Introduction to Glaucoma

ByMutahir ShahM Phil Vision SciencesPakistan Institute of Community OphthalmalogyIntroduction to GlaucomaPOAG, NTG and Ocular Hypertension

Normal disc that obeys the ISNT rule

Intra Ocular PressureIntraocular pressure (IOP) is determined by the balance between the rate of aqueous production and its outflow The average IOP in the general population is around 16 mmHg on applanation tonometry, and a range of about 1121 mmHg Some patients develop glaucomatous damage with IOP less than 21 mm Hg whilst others remain unscathed with IOP well above this level. These include features influencing the IOP reading, such as corneal rigidity, and probably factors affecting the susceptibility of the optic nerve to damage, Such as the integrity of its blood supply and structural vulnerability to mechanical stress at the optic nerve head.

Fluctuation Normal IOP varies with time of day (diurnal variation), heartbeat, blood pressure and respiration.The diurnal pattern varies, with a tendency to be higher in the morning and lower in the afternoon and evening. Glaucomatous eyes exhibit greater than normal fluctuation, The extent of which is directly proportional to the likelihood of progressive visual field damage, A single reading may therefore be misleading.

Definition of GlaucomaA characteristic potentially progressive optic neuropathy that is associated with visual field loss as damage progresses, and in which IOP is a key modifiable factor. Classification of Glaucoma:Glaucoma may be congenital (developmental) or acquired. Open-angle and angle-closure types are distinguished based on the mechanism by which aqueous outflow is impaired with respect to the AC angle configuration.

EpidemiologyGlaucoma affects 23% of people over the age of 40 years; 50% may be undiagnosed. Primary open-angle glaucoma (POAG) is the most common form in white, Hispanic/Latino and black individuals; The prevalence is especially high in the latter. Primary angle closure (PAC) constitutes up to half of cases, and has a particularly high prevalence in individuals of Asian descent,

Risk factors of POAG IOP. The higher the IOP, the greater the likelihood of glaucoma. Asymmetry of IOP of 4 mmHg or more is also significant. Age. POAG is more common in older individuals. Race. It is significantly (perhaps four times) more common, more difficult to control in black individuals than in whites. Family history of POAG. First-degree relatives of patients with POAG are at increased risk. An approximate risk to siblings is four times and to offspring twice the normal population risk, though surveyed figures vary. Diabetes mellitus. Many studies suggest a correlation between diabetes and POAG. Myopia is associated with an increased incidence of POAG and myopic eyes may be more susceptible to glaucomatous

Contraceptive pill. Long term use of OC use may substantially increase the risk of glaucoma.Optic disc area. Large discs may be more vulnerable to damage, Ocular perfusion pressure is the difference between the arterial BP and the intraocular pressure (IOP), and has been shown in population studies to be linked to increased risk for the development and progression of glaucoma.

Primary Open Angle GlaucomaPrimary open-angle glaucoma (POAG) is a commonly bilateral disease of adult onset. Symptoms:Usually Asymptomatic until the later stage.Early Symptoms may include parts of a page missing.Tunnel vision and loss of central fixation typically do not occur until late.Signs:Raised IOP (Half the patient have an IOP of higher than 21mmHg.But still half of the patient have and IOP of 21 or lower at any one screening.Normal Angle Appearance

Disc Cupping & Notching usually follow ISNT rule.

concentrically enlarging Focal ischaemic inferior notch and disc haemorrhage;

Characteristic visual field loss as damage progresses.CDR asymetry >0.2 in the absence of a cause(e.g. anisometropia, Different nerve sizes.Bayoneting ( Sharp angulations(deviation from a straight line) of blood vessels as they exit the nerve)

Others include Large fluctuation in IOP

bayoneting of blood vessels;

DD of POAGOcular Hypertension : Normal VF and Optic NervePhysiological Cupping: static Enlarged CDR without rim notching and VF defects.Low Pressure Glaucoma: Same as POAG except normal IOPSecondary Open Angle Glaucoma: Have an identifiable cause may be lens induced , Inflammatory Exfoliative, Pigmentary or steroid induced. Optic Atrophy : Characterized by disproportionally more optic nerve pallor than cupping IOP normal color vision and central vision are usually affectedCongenital optic nerve defect(tilted disc, colobomas Optic nerve pit

Ocular HypertensionIn the general population the mean IOP is 16 mmHg; two standard deviations either side of this gives a normal IOP range of 1121 mmHgIt is estimated that 410% of the population over the age of 40 years have IOP >21 mmHg without detectable glaucomatous damage: ocular hypertension (OHT).Intraocular pressure. The risk of developing glaucoma increases with increasing IOP. Age. Older age is associated with greater risk. Central corneal thickness (CCT). The risk is greater in eyes with low CCT and lower in eyes with higher CCT. This is probably due to resultant under- and over-estimation of IOP Cup/disc (C/D) ratio. The greater the C/D ratio the higher the risk. This may be because an optic nerve head with a large cup is structurally more vulnerable, or it may be that early damage is already present.

TreatmentNo treatment in the absence of Optic nerve damage and VF loss if IOP is less than 24mmHg. Close observation is necessary.Patient having an IOP of greater than 24 to 30mmHg but otherwise normal examinations are candidates for pressure lowering therapy.

Normal Tension GlaucomaPAOG occurring in patients without IOP elevation usually regarded as a variant of POAG. It is characterized by: IOP consistently equal to or less than 21 mmHg. Signs of optic nerve damage in a characteristic glaucomatous pattern. An open anterior chamber angle. Visual field loss as damage progresses, consistent in pattern with the nerve appearance. No features of secondary glaucoma or a non-glaucomatous cause for the neuropathy.

The distinction between NTG and POAG is based on an epidemiologically derived range of normal IOPClinical features History and examination are essentially the same as for POAG but specific points warrant attention. History Migraine and Raynaud phenomenon. Episodes of shock. Head or eye injury. Headache and other neurological symptoms (intracranial lesion). Medication, e.g. systemic steroids, beta-blockers.

IOP is usually in the high teens, but may rarely be in the low teens. In asymmetrical disease the more damaged disc typically corresponds to the eye with the higher IOP. Optic nerve head The optic nerve head may be larger on average in NTG than in POAG. The pattern of cupping is similar, but acquired optic disc pits and focal nerve fibre layer defects may be more common. Peripapillary atrophic changes may be more prevalent. Pallor disproportionate to cupping should prompt a suspicion of an alternative diagnosis. Visual field defects are essentially the same as in POAG although there is some evidence that they tend to be closer to fixation, deeper, steeper and more localized.

Disc (splinter, Drance see Figs A B and C) haemorrhages may be more frequent than in POAG, and are associated with a greater likelihood of progression.

EtiologyControversial: Most investigators believe that IOP play an important role in LTG.Other proposed that include vascular dysregulation(e.g. systemic or nocturnal hypotension, vasospasm or loss of autoregulation) microischemic disease and autoimmune disease.Treatment:Research suggests that further lowering of IOP plays an important role in preventing progression of low pressure POAG.Target IOPs are at least 30% lower than the level at which progressive damage was occurring.Avoid use of Antihypertensive drugs at bedtime and use preferentially in the morning

Refrences J Kanski 8th Edition and Wills Eye ManualThank you