Medical management of glaucoma
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Glaucoma refers to a group of diseases characterized by optic neuropathy, visual field defects, and raised intraocular pressure. The document discusses the medical management of glaucoma including targeting intraocular pressure, evaluating patients, and selecting initial treatments such as beta blockers, prostaglandin analogues, adrenergic agonists, cholinergic drugs, carbonic anhydrase inhibitors, and hyperosmotic agents. Neuroprotective drugs that may help preserve vision by various mechanisms including blocking glutamate receptors and calcium channels are also reviewed. The ultimate goal of glaucoma treatment is to preserve vision and quality of life through long term management and control of intraocular pressure.
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Medical management of glaucoma
- 1. MEDICAL MANAGEMENT OF GLAUCOMA Dr. Amrutha
- 2. GLAUCOMA Glaucoma refers to a group of diseases characterised by Optic neuropathy Specific pattern of visual field defects Raised iop
- 3. AQUEOUS PRODUCTION & DRAINAGE SECRETION is from ciliary body Route of drainage Trabecular meshwork Uveoscleral outflow
- 4. MANAGEMENT is by EVIDENCE BASED APPROACH FACTORS TO BE CONSIDERED : Making an accurate clinical diagnosis Assessing the stage of disease Assessing the risk factors for disease progression Understanding the patient's access to health care and related factors Considering the patient's lifestyle, health status, and life expectancy Implementing a treatment strategy To achieve the target IOP range To minimise the progression of glaucomatous optic neuropathy
- 5. ULTIMATE GOAL OF GLAUCOMA TREATMENT IOP is a surrogate clinical end point Long term goal is to preserve vision and best quality of life for the patient.
- 6. APPROACH TO A NEW PATIENT Ocular and medical history Testing visual acuity and refraction Performing tonometry and pachymetry Conducting an external examination with evaluation of the pupillary reaction Slitlamp biomicroscopy and gonioscopy Assessing the retina and optic nerve head with photographic documentation Testing the visual field
- 7. IN AN ESTABLISHED PATIENT Evaluate adherence to glaucoma medical treatment Evaluate tolerance to the treatment Assess stability of the optic nerve head and visual function. If the patient has had a surgical intervention, the surgical site should be examined carefully for signs of tissue breakdown or infection
- 8. HOW TO START TREATMENT?? Establishing the target IOP or IOP range Selecting the appropriate medication, Educating and instructing the patient, and Establishing the efficacy and safety of the treatment at follow-up evaluations.
- 9. TARGET PRESSURE Elevated IOP is the most important causative risk factor for glaucoma development and progression, and it is the only one for which we have proven treatment. The IOP target is based on the status of the optic nerve head and other risk factors for progression. reducing the IOP by 20% to 30% from baseline is recommended
- 10. TARGET IOP Minimal damage Early neural rim thinning without field loss Middle-high teens Moderate damage Cupping to the disc margin Early field loss Low – mid teens Advanced damage Extensive cupping Field loss Single digit – low teens
- 11. Initial medical therapy remains the standard for most patients with newly diagnosed glaucoma. The therapeutic goal is to use the Least amount of medication that will give The desired therapeutic effect with Fewest adverse reactions and Affordable for the patient.
- 12. EXCEPTIONS TO MEDICAL THERAPY Very high iops that are immediate threat to vision Intolerable side effects with medications Problems with adherence Acute angle closure glaucomas Childhood glaucomas
- 13. Mechanisms of action of anti glaucoma agents
- 14. SELECTING INTIAL MEDICATION CHOLINERGIC AGONISTS PILOCARPINE CARBACHOL ADRENERGIC AGONISTS SELECTIVE • APRACLONIDINE BRIMONIDIDNE NON SELECTIVE •EPINEPHRINE • DIPIVEFRINE BETA BLOCKERS SELECTIVE •BETAXOLOL NON SELECTIVE •CARTEOLOL •LEVOBUNOLOL •METIPRANOLOL •TIMOLOL CA INHIBITORS TOPICAL •BRINZOLAMIDE •DORZOLAMIDE SYSTEMIC •ACETAZOLAMIDE •DICHLORPHENAMIDE •METHAZOLAMIDE PROSTAGLANDIN ANALOGUES BIMATOPROST •LATANOPROST •TRAVOPROST •UNOPROSTONE
- 15. BETA BLOCKERS First drug of choice for POAG Lowers iop by reducing aqueous secretion due to their effect on β2 receptors Antagonises the effect of catecholamines by reducing the aqueous production.
