This document discusses steroid-induced glaucoma, including its definition, prevalence, screening, risk factors, and management. Some key points: - Steroid-induced glaucoma occurs when elevated intraocular pressure (IOP) caused by steroid use leads to optic nerve damage and vision loss. Steroids can increase IOP through various mechanisms affecting tissues in the eye. - The risk of developing glaucoma is higher in those with a family history or existing open-angle glaucoma. Thinner corneas also increase risk. - Screening includes comprehensive eye exams measuring IOP, optic nerve evaluation, and visual field tests. Risk should be stratified based on factors like age and IOP levels

1. GLAUCOMA
SUSPECT,OCULAR
HYPERTENSION,
STEROID INDUCED
Bipin Bista
Resident
National Medical
College
& Teaching Hospital
Ophthalmology

2. DEFINITION
Open angle by gonioscopy and one of the following in at least one
eye:
•IOP consistently >21mm Hg by applanation tonometry
•Appearance of the OD or RNFL s/o glaucomatous damage
•Diffuse or focal narrowing or sloping of the disc rim
•Diffuse or localised abnormalities of the nerve fiber layer, especially
at superior and inferior poles
•Disc haemorrhage
•Asymmetric appearance of the disc or rim between fellow eyes (C/D
difference >0.2)
•VF suspicious foe early glaucomatous damage.
*American academy of Ophthalmology,2005

3. PREVALENCE &
DEVELOPMENT OF COAG
The cumulative probability of developing COAG over 5 years was
about 1% in medication group and about 2% per year in observation
group.

4. SCREENING AND EARLY
DETECTION
Comprehensive Eye Examination
IOP -
Pachymetry – Thinner CCT is a strong risk factor for COAG
Slitlamp Examination and Gonioscopy
Fundus Examination
Skilled Optic Nerve Evaluation- HRT, OCT, GDx – ON Head and RNFL
Standard automated Perimetry (SAP)
Short Wavelength Automated Perimetry(SWAP)
Ocular Blood Flow : Reduced Blow Flow in GS in the course of COAG.
(Superotemporal rim-16%, cup -35% and inferotemporal rim – 22%).

5. RISK FACTORS
•IOP > 30 mmHg.
•Thin CCT
•Vertical C/D > 0.7
•Older Age
•Abnormal VF : Increased Pattern Deviation
•Presence of exfoliation or Pigment Dispersion Syndrome
•Disc Hemorrhage
•Family History
•Fellow eye of patient with severe unilateral glaucoma
•Additional – suspicious disc appearance, myopia, Low ON perfusion pressure, Steroid user,
African Ancestor, sleep apnea, DM, Hypertension, CVS disease, Hypothyroidism, Migraine
headache, vasospasm.

6. RISK CALCULATORS
Ocular hypertension treatment study
European Glaucoma Prevention Society
Diagnostics Innovations in Glaucoma Study

7. WHEN TO TREAT
Every attempt should be made to engage the patient in decision-making process.
Elevated IOP should be stratified into low, moderate and high risk for progression.
Patients at high risk for progression warrant treatment to prevent Optic nerve damage,
whereas low risk should should be observed at periodic intervals. Moderate can initiate
treatment if appropriate, or monitor closely.
CAREFUL CONSIDERATION :
Greater age and life expectancy
Psychological factors
Convictions
Social environment
Follow-up availability
Pregnancy.

8. GUIDELINES FOR FOLLOW-
UP
Follow-up is necessary to determine whether there is a change in the
IOP, ONH, or VF status.
Follow-up of Glaucoma Suspects should be at least every 6 to 12
months & frequently more in high risk patients.
VF should be observed every 6 to 18 months and compared with the
baseline.
Gonioscopy : In suspicion of angle closure.

9. STEROID INDUCED
GLAUCOMA

10. HISTORY
First reported by Mclean in 1950, after administration of
corticotropine and cortisone systematically.
Later françois also evaluated after local administration of cortisone.
Occurs more commonly in patient with COAG or a family history of
the disease.
Whether given by the topical, systemic , periocular, or intraocular
route, and the IOP elevation can lead to GOA and loss of vision . Such
a condition is referred to as Steroid-induced glaucoma.

