glaucoma management,dr.a.r.rajalakhmi,11.05.16

Management of Glaucoma

Dr AR Rajalakshmi

• Aim of Glaucoma management• When and how to treat• Various treatment modalities

Glaucoma Management

AIM:• to prevent functional impairment of vision.

• Currently the only proven method of achieving this is the lowering of IOP.

MECHANISM

• Decreased aqueous production

• Increased facility of outflow (trabecular / uveoscleral)

• Intraocular osmotic fluid reduction

Treatment goals

Target pressure:• An IOP level is identified below which further damage

is considered unlikely

• To Assess: – the severity of existing damage (particularly a greater vertical

C/D ratio and a greater mean deviation on visual fields), – the level of IOP, CCT, – the rapidity with which damage occurred if known, and – the age and general health of the patient;

Classification

I. Prostaglandin analogues

II. Beta Blockers

III. Alpha-2-agonists

IV. Carbonic anhydrase inhibitors

V. Miotics

VI. Osmotic agents

Prostaglandin derivatives

Mode of Action:• preferred first-line treatment for glaucoma• enhancement of uveo-scleral aqueous outflow• Duration of action: several days• Administration once/day (at bedtime) • IOP by 25 –34 %

Agents Latanoprost 0.005%• fewer ocular adverse

events than other PG agents

• Often used first line

Travoprost 0.004%• Similar to latanoprost, • May lower IOP to a

slightly greater extent, particularly in black patients

Bimatoprost 0.03%• Shown to have a greater IOP-

lowering effect than the other PG agents

• More conjunctival hyperaemia & less iris hyperpigmentation

Tafluprost • Newer prostaglandin derivative,• Well tolerated and cause less

disruption of the ocular surface.

Side effectsOcular• Conjunctival hyperaemia • Eyelash lengthening, thickening,

hyperpigmentation • Irreversible iris

hyperpigmentation • Periorbital fat loss • deepening of the upper lid

sulcus• Hyperpigmentation of periocular

skin – Common but reversible

Systemic side effects • occasional headache, • precipitation of migraine in susceptible

individuals,• malaise, myalgia,• skin rash and • mild upper respiratory tract symptoms.

• C/I: Uveitic glaucoma, H/O herpes keratitis

Beta Blockers

• Act by decreasing aqueous production

• Eg: Timolol (0.5%), Betaxolol (Cardioselective),

Levobunolol, Carteolol, Metipranolol

• Most commonly used ocular hypotensive agent

especially in developing countries

• Given twice daily

• S/E: Ocular: Tachyphylaxis, allergy, punctate keratitis

Systemic: Bronchospasm (nonselective agents), bradycardia, nocturnal hypotension,worsening of heart failure and peripheral vascular disease, depression, impotence,dyslipidemia

• C/I: COPD, Heart failure, Diabetics(masking of hypoglycemia)

Timolol available forms- 0.25% and 0.5% solutions used twice daily• Gel-forming preparations of 0.1%,

0.25% and 0.5% are used once daily.

Betaxolol twice daily • lower hypotensive effect than

timolol. • optic nerve blood flow may be

increased due to a calcium-channel blocking effect, so that visual field preservation may be superior.

• Betaxolol is relatively cardioselective (beta-1 receptors), so causes less bronchoconstriction.

Levobunolol once or twice daily • similar profile to timolol.

Carteolol twice daily is similar to timolol • exhibits intrinsic

sympathomimetic activity. • more selective action on the eye

than on the cardiopulmonary system and lower systemic side effect incidence.

Metipranolol twice daily • similar to timolol • linked with granulomatous

anterior uveitis.

Alpha-2 agonists

• Decrease aqueous production by acting on the ciliary epithelium; also have some effect on uveo-scleral outflow

• Eg.Brimonidine (0.2%), Apraclonidine (1%)

• Apraclonidine is commonly used to treat transient IOP spikes following laser treatment of the anterior segement

• S/E: allergic conjunctivitis, uveitis, eyelid retraction, xerostsomia, fatigue

• C/I: in children less than 2 years as it crosses BB barrier and causes depression and hypotension, along with MOA inhibitors as they precipitate hypertensive crisis

Brimonidine 0.2% twice daily • Allergic conjunctivitis is

relatively common• Granulomatous anterior

uveitis - rare.