- 16. TIMOLOL 0.25,0.5% OD/BD CARTEOLOL 1%drop OD/BD LEVOBUNOLOL 0.25-0.50% OD BETAXOLOL 0.25% BD MOST COMMONLY USED • Iop dec by 20-28% • Peak 2-3hrs • Washout 1 month • SHORT TERM ESCAPE • Marked initial fall by transient rise with moderate fall in iop LONG TERM DRIFT Slow rise in iop in well controlled with many monts of therapy • Intrinsic sympatomimetic activity • Partially activates B receptors in absence of cat”s • ADVANTAGES • LESS Stinging • Best in pt with hyperlipidemias /CADs • ADVANTAGES: • LONGEST IN ACTION • Most reliable in OD usage CONTRAINDICATION • Predisposed to cardiac or resp disease SELECTIVE BETA BLOCKER • Indicated in pts with astma and pulmonary problems
- 17. OCULAR SIDE EFFECTS OF B BLOCKERS Allergic blepharoconjuctivitis Dry eye Macular edema in aphakics Uveitis Cataract progression
- 18. CONTRAINDICATIONS OF B BLOCKERS BRONCHIAL ASHTMA COPD BRADYCARDIA HEARTBLOCK CARDIAC FAILURE CHILDREN& INFANTS
- 19. ADRENERGIC AGONISTS APRACLONIDINE 1% 0.5% BD Para amino derivative of clonidine IOP control : 20 % -30 % Maximal effect is produced 3-5 hours after dosing Not used as primary treatment due to significant tachyphylaxis Mainly indicated in acute pressure spikes in case of laser iridotomy, trabeculoplasty, and posterior capsulotomy BRIMONIDINE 0.2% BD/TID Small effect on uveoscleral outflow Neuroprotection IOP control: 20-30% Advantage Can be used as primary drug in POAG Less tachyphylaxis & less rate of allergic reactions than apraclonidine
- 20. SIDE EFFECTS SYSTEMIC Dry mouth Fatigue Drowsiness Headache hypotension Bradycardia & hypothermia in neonates OCULAR Allergy Contact dermatitis Blurred vision Stinging Follicular conjunctivitis Hyperaemia Photophobia
- 21. CHOLINERGIC DRUGS MOA Contraction of the iris sphincter: Constricts the pupil (miosis) contraction of the longitudinal fibers of the ciliary muscle, producing tension on the scleral spur:(Openingthe trabecular meshwork) and facilitating aqueousoutflow Contraction of the circular fibers of the ciliary muscle, relaxing the zonular tension onthe lens equator :Accommodation
- 22. PILOCARPINE Derived from the plant Pilocarpus Microphyllus IOP decrease : 15-25% Peak : 1 ½ - 2hrs Effect lasts up to : 6-8 hrs Gel form at bedtime Concentration : 0.25- 10% drop QID, 4% gel, ocusert:20-40µg/hr
- 23. Ocular pigmentation influences Blue eyes show maximal ocular hypotensive responses Darkly pigmented eyes demonstrate a relative resistance to IOP reduction may require pilocarpine solutions in concentrations exceeding 4%
- 24. INDICATIONS Acute and chronic narrow angle glaucoma Open angle glaucoma For prophylaxis of primary angle-closure glaucoma until a peripheral iridotomy can be performed CONTRAINDICATIONS Presence of cataract Patients younger than 40 years of age Neovascular and uveitic glaucoma History of retinal detachment Asthma or history of asthma High myopia Known hypersensitivity to the drug
- 25. SIDE EFFECTS OCULAR Accommodative spasm Miosis Follicular conjunctivitis Pupillary block with secondary angle-closure glaucoma Band keratopathy Allergic blepharoconjunctivitis Retinal detachment Conjunctival injection Anterior subcapsular cataract Iris cyst formation SYSTEMIC Headache Browache Marked salivation Profuse perspiration Nausea Vomiting Bronchospasm Pulmonary edema Systemic hypotension Bradycardia Generalized muscular weakness Abdominal pain, diarrhea
- 26. PROSTAGLANDIN ANALOGUES Hypotensive lipids Pro drugs INCREASE UVEOSCLERAL OUTFLOW PG stimulates collagenase and metalloproteinase to degrade the extracellular matrix between ciliary muscle bundles, which in turn leads to the reduction of hydraulic resistance to uveoscleral flow. High concentration – inc IOP and inflammation Low concentration – decreases IOP Lack of cardiopulmonary side effects Additive to other anti glaucoma medications
- 27. LATANOPROST BIMATOPROST TRAVOPROST 0.005% OD 0.03% OD evening 0.004% OD evening Lowers IOP 27-30% with peak at 10-14 hrs Maximum effect usually by 4-6 weeks, may have further decrease after 3- 4 months Latanoprost tends to be less effective in lowering IOP in children than in adults • better IOP control than latanoprost • Maximum iop lowering effect in 1-2 weeks • Lowers iop by 7- 9mmhg • Maximum iop lowering effect achieved within 2 weeks
