Glacucoma
Glacucoma
Sorce : Rapid Ophthalmology
Glaucoma, acute primary angle-closure DEFINITION An optic neuropathy caused by an acute rise in intraocular pressure (IOP) secondary to closure of the irido-corneal angle. This is an ophthalmic emergency.
AETIOLOGY
Aqueous fluid normally flows from the posterior chamber, though the pupil into the anterior chamber, and then out through the trabecular meshwork which is located between angle formed by the peripheral iris and the cornea. Forward movement of the iris can block this angle and thus prevent drainage of the fluid leading to an acute rise in IOP.
ASSOCIATIONS/RISK FACTORS
Hypermetropia (which is often characterized by eyes with crowded structures owing to their relatively small size), increased age, females affected more commonly than males (4:1), family history, shallow anterior chamber. Rarely complicates pharmacological pupil dilation in at risk individuals.
EPIDEMIOLOGY
Common in Eskimos and Asians. Uncommon in Blacks.
HISTORY
Severe eye pain, nausea, vomiting, (may misleadingly present as an acute abdomen), headache, red eye, rainbow halos around lights, decreased vision. There may be a preceding history of intermittent blurred vision, and halos around lights, for example after an evening in a dark environment, due to transient closure of the irido-corneal angle caused by pupil dilation.
EXAMINATION
Poor visual acuity, red eye (ciliary flush), cloudy cornea (secondary to corneal oedema), fixed and mid-dilated oval shaped pupil, eye that is stone hard on palpation, shallow anterior chamber, RAPD – if optic nerve damage has occurred.
PATHOLOGY/PATHOGENESIS
The posterior iris becomes appositional with the anterior lens. This causes a block of aqueous outflow through the pupil. There is a resultant increase in pressure of the posterior chamber relative to the anterior chamber which causes bulging forward of the peripheral iris; leading it to block the angle as described above.
The acute and significant rise in IOP damages ocular structures. The corneal endothelial pump, which maintains hydration and subsequently clarity of the cornea, ceases to function causing corneal oedema. The pressure rise also causes damage to the optic nerve which can be permanent and blinding.
Age is a risk factor because the lens, as it develops cataract, increases in size thus promoting pupil block.
Glaucoma, acute primary angle-closure
INVESTIGATIONS N/A
intraocular pressure assessment, slit lamp examination and gonioscopy (examination of the irido-corneal angle using a contact lens) will be performed by an ophthalmologist.
MANAGEMENT
Urgent referral to ophthalmology: For assessment and immediate reduction of IOP with agents including parenteral/oral acetazolamide, topical pilocarpine, dexamethasone, timolol and iopidine. Peripheral laser iridotomy (PI) in the fellow eye is performed as an urgent prophylactic measure and is performed in the affected eye as soon as corneal clarity is restored.
Cataract extraction and prophylactic PI can be performed in eyes that have narrow, and therefore potentially occludable angles.
COMPLICATIONS
There is a risk of further pressure rise unless definitive PI is performed. Over 50% will develop acute angle closure glaucoma in the fellow eye if not prophylactically treated.
PROGNOSIS
Severe attacks, especially if not promptly treated, can lead to irreversible damage to the optic nerve head and consequent blindness. There can be IOP rises over time due to damage sustained to the trabecular meshwork during the acute attack (a form of chronic open angle glaucoma). This necessitates long term follow-up.
Glaucoma, chronic open angle
DEFINITION
A chronic and progressive condition that causes an optic neuropathy with characteristic visual field loss.
AETIOLOGY
Glaucoma can exist in the presence of normal intraocular pressure (normal tension glaucoma). There can be raised intraocular pressure without signs of optic nerve damage (ocular hypertension).
Raised intraocular pressure in primary open angle glaucoma is due to resistance, of unknown cause, of aqueous outflow through the drainage pathways.
Secondary open angle glaucoma is due to a known aetiological factor causing restriction of aqueous outflow through the trabecular meshwork, for example inflammatory cells, blood cells (from a hyphaema), steroid use or pigment. Secondary causes may be related to trauma.
ASSOCIATIONS/RISK FACTORS
Raised intraocular pressure, increased age, race - more severe and more common in Blacks, family history, diabetes mellitus, myopia, thin cornea, nocturnal hypotension, migraine, Raynaud’s phenomenon.
EPIDEMIOLOGY
The second most common cause of blindness in the world.
HISTORY
Usually asymptomatic. Patient reported field loss (tunnel vision) only in severe late stage disease. Most are detected on routine examination at the optometrist or by screening those with a family history.
EXAMINATION
Visual acuity, visual fields, RAPD (present in severe optic nerve damage), optic disc cupping/pallor/atrophy. Ophthalmologists will check intraocular pressure (IOP) by Goldmann applanation tonometry – pressure >21 mmHg is a risk factor for glaucoma.
PATHOLOGY/PATHOGENESIS
The optic nerve axons in patients with glaucoma are susceptible to either direct pressure effects or ischaemia associated with impaired flow through the microvasculature supplying them. The retinal ganglion cells undergo apoptosis.
INVESTIGATIONS
Automated visual field assessment, optic disc imaging, central corneal thickness. Blood glucose and BP (including 24 hour monitoring) if normal tension glaucoma suspected.
Credit :
Rapid Ophthalmology
Dr Zahir Mirza, BSc, MBChB Ophthalmic Specialist Trainee
Western Eye Hospital, Imperial NHS Trust London, UK
Mr Andrew Coombes, BSc, MBBS FRCOphth Consultant Eye Surgeon
Barts and the London NHS Trust
