Glaucomas are ocular disorders that lead to an optic neuropathy characterised by changes in the optic nerve head (optic disc) that is associated with loss of visual sensitivity and field.
WHAT ARE THE CAUSES OF GLAUCOMA?
There are two major types of glaucoma: primary open-angle glaucoma (POAG) or ocular hypertension, which accounts for most cases and is, therefore, the focus of this chapter, and primary angle closure glaucoma (PACG). Either type can be a primary inherited disorder, congenital, or secondary to disease, trauma, or drugs.
In POAG, the specific cause of optic nerve damage is unknown. Increased intraocular pressure (IOP) was historically considered to be the sole cause. Additional contributing factors include increased susceptibility of the optic nerve to ischemia, excitotoxicity, autoimmune reactions, and other abnormal physiologic processes.
Although IOP is a poor predictor of which patients will have visual field loss, the risk of visual field loss increases with increasing IOP. IOP is not constant; it changes with the pulse, blood pressure, forced expiration or coughing, neck compression, and posture. IOP demonstrates diurnal variation with a minimum pressure around 6 pm and a maximum pressure upon awakening.
The balance between the inflow and outflow of aqueous humour determines IOP. Inflow is increased by β-adrenergic agents and decreased by α2- and β-adrenergic blockers, dopamine blockers, carbonic anhydrase inhibitors (CAIs), melatonin-1 agonists, and adenylate cyclase stimulators. The outflow is increased by cholinergic agents (e.g., pilocarpine), which contract the ciliary muscle and open the trabecular meshwork, and by prostaglandin analogues and β- and α2-adrenergic agonists, which affect uveoscleral outflow. Secondary OAG has many causes, including exfoliation syndrome, pigmentary glaucoma, systemic diseases, trauma, surgery, ocular inflammatory diseases, and drugs. Secondary glaucoma can be classified as trabecular (normal meshwork is covered and prevents the outflow of aqueous humour), trabecular (meshwork is altered, or material accumulates in the intertrabecular spaces), or most trabecular (episcleral venous blood pressure is increased).
Many drugs can increase IOP (Table 1–1). The potential to induce or worsen glaucoma depends on the type of glaucoma and on whether it is adequately controlled.
PACG occurs when there is a physical blockage of the trabecular meshwork, resulting in increased IOP.
WHAT ARE THE SIGNS AND SYMPTOMS OF GLAUCOMA?
POAG is slowly progressive and is usually asymptomatic until the onset of substantial visual field loss. Central visual acuity is maintained, even in late stages.
Patients with PACG typically experience intermittent prodromal symptoms (e.g., blurred or hazy vision with halos around lights and, occasionally, headache). Acute episodes produce symptoms associated with a cloudy, edematous cornea; ocular pain; nausea, vomiting, and abdominal pain; and diaphoresis.
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