Risk factors
In general, elevated IOP is a major risk factor in the development of secondary glaucoma. However, there are several risk factors contributing to the fluctuation in IOP levels. Uveitis
Secondary glaucoma is commonly associated with uveitis. Uveitis is the inflammation of the uvea, a middle layer tissue of the eye consisting of the ciliary body, choroid and iris. Various causes have been identified as potential risk factors contributing to the occurrence of secondary glaucoma. These include viral anterior uveitis due to cytomegalovirus infection, and herpetic anterior uveitis caused by herpes simplex virus. The observed pathophysiology of secondary glaucoma in uveitis is found to be linked to the increase and fluctuation of IOP. Inflammation of eye tissues contributes to the blockage of IOP produced in the ciliary body. This results in the accumulation of aqueous and thus elevated IOP, which is a common risk factor for the progression of secondary glaucoma. Paediatric congenital cataract surgery
Paediatric congenital cataract surgery is also identified as a risk factor for the progression of secondary glaucoma. Cataract is an ocular disease, identified by the progressive clouding of the lens. Surgical procedures are often employed to replace the lens and allow for clear vision. However, there is an increased risk of secondary glaucoma development in children due to the secondary IOL implantation procedure. The increased inflammatory sensitivity in the anterior chamber angle may contribute to the risks of secondary glaucoma. Intraocular tumour
Intraocular tumours (uveal and retinal tumours) are also found to be closely associated with the development of secondary glaucoma.
Other side effects include increased risk of miosis-induced headaches, blurred vision, retinal detachment and damage to the blood-aqueous barrier.Alternative drugs which can reduce the synthesis of aqueous humour, called aqueous suppressants, or increase the drainage of aqueous humour emerged as effective first-line treatments. Aqueous suppressants include beta-blockers, alpha-agonists and carbonic anhydrase inhibitors. They are particularly effective in treating corticosteroid, uveitic, aphakic, pseudophakic, ghost-cell and post-traumatic glaucoma. Prostaglandin analogues increase aqueous drainage and are thus used in the reduction of IOP. There are contradictory findings regarding the occurrence of prostaglandin analogue mediated side effects in the treatment of uveitic glaucoma. It was previously identified that the side effects comprise damage to the blood-aqueous barrier, cystoid macular oedema, risk of developing anterior uveitis and recurrence of keratitis caused by herpes simplex virus. However, current scientific evidence only supports the reactivation of herpes simplex keratitis among the other side effects.In uveitic and inflammatory glaucoma, reduction in inflammation is a critical step during the treatment and management process. This is commonly done using corticosteroids coupled with immunosuppressants. Steroidal treatment is also used in management of aphakic, pseudophakic, and post-traumatic glaucoma. Inflammatory glaucoma may further be treated using cycloplegics, a class of drugs that treats pain, ciliary spasm, uveoscleral tract blockage and disrupted blood-aqueous barrier linked with this form of glaucoma. While some studies recommend the use of anti-vascular endothelial growth factor drugs for inhibition of neovascularization in neovascular glaucoma, there is a lack of substantial evidence for the effectiveness of this treatment method.