Glaucoma
Dr Jennifer Shum
Introduction
Glaucoma is a neurodegenerative disease characterized by the progressive death of retinal ganglion cells (RGC) and their axons, leading to characteristic optic nerve structural damage and visual field deficits. It is the second leading cause of blindness in developed countries.
Risk factors
A high intraocular pressure (IOP) is the strongest risk factor for glaucoma. It has a dose-response relationship with the risk of glaucomatous damage and thus lowering the IOP remains the mainstay of glaucoma treatment. The normal range of IOP is 10-21mmHg. Ocular hypertension is where the intraocular pressure is elevated without glaucomatous damage, and normal tension glaucoma refers to glaucomatous damage occurring within a normal IOP range.
Other risk factors include a family history of glaucoma, history of trauma or steroid use and high myopia. Medical conditions that cause a decrease in perfusion may also contribute to glaucoma, such as hypertension, low diastolic pressure, diabetes, obstructive sleep apnoea, migraine, arrhythmia etc.
Optic disc findings
Cup, color, contour
- Increased vertical cup-disc ratioRGC axons run in a characteristic pattern towards the optic disc which respects the horizontal meridian. Axons from the superior, inferior and nasal retina take a relatively straight path while those from the temporal retina travel in an arcuate pattern. Thus, as axons degenerate, the vertical cup-disc ratio increases (Figure 1). Cup-disc ratio asymmetry of 0.2 or more is highly suspicious.
- Increased vertical cup-disc ratio to 0.7 delineating the cup
- Thinning of inferior neuro-retinal rim
- Pink rim
Tip: you can tell this is the right eye by the orientation of the arcade vessels,
the temporal arcade vessels run more horizontally to “hug” the macula
- Colour: do not mistake the cavernous cupping in glaucoma for disc pallor. In most cases of glaucoma, the rim tissue remains well-perfused and pink. Although there may be optic disc pallor in end-stage cupping, glaucoma is characterized by cupping rather than pallor. If pallor is more evident then cupping, rule out compressive lesions and other causes of optic atrophy.
- Contour: pay attention to the contour of the neuro-retinal rim. Focal notching or thinning is characteristic. Remember the “ISNT rule”, the normal neuroretinal rim is thickest inferiorly, then superiorly and nasally, with the thinnest area temporally.
Vessels and haemorrhage
Sharp bending bayonetting vessels may be seen at the rims. There may be nasalization of vessels as the cupping deepens. Disc splinter haemorrhages signal glaucoma activity and progression, and usually precede focal neuro-retinal rim notching.
Visual field deficit and nerve fibre layer thinning
RGC axons subserve the opposite visual field, i.e. the superior axons subserve the inferior visual field, inferior axons the superior field and so on. Glaucomatous visual field defects respect the horizontal meridian. Characteristic glaucomatous field defects include superior or inferior arcuate defect (Figure 2), nasal stepping, para-central scotoma and generalized depression. RGC axonal death is reflected structurally by thinning of the nerve fibre layer (Figure 3).
Figure 2. Humphrey visual field of the right eye showing a superior arcuate visual field defect
Tip: you can tell that this is the right eye by the blind spot, which lies 15° temporally from fixation
Figure 3. OCT (Optical coherence tomography) of the retinal nerve fibre layer
The right eye shows thinning of the inferior retinal nerve fibre layer
Laser and surgical intervention
Signs of laser and surgical intervention may be observed by looking closer at the anterior segment.
Use the retro-illumination technique to shine a focused light beam through the lens to look for laser peripheral iridotomies (Figure 4). You may have to lift the upper eyelid to look for evidence of glaucoma filtration surgery (Figures 5 & 6).
Figure 4. Retroillumination technique revealing the laser peripheral iridotomy
Figure 5. Tube of glaucoma drainage device , surgical iridotomy
Figure 6. Trabeculectomy bleb