Contributor: Gordon K. Klintworth
Secondary glaucoma is a form of glaucoma that develops in individuals with an underlying ocular pathologic process. Secondary glaucoma is subdivided into secondary open angle glaucoma [glaucoma - secondary open angle] and secondary closed angle glaucoma [glaucoma - secondary closed angle] types depending on whether the iridocorneal angle appears open or closed.
In secondary open angle glaucoma the aqueous-outflow and trabecular meshwork are occluded by a variety of cells and debris. These include blood and macrophages that have ingested degenerated lens material, blood breakdown products or melanosomes from necrotic tumors. Melanin released from the iris pigment epithelium by zonular abrasion accumulates in the trabecular meshwork as in the pigment dispersion syndrome. The exfoliation syndrome is a relatively common cause of a special type of secondary open angle glaucoma in elderly patients [glaucoma - capsular].
melanomalytic glaucoma, trabecular blockade occurs primarily by the following mechanism.
Secondary glaucoma may be caused by a variety of tumors by different mechanisms. Malignant intraocular tumors (melanoma, retinoblastoma, metastatic carcinoma) can cause secondary glaucoma by directly infiltrating the trabecular meshwork. Malignant cells may also be shed into the intraocular cavities and become carried in the outflow system and when sufficient numbers of these cells become trapped within the trabecular meshwork, a secondary open angle glaucoma occurs. Some tumors can cause glaucoma by another mechanism after undergoing necrosis. If cellular debris from a necrotic melanoma [melanoma - necrotic] becomes dispersed intraocularly and phagocytosed by macrophages these melanin- laden scavengers can obstruct the anterior chamber angle and trabecular meshwork and cause melanomalytic glaucoma [glaucoma - melanomalytic]. The same phenomenon occasionally takes place when a melanoctoma undergoes necrosis causing melanocyomalytic glaucoma [glaucoma - melanocytomalytic].
Iris neovascularization is a feature of neovascular glaucoma [glaucoma - neovascular] (the most common and clinically significant form of secondary closed angle glaucoma).
Glaucoma secondary to some ocular pathologic process can occur in eyes with open or closed angles.
The causes of secondary glaucoma are many and include inflammation, hemorrhage, neovascularization of the iris, and adhesions. In secondary glaucoma the anterior chamber angles may be open or closed. Because the underlying disorder is usually limited to one eye, secondary glaucoma is usually unilateral. Causes of secondary open angle glaucoma include developmental anomalies, injuries, inflammatory reactions and neoplasms. Anterior uveitis can cause secondary glaucoma by producing posterior synechiae that partially or completely occlude the pupil (pupillary block). Scarring induced by chronic inflammation or repeated anterior chamber hemorrhages can impede aqueous outflow. An ocular contusional injury often tears the ciliary body between its longitudinal and radial muscles and disrupts the greater arterial circle of the iris causing hyphema. After healing a significant number of patients with post-contusion angle recession develop unilateral glaucoma. Such eyes often have a new layer of Descemet's membrane on the inner surface of the trabecular meshwork, which may cause the glaucoma.
Glaucoma is associated with as many as 25% of cases of chronic uveitis. This may be secondary to mechanical obstruction from exudation of inflammatory cells or release of hydrolytic enzymes, prostaglandins, cytokins, and other materials from leukocytes and damaged tissues. Eventually, there is loss of trabecular meshwork cells, degeneration of trabecular cores, and reactive fibrosis. Pigment dispersion syndrome is rare occurrence in young myopic males and rarely, females. It is thought that pigment epithelium of the iris atrophies and is later detached, with release of melanin granules into the aqueous. Such liberated pigment can obstruct the aqueous flow and give rise to secondary open angle glaucoma.
Ocular trauma resulting in release of a number of inflammatory mediaters and mechanical blockage by inflammatory cells may result in secondary open angle glaucoma. If the lens is dislocated in an ocular concussion, mechanical pupillary block or angle deformation obstructs aqueous outflow resulting in secondary closed-angle glaucoma. Lens displacement can also occur in advanced retinal detachment or after miotic use. The lens displacement has been attributed to constriction of the ciliary body around the lens by overaction of the sphincter component of the ciliary muscle and to the accumulation of aqueous within the vitreous.
Glaucoma [glaucoma - capsular] occurs in many patients with exfoliation syndrome. It is unclear whether glaucoma occurs secondary to in coexistence with the exfoliation syndrome.
Long term use of topical or systemic corticosteroids results in "corticosteriod glaucoma" from raised intraocular pressure and signs similar to those of primary open-angle glaucoma.
