitis.Anterior granulomatous uveitis with smalldiffuse stellate KP, iris heterochromia(Figure 4) and cataract are majordiagnostic elements. Heterochromia isvariable depending on the intensity of theinflammation, the initial iris color andamount of pigment in the iris pigmentepithelium. Iris nodules and vitritis maybe observed but posterior synechiae andmacular edema are excluding criteria.Since the early 2000s, Fuchs’ uveitis has

Glaucoma Now - Issue No 1, 2019. www.glaucoma.org.au 3

Table 1. Clinical characteristics of major viral ocular inflammatory entities involving the anterior segment and inducing OHT or glaucoma.

Previous keratitis

Scleritis

Keratic Precipitates

Posterior synechiae

Heterochromia

Iris atrophy

Iris nodules

OHT at presentation

Glaucoma

Cataract at presentation

Vitreous cells

+

++

Brown in Arlt’s triangle

+

-

Sectoral

-

++

+/-

-

+

Chorioretinal scars -

+

++

Brown in Arlt’s triangle

+

-

Sectoral

-

++

+

-

+

-

+

-

White central in PSS orBrown in CAU

-

-

Sectoral (rare)

-

+++

+

-

-

-

-

HSV VZV CMV RUBELLA VIRUS

-

White-gray, Stellate, diffuse

-

+++

Diffuse

+

+

+

++

+++

+


been strongly associated with rubellavirus infection.[10-12] Topicalcorticosteroids have no efficacy on thisviral-induced inflammation and are oftenthe cause of OHT. Disease progression ormisuse of topical corticosteroids may leadto glaucoma in 20 to 60% of cases. In theabsence of anti-rubella drugs, the use of

corticosteroids must be avoided.Molecular analysis of the aqueous humorand a few clinical signs may be predictiveelements of secondary glaucoma.Additional information on themanagement of Fuchs’ corneal dystrophymay be found in the Practical Tips section.

2- Other infectious diseases

Toxoplasmic retinochoroiditis may induceOHT. The peripheral location of lesionsand their size are more frequentlyassociated with a severe panuveitis andOHT. Ocular pressure is rapidlynormalized with antibiotics and systemiccorticosteroids. Tuberculous uveitis orscleritis may involve the anterior segmentwith large KP, extensive posteriorsynechiae and different types ofgranulomas on the iris or the trabeculum.OHT is commonly observed in severeanterior inflammation from tuberculosis(TB), due to different pathophysiologicmechanisms, with significant ocularmorbidity.[13] Syphilitic uveitis is anothergranulomatous anterior uveitis in thesecondary or tertiary phase of infection.All three conditions require a promptdiagnosis before specific therapy. Topicalcorticosteroids may be helpful inassociation with specific antibiotics. Theirshort-term use explains the absence ofOHT or glaucoma secondary to steroids.

3- Two special entities: BADI and BAIT

Bilateral acute depigmentation of the iris(BADI) and bilateral acute iristransillumination (BAIT) are two recentlydescribed entities with anterior segmentinflammation and OHT. BADI ischaracterized by acute onset ofdepigmentation of the iris stroma. Irispigment is deposited heavily in theiridocorneal angle, decreasing aqueousoutflow.[14] OHT is usually transient. Acase of simultaneous BADI in 2 siblingshas been recently reported.[15] On the otherhand, BAIT patients present with iristransillumination and a mydriatic atonicpupil, even though the pathophysiology ofOHT and secondary glaucoma remainssimilar. Recent systemic antibiotic(fluoroquinolone) use or a prior upperrespiratory tract infection are frequentlyreported prior to BAIT onset. Damagesare more frequent in BAIT patients witha higher rate of secondary glaucoma.

B- Noninfectious uveitis

1- Juvenile idiopathic arthritis-associated uveitis (JIAU)

Secondary glaucoma is one of the mostsevere complications in children withJIAU.[16] More information on

Fig 3. Extensive but sectoral iris atrophy in a VZV anterior uveitis

Fig 2. White, central keratic precipitates without posterior synechiae in animmunocompetent patient with CMV-associated Posner Schlossman syndrome


epidemiology, etiology and treatment ofpediatric uveitic glaucoma maybe foundin the Clinical Issues section. It should beadded that laser flare photometry is usefulfor the management of severe cases as itmay provide a more quantitative andreproducible evaluation of anteriorchamber flare, avoiding overtreatmentwith topical steroids.

2- Sarcoidosis

Both uveitis and scleritis may beassociated with sarcoidosis. Oculardisease may occur without detectablesystemic involvement. Prevalence rangeswidely in different geographic areas.[17]

Diagnostic criteria have been recentlyrevised.[18] Granulomatous nodules on thetrabecular meshwork and/or tent-shapedperipheral anterior synechiae may explainOHT and secondary glaucoma. In a seriesof 88 biopsy-proven sarcoid patients,ocular disease was present in 36.4% ofcases and the prevalence of glaucoma hasbeen estimated at 5.7%.[19]

III- Pathophysiology andpathomechanisms

Understanding the pathophysiology ofOHT or secondary glaucoma in patientswith ocular inflammation is challengingbut remains necessary to determine anappropriate therapeutic strategy.

Angle closure glaucoma may be missed,masquerading as an acute anterior uveitiswith OHT. It is vital to examine the angleand use tests like anterior segment ultra-sound , if necessary. Posterior synechiaecan point to previous episodes of angleclosure. Appropriate laser or surgicaltreatment may avoid irreversible damage.

Uveitic glaucoma is caused by fourprincipal mechanisms. Open angleglaucoma is the most common form.Trabecular meshwork blockade due toinflammatory cells, fibrin, proteins andother debris is the main reason forincreased resistance to aqueousoutflow.[20] Protein accumulation in theaqueous hunour (AH) follows a disruptedblood-aqueous barrier. Permanent damageto trabeculum varies among patients anddepends on the type of uveitis.

