Glaucoma - Open angle


    • Neurodegenerative condition primarily due to dysfunction in outflow of aqueous humour

    • Open-angle glaucoma is characterised by an anatomically open angle

      • but with an obstructed and slowed drainage system outflow

    • The mechanism of blockage is unclear.

    • A rise in increased intra-ocular pressure results, characterised by retinal ganglion cell damage, then peripheral vision loss in early disease and central vision loss in late disease. [1]

Risk Factors

    • High intra-ocular pressure

      • >23 mmHg

    • Age >50

    • FHx

    • Black ethnicity

    • Myopia?

      • > -6 diopters

Differential diagnosis

    • Low-tension glaucoma

    • Closed-angle glaucoma

    • High myopia

    • Ocular hypertension

    • Characterised by increased intra-ocular pressure in the absence of evidence of damage to the nerve fibre layer

    • Normal visual field test and no enlargement of the cup-to-disc ratio over time.


    • Glaucoma is the second leading cause of blindness in the world, causing permanent vision loss. [1]

    • Open-angle glaucoma accounts for two-thirds of those affected.

    • In black people, glaucoma is the main irreversible cause of blindness

      • presents at a younger age with higher intra-ocular pressures and often behaving more aggressively. [2]

    • In the white population, glaucoma is found in 1% to 2% of those >40 years of age and 5% of those >70 years of age. [2]

    • In the US, 2.3 million people have glaucoma

      • prevalence of 5.6% in black patients and 1.7% in white patients. [3] [4]

    • In the UK, glaucoma-related blindness is responsible for 8% of new blind registrations. [2]

    • Worldwide, 66.8 million people were estimated to have the disease in 2000. [5]

      • Of these, 6.8 million are blind bilaterally


  • Open-angle glaucoma is a neurodegenerative process wherein retinal ganglion cells slowly degenerate

  • Perhaps due to hereditary factors.

  • A gene at the GLC1A locus is associated with adult- and juvenile-onset open-angle glaucoma

Clinical features

    • presence of risk factors

      • intra-ocular pressure >23 mmHg, age >50 years

      • FHx of glaucoma

      • black ethnicity

    • peripheral vision loss

      • Shown by missing areas in the field of vision, in the absence of other identifiable causes

      • Indicates advanced disease. [1]

    • cup-to-disc ratio >0.4

      • Cup-to-disc ratios >0.4 carry a greater risk.

      • However a ratio of 0.7 may be a normal anatomic variant, while a ratio of 0.3 may indicate glaucoma if the ratio started out at 0.1.

      • Documenting an increase is far more meaningful than the ratio seen on one visit. [1]

      • Ratios in this range shown to increase disease progression in the Ocular Hypertension Treatment Study (OHTS). [10]

    • notching of optic nerve cup

      • Almost pathognomonic of disease. [1]

    • increased intra-ocular pressure

      • Although commonly seen, 50% of undiagnosed patients may have a normal measurement at the time of diagnosis. [11]

    • scotomas

      • Found on visual field testing

    • loss of nerve fibre layer

      • Now used in many practices as a diagnostic factor. [1]

    • retinal haemorrhage

      • Appears on, or adjacent to, the optic nerve.


    • The slow, degenerative process is characterised by retinal ganglion cell death

      • elevated intra-ocular pressure clearly leads to cell death.

    • The exact pathophysiology is not understood as clinical research is limited in humans

    • The process may occur at a faster rate because of a localised vascular insufficiency compromising key ocular structures. [6]

    • The degeneration is well known to occur faster in the presence of increased intra-ocular pressure

      • The mechanism may involve deformation and stress to the lamina cribrosa, compressing retinal ganglion cell axoplasmic flow. [1]

    • This pressure balance is maintained by the flow of aqueous humour.

      • Fluid is secreted by the ciliary body into the posterior chamber, flows to the iris and through the pupil into the anterior chamber, and then leaves through the trabecular meshwork or uveoscleral outflow routes.

      • Intra-ocular pressure is most often elevated, but is normal in some cases.

      • On clinical examination, the obstruction of fluid outflow is not seen.

      • The pressure gradient across the trabecular meshwork is increased, causing stress to the lamina cribrosa and retinal ganglion cells and their eventual destruction.

    • Additionally, the compression of axons may lead to impaired axonal transport, which causes cell death due to an insufficiency of trophic factors.