Secondary glaucoma is a form of glaucoma that develops in individulas with an underlying ocular disease [glaucoma - secondary]. Secondary glaucoma is subdivided into secondary open angle glaucoma [glaucoma - secondary open angle] and secondary closed angle glaucoma [glaucoma - secondary closed angle] types depending on whether the iridocorneal angle appears open or closed. In secondary open angle glaucoma
the aqueous-outflow and trabecular meshwork are occluded by a variety of cells and debris. These include blood and macrophages that have ingested degenerated lens material, blood breakdown products or melanosomes from necrotic tumors. Melanin released from the iris pigment epithelium by zonular abrasion accumulates in the trabecular meshwork as in the pigment dispersion syndrome. The exfoliation syndrome is a relatively common cause of a special type of secondary open angle glaucoma in elderly patients [glaucoma - capsular].
melanomalytic glaucoma, trabecular blockade occurs primarily by the following mechanism.
Secondary glaucoma may be caused by a variety of tumors by different mechanisms. Malignant intraocular tumors (melanoma, retinoblastoma, metastatic carcinoma) can cause secondary glaucoma by directly infiltrating the trabecular meshwork. Malignant cells may also be shed into the intraocular cavities and become carried in the outflow system and when sufficient numbers of these cells become trapped within the trabecular meshwork, a secondary open angle glaucoma occurs. Some tumors can cause glaucoma by another mechanism after undergoing necrosis. If cellular debris from a necrotic melanoma [melanoma - necrotic] becomes dispersed intraocularly and phagocytosed by macrophages these melanin- laden scavengers can obstruct the anterior chamber angle and trabecular meshwork and cause melanomalytic glaucoma [glaucoma - melanomalytic]. The same phenomenon occasionally takes place when a melanoctoma undergoes necrosis causing melanocyomalytic glaucoma [glaucoma - melanocytomalytic].
Iris neovascularization is a feature of neovascular glaucoma [glaucoma - neovascular] (the most common and clinically significant form of secondary closed angle glaucoma).
Glaucoma secondary to some ocular pathologic process can occur in eyes with open or closed angles.
The causes of secondary glaucoma are many and include inflammation, hemorrhage, neovascularization of the iris, and adhesions. In secondary glaucoma the anterior chamber angles may be open or closed. Because the underlying disorder is usually limited to one eye, secondary glaucoma is usually unilateral. Causes of secondary open angle glaucoma include developmental anomalies, injuries, inflammatory reactions and neoplasms. Anterior uveitis can cause secondary glaucoma by producing posterior synechiae that partially or completely occlude the pupil (pupillary block). Scarring induced by chronic inflammation or repeated anterior chamber hemorrhages can impede aqueous outflow. An ocular contusional injury often tears the ciliary body between its longitudinal and radial muscles and disrupts the greater arterial circle of the iris causing hyphema. After healing a significant number of patients with post-contusion angle recession develop unilateral glaucoma. Such eyes often have a new layer of Descemet's membrane on the inner surface of the trabecular meshwork, which may cause the glaucoma.
Histopathology. In secondary closed angle glaucoma the anterior chamber angle is obstructed by adhesions between the iris and the posterior surface of the cornea (peripheral anterior synechiae) caused by a fibrovascular membrane on the anterior iris (neovascular glaucoma) [glaucoma - neovascular] or an intraocular proliferation of corneal or conjunctival epithelium after intraocular surgery or perforating trauma (epithelial ingrowth). In the iridocorneal endothelial syndrome abnormal corneal endothelial cells proliferate, causing unilateral closed angle glaucoma and a characteristic spectrum of iris abnormalities including full-thickness holes. Eyes with advanced posterior segment tumors may cause secondary angle closure glaucoma by iris neovascularization or pupillary block.
Glaucoma is associated with as many as 25% of cases of chronic uveitis. This may be secondary to mechanical obstruction from exudation of inflammatory cells or release of hydrolytic enzymes, prostaglandins, cytokins, and other materials from leukocytes and damaged tissues. Eventually, there is loss of trabecular meshwork cells, degeneration of trabecular cores, and reactive fibrosis. Pigment dispersion syndrome is rare occurrence in young myopic males and rarely, females. It is thought that pigment epithelium of the iris atrophies and is later detached, with release of melanin granules into the aqueous. Such liberated pigment can obstruct the aqueous flow and give rise to secondary open angle glaucoma.
Ocular trauma resulting in release of a number of inflammatory mediaters and mechanical blockage by inflammatory cells may result in secondary open angle glaucoma. If the lens is dislocated in an ocular concussion, mechanical pupillary block or angle deformation obstructs aqueous outflow resulting in secondary closed-angle glaucoma. Lens displacement can also occur in advanced retinal detachment or after miotic use. The lens displacement has been attributed to constriction of the ciliary body around the lens by overaction of the sphincter component of the ciliary muscle and to the accumulation of aqueous within the vitreous.
Glaucoma [glaucoma -capsular] occurs in many patients with exfoliation syndrome. It is unclear whether glaucoma occurs secondary to in coexistence with the exfoliation syndrome.
Long term use of topical or systemic corticosteroids results in "corticosteriod glaucoma" from raised intraocular pressure and signs similar to those of primary open-angle glaucoma.

Secondary glaucoma  may develop in persons with X-linked retinoschisis  due to closure of the angles by anterior ballooning of the cyst.