A second mechanism for decreasedaqueous outflow is steroid responsiveness,aggravating other damage.Corticosteroids response occurs in up toone third of patients;[21] while it usuallydevelops 2 - 6 weeks after initiatingtherapy, it may occur later in the course of

the disease. Prevalence of steroidresponsiveness seems higher in the groupof patients with uveitis compared with thegeneral population. Perhaps this is due toan already altered trabecular meshworkand a cumulative effect. Extremes of agesare more frequent steroid responders. Thetype of steroid molecule and its dosageare relevant.

Secondary angle-closure glaucoma israrer but significant mechanism. Pupillaryseclusion or block happens when chronicinsidious inflammation has not beendiagnosed rapidly and/or not treatedappropriately. Sarcoidosis, tuberculosis,JIAU and chronic Vogt-Koyanagi-Haradadisease are at high risk of pupillaryseclusion, block and iris bombé (Figure5). Inflammatory induced anterior

Fig 4. Fuchs uveitis of the left eye with heterochromia (4a) and small and diffuse stellate keratic precipitates (4b)

Fig 5. Chronic granulomatous uveitis with pupillary seclusion and iris bombé


synechiae can also result in total closureof the angle. Finally, transient anatomicalterations observed during Vogt-Koyanagi-Harada disease such as ciliarybody rotation may induce non-pupillaryblock angle closure glaucoma. Posteriorscleritis may be associated with angleclosure glaucoma.[22] Diagnosis is easilymade due to presence of choroidalthickening, sub-Tenon effusion and theclassical "T" sign observed onultrasonography.

Finally, neovascular glaucoma may occurin uveitis patients with episodes ofextensive retinal vein occlusion associatedwith different types of disease such assevere Behçet’s disease, sarcoidosis andidiopathic retinal vasculitis. Carefulexamination of the iris and chamber angleis mandatory; it guides developing anappropriate therapeutic approach.

IV - Conclusion

Inflammatory diseases have multiplecauses and mechanisms, which maychange during the course of management.A multi-disciplinary approach todiagnosis and treatment achieves optimalmanagement strategies for the underlyinginflammation and the superimposedglaucoma.

References:

1. Honik, G., I.G. Wong, and D.C. Gritz,Incidence and prevalence of episcleritisand scleritis in Northern California.Cornea, 2013. 32(12): p. 1562-6.

2. Heinz, C., et al., Ocular hypertensionand glaucoma incidence in patientswith scleritis. Graefes Arch Clin ExpOphthalmol, 2013. 251(1): p. 139-42.

3. Siddique, S.S., et al., Glaucoma anduveitis. Surv Ophthalmol, 2013. 58(1):p. 1-10.

4. Bodaghi, B., et al., Chronic severeuveitis: etiology and visual outcome in927 patients from a single center.Medicine (Baltimore), 2001. 80(4): p.263-70.

5. Pathanapitoon, K., et al., Prevalenceand Visual Outcome of Glaucoma WithUveitis in a Thai Population. JGlaucoma, 2017. 26(3): p. 247-252.

6. Groen-Hakan, F., et al., Challengesof Diagnosing Viral Anterior Uveitis.Ocul Immunol Inflamm, 2017. 25(5): p.710-720.

7. Miserocchi, E., et al., Visual outcomein herpes simplex virus and varicellazoster virus uveitis: a clinical evaluationand comparison. Ophthalmology,2002. 109(8): p. 1532-7.

8. Chan, N.S., et al., Clinical Featuresof CMV-Associated Anterior Uveitis.Ocul Immunol Inflamm, 2018. 26(1): p.107-115.9. Touhami, S., et al., CytomegalovirusAnterior Uveitis: Clinical Characteristicsand Long-term Outcomes in a FrenchSeries. Am J Ophthalmol, 2018. 194:p. 134-142.

10. Quentin, C.D. and H. Reiber, Fuchsheterochromic cyclitis: rubella virusantibodies and genome in aqueoushumor. Am J Ophthalmol, 2004.138(1): p. 46-54.

11. Groen-Hakan, F., et al., ClinicalManifestations, Prognosis AndVaccination Status Of Patients WithRubella Virus-Associated Uveitis. Am JOphthalmol, 2019.

12. Wensing, B., et al., Comparison ofrubella virus- and herpes virus-associated anterior uveitis: clinicalmanifestations and visual prognosis.Ophthalmology, 2011. 118(10): p.1905-10.

13. Gunasekeran, D.V., et al., VisualMorbidity and Ocular Complications inPresumed Intraocular Tuberculosis: AnAnalysis of 354 Cases from a Non-Endemic Population. Ocul ImmunolInflamm, 2018. 26(6): p. 865-869.

14. Tugal-Tutkun, I., et al., Bilateralacute depigmentation of the iris: reportof 26 new cases and four-year follow-up of two patients. Ophthalmology,2009. 116(8): p. 1552-7, 1557 e1.

15. Amin, R., A. Nabih, and N. Khater,Bilateral acute depigmentation of theiris in two siblings simultaneously. Am JOphthalmol Case Rep, 2018. 10: p.257-260.

16. Gueudry, J., et al., Therapeuticadvances in juvenile idiopathic arthritis- associated uveitis. Curr OpinOphthalmol, 2019.

17. Pasadhika, S. and J.T.Rosenbaum, Ocular Sarcoidosis. ClinChest Med, 2015. 36(4): p. 669-83.

18. Mochizuki, M., et al., Revisedcriteria of International Workshop onOcular Sarcoidosis (IWOS) for thediagnosis of ocular sarcoidosis. Br JOphthalmol, 2019.

19. Radosavljevic, A., et al., ClinicalFeatures of Ocular Sarcoidosis inPatients with Biopsy-proven PulmonarySarcoidosis in Serbia. Ocul ImmunolInflamm, 2017. 25(6): p. 785-789.