- 28. INDICATIONS CONTRAINDICATIONS • Primary open angle glaucoma • Normal tension glaucoma • Chronic closed angle glaucoma • Pigment dispersion syndrome • Pseudoexfoliation glaucoma • Allergy • Pregnant & nursing mother • Children • Uveitic glaucoma • Immediate post operative period • Healed or active herpes simplex keratitis
- 29. SIDE EFFECTS OCULAR SYSTEMIC • CORNEA: • punctate erosions • pseudodendrites • recc herpes keratitis • CONJUCTIVAL hyperaemia • EYELASH hyperpigmentation • Iris hyper pigmentation • Periorbital skin • CME after cataract sx • Allergy • Anterior uveitis • Occasional headache • Skin rash • URTI • Precipitates migraine
- 30. CARBONIC ANYDRASE INHIBITORS Inhibit carbonic anhydrase enzyme Reducing aqueous humor formation Lower iop
- 31. ACETAZOLAMIDE Oral , Iv prep Iop decreases by 15-20% Peak 2-4hrs – oral 30 mins iv Wash out 12 hrs oral, 4hrs iv Oral – 125, 250mg tablets 6hrly 500mg sustained release caps Iv use- 500mg METHAZOLAMIDE MORE POTENT Imp intraocular penetration Inc halflife, plasma conc 25-50mg BD.TDS In chronic In chronic IOP reduction
- 32. TOPICAL CA INHIBITORS DORZOLAMIDE 2% % BRINZOLAMIDE 1% Iop decreases by 15-20% Peak at 3-4 hrs Wash out 10-18hrs Dose – BD/TDS
- 33. SIDE EFFECTS OCULAR SYSTEMIC • Induced myopia • Stinging sensation • Keratitis, conjunctivitis • Dermatitis • Choroidal efusion • Numbness and tingling of extremities and perioral region • Metallic taste • Fatigue • Malaise • Weight loss • Hypokalemia • Renal calculi • Steven johnson syndrome • Blood dyscrasias • Dermatitis
- 34. HYPEROSMOTIC AGENTS IV – MANNITOL , UREA ORAL – GLYCEROL, ISOSORBIDE Increase blood osmolality Osmotic gradient b/w blooad & vitreous Water is drawn out of vitreous
- 35. MANNITOL GLYCEROL ISOSORBIDE 20%solution Onset 15-30 mins Peak 30-60min 50%solution Onset 20 min Peak 45min-2hr Caution in DM 45%solution 1.5-4ml/kg
- 36. SIDE EFFECTS GIT : nausea , vomiting, abdominal cramp CVS : CHF , angina CNS : subdural hematoma, headache, confusion, disorientation, fever RENAL : diuresis , anuria, potassium ions Diabetic ketoacidosis, urticaria.
- 37. NEURO PROTECTIVE DRUGS IN GLAUCOMA
- 38. RATIONALE FOR NEUROPROTECTION Intra retinal or intravitreal glutamate levels are neurotoxic to ganglion cells plays a role in glaucoma Neuroprotective drugs Enhance the vascular supply Decrease pro apoptotic factors
- 39. METHODS OF NEUROPROTECTION PHARMACOLOGIC • MemantineNMDA receptor antagonists • NimodipineCalcium channel blockers • AminoguanidineNO synthetase inhibitors • BrimonidineAlfa agonists • Cytochrome C release inh • Capsase inhibitors Apoptosis inibitors Neurotropin 3 Vasodilators Antioxidants
- 40. IMMUNE MODULATION PRECONDITIONING NEUROREPAIR & REGENERATION
- 41. MEMANTINE N-Methyl D-Aspartate (NMDA) receptor antagonist NMDA ion channel Activated by glutamate Allows EC Ca+2 to enter the cell Memantine blocks glutamate stimulation of retinal ganglion cell Protects from calcium mediated apoptosis
- 42. AMINOGUANIDINE NO SYNTHASE INHIBITOR Optic nerve astrocytes and microglia – iNOS cause optic nerve damage INHIBITS inducible iNOS prevents retinal ganglion cell loss ROLEOFNOineye AMINOGUANIDINE
- 43. NIMODIPINE INHIBITS entrance of calcium ion into vascular smooth muscle cells VASODILATION Protects optic nerve head by increasing vascular perfusion
- 44. EDUCATING AND INSTRUCTING THE PATIENT Regarding the disease , prognosis, treatment Explain the patient on how to instill eyedrops properly And the spacing between the doses
- 45. DISEASE: Total and irreversible blindness but blindess can be prevented wit proper treatment NEED FOR MEDICATION To lower the IOP Treatment will not improve visual acuity FOLLOW UP Evaluation of efficacy by checking the iop reduction and side effects
- 46. WHEN AND HOW TO CHANGE OR COMBINE MEDICATIONS When target iop is no longer being maintained with a particular drug. Replace or add or move on to surgery In adjunctive therapy , check if each drug is making a significant iop lowering contribution QUITTING MEDICAL THERAPY Inability to maintain target iop Progressive glaucomatous damage despite treatment Inability to tolerate or adhere to medical regimen.