    • Another possibility is that ischaemia, due to faulty blood flow to the retina, may cause cell death and eventual blindness.

    • The results of increased intra-ocular pressure are an enlarged cup-to-disc ratio and loss of peripheral vision as demonstrated on automated visual field testing. [1]


    • Tonometry

      • Most common, accurate, and most expensive method is Goldmann tonometry.

      • Another method entails use of the Tono-Pen, a portable device also used with a topical anaesthetic and a sterile cover.

      • The most basic is the Air Jet tonometer.

        • A blast of air on the cornea measures the rate of fluid rebound.

        • A pressure readout results.

        • No eye drops are needed.

    • Fundoscopy

    • Gonioscopy

    • Visual field testing

    • Pachymetry

      • Provides measurement of corneal thickness, which is predictive of high intra-ocular pressures proceeding to glaucoma.

      • A thick cornea can falsely decrease the intra-ocular pressure reading.

      • In addition, a thin central corneal thickness can predict progression from high IOP to glaucom


a) conservative

    • The goal is to slow or halt neurodegeneration by lowering intra-ocular pressure. [18]

    • Specifically, optic nerve health is tracked by assessment of the optic disc, retinal nerve fibre layer, and visual field.

    • Additionally, the pressure is tracked and maintained at a target level via measurement and medicine and/or interventions.

    • If already high and retinal damage has occurred, the aim is to lower the pressure to the target level.

    • The target value is based on the degree of advancement of the disease.

    • Additionally, treatment is given if visual changes and retinal damage are seen, regardless of intra-ocular pressure

b) medical

    • Generally, medicines are started in the form of eye drops.[A Evidence]

    • All ophthalmic medicines have local adverse effects, which can be managed by changing to a different medicine when these effects are severe.

    • Additionally, the clinician tends to start one medicine based on clinical judgement and patient agreement, and then the clinician either changes medicines or adds another eye drop if the pressure does not reduce to a satisfactory level or signs of progression occur.

    • A satisfactory level is determined by many factors specific to each patient.

    • Progression is determined by examination techniques.

    • The timing of medicine changes and additions depends on the clinician's judgement.

    • Many different combinations are used based on patient allergies, compliance, past medical history, and other factors.

    • Some of the newer formulations of eye drops combine more than one class of medication, which may improve compliance.

    • Some eye drops (for example, beta-blockers) may cause systemic adverse effects and may prove incompatible with patients who have severe cardiovascular or pulmonary disease.

c) surgical

    • Laser therapy

      • Laser treatments to the trabecular meshwork may also be used to increase drainage of the aqueous humour.

      • This treatment is selected if eye drops fail to lower pressure.

      • Some laser treatments may damage the trabecular meshwork and elevate pressure transiently.

    • When medicine and laser fails or the patient is unable to comply, surgery is performed to create a new passageway for the drainage of aqueous humour.

    • Surgery lowers intra-ocular pressure, providing filtration for aqueous outflow.[C Evidence]

    • If the patient has cardiovascular or pulmonary disease prohibiting use of eye drops, and rapidly progressing disease, surgical intervention may be the first line. [19]

    • The common surgical techniques are trabeculectomy or tube shunt.

    • Other options include thermal sclerostomy, posterior or anterior lip sclerotomy, and trephination.

    • Surgeries can cause some loss of vision and make the eye more susceptible to infection and inflammation.[A Evidence]

    • Infections are treated aggressively with ophthalmic and intra-ocular antibiotics.

    • Inflammation will subside as infection subsides.

    • Mild loss of vision may resolve in time or be permanent.

    • In advanced disease, when vision is poor, ablation of the ciliary body is performed to decrease aqueous humour production.


    • Glaucoma is a slowly progressive, lifelong disease that may be slowed or halted with treatment. [1]

    • Prognosis is based on the degree of disease at diagnosis, the response to treatment, the patient's compliance, and the patient's life expectancy.

    • At diagnosis, 20% of people have already lost significant peripheral vision.

    • If the condition is left untreated and intra-ocular pressure stays at ≥30 mmHg, blindness may occur in 3 years or less.

    • Affected people will complain of trouble in visually accommodating from bright to dark rooms, and in navigating street kerbs and objects in their periphery. [2]

    • Most compliant patients who respond well to treatment can expect to maintain a functional level of vision for the remainder of their life. [27]