20. Moorthy, R.S., et al., Glaucomaassociated with uveitis. SurvOphthalmol, 1997. 41(5): p. 361-94.21. Becker, B., Intraocular PressureResponse to Topical Corticosteroids.Invest Ophthalmol, 1965. 4: p. 198-205.

22. Ugurbas, S.H., A. Alpay, and S.C.Ugurbas, Posterior scleritis presentingwith angle closure glaucoma. OculImmunol Inflamm, 2012. 20(3): p. 218-20.


What’s New:

Principles of medical and non-medical managementof glaucoma in dry eye patientsChristophe Baudouin, MD,PhDQuinze-Vingts National Ophthalmology Hospital, and Vision Institute, Paris, France

Core Concepts

• The ocular surface is frequentlydamaged in glaucoma patients onlong term topical medical treatment

• Active compound, preservative andindividual patient sensitivities mayinteract to cause or aggravate ocularsurface disease (OSD)

• The preservative benzalkoniumchloride (BAK) may play an importantrole in dry eye through its ownchemical properties

• The number of BAK-containingeyedrops instilled each day is asignificant risk factor for failure inglaucoma surgery

• In patients with OSD it is advisableto use preservative-free or at leastBAK-free eye drops

• Removal of the causativecompound(s) is more effective thanadding eye drops to counteract OSD(subtractive preferred to additivestrategy) Figure 1: Clinical example of toxic keratopathy.

I- Ocular surface changes in glaucoma

Both basic science and clinical researchdemonstrate frequent and significantocular surface changes from long-termeye drop use.1 In patients treatedchronically with topical glaucomamedications, signs of low-grade, chronicinflammation occur, with variousclinical manifestations. Suchmedications, often used for decades inclinical practice, may cause and/orexacerbate pre-existing ocular surfacedisease (OSD), such as dry eye,meibomian gland dysfunction, andchronic allergy, further depressingquality of life, adherence, and surgicaloutcomes. Several consistentobservational studies on the ocularsurface in glaucoma patients highlight amuch higher prevalence of OSD thanthat found in the general population.2-4

Signs and symptoms of OSD areobserved in 35–50% of glaucomapatients, according to the criteria

analyzed, which is substantially morecommon than could be expected fromdry eye prevalence.5 An observationalstudy confirmed a prevalence of OSD inglaucoma patients reaching 35-40%,with 35% of patients repeatedly usingtear substitutes adjunctively.Interestingly, this study also evaluatedthose patients suffering from OSD (dryeye or allergy) prior to the initiation ofantiglaucoma treatment. As expected,the prevalence was 10 to 15%, which isconsistent with dry eye diagnosis in thegeneral population.6 The difference istherefore that induced by glaucomatherapy, which points out the importanceof drug-induced OSD. In 2017 The DryEyeWorkShop II emphasized the role ofmedical or surgical interventions ininducing dry eye, and dedicated achapter to iatrogenic causes of dry eye.7

The importance of topical treatments,and especially the role of preservativesin inducing OSD deserved specialattention (Figure 1).

II- The role of preservatives in ocularsurface disease

Several studies have correlated signs andsymptoms of OSD with the number ofconcomitantly used eye drops containingbenzalkonium chloride (BAK), the mostfrequently used preservative in eyedrops.2,3 Signs and symptomssignificantly improved withdiscontinuation of the BAK-preserveddrops and substitution with non-preserved drops.2,8 BAK impairs the tearfilm because of its surfactant properties(Figure 2). It also has proinflammatory,and cytotoxic properties for epithelialand goblet cells1,9 and may causeincreased tear hyperosmolarity.10 Its usein dry eye patients therefore mayaggravate ocular surface disorders. Thisis why most tear substitutes availableworldwide have been developed aspreservative-free or BAK-freeformulations.


Interestingly, this can be modeled in vitro,where BAK’s deleterious effects weresignificantly increased when conjunctivalcells were stressed osmotically.11 Thisprocess may mimic the enhanced toxicityof the preservative in dry eye patients,compared with normals.

Through the loss of its protectiveproperties, an impaired tear film provokesdry eye symptoms with corneal damageand convey cytotoxic inflammatorymediators across the ocular surface. Tearfilm alterations may even stimulate aseries of biological changes in the ocularsurface, leading to subsequent neurogenicinflammation and further impairment ofthe tear film, actually creating a viciouscircle.12

BAK has also been shown to beneurotoxic13, causing cornealhypoesthesia and nerve damage. In astudy comparing the effect of variousantiglaucoma treatments on cornealnerves, abnormal nerve morphology andcorneal hypoesthesia were consistentlyfound in patients receiving preservedcompared with unpreservedmedications.14 BAK’s nerve-damagingeffects could contribute to the overall falsecomfort of patients receiving BAK-

containing eyedrops, with cornealhypoesthesia masking corneal damageand explaining a misleading apparently“good” tolerance. Indeed tolerance ofglaucoma therapy is usually considered asquite good, despite a high rate of dry eyedisease, tear instability and meibomiangland dysfunction in glaucoma patients.BAK was already identified as delayingcorneal wound healing and should thus beavoided in patients with damagedcornea.15,16

III- Glaucoma in dry eye patients

Dry eye disease is quite prevalent in theelderly population, frequency rangingbetween 10 and 30%, depending on thecriteria considered.5 Therefore glaucomamay occur in significant numbers ofpatients suffering from OSD: aretrospective case series showed theincidence of glaucoma was 20.4%,ranging from 13.6% to 60% in patientswith coinciding OSD.17 In these patients,it is advisable either to avoid preservative-containing IOP-lowering agents or to limittheir use.

