What is glaucoma?

Glaucoma is an optic neuropathy where intraocular pressure (IOP) is one of the main risk factors. It is the leading cause of irreversible vision loss in adults in Australia. Patients typically gradually lose peripheral vision without noticing until it encroaches on the central vision.

Common types of glaucoma are Ocular Hypertension, Primary open angle glaucoma Acute angle closure glaucoma Primary Angle Closure glaucoma Secondary glaucoma and Normal Tension Glaucoma or Normal Pressure Glaucoma

Ocular hypertension just means high IOP. A normal IOP is around 10-20mmHg and anything over 21mmHg is usually considered to be above normal. OHT implies a healthy optic nerve and therefore is not technically glaucoma, but OHT is often grouped with glaucoma as these patients will need monitoring for the risk of progression to glaucoma. The risk of conversion to glaucoma from OHT is around 10% over 5 years, therefore most practitioners do not treat OHT, unless they have additional risk factors.

Primary Open Angle Glaucoma is the most common form of glaucoma, it usually occurs in patients over the age of 40 years old. It is thought to be caused by reduced outflow at the drainage angle due to blockage at the cellular level, which in turn causes raised IOP and subsequently optic nerve damage. Glaucoma patients also seem to have a particularly susceptible optic nerve, such that they tend to be damaged more easily than others at moderately elevated IOP levels. Other factors such as mechanical stress, inflammation and reduced blood flow have also been associated with glaucoma.

Primary Angle Closure Glaucoma is a chronic form of glaucoma where the increased IOP is caused by a mechanical closing of the drainage angle by the iris due to abnormal morphology and overcrowding at the angle. This overcrowding may be due to a cataract or patients with small eyes (long sighted patients). Asian patients have a higher risk due to their abnormal iris morphology.

Acute Angle Closure Glaucoma happens when the drainage angle suddenly closes and the IOP goes up to a high level (around 40-50mmHg) in under an hour. The iris is pushed forward against the cornea due to a pressure shift. This is a very painful condition with associated redness, fixed mid dilated pupil, rock hard globe, vomiting and loss of vision. This is a medical emergency and requires an urgent referral.

Secondary Glaucoma is usually an increased IOP caused from ischaema (neovascular or rubeotic glaucoma), inflammation (uveitic glaucoma) or trauma (traumatic glaucoma). The mechanism here is again damage to the outflow channels.

Normal Tension Glaucoma (NTG) is thought to be a less IOP depended form of glaucoma, although lowering IOP still can prevent progression of glaucoma in many (but not all) cases. Here other factors also come into play to cause the optic neuropathy. Such as blood supply, mechanical stress and IOP fluctuations. Nocturnal hypotension is thought to be a major culprit in many cases and the role of 24 hr BP monitoring to reduce the noturnal BP dip may improve optic nerve perfusion. Obstructive sleep apnoea has been associated with NTG and the management of this condition with CPAP is thought to help. Other risk factors for NTG are migranes, Raynauld’s and anaemia.

How is glaucoma monitored?

Patients will have an automated Humphrey’s Visual Field test and OCT scan done of the nerve at most glaucoma follow up visits. The HVF tests the peripheral vision and tests the “functional” or subjective performance of the patient’s glaucoma. The OCT measures the thickness of the optic nerve and assesses the “structure” of the optic nerve. The eye specialist will assess the “structure” and “function” of the optic nerve to look for evidence of progression of the disease, where the nerve rim becomes more thin and the visual field defect becomes deeper and larger.

Patient undergoing OCT scan

Patient undergoing OCT scan

What is a disc suspect or glaucoma suspect?

You may see these 2 terms used in correspondence letters. This means that the Ophthalmologist has examined the optic nerve’s “structure” and “function” and decided that there is a feature suspicious  of glaucoma but no definite glaucoma diagnosis. The differential diagnosis is usually physiological cupping, physiological disc asymmetry or myopic tilt of the nerve. These patients usually have eye pressure in the normal range and are specifically normal tension glaucoma suspects. In this situation most specialists would choose to monitor patients for evidence of structure/function progression or evidence of IOP fluctuations. If there is no evidence of progression after several years, then the diagnosis of NTG can be excluded.

If there is optic neuropathy with visual field loss in the absence of any risk factors for glaucoma, then the specialist will need to be mindful of other causes. This would include compressional, toxic, inflammatory and infiltrative causes and the appropriate investigations would need to be done.

What is the treatment for glaucoma?

Eye drops are the most common treatment for glaucoma. There are 4 main categories of eye drops with Xalatan/latanoprost (prostaglandin analogue) the most common first line treatment. Its main side effects are redness, irritation, lash growth, increase pigmentation of the surrounding skin and cystoid macular oedema. Timolol (B-Blocker) is the most common second line treatment with shortness of breath and bradycarida the most common side effect. Other glaucoma medications include Alphagan (alpha-agonist) and azopt (carbonic anhydrase inhibitor).

Laser (selective laser trabeculoplasty – SLT) is also a good option for the treatment of open angle glaucoma. It has similar efficacy as Xalatan/latanoprost and can be used instead of drops to allow patients to be drop-free for several years, or in addition to drops in patients refractory to drops alone. SLT works by stimulating the outflow channel cells to increase outflow and reduce the eye pressure. It is important to note that the effects of the laser tend to wear off after a few years, after which the patient may need to start drops or have a repeat SLT treatment. Around 20% of patients do not respond or respond poorly to this laser. The laser is very safe, with most side effects such as inflammation and pressure spikes having a transient effect.

Laser Peripheral Iridotomy is a different laser ONLY used in primary angle closure glaucoma. It involved making a small hole in the peripheral iris to stop the mechanical obstruction of the channel by the iris. In angle closure, the pressure behind the iris pushes the iris forward, blocking off the drainage outflow angle. The iridotomy releases this pressure differential and the iris naturally falls posteriorly and opens up the angle. The management there after becomes similar to open angle glaucoma.

Trabeculectomy with Mytomycin C is a filtration operation, to create a channel to reduce the eye pressure. The channel allows fluid to enter the subconjunctival space forming a “bleb” which sits under the upper lid. This operation is usually reserved for patients who do not respond to drops and laser. There is a potential long term risk patients having a bleb. The bleb can thin out and begin to leak or become infected (blebitis) and this needs to be managed as an emergency.

Newer glaucoma procedures are known as MIGS – minimally invasive glaucoma surgery. These operations are safer than the traditional trabeculectomy but also do not work as well or as long. They are stents that bypass the blocked outflow filter (trabecular meshwork), to allow flow back into the normal drainage pathway. There are 2 stents on the market at the moment – iStent and Hydrus implants. Both currently need to be used in combination with cataract surgery due to government rebate regulations, but will likely be used as a stand alone operation in the near future. They reduce the IOP by small amounts and can often reduce the number of medications being used by 1. Therefore, they do not replace traditional surgery, but give a new option for patients with mild to moderate glaucoma.


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