Primary Open Angle Glaucoma - Standard Treatment Guideline

POAG is most common form of glaucoma world wide. It is estimated that 45 million people worldwide have POAG. With the exception of Asia, Primary open angle glaucoma (POAG) is far more common than Primary angle-closure glaucoma (PACG) worldwide.

Ministry of Health and Family Welfare, Government of India has issued the Standard Treatment Guidelines for Primary Open Angle Glaucoma. Following are the major recommendations :

Case definition:

It is a chronic progressive anterior optic neuropathy characterised by acquired loss of retinal ganglion cell loss, visual field loss, open angles with no obvious causative ocular or systemic condition.

Incidence of The Condition In Our Country

In India, Primary open angle glaucoma is estimated to affect 6.48 million persons. Aravind comprehensive eye survey found a prevalence (95% confidence interval) of POAG it was 1.7% (1.3, 2.1) in rural population. The prevalence of POAG in rural south Indian population as evaluated by Chennai glaucoma study group 1.62%. The prevalence increased with age, and 98.5% were not aware of the disease. Vellore eye study found a prevalence (95% CI) of POAG 4.1 (0.08-8.1) in urban south Indian population. Andhra Pradesh eye disease study found a prevalence (95% confidence interval) of 1.62% (0.77%-2.48%) in urban south Indian population. Studies comparing the prevalence in urban and rural population – Chennai glaucoma study found prevalence of POAG in south Indian urban population was 3.51%, higher than that of the rural population. Andhra Pradesh eye disease study also found the prevalence to be greater in urban population (4% vs 1.6%; P<0.001).

Differential Diagnosis

• Optic nerve anomalies: coloboma, pits, oblique insertion


• Primary optic atrophy


• Past history of steroid usage


• Past history of trauma or surgery


• Ischemic optic neuropathy (arteritic/non arteritic)

Prevention And Counseling

Once the blindness of glaucoma has occurred there is no treatment that will restore the lost vision. In nearly all cases blindness from glaucoma is preventable, which requires early diagnosis and proper treatment. Detection depends on the ability to recognize the early clinical manifestations of various glaucomas. Appropriate treatment requires an understanding of the pathogenic mechanisms involved, detailed knowledge of drugs and operations that control IOP. Infact sometimes, a patient needs to be followed up for an extended period of time before a decision to treat can be made. Retinal nerve fiber layer loss precedes measurable optic nerve head and conventional white on white perimetry changes in early glaucoma.Hence patients should be counseled regarding the asymptomatic nature of the disease, importance of treatment, correct technique of eye drop application and regular follow up. Each patient should be educated about different modalities of treatment.

Optimal Diagnostic Criteria, Investigations, Treatment & Referral Criteria

*Situation 1: At Secondary Hospital/ Non-Metro situation: Optimal Standards of Treatment in Situations where technology and resources are limited

Clinical Diagnosis :

Diagnosis: based on comprehensive initial ophthalmic evaluation-

• History (ocular and systemic)


• Family history of Glaucoma ( Severity and Outcome)


• IOP recording by applanation tonometer.


• Larger diurnal variation in IOP either by daytime phasing or 24 hour diurnal phasing.


• Gonioscopy to exclude angle closure disease and causes of secondary open angle glaucoma


• Steroscopic ONH evaluation (Preferably through dilated pupil) with pictoric fundus diagram.

Investigations :

• Pachymetry : central corneal thickness affects IOP measurements with higher IOP in thick corneas and lower IOP in thin corneas.


• Fundus photography aids in documentation of optic nerve head at baseline and follow up visits.


• Visual field analysis

Treatment:

Management Goals:

• Stable ONH and RNFL status


• Controlled IOP


• Stable visual fields

Standard Operating procedure

In Patient :Surgical treatment is indicated

• IOP not controlled with maximal medical therapy


• Contraindication to medical therapy


• Poor compliance

Surgical options: Trabeculectomy and combined glaucoma and cataract surgery.

Out patient : Medical management : Most appropriate medication with greatest chance of reaching target IOP, with good safety profile, convenient dosing and affordable medication should be chosen. Details of the medications, dosage, its adverse effects and follow up schedule are mentioned below.

Day Care
Not applicable

Referral criteria:

1.High suspicion of secondary glaucoma is present requiring evaluation for secondary causes
2.For optimal investigations and treatment
3.For management of difficult cases and Post-operative complications

*Situation 2: At Super Specialty Facility in Metro location where higher-end technology is available

Clinical Diagnosis: Comprehensive ophthalmic evaluation including

• History special attention to factors including systemic diseases that influence diagnosis, course and treatment of POAG.