When dry eye has progressivelydeveloped over time with antiglaucomatreatments, switching to preservative-free

medications should be the first choice,rather than adding tear substitutes or anti-inflammatory agents. This wouldemphasize a “subtractive strategy”, whichis likely more effective, because it targetsthe origin of the disease or one of its co-factors, rather than an "additive strategy"consisting of adding medications tocounteract the iatrogenic effects of otherdrugs. Data from studies where suchswitches have taken place suggestreversible drug-induced ocular surfacechanges, which may improve when thecausative or aggravating factor isremoved8 or even just decreased.2

However, removal of an aggravatingfactor may not be sufficient to treat dryeye associated with glaucoma. Specificdry eye therapy may be necessary, such aspreservative-free tear substitutes,osmoprotectants or topical cyclosporine,to counteract inflammatory reactionsoften associated with dry eye. In aqueous-deficient dry eye, punctual plugs may behelpful, but it is advisable to minimize orremove potentially toxic compounds thatwould be retained on the ocular surface.In addition, surface inflammation as wellas toxic compounds may diffuse from thesurface into deeper ocular structures, likesubconjunctival tissue, which maynegatively influence the outcome ofglaucoma surgery, as suggested byBroadway et al. as early as in the 90s, andconfirmed by the PESO study that clearlyidentified the number of BAK-containingeyedrops instilled each day as asignificant risk factor of failure.18,19

Moreover BAK may penetrate to thetrabecular meshwork and there exert toxicand/or proinflammatory effects.20

Specifically treating the ocular surfaceand removing toxic compounds not onlyreduced surface inflammation but alsoreduced intraocular pressure; suchinflammation could cause an iatrogenictrabeculitis.21,22

IV- Which patients may benefit mostfrom preservative-free drugs and howto identify them?

Not all patients are sensitive topreservatives and not all side effectsobserved with antiglaucoma medicationsare induced by preservatives. Threefactors must in fact be considered: theactive compound, the preservative, and the

Figure 2: Illustration of tear film break up time (TBUT) testing


patient’s ocular surface. Patients withexisting OSDwhen glaucoma treatment isinitiated, as well as those developing dryeye or ocular irritation during glaucomatherapy, should be identified and receiveparticular attention. Simple clinical testsmay help the clinician detect ocularsurface disease, such as assessment ofsymptoms of irritation or dryness, eyelidmargin redness, positive corneal andconjunctival fluorescein staining, andrapid tear film break-up time.

In such cases, quality of life, adherence,surgical outcome, and overall glaucomacare may be adversely affected. Considertreatment alternatives, such as removingthe preservative when possible or at leastdecreasing the number of preservedeyedrops by using fixed combinations orusing medications with preservativesother than BAK, treating the ocularsurface with unpreserved tear substitutes,and considering laser trabeculoplasty orsurgery to decrease the number ofeyedrops.

V- Conclusion

Definitively glaucoma should beconsidered a high risk for ocular surfacedisease that deserves specific attention soas to manage safely and effectively thissight-threatening disease for the long-term.

References:

1. Baudouin C, Labbé A, et al.Preservatives in eyedrops: the good,the bad and the ugly. Prog Retin EyeRes. 2010;29:312-334.

2. Pisella PJ, Pouliquen P, Baudouin C.Prevalence of ocular symptoms andsigns with preserved and preservativefree glaucoma medication. Br JOphthalmol. 2002;6:418-423.

3. Leung EW, Medeiros FA, WeinrebRN. Prevalence of ocular surfacedisease in glaucoma patients. JGlaucoma. 2008;17:350-355.

4. Fechtner RD, Godfrey DG, et al.Prevalence of ocular surfacecomplaints in patients with glaucoma

using topical intraocular pressure-lowering medications. Cornea.2010;29:618-621.

5. Dry Eye WorkShop. Theepidemiology of dry eye disease: reportof the Epidemiology Subcommittee ofthe International Dry Eye WorkShop.Ocul Surf. 2007;5:93-107.

6. Lemij HG, Hoevenaars JG, van derWindt C, Baudouin C. Patientsatisfaction with glaucoma therapy:reality or myth? Clin Ophthalmol.2015;9:785-793.

7. Gomes JAP, Azar DT, et al. TFOSDEWS II iatrogenic report. Ocul Surf.2017;15:511-538.

8. Uusitalo H, Chen E, et al. Switchingfrom a preserved to a preservative-freeprostaglandin preparation in topicalglaucoma medication. ActaOphthalmol. 2010;88:329-336.

9. Kahook MY, Noecker R. Quantitativeanalysis of conjunctival goblet cellsafter chronic application of topicaldrops. Adv Ther. 2008;25:743-751.

10. Labbé A, Terry O, et al. Tear filmosmolarity in patients treated forglaucoma or ocular hypertension.Cornea. 2012;31:994-999.

11. Clouzeau C, Godefroy D, et al.Hyperosmolarity potentiates toxiceffects of benzalkonium chloride onconjunctival epithelial cells in vitro. MolVis. 2012;18:851-863.

12. Baudouin C, Aragona P, et al. Roleof Hyperosmolarity in the Pathogenesisand Management of Dry Eye Disease:Proceedings of the OCEAN GroupMeeting. Ocul Surf. 2013;11:246-258.

13. Sarkar J, Chaudhary S, et al.Corneal neurotoxicity due to topicalbenzalkonium chloride. InvestOphthalmol Vis Sci. 2012;53:1792-1802.

14. Martone G, Frezzotti P, et al. An invivo confocal microscopy analysis ofeffects of topical antiglaucoma therapy

with preservative on corneal innervationand morphology. Am J Ophthalmol.2009;147:725-735.

15. Nagai N, Murao T, Okamoto N, ItoY. Comparison of corneal woundhealing rates after instillation ofcommercially available latanoprost andtravoprost in rat debrided cornealepithelium. J Oleo Sci 2010;59:135-141.

16. Kossendrup D, Wiederholt M,Hoffmann F. Influence of cyclosporin A,dexamethasone, and benzalkoniumchloride (BAK) on corneal epithelialwound healing in the rabbit and guineapig eye. Cornea 1985;4:177-181.

17. Tsai JH, Derby E, Holland EJ,Khatana AK. Incidence and prevalenceof glaucoma in severe ocular surfacedisease. Cornea. 2006;25:530-532.

