Glaucoma

Entitlement Eligibility Guideline (EEG)

Date reviewed: 22 January 2025

Date created: February 2005

ICD-11 code: 9C61

VAC medical code: 00640 Glaucoma

This publication is available upon request in alternate formats.
Full document – PDF Version

Definition

Glaucoma is a chronic, progressive atrophy of the optic nerve seen on fundoscopic exam of the optic disc. Typically the resulting loss of vision is found on changes on visual field testing. These changes are usually found in the presence of increased intraocular pressure (IOP).

There are two major types of glaucoma:

  1. Open angle glaucoma occurs when pressure builds in the eye as the result of an inability of the eye to drain properly. The increased pressure due to fluid accumulation can cause damage to the optic nerve. Open angle glaucoma is the most common type of glaucoma.
  2. Angle closure glaucoma occurs when the iris of the eye is too close to the drainage angle of the affected eye. The iris can block the drainage in the eye causing a rise in eye pressure to occur.

Note:

  1. A diagnosis of glaucoma suspect may be made by ophthalmologists with the following findings:

    • normal optic disc and visual field associated with elevated IOP
    • suspicious optic disc and/or visual field with normal IOP
    • abnormal drainage angle
    • strong family history of severe glaucoma.

    The diagnosis of glaucoma suspect is not included in this entitlement eligibility guideline (EEG).

  2. When an ophthalmologist has provided the diagnosis of glaucoma for the following findings, Veterans Affairs Canada (VAC) will accept the diagnosis of glaucoma for entitlement and assessment purposes:
    • a finding of elevated IOP with no changes on fundoscopic examination or losses of visual acuity
    • unexplained visual field defect(s) consistent with glaucoma with no changes on fundoscopic examination or elevated IOP
    • characteristic changes on fundoscopic examination with no elevated IOP or visual field defects.
  3. Glaucoma is entitled as a bilateral condition, unless associated with trauma, surgery, or intra-orbital hemorrhage in the affected eye.

Diagnostic standard

Diagnosis by a qualified ophthalmologist is required.

Required investigations include visual acuity, visual field (perimetry), and intraocular pressure (tonometry). Reports must be submitted with the application.

Anatomy and physiology

The eye has three chambers: the anterior chamber in front of the iris, the posterior chamber between the iris and the lens, and the vitreous chamber behind the lens (Figure 1: Eye anatomy).

IOP is maintained by a balance between inflow and outflow of the aqueous humour, the fluid in the anterior and posterior chambers of the eye, which nourishes the transparent structures of the eye. Aqueous humour is produced and secreted by the ciliary body, a gland behind the iris of the eye. Aqueous humour enters the anterior chamber of the eye through the pupil, and leaves by passing through the trabecular meshwork in the iridocorneal angle (drainage angle) of the anterior chamber, and back into venous circulation through the canal of Schlemm.

The vitreous chamber is between the lens and the retina and contains a jelly type substance, the vitreous humour. Increased IOP in the anterior chamber is transferred to the retina and optic nerve by the vitreous.

Figure 1: Eye Anatomy

Top image: A frontal view of the eye, highlighting the iris, pupil, sclera, and conjunctiva. Bottom image: A cross-sectional view showing the same parts, along with additional internal structures: the ciliary body, lens, cornea, and anterior chamber. The back of the eye includes the choroid, retina, macula, vitreous body, optic nerve, and optic disc. Source: Veterans Affairs Canada (2024).

A number of classification schemes for glaucoma have been proposed. They are based on the age of the person (infantile, juvenile, adult), the site of obstruction to aqueous outflow (pre-trabecular, trabecular, post-trabecular), the tissue principally involved (for example, glaucoma caused by diseases of the lens), and etiology. Although each of these systems has value, the classification scheme that separates angle closure glaucoma from open angle glaucoma has been used most widely; it focuses on pathophysiology and points to proper clinical management.

