Damage to the optic nerve due to a rise in intraocular pressure (IOP) is referred to as glaucoma. There are many subtypes of glaucomas, but broadly we can divide them into primary and secondary glaucomas.
Primary glaucomas
- Primary open-angle glaucoma
- Angle-closure glaucoma
- Normal tension glaucoma - damage to optic nerve without any change to IOP.
- Congenital glaucoma
Secondary glaucomas
- Neovascular glaucoma
- Pigmentary glaucoma
- Uveitic glaucoma
- Exfoliation glaucoma
We will solely be discussing open-angle glaucoma (OAG) and angle-closure glaucoma (ACG).
Pathophysiology
First let’s recap our anatomy of the eye:
Ciliary body produces aqueous humour to provide nutrition to the eye and also to maintain the eye in a pressurised state of 10-21mmHg.
This aqueous humour flows from the posterior chamber (lens → iris) through the anterior chamber (iris → cornea) and then travels to the trabecular meshwork into the canal of Schlemm.
From the canal of Schlemm it drains into the episcleral veins to re-enter into the general circulation. This is known as the Trabecular outflow pathway.
Ciliary epithelium has B-receptors that increase production of aqueous humour. There are also a-receptors that decrease the production of aqueous humour.
There is also another pathway known as the uveoscleral outflow pathway. This essentially allows the passage of aqueous humour through gaps in the ciliary epithelium to allow it to enter into the orbital veins to return to circulation.
It is the most common type of glaucoma, affecting 1 in 200 (0.5%) of patients >40 years old. It is the second leading cause of blindness in the UK.
Pathophysiology
In open-angle glaucoma there is an increase in resistance in our trabecular outflow pathway due to some sort of blockage within the trabecular meshwork or the canal of Schlemm. This makes it difficult for the aqueous humour to leave the eye and as a result we get a chronic and slow increase in the buildup of pressure.
This leads to damage to the optic nerve cells and leads to an increased cup:disk ratio.
⚠️ Risk factors
- Increasing age - this is the biggest risk factor.
- Genetics - there is a 16% increased risk if a first-degree relative had glaucoma.
- Myopia - changes to the shape of the eye increase the risk due to structural changes obstructing our outflow.
- Hypertension
- Diabetes - increases risk for neovascular glaucoma.
- Corticosteroids
😷 Presentation
It is insidious and is often detected incidentally with routine optometry.
Some symptoms include:
- Peripheral vision loss
- Decreased visual acuity
Fundoscopy may show:
- Increased CDR >0.7
- Optic disk pallor - indicative of optic nerve atrophy.
- Bayoneting of vessels - kinking or sharp turning of vessels when passing over the edge of the cup.
🔍 Investigations
- Visual field assessment
- Optic nerve assessment
- Intraocular pressure
- Anterior chamber depth (ACD assessment)
- Central corneal thickness measurement
💡 NICE recommends that patients with a 1º relative with glaucoma should be screened annually from 40 years onwards.
🧰 Management
- Prostaglandin analogues - increases uveoscleral outflow by activation of MMPs to increase permeability and outflow.
- 🥇 Latanoprost
- B-blockers - reduces aqueous humour production by binding to B1 receptors in ciliary epithelium.
- 🥈 Timolol
- Sympathomimetics - increases aqueous humour outflow and reduces the production of it through binding of the a2 receptor.
- 🥈 Brimonidine
- Carbonic anhydrase inhibitors - they reduce aqueous humour production.
- 🥈 Acetazolamide (-zolamides)
- Miotics - increases uveoscleral outflow by binding to the M3 receptor which causes ciliary muscle contraction and pulls the lens backwards to increase the outflow.
- 🥈 Pilocarpine
ACG is a medical emergency as a result of the rapid increase in IOP.
Pathophysiology
It occurs due to the bulging of the iris forward which blocks off the trabecular meshwork and prevents aqueous humour drainage from the anterior chamber which leads to a build up of pressure (especially in the posterior chamber).
⚠️ Risk factors
- Hypermetropia
- Pupillary dilatation
- Lens growth
- Medications
- Adrenergics - such as noradrenaline as they increase aqueous humour production.
- Anticholinergics - such as oxybutinin as they increase pupillary dilation.
- TCAs - such as amitryptaline as they also have anticholinergic effects.
😷 Presentation
- Severe ocular pain ± headache
- Blurred vision
- Mydriasis worsens symptoms
- Halos around lights
- Nausea and vomiting may be associated
On examination we may see:
- Red eye
- Teary eye
- Hazy cornea - due to oedema.
- Dilation of the affected pupil
- Unreactive pupil
- Firm pupil (hard eye)
🧰 Management
As a lot of patients come into primary care and so they need an urgent same-day referral to ophthalmology.
However, if they are unable to be admitted, there are some things one can do in primary care:
- Lie the patient flat on their back to allow the lens to fall back.
- Pilocarpine drops (2% for blue eyes and 4% for brown eyes) - constricts pupil.
- Acetazolamide - 500mg orally. Prevents aqueous humour production.
- Analgesia and antiemetics if need be.
- IV acetazolamide
- Topical pilocarpine
- Timolol
- Steroids
This is our initial management.
Surgical procedures can be performed such as:
- Iridotomy - creating a tiny hole in the peripheral iris to enable aqueous humour flow.
- Phacoemulsification - uses ultrasound waves to emulsify the lens.
- Iridoplasty - molds the iris to allow flow temporarily.