Apraclonidine 1% (or 0.5%) • used principally to prevent

or treat an acute rise in IOP following laser surgery on the anterior segment. The

• It is generally not suitable for long-term use

• because of a loss of therapeutic effect over weeks to months and a

• high incidence of local side

Carbonic Anhydrase Inhibitors• Inhibit aqueous secretion; supplementary neuroprotective

effect

• Acetazolamide (oral) 250-1000mg in divided doses. Also

available as sustained release tablets. Another oral drug is

Methazolamide

• Useful particularly in acute glaucoma for immediate short

term control of IOP• Topical forms include Dorzolamide 2%, Brinzolamide 1%

which are commonly used twice daily.

• S/E: Ocular: allergic

blepharoconjunctivitis, corneal decompensation (esp in patients with endothelial dysfunction), transient stinging sensation and bitter taste. Rarely choroidal effusion.

Systemic: Paresthesia, hypokalemia, GI symptoms, dose-related bone marrow suppression and aplastic anemia

• C/I: sulpha allergy (relative)

Miotics

• Cholinergic agonists used in treatment of angle closure glaucoma to terminate an acute attack.

• 2 main mechanisms: 1)Pull the peripheral iris away from the trabeculum

thereby opening the angle(useful in PACG). 2) Contraction of longitudinal muscle of ciliary body

hence increasing outflow (useful in POAG).

• Eg: Pilocarpine 1% qid was used previously for POAG, Carbachol

• S/E: Miosis, browache, myopic shift and exacerbation of symptoms of nuclear cataract.

• Systemic side effects include bradycardia, bronchospasm, GI symptoms, salivation

Osmotic agents• They reduce IOP by drawing water into the blood. • The effect is short term and is used in resistant

acute angle closure and prior to intraocular surgery to reduce high IOP.

• Mannitol intravenously 1gm/kg of a 20% solution over 30-60 minutes

• Glycerol orally 1g/kg of a 50% solution• Isosorbide is a safer alternative in diabetics than

glycerol

• S/E: CVS overload, headache, nausea, confusion

• C/I: in cardiac and renal patients for risk of volume overload, glycerol in uncontrolled diabetes

Combined preparations • Combined preparations with similar ocular hypotensive

effects to the sum of the individual components • improve convenience and patient compliance. • cost effective

• Cosopt®: timolol and dorzolamide, administered twice daily. • Xalacom®: timolol and latanoprost once daily. • TimPilo®: timolol and pilocarpine twice daily. • Combigan®: timolol and brimonidine twice daily. • DuoTrav®: timolol and travoprost once daily. • Ganfort®: timolol and bimatoprost once daily. • Azarga®: timolol and brinzolamide twice daily. • Simbrinza®: brimonidine and brinzolamide; a new combination – the only one that does not contain the beta-blocker timolol; administered twice daily.

Class/Compound Conc Dose Mech of action IOP Reduction

Ocular S/E Systemic S/E Comments

PG ANALOGUESLatanoprost

Travoprost

Unoprostone

Bimatoprost

Tafluprost

0.005%

0.004%

0.15%

0.03%

0.0015%

HS

HS

Bd

HS

HS

uveo scleral outflow

Both trabecular and uveoscleral outflow

25-32%

13-18%

Hyperpgt of iris/lashesHypertrichosisBlurred vision, Keratitis, CME, anterior uveitis, conjunctiva!hyperemia, exacerbation ofherpes keratitis

Flu like symptom, joint pain,headache

Peak-10-14 hrs

Washout:4-6 wks

Peak & wahout period unknown



BETA BLOCKERSNon selectiveTimolol

Levobunolol

Metipronolol

CarteololHydrochloride

SelectiveBetoxolol

0.5%

0.5%

0.3%

1.0%

0.25%

Bd

Aqueous production 20-

30%

15-20%

Blurring, irritation, cornealanesthesia, punctate keratitis,allergy;

Bradycardia, heart block,bronchospasm,loweredblood pressure, decreasedlibido, CNS depression,mood swings, reducedexercise ToleranceIntrinsic sympathomimetic

Fewer pulmonary complications

Peak: 2-3 hoursWashout: 1 month

Peak: 2-6 hours

Peak: 2 hours

Peak: 4 hoursWashout: 1 month

Peak: 2-3 hoursWashout: 1 month



Alpha-Adrenergic agonistsSelectiveApraclonidinehydrochloride

Brimonidinetartrate 0.2%

0.5%

0.2%

TDS

TDS

Decrease aqueous production,decreaseepiscleralvenous pressure

Decreases aqueousproduction,increasesuveoscleraloutflow

20-30%

20-30%

Irritation, ischemia, allergy,eyelid retraction, conjunctiva!blanching, follicularconjunctivitis, puritis,dermatitis, ocular ache,photopsia, miosisBlurring, foreign-bodysensation, eyelid edema,dryness, less ocularsensitivity/allergy than withapraclonidine