A classification outline for open angle, angle closure, combined-mechanism, and childhood glaucoma follows:

Open angle glaucoma occurs when pressure builds in the eye as the result of an inability of the eye to drain properly. The increased pressure due to fluid accumulation can cause damage to the optic nerve. Open angle glaucoma is the most common type of glaucoma.

Angle closure glaucoma occurs when the iris of the eye is too close to the drainage angle of the affected eye. The iris can block the drainage in the eye causing a rise in eye pressure to occur. The increased pressure due to fluid accumulation can cause damage to the optic nerve. The rise in pressure generally occurs over time and is asymptomatic. With acute angle closure glaucoma, the rise in pressure can also occur acutely, most notably with medication use and may result in pain and visual loss. Acute angle closure glaucoma can cause blindness if not treated promptly.

  1. Open angle glaucoma may present as:
    • Primary open angle glaucoma with:
      • optic nerve damage and visual field loss associated with increased IOP
      • trabecular obstruction, cause not known.
    • Normal-tension glaucoma with optic nerve damage and visual field loss associated with normal IOP.
    • Secondary open angle glaucoma with:
      • increased resistance to trabecular meshwork outflow associated with another condition, for example, pigmentary glaucoma, phacolytic glaucoma, steroid-induced glaucoma, ocular inflammation, and ghost cell glaucoma
      • increased post-trabecular resistance secondary to elevated episcleral venous pressure, for example, carotid-cavernous sinus fistula.
  2. Angle closure glaucoma may present as:
    • Primary angle closure glaucoma with relative pupillary block where the aqueous humour from posterior chamber to anterior chamber is restricted and the peripheral iris is in contact with trabecular meshwork.
    • Primary angle closure glaucoma without pupillary block, for example plateau iris.
    • Secondary angle closure glaucoma with pupillary block, for example swollen lens or secluded pupil.
    • Secondary angle closure glaucoma without pupillary block.
    • Posterior pushing mechanism where the lens iris diaphragm is pushed forward, for example with posterior segment tumor, scleral buckling procedure, and uveal effusion.
    • Anterior pulling mechanism where the anterior segment process pulls the iris forward to form peripheral anterior synechiae, for example with iridocorneal endothelial syndrome, neovascular glaucoma, and inflammation.
  3. Combined-mechanism glaucoma is a combination of two or more forms of glaucoma, for example open angle glaucoma in a person who develops secondary angle closure following a scleral buckling procedure.
  4. Childhood glaucoma may present as:
    • primary congenital/infantile glaucoma
    • juvenile glaucoma
    • glaucoma associated with congenital anomalies:
      • associated with ocular disorders, for example anterior segment dysgenesis and aniridia
      • associated with systemic disorders, for example rubella and Lowe’s syndrome
    • secondary glaucoma in infants and children, for example glaucoma secondary to retinoblastoma or trauma.

Clinical features

Glaucoma is a leading cause of blindness. There is usually a strong familial pre-disposition to glaucoma.

An IOP of 21 mmHg or greater is associated with glaucoma. This increased pressure may damage the optic nerve, the head of which is known as the optic disc. The disc may develop cupping and pallor which results in “blind spots,” or scotomata, in the person’s field of vision. These scotomata may enlarge, coalesce, and eventually lead to blindness.

An IOP of 21 mmHg or more does not necessarily mean a diagnosis of glaucoma, as the person also needs to demonstrate a glaucomatous visual field defect or optic nerve damage. There are individuals with an IOP over 21 who never develop glaucoma, as well as people with sensitive eyes who develop glaucomatous visual field defects with pressures less than 21.

While the peripheral visual field gradually shrinks, fixation and the ability to track remains unaffected until the late stages of the disease.

Open angle glaucoma is asymptomatic in its early stages, but if left untreated, blindness can eventually result. It does not usually cause pain or a red eye and has only moderately elevated intraocular pressure. It is bilateral, insidious in onset, and slowly progressive. By the time the person notices visual loss, there is substantial irreversible damage to peripheral vision.