18. Broadway DC, Grierson I, O'BrienC, Hitchings RA. Adverse effects oftopical antiglaucoma medication. II.The outcome of filtration surgery. ArchOphthalmol. 1994;112:1446-1454.

19. Boimer C, Birt CM. Preservativeexposure and surgical outcomes inglaucoma patients: The PESO study. JGlaucoma. 2013;22:730-735.

20. Baudouin C, Denoyer A, et al. Invitro and in vivo experimental studieson trabecular meshwork degenerationinduced by benzalkonium chloride (anAmerican Ophthalmological Societythesis). Trans Am Ophthalmol Soc.2012;110:40-63.

21. Batra R, Tailor R, Mohamed S.Ocular surface disease exacerbatedglaucoma: optimizing the ocularsurface improves intraocular pressurecontrol. J Glaucoma. 2014;23:56-60.

22. Dubrulle P, Labbé A, et al. Influenceof treating ocular surface disease onintraocular pressure in glaucomapatients intolerant to their topicaltreatments: a report of 10 cases. JGlaucoma. 2018;27:1105-1111.


I- Introduction

Paediatric uveitis is most commonlyidiopathic, followed closely by uveitisassociated with juvenile idiopathicarthritis (JIA)1. Approximately 12-38%of children with JIA develop uveitis(JIA-U)2. There are a number ofarthritides associated with paediatricuveitis and subsequent secondaryuveitic glaucoma. These are highlightedin Tables 1 and 2. Initial screening of achild diagnosed with these subclassesshould be within 6 weeks of referralfollowed by two monthly intervals fromonset of arthritis for 6 months. Then allchildren should be screened until 11years of age irrespective of the subclassof diagnosis3.

Management of paediatric uveitis posesmany challenges. Despite severeinflammation, children may remainasymptomatic or have difficultyexpressing their symptoms. They oftenpresent with advanced disease, whichcan lead to a lifetime of visualimpairment and amblyopia4,5. Visionloss in paediatric uveitis is morecommon than in adults. Structuralcomplications from the disease includeinflammatory mediated (cystoidmacular oedema and optic discswelling) and non-inflammatorymediated (elevatedIOP/glaucoma/glaucomatous opticn e u r o p a t h y / c a t a r a c t / b a n dk e r a t o p a t h y / p o s t e r i o rsynechiae/hypotony). These can be

Clinical Issues:

Paediatric Uveitic GlaucomaSophia L Zagora MD FRANZCO1,2,3, John Grigg MD FRANZCO1,2,31 Discipline of Ophthalmology, University of Sydney, Sydney Australia2 Sydney Eye Hospital, Sydney Australia3 Children’s Hospital Westmead, Sydney Australia

Core Concepts

• Paediatric uveitis is rare, 5-10% ofthe uveitis burden

• Although many cases are idiopathic,41–67% of uveitis in children is linkedwith Juvenile Idiopathic Arthritis (JIA)and 3–6% with Sarcoidosis

• Systemic management of theintraocular inflammation is crucial toreduce the vision threateningcomplications of paediatric uveiticglaucoma

• While screening guidelines remainthe same the 2018 EULAR guidelinesand the Sycamore trial highlightmultidisciplinary care and use ofbiologics to control disease to reducethe incidence of secondary uveiticglaucoma

27-56%

11-28%

4-17%

2-7%

2-11%

3-11%

11-21%

Arthritis affecting 1- 4 joints during first 6 months disease

Arthritis affects 5 or more joints in first 6 months of disease. Tests for RF are negative

Arthritis in one or more joints with or preceded by fever of at least 2 weeks+ 1) Rash2) Lymphadenopathy 3) Hepatomegaly or splenomegaly 4) Serositis

Arthritis affects 5 or more joints in first 6 months of disease. Tests for RF are positive

Arthritis and psoriasis

Arthritis or enthesis plus two of 1) sacroiliac tenderness of lumbosacral pain 2) HLA B27 antigen 3) arthritis M> 6 yrs 4) AAU 5) Family Hx HLA B 27 disease

Arthritis that fulfills criteria in no category or in two or more of above categories

Earlychildhood

Peak 2-4 yrs

BiphasicEarly 2-4 yrs,later 6-12 yrs

Childhood

LateChildhood

BiphasicEarly 2-4 yrsand 9-11 yrs

Latechildhood oradolescence

F>M

F>M

F>M

F>M

F>M

M>F

Oligoarticular JIA

Polyarthritis(RH-negative)

Systemic onset JIA

Polyarthritis(RH-positive)

Psoriatic arthritis

Enthesis relatedarthritis

Undifferentiatedarthritis

Table 1 – International League of Associations for Rheumatology Classification of JIA3

Sex RatioAge of OnsetFrequencyDefinitionCategory


Table 2 - AAO Paediatric guidelines for screening eye examinations3

Oligoarticular or polyarticular, onset < 7 years of age and ANA +ve High risk

Medium risk

Medium risk

Low risk

Every 3-4 months

Every 6 months

Every 6 months

Every 12 months

Oligoarticular or polyarticular, onset < 7 years of age and ANA +ve



Examination frequencySubtype risk of iritisJIA

Figure 1 - An approach to the management of Paediatric uveitic glaucoma adapted from Joos et al 2013 16


present at diagnosis or develop duringthe chronic course of the disease.Children appear to be more susceptibleto these structural complications and upto 20% develop glaucoma5,6.

Paediatric uveitic glaucoma ischallenging because of themultifactorial nature of the elevatedIOP7 (Figure 1). Medical treatmentshould be commenced early with anyelevated IOP, even if the optic discs arenormal. Glaucoma surgery is oftenrequired: options includetrabeculectomy, glaucoma drainagedevices and cyclodiode (rarely, as it ispro-inflammatory). To reducecomplications, it is important to operateon a ‘quiet eye’. Surgical risks include:increased inflammation, cataract,corneal decompensation, ciliary body“shutdown”, retinal detachment, cystoidmacular edema, choroidal effusion, flatanterior chamber, encapsulated bleb,extruded glaucoma drainage device andinfection. Hypotony is a commonproblem in paediatric uveitic patientspost glaucoma surgery even in theabsence of over-drainage.

