Ophthalmology - Glaucoma Flashcards
How do patients with acute angle closure glaucoma (AACG) present?
Patients with AACG present with severe ocular and periorbital pain and reduced vision in the affected eye(s). Patients may be vomiting and usually feel extremely unwell. The eye on the side with AACG is often injected with a hazy oedematous cornea and a vertically oval, non reactive, mid dilated pupil. A history of prodromal subacute attacks of angle closure may be present with intermittent episodes of red painful eyes or of seeing haloes around bright lights. After an abortive attack (which may settle overnight) there may be minimal residual signs of the episode. Therefore, an accurate history is ESSENTIAL.
What patients are at an increased risk of developing glaucoma?
People, particularly women, with hypermetropia are at an increased risk of developing AACG. Glaucoma is a disease of middle years in general and is commoner in Asia.
What is the pathology of acute angle closure glaucoma?
Open angle glaucoma can occur as a primary degenerative condition in the elderly, when the progressive accumulation of collagen within the trabeculae and extracellular space of the outflow system increases the resistance to flow of aqueous fluid from the anterior chamber and out via the canal of Schlemm. This causes a slow increase in intraocular pressure that often presents as a central visual field defect.
The iris presses forwards to narrow the closure angle and obstructs circulation of the aqueous humour.
Pupil dilatation at night worsens this. Intraocular pressure then rises to >30 mmHg (normal is 15-20), the pupil becomes fixed and dilated and axonal death occurs. A shallow anterior chamber may be a predisposing factor.
How should acute angle closure glaucoma be managed?
Pilocarpine drops 2-4% (miosis opens a blocked “closed” drainage angle) and 500mg of acetazolomide stat should be given alongside an ophthalmology referral for gonioscopy. Analgesia and anti-emetics may be used. Admit to monitor IOP. Mannitol may be needed.
Topical steroids and antihypertensive drops (beta blockers, prostaglandins, alpha adrenergic agonists) are used. Peripheral iridectomy (laser or surgery) is done once IOP is controlled (rarely as an emergency if IOP is uncontrollable). A piece of iris is removed in both eyes to allow aqueous flow.
What is gonioscopy?
Gonioscopy is a technique which enables the ophthalmologist to examine the drainage angle of he eye, by using a specially designed contact lens. Patients with glaucoma can be grouped into two broad categories on the basis of this examination: open angle glaucoma and closed angle glaucoma, depending on whether the drainage angle structures are visible or not. The distinction between open and closed angle glaucoma is critical because both treatment and prognosis are different in the two groups. Primary open angle glaucoma (POAG) is the most common form of glaucoma in the western world, and affects about 2% of the population over the age of 60.
In acute angle closure glaucoma (AACG) the drainage angle is narrow as the iris blocks the flow of aqueous fluid out of the anterior chamber via the canal of Schlemm.
What is a YAG laser iridotomy?
In cases of acute or chronic angle closure glaucoma, relative pupil block can often be alleviated by creating a full thickness hole through the peripheral iris, a procedure called peripheral iridotomy (PI). This procedure can be performed as an out-patient with the photodisruptive YAG laser which vaporises tissue. The procedure can also be performed prophylactically in eyes at risk of angle closure glaucoma, for example high hypermetropes.
What are the important features of a normal optic disc?
The neural rim tissue should be pink and clearly defined. The optic cup is small and sits inside a well demarcated optic disc. There is often a high degree of symmetry between the disc morphology in the two eyes, particularly with reference to the vertical cup:disc ratio (C/D ratio). A large percentage of the population have a C/D ratio of 0.5 or less. Studies have shown that if one has a C/D ratio of 0.6 or greater, or a difference in C/D ratio of greater than 0.2 between the two eyes, then there is a significant risk of developing glaucoma.
What is the appearance of the optic disc in glaucoma?
The classical feature of damage to the optic nerve in glaucoma is cupping. The most important risk factor for the development of optic disc cupping is elevated intraocular pressure. Reduced blood flow to the optic nerve head is also thought to be a factor in some patients.
