Beyond Eye Pressure: Exploring Other Factors Contributing To Glaucoma - Dr Meenakshi Yadav Dhar

Glaucoma implied an elevated eye pressure and vice versa up until 1995 when the new definition of glaucoma was established. It is now defined as a type of optic neuropathy with characteristic optic nerve head & visual field changes, where intraocular pressure is the only modifiable risk factor.

To explain further, it is a group of eye diseases that causes progressive damage to the optic nerve at the point where it leaves the eye to carry visual information to the brain. It is neither contagious nor is it an infection, but unfortunately the damage is irreversible.

It is the second leading cause of blindness in the world and, in fact, the most common cause of irreversible visual loss. Furthermore, it is referred to as the silent killer of vision, since it doesn't produce any symptoms until the late stage of the disease is reached.

It is a disease that the needs to be evaluated at the earliest when suspected, and followed up frequently -the aim of treatment being to keep it under control, without further progression of the disease.

Glaucoma is classified into narrow and open angle based on the configuration of the angle between the transparent cornea in front and the pigmented iris behind-this is evaluated by gonioscopy.

Majority of the glaucoma patients have glaucoma damage with high Intraocular Pressure [IOP], but there is a minority that have the same optic nerve damage with normal eye pressures who are referred to as Normotensive glaucoma[NG] and then, a subset of population has high IOP but with no glaucoma damage who are referred to as Ocular hypertensives, the rest of the population has both normal IOP[<21mmHg] and optic nerve.

Intraocular pressure [IOP] is the pressure maintained within the eye, and its rise is classically associated with glaucomatous damage. The best way to assess IOP is Applanation Tonometer mounted on a slit lamp.

Damage to retinal ganglion cells, is either by mechanical pressure or by hindering the blood supply which brings in oxygen to these delicate cells. It can occur in one or both eyes.

According to the vascular theory, glaucomatous loss occurs when the ganglion cells of the retina are damaged by impediment in its blood supply, which can occur in Hypotension especially acute like in acute severe blood/ fluid loss.

Both our IOP and blood pressure [BP] follow a circadian rhythm, with our IOP being highest between 2-4 pm and blood pressure being lowest at that time. So there is lesser blood supply to the globe at this hour and the resistance to its flow within the eye is more as the IOP is higher.

Nocturnal Hypotension is known to accelerate visual field damage in glaucoma, probably due to the nocturnal dip in BP, especially if patients are taking their blood pressure [BP] lowering medication in the evening.

We must calculate the Ocular Perfusion Pressure[OPP] in patients with Normotensive glaucoma. It is the pressure difference between systemic BP and IOP, wherein a low OPP -lower than 50 mmHg had a four times greater risk of developing glaucoma and its progression.

Another way of assessing the blood supply to the eye is assessment of Ocular blood flow [OBF] using the Doppler ultrasound. The factor considered relevant in this study is the Resistive Index which, if found high, is associated with glaucoma progression in spite of good control of IOP.

Disturbed ocular blood flow has emerged as an increasingly prevalent glaucoma risk factor in large population-based trials. Lower systolic perfusion pressure, lower systolic blood pressure, and cardiovascular disease history are the new predictors of Open angle glaucoma disease progression.

Patients of Sleep Apnea are also found to have changes similar to those in glaucoma, with similar visual field defects and optic nerve head changes in the presence of normal eye pressure. This also happens in any situation where a positive pressure affects the vulnerable retinal ganglion cells [RGC] of the retina, which have a very low threshold for ischaemic damage.

Valsalva’s manoeuvre, breath holding in Yoga or regularly playing conchs or air instruments like flute, a similar scenario for optic nerve head damage mimicking glaucoma arises. Here again blood supply is impeded.

Dysfunction of the autoregulation also occurs in glaucoma, which is accentuated in diseases with vascular spasms like migraine. All these become risk factors in glaucoma patients and increase their vulnerability to more severe damage to ganglion cells of the optic nerve and visual field defects.

Thus, these non IOP factors should be looked for in patients, glaucoma progresses in spite of IOP control or glaucoma like damage is seen without high intraocular pressure.