11. CLINICAL FEATURES
IOP elevation usually develops within a few weeks with potent topical
or intraocular corticosteroids or in months with weaker steroids.
Clinical picture resembles with COAG, with an open, normal-
appearing anterior chamber angle and absence of symptoms.
Children appear to have a lower incidence of positive steroid
responses than adults do.
IOP elevation was seen in treatment with external diseases in infants
with corticosteroids, with nasal and inhalational steroids, after
strabismus surgery with use of topical dexamethasone.
May also mimic LTG when steroid induced pressure elevation has
damaged the optic nerve head and VF in the past.

12. THEORIES OF MECHANISM
1. Nuclear transport of Glucocorticoid receptor
2. Influence of ECM
3. Influence on Phagocytosis
4. Genetic Influence
5. Outflow Obstruction by Steroid Particles

13. NUCLEAR TRANSPORT OF
GLUCOCORTICOID
RECEPTOR
Glucocorticoids have shown alter TM cell morphology by causing an
increase in nuclear size and DNA content.
Experiments on TM cells exposed to Dexamethasone have
demonstrated that the FK506-binding immunophilin FKBP51
mediates nuclear transport of the human glucocorticoid receptor.

14. INFLUENCE OF ECM
François postulated that GAG in the polymerised form become
hydrated, producing a ‘biologic edema’ that may increase resistance
to aqueous outflow.
Hyaluronidase in lysosomes depolymerizes hyaluronate , and
corticosteroids stabilize the lysosomal membrane, which may lead to
an accumulation of polymerised GAGs in the TM.
Topical Dexamethasone induced IOP elevation associates with
increase chondroitin sulphate but decrease in hyaluronic acid.
Dexamethasone can decrease the synthesis of collagen in Normal
human TM decreases and decrease the EC activity of TPA.

15. INFLUENCE ON
PHAGOCYTOSIS
Endothelial cells lining the TM have phagocytic properties, may help
to clean the aqueous debris before it reaches the inner wall of the
Schlemm canal.
Corticosteroids are known to suppress phagocytic activity, and
suppressed phagocytosis of the trabecular endothelium may allow
debris in the aqueous to accumulate in the meshwork and act as a
barrier to outflow.
Experiments shows formation of cross-linked actin networks in the
networks in the TM cytoskeleton with exposure to dexamethasone.

16. GENETIC INFLUENCE
Experiments have revealed multiple genes that may be involved in
protective and damaging mechanisms with IOP elevation.
Examples :α1- antichymotrypsin, pigment epithelium derived factor, cornea derived
transcript 6, prostaglandin D2 synthase, growth arrest specific 1, decorin , insulin-
like growth factor binding protein 2, ferritin light chain, and fibulin -1C.
Much works needs to be done to determine which of these genes are upregulated
in vivo and which of these and other genes play a role in increasing outflow
resistance in response to steroid application .

17. OUTFLOW OBSTRUCTION BY
STEROID PARTICLES
Peculiar finding was the presence of white crystals in the angle.
Obstruction of the TM with crystalline steroid particles.

18. PREVENTION
Patient Selection : Individuals with COAG or a family history of the
disease respond to long-term , Similarly for Myopics, old-aged
persons, DM , Connective tissue disease.
Avoid steroid use, if must then provide lowest possible amount of
drug over the shortest duration needed.
Drug Selection : advice for drug with lowest concentration with the
fewest potential adverse reactions.

19. ROUTES OF ADMINISTRATION
Topical therapy : Occurs more
Periocular therapy : dangerous route, repository is more dangerous
d/t prolonged duration of action.
Intravitreal therapy : triamcinolone acetonide to treat IO neovascular /
inflammatory diseases.
Systemic therapy : Least likely to introduce glaucoma, nasal or
inhalational corticosteroids are associated with increased IOP.

20. PRESSURE EFFECTS IN
SOME IMPORTANT DRUGS
1. Fluorometholone (0.25%) is least likely to increase IOP than
dexamethasone. Formulation with acetate appears to be more
effective, as effective as Prednisolone acetate (1.0%) .
2. NSAIDs : Topical oxyphenbutazone, flurbiprofen, and diclofenac
indicates that these NSAID agents don’t cause an elevation of IOP.

21. MANAGEMENT
oDiscontinuation of steroid Use
oExcision of Depot Steroid
oGlaucoma Therapy

22. THANK YOU
Refrence from:
1.Glaucoma – Shield
Textbook of Glaucoma
2.Recent advances –
Curbside Consultation in
Glaucoma : Steven J. Gedde
3.Myron yanoff and jay s
duker4th edition