Normal cups are similar in shape and occupy <50% of the disc. In glaucomatous cupping the amount of pink, healthy neural rim tissue is decreased resulting in an increased cup:disc ratio. Diffuse neural tissue loss results in a concentrically enlarged cup, but focal neural loss may also occur resulting in a focal notch in the neural rim. As the cup widens and deepens, vessels emerging from the disc appear to have breaks as they disappear into the cup and are then seen at the base again.
If there is asymmetrical optic disc cupping, or marked pallor of the discs, one should consider the possibility of glaucoma. Splinter haemorrhages on the disc indicate the site of future nerve fibre layer damage.
What is chronic simple (open angle) glaucoma?
In this form of open angle glaucoma, the classical features of cupping of the optic nerve head are seen in the absence of statistically elevated intraocular pressure. The resistance to outflow through the trabecular meshwork gradually increases, for reasons not fully understood, and the pressure in the eye slowly rises causing damage to the nerve.
By definition, glaucoma is present when on visual field testing 3 or more locations are outside the normal limits, and the cup:disc ratio is greater than that seen in 97.5% of the population. IOP may be raised but this is NOT part of the definition.
Glaucoma implies optic neuropathy with death of many retinal ganglion cells and their optic nerve axons. It is asymptomatic until visual fields are badly impaired - roughly corresponding to loss of 30-50% of fibres in the optic nerve. Hence the need for screening. If raised IOP is found, lifelong follow up is needed.
What is normal (low) tension glaucoma (NTG)?
This may be associated with vasospastic diseases such as migraine and Raynaud’s phenomenon and there may be a history of previous hypotensive episode or blood loss.
Management of normal tension glaucoma involves lowering IOP.
What is IOP phasing?
Patients often require IOP phasing, in which multiple IOP measurements are made throughout the day to exclude undetected spikes of raised IOP. Management is initially aimed at lowering the IOP since there is now evidence that lower IOP correlates with improved visual function in progressive disease.
Name some symptoms of primary open angle glaucoma?
Because the visual loss is gradual, patients do not usually present until severe damage has occured. The disease can be detected by screening high risk groups for the signs of glaucoma. At present, most patients with primary open angle glaucoma are detected by optometrists on routine examinations.
What groups are at risk of primary open angle glaucoma?
Prevalence of POAG increases with age. Those with an increased risk include first degree relatives of patients, patients with ocular hypertension (particularly those with thin corneas), people with myopia, and people of Afrio-Caribbean origin.
What are the signs of POAG?
The eye is white and on superficial examination looks normal. The best signs for the purposes of detection, are optic disc changes. The cup:disc ratio increases as the optic nerve fibres atrophy. Asymmetry of the cupping is also important, as the disease is often more advanced in one eye than the other. Haemorrhages on the optic disc are a poor prognostic sign. Longer term changes in disc cupping are best detected by serial photography.
Visual field loss is difficult to pick up clinically without specialised equipment until considerable damage has occurred. Computer field testing equipment may detect nerve fibre damage earlier.
The classical signs of glaucoma (visual field loss and optic disc cupping) are often seen in patients who have pressures lower than the statistical limit of normal. But many clinicians now feel that these two glaucomas are part of the same spectrum of pressure dependent optic neuropathies, although these patients are sometimes referred to as having normal tension glaucoma.
What other conditions can cause glaucoma?
If there is inflammation in the eye (anterior uveitis), adhesions may develop between the lens and the iris (posterior synechiae). These adhesions will block the flow of aqueous between the posterior and anterior chambers and result in forward ballooning of the iris and a rise in the IOP. Adhesions may also develop between the iris and cornea (peripheral anterior synechiae), covering up the trabecular meshwork.
Inflammatory cels may also block the meshwork. Topical steroids may cause a gradual asymptomatic rise in IOP that can lead to blindness.
The growth of new vessels in the iris (rubeosis) occurs both in diabetic patients and after occlusion of the central retinal vein resulting in retinal ischaemia. These vessels also block the trabecular meshwork causing rubeotic glaucoma, which is extremely difficult to treat.
The trabecular meshwork itself may have developed abnormally (congenital glaucoma) or been damaged by trauma to the eye. Patients who have had eye injuries have a higher chance than normal of developing glaucoma in later life.