• Evaluation of visual function: with respect to difficulties in night driving, near vision
and outdoor mobility.

• Visual acuity measurement


• Pupil examination: to detect Relative afferent pupillary defect, which is a function of optic nerve


• Anterior segment examination by Slit lamp biomicroscopy


• Intraocular pressure measurement by Goldmann applanation tonometry

o Gonioscopy: Is pre-requisite for diagnosis of glaucoma to rule out secondary causes like angle closure, angle recession, pseudoexfoliation, pigment dispersion, peripheral anterior synechiae, new vessels, blood in schlemm's canal and inflammatory precipitates.

• Optic nerve head and retinal nerve fiber evaluation by 90D stereopscopic examination:

1. Disc size.


2. Neuroretinal rim


3. Disc haemorrhage


4. Nerve fiber layer defect.


5. Peripapillary atrophy.


6. Vascular pattern.

• Central corneal thickness measurement (CCT)

Thicker CCT overestimates IOP readings and thinner CCT underestimates. There is no generally accepted correction formula. Thinner CCT is independent risk factor for conversion of ocular hypertensive to POAG as proven in Ocular Hypertensive Treatment Study.

• Visual field evaluation: characteristics of glaucomatous visual field defects

1. Asymmetrical across horizontal midline.


2. Located in midperiphery.(5-25 degrees from fixation).


3. Reproducible.


4. Not attributable to other pathology.


5. Clustered in neighbouring test points.


6. Defect should correlate with the ONH damage.

• Optic nerve head and retinal nerve fiber layer analysis

1. Slit lamp indirect ophthalmoscopy using 90 D and 78 D lenses.


2. Fundus diagrams.


3. Stereoscopic disc photographs.


4. Red free fundus photography.


5. Confocal scanning laser ophthalmoscopy.(HRT)


6. Scanning laser polarimetry (GDx)


7. Optical coherence tomography.

POAG is chronic progressive optic neuropathy that is bilateral and asymmetric in presentation
• Evidence of Optic Nerve Head damage

• Optic disc and retinal nerve fiber layer damage

1. Diffuse thinning, focal narrowing or notching of neuroretinal rim (NRR) especially at inferior or superior poles


2. Progressive thinning of NRR with increased cupping


3. Diffuse or focal peripapillary nerve fiber layer defects especially at poles


4. Peripapillary splinter hemorrhages

• Reliable and reproducible visual field abnormality

1. Visual field defects corresponding to retinal nerve fiber layer damage (nasal step, arcuate scotoma, paracentral scotoma)


2. Adult onset (more than 18yrs of age)


3. Elevated Intraocular pressure > 22 mm Hg in majority of cases on two successive occasions


4. Diagnosis of exclusion (to exclude pigment dispersion, pseudoexfoliation and other secondary open angle glaucomas)

Severity of glaucoma:

• HAP Visual Field Severity Score (Based on visual field damage)

Criteria for early defect

1. Mean deviation no worse than −6 dB


2. On pattern deviation plot, _25% of points depressed below the 5% level and _15% of points depressed below the 1% level


3. No point within central 5° with sensitivity _15 dB

Criteria for moderate defect

1. Mean deviation worse than −6 dB but no worse than −12 dB


2. On pattern deviation plot, _50% of points depressed below the 5% level and _25% of points depressed below the 1% level


3. No point within central 5° with sensitivity _0 dB


4. Only 1 hemifield containing a point with sensitivity _15 dB within 5° of fixation

Criteria for severe defect

1. Mean deviation worse than −12 dB


2. On pattern deviation plot, _50% of points depressed below the 5% level or _25% of points depressed below the 1% level


3. Any point within central 5° with sensitivity _0 dB


4. Both hemifields containing point(s) with sensitivity _15 dB within 5° of fixation

Investigations:

1. Pachymetry


2. Visual field


3. Optic nerve head and retinal nerve fiber layer analysis


4. Slit lamp indirect ophthalmoscopy using 90 D and 78 D lenses.


5. Fundus diagrams.


6. Stereoscopic disc photographs.


7. Red free fundus photography.


8. Confocal scanning laser ophthalmoscopy.(HRT)


9. Scanning laser polarimetry (GDx)


10. Optical coherence tomography.


11. Additional Investigations to rule out secondary causes:


12. B scan, UBM


13. Fluorescein angiography

Standard Operating procedure

a. In Patient

Surgical treatment when

• target IOP not achieved with medical therapy


• Any contraindication to medical therapy exists.


• Has an edge over medical therapy in advanced glaucomas.