II-What is new?

1. Recent EULAR8 guidelines andrandomised control trials highlight theneed for multi-disciplinary clinics, withopen communication betweenophthalmologists (paediatric, glaucomaand uveitis) and the paediatricrheumatologist concerning changes indisease activity, adjustments orescalation of any treatment9-13.2. The Sycamore10 study was arandomised control trial comparing 90children with JIA uveitis treated witheither Adalimumab and Methotrexateversus Methotrexate alone. The trial wasstopped after one year of recruitmentwith a difference in relapse rate 27%Adalimumab and Methotrexate versus60% Methotrexate alone. Biologics arethe next step being increasingly usedwhen uveitis is poorly responsive tosystemic immunomodulating drugtherapy.3. Glaucoma surgery should beconducted prior to cataract surgery, as

there is ofteni n c r e a s e dinflammation aftercataract surgery,requiring increasedshort-term steroidthat subsequentlycan increase the IOP.If trabeculectomy isperformed, tightscleral flap suturesare mandatory. Non-flow restrictedglaucoma drainagedevices (GDD)should have anintraluminal stent inaddition to anextraluminal occlusivesuture (e.g. 6/0 Coatedpolyglactin 910Ethicon USA), to reduce the risk ofpost-operative hypotony. Werecommend a Baerveldt tube 350mm(Johnson & Johnson Vision USA)independent of age to reduce the risk ofthe child outgrowing the tube and a 3.0nylon intraluminal stent to reduce flowand risk of hypotony14 (see Figure 2).

4. We advocate for an IOL duringcataract surgery especially when thereis adequate systemicimmunosuppression and the child hasbeen free from inflammation for >3months15. This reduces the risks of bothamblyopia and aphakic glaucoma. Anintravitreal triamcinolone injection(2mg) at time of surgery improves post-operative inflammatory control withoutthe need for additional systemicsteroids. Heparin 1 Unit per ml ofBalanced Salt Solution (BSS) in theinfusion line further reducesinflammation in the early post-operativeperiod.

III- Conclusion

Managing uveitic glaucoma in childrenis challenging. Adequateimmunosuppression is crucial in themanagement of these children. Thismeans early recognition of poor controlwith topical agents with institution ofsystemic steroid sparing agents.

References:

1. Keino H, Watanabe T, Taki W,Nakayama M, Nakamura T, Yan K,Okada AA. Clinical features of uveitisin children and adolescents at atertiary referral centre in Tokyo. BritishJournal of Ophthalmology 2017; 101:406-10.2. Ferrara M, Eggenschwiler L,Stephenson A, Montieth A, NakhoulN, Araùjo-Miranda R, Foster CS. TheChallenge of Pediatric Uveitis: TertiaryReferral Center Experience in theUnited States. Ocular immunologyand inflammation 2018: 1-8

3. Saboo US, Metzinger JL, RadwanA, Arcinue C, Parikh R, Mohamed A,Foster CS. Risk factors associatedwith the relapse of uveitis in patientswith juvenile idiopathic arthritis: apreliminary report. Journal ofAmerican Association for PediatricOphthalmology and Strabismus2013; 17: 460-4.

4. Ravelli A, Martini A. Juvenileidiopathic arthritis. Lancet.2007;369:767–78.

5. Jabs DA, Nussenblatt RB,Rosenbaum JT. Standardization ofuveitis nomenclature for reportingclinical data. Results of the First

Figure 2 - Baerveldt Tube insertion with intraluminal and extraluminaltie (thin arrow). Tube in the anterior chamber (thick arrow).


International Workshop. Americanjournal of ophthalmology 2005; 140:509-16.

6. Zierhut M, Heiligenhaus A, deBoerJ, Cunningham ET, Tugal-Tutkun I.Controversies in juvenile idiopathicarthritis-associated uveitis. Ocularimmunology and inflammation 2013;21: 167-79.

7. Sen ES, Dick AD, Ramanan AV.Uveitis associated with juvenileidiopathic arthritis. Nature ReviewsRheumatology 2015; 11: 338.

8. Constantin T, Foeldvari I, Anton J,de Boer J, Czitrom-Guillaume S,Edelsten C, Gepstein R, HeiligenhausA, Pilkington CA, Simonini G.Consensus-based recommendationsfor the management of uveitisassociated with juvenile idiopathicarthritis: the SHARE initiative. Annalsof the rheumatic diseases 2018:annrheumdis-2018-213131.

9. Jaffe GJ, Dick AD, Brézin AP,Nguyen QD, Thorne JE, Kestelyn P,Barisani-Asenbauer T, Franco P,Heiligenhaus A, Scales D.Adalimumab in patients with activenoninfectious uveitis. New EnglandJournal of Medicine 2016; 375: 932-43.

10. Ramanan AV, Dick AD, Jones AP,McKay A, Williamson PR,Compeyrot-Lacassagne S, HardwickB, Hickey H, Hughes D, Woo P.Adalimumab plus methotrexate for

uveitis in juvenile idiopathic arthritis.New England Journal of Medicine2017; 376: 1637-46.

11. Nguyen QD, Merrill PT, Jaffe GJ,Dick AD, Kurup SK, Sheppard J,Schlaen A, Pavesio C, Cimino L, VanCalster J. Adalimumab for preventionof uveitic flare in patients with inactivenon-infectious uveitis controlled bycorticosteroids (VISUAL II): amulticentre, double-masked,randomised, placebo-controlledphase 3 trial. The Lancet 2017; 388:1183-92.