Angle closure glaucoma occurs when the iris of the eye is too close to the drainage angle of the affected eye. The iris can block the drainage in the eye causing a rise in eye pressure to occur. The increased pressure due to fluid accumulation can cause damage to the optic nerve. The rise in pressure generally occurs over time and is asymptomatic. With acute angle closure glaucoma, the rise in pressure can also occur acutely, most notably with medication use and may result in pain and visual loss. Acute angle closure glaucoma can cause blindness if not treated promptly.

Congenital glaucoma is due to a congenital malformation of the iridocorneal angle. Most of these cases are diagnosed within the first three months of life.

There is a slightly increased incidence of open angle glaucoma in males as compared to females.

There is an increased incidence of angle closure glaucoma in females as compared to males.

Entitlement considerations

In this section

Section A: Causes and/or aggravation

For VAC entitlement purposes, the following factors are accepted to cause or aggravate the conditions included in the Definition section of this EEG, and may be considered along with the evidence to assist in establishing a relationship to service. The factors have been determined based on a review of up-to-date scientific and medical literature, as well as evidence-based medical best practices. Factors other than those listed may be considered, however consultation with a disability consultant or medical advisor is recommended.

The timelines cited below are for guidance purposes. Each case should be adjudicated on the evidence provided and its own merits.

Factors

Note: Unless indicated or otherwise, the following factors may be associated with angle closure glaucoma and open angle glaucoma.

  1. The cause may be of an unknown or idiopathic nature.
  2. Having uveitis or scleritis within three months prior to the clinical onset or aggravation of glaucoma. Uveitis is an inflammation of the vascular middle coat of the eyeball, consisting of the iris, ciliary body, and choroid. Scleritis is inflammation of the sclera, the white fibrous outer layer of the eye that attaches to the edge of the cornea.
  3. Having sustained significant trauma to the affected eye, generally within several months, prior to the clinical onset or aggravation of glaucoma. Significant trauma to the eye includes a penetrating injury, blunt trauma, radiation injury, or acid burn injury to the affected eye resulting in intraocular inflammation, bleeding, or other tissue injury.
  4. Having a corneal transplant (keratoplasty) or other intraocular surgery of the affected eye at any time prior to the clinical onset or aggravation of glaucoma.

    Keratoplasty is an operative procedure in which the entire thickness of the cornea is removed and replaced by donor tissue.

    Note: Uncomplicated partial thickness surgery to the eye, such as those performed for errors of refraction, including photo-refractive keractectomy (PRK) and laser assisted in situ keratomileusis (LASIK), are not considered to cause glaucoma.

  5. Having pseudoexfoliation in the affected eye prior to the clinical onset or aggravation of glaucoma. Pseudoexfoliation occurs when flaky deposits of protein are seen on the lens surface, posterior iris surface, ciliary processes, and zonule, in the trabecular meshwork, and loose in the anterior chamber. This material deposits in the trabecular meshwork obstructing the outflow of aqueous humour, causing an increase in IOP.
  6. Having iridocorneal endothelial (ICE) syndrome, present in the affected eye at the time of clinical onset or aggravation of glaucoma. There are three subtypes of ICE: Chandler syndrome, Cogan-Reese syndrome, and progressive iris atrophy.
  7. Insertion of silicone oil in the affected eye prior to the clinical onset or aggravation of glaucoma. Silicone oil may be injected into the eye during treatment of retinal detachment.
  8. Inability to obtain appropriate clinical management of glaucoma.

For angle closure glaucoma only:

  1. Having a cataract of the affected eye at the time of clinical onset or aggravation of angle closure glaucoma.
  2. Having an anterior subluxation or dislocation of the lens of the affected eye at the time of clinical onset or aggravation of angle closure glaucoma.
  3. Using medication just prior to the clinical onset or aggravation of angle closure glaucoma. Medication can cause glaucoma through multiple mechanisms and for many of these medications, the incidence of glaucoma may be quite low. Medication as a cause of glaucoma is best determined by the treating ophthalmologist.

