User:Bloominghibiscus/sandbox/Secondary Glaucoma

Secondary glaucoma is a collection of progressive optic nerve disorders associated with a rise in intraocular pressure eventually resulting in the loss of vision. In clinical settings, secondary glaucoma is defined in the occurrence of intraocular pressure (IOP) above 21 mmHg requiring the prescription of IOP-managing drugs7. It can be broadly divided into two subtypes: secondary open-angle glaucoma and secondary angle-closure glaucoma, depending on the closure of the angle between the cornea and the iris. It can be further classified based on the cause of glaucoma. Principal causes of secondary glaucoma include optic nerve trauma or damage, eye disease, surgery, neovascularization, tumours and use of steroid and sulfa drugs.

Typical diagnostic tools for secondary glaucoma are similar to primary glaucoma. They involve the detection of optic neuropathy, using ophthalmological examination and gonioscopy, and evaluation of the patient’s medical history. Common treatments are designed to treat secondary glaucoma according to the type (open-angle or angle-closure) and the underlying causative condition, in addition to the consequent rise in intraocular pressure (IOP). These include drug therapy, like the use of miotics, surgery or laser therapy.

Mechanism
In pediatric congenital cataract patients under the age of two, cataract surgery is frequently considered and employed as the primary treatment. There are two types of therapeutic combination, primary and secondary intraocular lens implantation (IOL)1. In primary IOL, cataract surgery is performed alongside immediate implantation of intraocular lens (IOL). However, in secondary IOL implantation, the patient is prescribed aphakic glasses or contact lenses till the implantation of IOL after a varied period of time between a few months or years. According to studies conducted, secondary IOL implantation poses a high risk for the development of secondary glaucoma1. On the other hand, primary IOL implantation is observed to significantly reduce and avoid the occurrence of secondary glaucoma in pediatric patients under the age of two1.

Based on the onset of secondary glaucoma in pediatric patients, it can be classified into early-stage and late-stage glaucoma cases. Early-stage secondary glaucoma observed as angle-closure glaucoma results from the blockage and inflammation of the peripheral anterior synechiae structure1. However, early-stage secondary glaucoma rarely occurs with the readily available prescription of anti-inflammatory medications. On the other hand, for late-stage glaucoma which is commonly associated with open-angle glaucoma, the mechanisms are currently unconfirmed. Yet, it is believed to be closely related to the onset of trabeculitis or vitreous toxicity1.

In patients diagnosed with herpic anterior uveitis (HAU), elevated intraocular pressure (IOP) and secondary glaucoma is often detected. This is due to two main reasons, the blockage of vitreous flow resulting from inflammation in the structures of the trabecular meshwork, and the sedimentation of inflamed cells. Specifically for viral anterior uveitis (VAU), patients with IOP levels above 30 mmHg are often suffering from secondary glaucoma caused by cytomegalovirus (CMV).

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.

Secondary glaucoma is commonly associated with uveitis8. 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 Virus-associated anterior uveitis (VAU) due to cytomegalovirus (CMV) and herpetic anterior uveitis (AU) caused by herpes simplex virus (HSV). The observed pathophysiology of secondary glaucoma in uveitis is found to be linked to the increase and fluctuation of intraocular pressure (IOP). Inflammation of eye tissues contributes to the blockage of IOP produced in the ciliary body. This resulted in the accumulation of IOP and thus elevated IOP, which is a common risk factor for the progression of secondary glaucoma7.

Paediatric congenital cataract surgery is also identified as a risk factor for the progression of secondary glaucoma3. 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 procedure3. The understood mechanism of anterior chamber angle with increased inflammatory sensitivity is speculated to contribute to the risks of secondary glaucoma1.

Intraocular tumours (uveal and retinal tumours) are also found to be closely associated with the development of secondary glaucoma. The pathophysiology of secondary glaucoma in these cases are affected by the type of tumour, location and other tumour-associated factors. Among the many subtypes of uveal tumours, secondary glaucoma is the most prominent among patients of trabecular meshwork iris melanoma cases. The blockage of vitreous flow due to inflammation in the structures of the trabecular meshwork mechanism is supported by the proposed mechanism in herpic anterior uveitis (HAU) patients. In addition to this, angle invasion6 is a mechanism that is observed to contribute greatly to the development of secondary glaucoma in patients of iris tapioca melanoma, iris lymphoma, choroidal melanoma, and medulloepithelioma.