12. Papadopoulou C, Kostik M,Böhm M, Nieto-Gonzalez JC,Gonzalez-Fernandez MI, Pistorio A,Martini A, Ravelli A. Methotrexatetherapy may prevent the onset ofuveitis in juvenile idiopathic arthritis.The Journal of pediatrics 2013; 163:879-84.

13. Thorne JE, Woreta FA, Dunn JP,Jabs DA. Risk of cataractdevelopment among children withjuvenile idiopathic arthritis-relateduveitis treated with topicalcorticosteroids. Ophthalmology2010; 117: 1436-41.

14. Rososinski, A., D Wechsler, JGrigg. Retrospective review of parsplana versus anterior chamberplacement of Baerveldt glaucomadrainage device." Journal ofGlaucoma 2015; 24(2): 95-99.

15. Grajewski RS, Zurek-Imhoff B,Roesel M, Heinz C, Heiligenhaus A.Favourable outcome after cataractsurgery with IOL implantation inuveitis associated with juvenileidiopathic arthritis. Acta Ophthalmol2012; 90; 657-62.

16. Joos, K., et al. GlaucomaAssociated with Acquired Conditions.Childhood Glaucoma: The 9thConsensus Report of the WorldGlaucoma Association. R. Weinreb,A. Grajewski, M. Papadopoulos, J.Grigg and S. Freedman. Amsterdam,The Netherlands, KuglerPublications: 2013.199-232.


Practical Tips:

Glaucoma and concomitant eye diseasesStephanie Watson Bsc(Med), MBBS, PhD, FRANZCOSydney Medical School Foundation FellowThe University of Sydney, Save Sight Institute, Discipline of Ophthalmology, Sydney Medical School, Sydney, New South Wales, Australia

Core Concepts

• In ocular surface disease such asSjogren’s syndrome the treatment ofglaucoma can further compromise apatients’ quality of life

• To improve outcomes for yourpatient with ocular surface diseaseand glaucoma, avoid preservatives inand reduce the number of topicalmedications

• Ocular inflammation and/or it’streatment with steroids, can increaseintraocular pressure leading toglaucoma

• Patient’s with Posner Schlossmansyndrome, suffer with recurrentattacks of increased intraocularpressure and inflammation, long-termmonitoring is needed due to the riskof glaucoma

• In Fuch’s corneal dystrophy eventualfailure of the corneal endothelium ismost commonly managed with anendothelial keratoplasty. Thisprocedure can be performed inpatients with glaucoma, includingthose with drainage devices, but in thelong-term re-grafting maybe needed

Figure 1: Corneal staining in Sjogren’s syndrome dry eye shown with cobalt blue light and fluorescein.

I- Introduction

Glaucoma is the most frequent cause ofirreversible preventable blindnessworldwide; with increased prevalence inthe elderly. Due to its prevalence, otherocular conditions can co-exist withglaucoma or be directly caused orexacerbated by glaucoma or its treatment.When there is co-existent ocular disease,such as dry eye, the patient’s quality of lifemaybe further reduced. 1 Eye carepractitioners need to be aware of theinteraction between glaucoma and otherocular conditions to guide management.

II- Sjogren’s Syndrome

In Sjorgen’s syndrome, aqueous tearproduction is reduced from autoimmune-mediated inflammation of the lacrimalgland. It is typically accompanied by drymouth, but dry skin and nose may occur.Patients may suffer with fatigue, muscleand joint pains. For the eye, there is a thinmarginal tear strip and the effects on theocular surface are similar to other formsof dry eye with punctate corneal erosionstypically present in the palpebral fissure(Figure 1) and inflammation.2 Due to thepresence of ocular surface disease inSjogren’s syndrome clinicians, when

treating co-existent glaucoma, shouldavoid preservatives in topical therapy andreduce the number of topical glaucomamedications daily, as well as minimizeoral Diamox, which can have a dryingeffect. It may be appropriate to considernon-medical approaches to treatment suchas selective laser trabeculotomy, MIGS ordrainage surgery.

III- Posner Schlossman syndrome

Posner Schlossman syndrome, alsoknown as glaucomatocyclitic crisis, is arelatively uncommon condition in whichacute, recurrent attacks of raised


intraocular pressure and anterior chamberinflammation typically occur in one eye. Itshould be considered in patients, typicallymiddle-aged Asian men, with repeatepisodes of unilateral non-granulomatousanterior uveitis and raised intraocularpressure. It is important to identify aschronic secondary glaucoma can followand require management, most often withtopical therapy, but in some casessystemic therapy or possibly surgery areneeded. The diagnosis however is usuallyclinical although aqueous or bloodinvestigations may be undertaken ifinfection is suspected. Patients withPosner Schlossman syndrome requirelong term follow up to identify andmanage chronic glaucoma as well asocular inflammation.3

IV- Fuchs’ corneal dystrophy

Endothelial keratoplasty (EK) hasrevolutionized the management of cornealdecompensation in Fuchs’ cornealdystrophy (Figure 2).As in Fuchs’ cornealdystrophy, corneal oedema occursgradually due to endothelial cell loss. It isusually bilateral and characterized bydeposits on Descement’s membraneknown as guttate. EK offers faster andeasier visual rehabilitation, reduced riskof graft rejection, and avoidance of suturerelated complications such as microbialkeratitis, that can follow penetratingkeratoplasty. In eyes with a glaucomadrainage device, EK can still beperformed with simple adjustments to thesurgical technique and acceptable clinicalresults. Patients should be advised that re-grafting maybe required.4 Nonetheless,repeated EK has a reduced burden oftreatment compared with repeatpenetrating keratoplasty. If a repeat EK isrequired, there is emerging evidence thatthe presence of glaucoma or priorglaucoma surgery may not affect visualoutcomes. 5

V- Conclusion

In summary, glaucoma is a burden formany people but it is not just those withglaucoma who may suffer with itsconsequences. In Sjogren’s syndrome,ocular surface disease can be exacerbated

by glaucoma treatments and for patientswith Posner Schlossman they maydevelop glaucoma over time and requiremonitoring. Lastly, in corneal diseasesuch as Fuch’s corneal dystrophy whensurgery is required , glaucoma maydevelop or require adjustments to theprocedure.