Hypotension, vasovagalattack, dry mouth and nose,Fatigue

Headache, fatigue,hypotension, insomnia,depression, syncope,dizziness, anxiety, drymouth

Peak: <1-2 hoursWashout: 7-14 days

Peak: 2 hoursWashout: 7-14 days



Parasympathomimetic agents

Pilocarpine HCI 0.5,1 .0, 2.0, 3.0,4.0, 6.0%

2-4 times

Increasestrabecularoutflow

15-25%

Posterior synechiae, keratitis,miosis, brow ache, cataractgrowth, angle-closurepotential, myopia, Retinal tear/detachment dermatitis,change in retinal sensitivity,color vision changes,epiphora

Increased salivation,increased secretion(gastric), abdominal cramps

Peak: 1 1/2 -2 hoursWashout: 48 hours

Class/Compound Conc DosePerday

Mech of action

IOP Reduction


Carbonic anhydrase inhibitorsOralAcetazolamide

Acetazolamide(parenteral)

Methazolamide

250 mg

500 mg

500 mg5-10 mg/kg

25, 50, 100 mg

2-4 times

2 times

6-8 hrly

2-3 times

Decrease aqueous production

15-20% None

Acidosis,depression, malaise,hirsutism, flatulence,paresthesias, numbness,lethargy, blood dyscrasias,diarrhea, weight loss,renal stones, loss of libido,impotence, bone ma rrowdepression, hypokalemia,cramps, anorexia, alteredtaste, increased serumurate, enuresis

Caution insulfaallergy


Mech of action

IOP Reduction


Carbonic anhydrase inhibitorsTopical

Dorzolamide

Brinzolamide

2%

1 %

2-3 times

2-3 times

Decrease aqueous production

15-20%

Induced myopia, blurredvision, stinging, keratitis,conjunctivitis, dermatitis

Same as above, except lessstinging when compared todorzolamide

Less likely

Bitter tastePeak: 2-3 hoursWashout: 48 hours


Mech of action

IOP Reduction


Hyperosmotic agents

Mannitol (parenteral)

Glycerol (oral)

20%

50%

0.5-2.0 g/kgB Wt

2-3 times

1-1.5gm/Kg

Creates osmotic gradientDehydrates vitreous

15-20%

Rebound increase in IOP

Urinary retention, headachecongestive heart failureexpansion of blood volumediabetic complicationsnausea, vomiting, diarrheaelectrolyte disturbancerenal failure, mental confusion, backachemyocardial infarction

Caution in DM

C/I in heart failure,renal failure

Useful in acute rise in IOP

Can ppt DKA

Laser treatment of glaucoma • Laser Trabeculoplasty:Involves delivery of laser to the trabecular meshwork

with the aim of improving outflow.Done using the conventional Argon laser (ALT) or Nd-

Yag laser (Selective Laser Trabeculoplasty)

• Laser Iridotomy:Used principally in treatment of primary angle

closure and secondary angle closure with pupillary block.

An opening is created between 11 to 1 o clock on the outer third of the iris preferably over a crypt.

• Other uses of laser:

1. Diode laser cycloablation

2. Laser iridoplasty

Trabeculectomy

• It is a filtration surgery that lowers IOP by creating a

fistula between the anterior chamber and sub-Tenons

space.

• Indications: failure of medical therapy, avoidance of

medical polytherapy, primary therapy especially in

younger patients

• Technique

1. Limbal or fornix based flap of conjunctiva and Tenons capsule

fashioned superiorly

2. A trapdoor lamellar scleral flap incision usually triangular and

rectangular in shape

3. AC entered, peripheral iridectomy done and superficial scleral

flap and conjunctival flap are sutured and a bleb is created

Complications:• shallow anterior chamber,• failure of filtration,• Bleb leakage,• blebitis & endophthalmitis

Other surgeries

Non penetrating Surgeries• Deep sclerectomy

• Viscocanalostomy

• Canaloplasty

Drainage Shunts

• Classification of anti glaucoma medications• Mechanism of action, Side effects,

contraindications• Name the Laser procedures for glaucoma• Name the surgical procedure for glaucoma.

glaucoma management,dr.a.r.rajalakhmi,11.05.16

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