    If it is claimed a medication resulted in the clinical onset or aggravation of angle closure glaucoma, the following must be established:

    • the treating ophthalmologist has indicated the medication is the cause of the onset or aggravation of the angle closure glaucoma
    • the medication was prescribed to treat an entitled condition
    • the individual was receiving the medication at the time of the clinical onset or aggravation of the angle closure glaucoma.

    Note: For corticosteroids, please see Factor #12 below.

For open angle glaucoma only:

  1. Using corticosteroids, via the following routes only, at the time of clinical onset or aggravation of secondary open angle glaucoma:
    • long term aerosolized inhaled corticosteroids (does not include multidose inhaler/puffer)
    • long term high potency topical application to skin adjacent to the eye
    • topical in the eye (eye drops or ointment)
    • intravitreal (injected into the eye)
    • systemically long term.

    Steroids can increase IOP by increasing resistance to aqueous outflow at the trabecular mesh.

  2. Having an intraorbital hemorrhage at the time of, or just prior to, clinical onset or aggravation of secondary open angle glaucoma. Obstruction to aqueous outflow by degenerated red blood cells devoid of hemoglobin (ghost cells) can occur causing ghost cell glaucoma. Intraorbital hemorrhage includes but is not limited to:
    • vitreous hemorrhage
    • hyphema and microhyphema
    • having intraocular surgery involving the affected eye prior to clinical onset of intraorbital hemorrhage.
  3. Having leakage of lens protein at the time of, or just prior to, clinical onset or aggravation of secondary open angle glaucoma. The proteins can cause obstruction of the trabecular mesh and decrease aqueous outflow, causing lens-induced glaucoma. Lens-induced glaucoma includes:
    • Phacolytic glaucoma which results from leakage of lens protein into the aqueous humour from a mature cataract.
    • Lens particle glaucoma which results from leakage of lens protein into the aqueous humour from disruption of the lens capsule. This may occur after disruption of the lens such as lens injury, cataract removal or laser surgery to the posterior capsule of the lens.
    • Phacoantigenic glaucoma which results from an inflammatory reaction against eye protein exposed through disruption of the lens such as lens injury, cataract removal, or laser surgery to the posterior capsule of the lens.
  4. Having pigment dispersion syndrome (PDS) at the time of clinical onset or aggravation of secondary open angle glaucoma. PDS results in the release of pigment from the cells of the iris. The pigment can cause obstruction of the trabecular mesh and decrease aqueous outflow.
  5. Having elevated episcleral venous pressure causing increased post-trabecular pressure at the time of clinical onset or aggravation of secondary open angle glaucoma. Causes include:
    • venous obstruction (for example: superior vena cava obstruction, tumor behind the eye)
    • arteriovenous abnormality (for example: carotid-cavernous sinus fistula).
  6. Having neovascularization of the iridocorneal angle of the affected eye at the time of clinical onset or aggravation of secondary open angle glaucoma. Neovascularization is a growth of new blood vessels. Conditions that may cause this include but are not limited to:
    • central retinal vein obstruction of the affected eye
    • proliferative diabetic retinopathy of the affected eye
    • ipsilateral carotid artery occlusive disease of the affected eye
    • retinal detachment of the affected eye
    • therapeutic radiation to the area of the affected eye.

Section B: Medical conditions which are to be included in entitlement/assessment

Section B provides a list of diagnosed medical conditions which are considered for VAC purposes to be included in the entitlement and assessment glaucoma. No Included medical conditions were identified at the time of the publication of this EEG.

Section C: Common medical conditions which may result, in whole or in part, from glaucoma and/or its treatment

No consequential medical conditions were identified at the time of the publication of this EEG. If the merits of the case and medical evidence indicate that a possible consequential relationship may exist, consultation with a disability consultant or medical advisor is recommended.

Related VAC guidance and policy:

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