References:

1. Skalicky SE, Goldberg I, McCluskeyP. Ocular surface disease and quality oflife in patients with glaucoma. Am JOphthalmol 2012; 153 (1):1-9.e2

2. Garcia DM, Reis de Oliveira F,Modulo CM, Faustino J, Barbosa AP,Alves, Rocha EM. Is Sjögren'ssyndrome dry eye similar to dry eyecaused by other etiologies?Discriminating different diseases by dryeye tests. PLoS One.2018;13(12):e0208420

3. Megaw R, Agarwal PK. Posner-Schlossman syndrome. SurvOphthalmol. 2017; 62(3):277-85

4. Birbal RS, Tong CM, Dapena I,Parker JS,Parker JS, Oellerich S,Melles GRJ. Clinical outcomes ofDescemet membrane endothelialkeratoplasty in eyes with a glaucomadrainage device. A J Ophthalmol. 2018Nov 28

5. Thompson JM, Truong AH, SternHD, Djalilian A, Cortina MS, Tu EY,Johnson P, Verdier DD, Rafol L, LubeckD, Spektor T, Jorgensen C, RubensteinJB, Majmudar PA, Talati R, Basti S,Feder R, Sugar A, Mian SI,Balasubramanian N, Sandhu J, GaynesBI, Bouchard CS. A Multicenter StudyEvaluating the Risk Factors andOutcomes of Repeat DescemetStripping Endothelial Keratoplasty.Cornea 2019; 38(2): 177 -182

Figure 2: Fuchs’ corneal dystrophy is characterized by central corneal guttate and can cause corneal oedema.Note that the endothelium has a typical ‘beaten metal appearance.


In order to maximize the learning effect, participants have the opportunityto register at our website and to answer a number of multiple choicequestions for each of the four sections covering the key points of eachsection. Shortly after test completion, participants receive electronicfeedback on successful accomplishment or failure. In case of failure theparticipant is encouraged to review articles and retake the test. Asuccessful test will earn the participant valuable CME credits needed fortheir continuous medical education efforts.

ACCREDITATIONSIndividual issues of Glaucoma Now are accredited for Continuing MedicalEducation (CME) by the Physicians' Chamber of Baden-Württemberg,Germany (Local Medical Responsible: Andreas Buchholz, MD, PhD,ROph). This accreditation automatically implies acceptance of creditsthroughout the European Union and associated countries.

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Since 2013 the program is recognized by the Brazilian Council ofOphthalmology. Brazilian physicians successfully taking CME tests on ourwebsite are automatically awarded CME points by CBO.

STATEMENT OF NEED AND PROGRAM DESCRIPTIONRecent months and years have seen significant advances in ourunderstanding of glaucoma. Much has been learned, not only aboutdamage mechanisms and pathogenesis, but also about diagnosis andmanagement. Treatment options – both medical and surgical – continueto expand. This program will review this new knowledge with an emphasison incorporating recent insights into day-to-day practice.

Date of original release: May 2019

Approved for a period of 12 months.

This issue is accredited for Continuing Medical Education (CME) by thePhysicians’ Chamber of Baden-Württemberg, Germany (Local MedicalResponsible: Andreas Buchholz MD, PhD, ROph)

DISCLAIMERParticipants have an implied responsibility to use newly acquiredinformation to enhance patient outcomes and professional development.

The information presented in this activity is not meant to serve as aguideline for patient care. Any procedures, medications, or other coursesof diagnosis or treatment discussed or suggested in this activity shouldnot be used by clinicians without evaluation of their patient’s conditionsand possible contraindications or dangers in use, applicablemanufacturer’s product information, and comparison withrecommendations of other authorities.

Contributors• Bahram Bodaghi MD, PhD is Professor at the Department ofOphthalmology, Sorbonne University, Coordinator of DHU ViewRestore,Pitié-Salpêtrière Hospital, Paris, France. He has no commercialrelationships to disclose.

• Christophe Baudouin MD PhD is a dry eye specialist and Professor ofOphthalmology at Quinze-Vingts National Ophthalmology Hospital, andVision Institute, Paris, France. He has no commercial relationships relatedto his current article. In general, he receives financial support from HorusPharma, Santen and Théa. Within the last 3 years he has also acted as aconsultant to Alcon, Allergan, Dompé, Horus Pharma, Santen, Sifi andThéa.

• John Grigg MD FRANZCO is Professor at Discipline of Ophthalmology,University of Sydney, Sydney, NSW, Australia. He is affiliated to SydneyEye Hospital, Sydney and The Children’s Hospital at Westmead, Sydney.He has no commercial relationship to disclose.

• Sophia L. Zagora MD FRANZCO works at Discipline of Ophthalmology,University of Sydney, Sydney, NSW, Australia. She is also affiliated toSydney Eye Hospital, Sydney and The Children’s Hospital at Westmead,Sydney. She also has no commercial relationship to disclose.

• Stephanie Watson Bsc(Med) MBBS PhD FRANZCO is Professor and aFellow at Sydney Medical School Foundation, The University of Sydney,Save Sight Institute, Discipline of Ophthalmology, Sydney Medical School,Sydney, NSW, Australia. She has no commercial relationships to disclose.

DISCLOSURE STATEMENT EDITORIAL BOARDIvan Goldberg serves on the Faculty and Advisory Boards of the followingcompanies: Novartis, Allergan, Mundipharma and Pfizer.

Remo Susanna served on the Faculty and Advisory Boards of thefollowing companies: Alcon, Allergan, Merck and Pfizer.

For each issue 4 CME credits can be obtainedby successfully passing the multiple choice test on our website!

main topic: “glaucoma and concomitant eye diseases” · uveitis and scleritis are the main...

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