• Poor compliance

Surgical options:

Trabeculectomy, Combined cataract and glaucoma surgery, non penetrating glaucoma surgeries and aqueous drainage devices.

b. Out Patient: Medical and laser therapy :

• Medical therapy.


• Effective for majority of patients.


• Most widely acceptable


• Widely available.


• Most appropriate medication with greatest chance of reaching target IOP, with good safety profile, convenient dosing and affordable medication should be chosen

Drug	Methods of action	IOP	Side- effects	Contraindications
Prostaglan	Increased uveoscleral outflow	25-33%	Cystoids macular edema conjunctival injection periocular hyperpigmentation eyelash growth iris colour change, uveitis possible herpes virus reactivation	Macular edema history of herpes keratitis
Beta- blockers	Decreased aqueous production	20-25%	Corneal toxicity allergic reactions congestive heart failure bronchospasm bradycardia depression impotence	COPD, asthma, bradycardia, first degree heart block, Myasthenia gravis CHF, hypotension
Alpha- adrenergic agonists	Non-selective: improve aqueous outflow Selective: decrease aqueous production, decrease episcleral venous pressure, increase uveoscleral outflow	20-25%	Conjuctival injection, allergic reaction, somnolosence, fatigue, headache	Monoamino oxide inhibitor therapy infants and children <2 yrs
Carbonic anhydrase inhibitors	Decrease aqueous production	15- 20%	Topical use: metallic taste Corneal edema, allergic dermatoconjunctivitis, Systemic use: Steven Johnson syndrome, aplastic anemaia, thrombocytopenia, renal calculi,metallic taste, malaise, anorexia, gastric irritation, depression, serum electrolyte disturbance	Sulfonamide allergy, aplastic anemia, Renal calculi and Renal failure, sickle cell disease
Parasyma pathomim metic agents	Increased trabecular outflow	20-25%	Myopia, brow ache, decreased vision, cataract, corneal toxicity, dermatoconjunctivitis, uveitis, development of peripheral anterior synechiae.	Neovascular glaucoma, malignant glaucoma, periodic retinal evaluation

Laser therapy: Selective Laser Trabeculoplasy by Frequency doubled Nd:YAG laser for ouflow enhancement and Diode Cyclophotocoagulation for end stage glaucoma

c Day Care

Trabeculectomy ,combined cataract and glaucoma surgeries, laser therapy, can be done on day care basis ensuring regular follow up.

WHO DOES WHAT? And TIMELINES

a. Doctor :

• Detailed history pertaining to ocular, systemic, past treatment should be obtained.


• Visual acuity and refraction should be reviewed.


• Detailed slit lamp evaluation with IOP recording, gonioscopy and stereoscopic optic nerve head evaluation should be performed.


• Interpretation and clinical correlation of the investigations requested.


• Accurate treatment as applicable and monitoring the follow up.

b. Nurse / Technician

• Brief ocular history with respect to chief complaints, treatment, compliance should be obtained.


• Visual acuity and refraction should be performed at each visit.


• Should be trained in obtaining fundus photographs, perimetry and imaging.

Situation	HUMAN RESOURCES	EQUIPMENT	DRUGS & CONSUMABLES	EQUIPMENT
1	Ophthalmologist -1 Optometrist/ Technician-1 OP Nurse-1	Visual fields Pachymetry Disc photographs (desirable)	Antiglaucoma medications Topical steroids Topical anaesthetics Fluorescien strips.	Slit lamp biomicroscope-1 Goldmann applanation tonometer-1 Indentation gonioscope-1 (preferable Sussman/ Posner/ Zeiss) 90D/ 78 D lens-1 Indirect ophthalmoscope-1 Pachymeter Automated perimeter-1 (preferably Humphrey/ Octopus)
2	Glaucoma specialist-1 Optometrist/ Technician-1 OPNurse-1 Scrub nurse OT nurse Ward nurse	Visual fields PachymetryOCT/GDX/HRT Fundus camera	Antiglaucoma medications Topical/Systemic steroids Topical anaesthetics. Fluorescein strips Anti – metabolites.	Slit lamp biomicroscope-1 Goldmann applanation tonometer-1 Indentation gonioscope-1 (preferable Sussman/ Posner/ Zeiss) 90D/ 78 D lens-1 Indirect ophthalmoscope-1 Pachymeter Disc photography-1 Automatedperimeter -1 (preferably Humphrey/ Octopus) Q switched frequency doubled Nd-Yag laser. Argon laser Diode laser. Glaucoma drainage devices

Guidelines by The Ministry of Health and Family Welfare :

Dr. Venkatesh Prajna Chief- Dept of Medical Education, Aravind Eye Hospitals, Madurai