Steroid Induced Glaucoma

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 by Leonard K. Seibold, MD on January 23, 2015.

Disease Entity

Steroid-induced glaucoma is a form of secondary open angle glaucoma that results from the use of steroids.


In steroid glaucoma, the IOP is elevated primarily due to increased outflow resistance. Increased responsiveness to steroids may be facilitated by upregulation of glucocorticoid receptors on trabecular meshwork cells. [1] In cultured human trabecular meshwork cells, glucocorticoids increased the expression of the extracellular matrix protein fibronectin, glycosaminoglycans, and elastin. [2] [3] Steroids also suppress phagocyctic activity which may lead to observations such as increased deposition of material in the juxtacanalicular meshwork of eyes with steroid induced glaucoma. [4] [5] Actual physical obstruction by the steroid medication has been postulated as well, based on the observation of white crystals in the angle in a patient who developed elevated IOP after intravitreal triamcinolone injection.[6]

Risk Factors

Anyone can be at risk for steroid induced glaucoma, and the risk of glaucoma increases as the duration of therapy increases.

A higher than average risk for steroid glaucoma is found in patients with:

  1. Primary open angle glaucoma (POAG)[7] [8]
  2. A first degree relative with POAG[9] [10]
  3. A history of previous steroid induced intraocular pressure (IOP) elevation
  4. Type 1 Diabetes Mellitus[11]
  5. Very young age (age less than six years old) or an older age[12]
  6. Connective tissue disease[13]
  7. Penetrating keratoplasty, especially in eyes with Fuchs endothelial dystrophy or keratoconus
  8. High myopia[14]

(Table 23.1 in Shields Textbook of Glaucoma, Sixth Ed. p. 346)

In this subset of patients, intraocular pressures should be monitored regularly. Care should be taken to avoid corticosteroids If possible. If corticosteroids are indicated, the judicious use of an adequate potency and duration should be considered.

Types of Steroids

Topical Ocular Preparations

IOP rise may occur with corticosteroid drops or ointment applied to the eye or with steroid preparations applied to the skin of the eyelids. The risk of IOP rise increases with duration of use and may be directly correlated to its anti-inflammatory effect. For example, dexamethasone and prednisolone increase the IOP more frequently than fluoromethalone, hydrocortisone, and rimexolone .[15] Fluoromethalone has poor intraocular penetration with less tendency towards IOP elevation.


This route of steroid delivery includes subconjunctival, sub-tenon’s, or retrobulbar injections. The elevation in intraocular pressure noted cannot always be predicted by the patient’s response to topical steroid treatment.[16] Sometimes, it is necessary to excise the depot of steroids in order to control the intraocular pressures. As a result, it may be useful to inject inferiorly as well as anteriorly when performing a subconjunctival or sub-tenon’s injection.


IOP elevation develops in about half the patients that receive intravitreal triamcinolone, usually developing between two to four weeks after the injection. In eyes that are pseudophakic or have undergone vitrectomy, the rise can happen more rapidly.[17] [18] [19] According to one study, IOP lowering treatment was needed for an average of six months after one intravitreal triamcinolone injection and for eight months after multiple injections.[20] Steroid implantation in the vitreous can also cause IOP elevation and necessitate treatment for glaucoma. One study showed that seventy five percent of eyes with fluocinolone acetonide implants required glaucoma treatment.[21]


Steroid induced glaucoma may develop after application of steroid preparations applied to the skin of the eyelids. This elevation occurs most frequently with chronic use, such as in patients with atopic dermatitis. Close IOP monitoring of these patients is essential and consideration of a non-steroidal topical medication, such as tacrolimus and pimecrolimus, should be considered as an alternative. Elevation in intraocular pressure has also been noted with application of steroids on skin that was not periocular, either from ocular contamination or systemic absorption. [22] Patients should be advised to wash their hands after applying dermatologic steroids or to use gloves.


Steroids by mouth (PO) can elevate the IOP as well. The elevation appears to be correlated to the patient’s IOP response to topical steroids.[23] [24] Though not common, elevation of IOP has also been noted with the use of inhalational and nasal corticosteroids [25] as well as after intraarticular steroid injections.


All patients receiving topical ocular steroids, periocular or intravitreal steroids need to be monitored regularly. Chronic ocular steroids should not be administered by non-ophthalmic physicians, unless patients are also being followed by an ophthalmologist. All patients using dermatologic steroids on the face should also have perioidic IOP measurements. Patients in the high risk groups mentioned above should use steroids judiciously and be monitored closely if the steroids are used long term.


  1. Discontinue steroids—In the acute form of IOP elevation from steroids, discontinuing steroids can cause the IOP to normalize in days. In the chronic form, elevation of IOP can last one to four weeks. [26] In a small subset of patients, the IOP may remain chronically elevated despite discontinuation of steroids. In one series, 2.8% of eyes converted to glaucoma. Interestingly, all of these patients had a family history of glaucoma.[27] The duration of steroid treatment seems to play a role as well. In one series, the IOP remained elevated in patients where the steroid was used for more than four years. [28]
  2. Removal of depot steroids—One can cause a decrease in IOP by excising depot steroids.[17] [29] [30]For intravitreal steroids, vitrectomy can also be used to reduce IOP.[18]
  3. Glaucoma treatment—Treatment of steroid glaucoma includes the use of topical glaucoma medications, laser trabeculoplasty, filtering surgery, glaucoma drainage implant surgery, or one of the other means of treatment of primary open angle glaucoma.


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  2. Johnson DH, Bradley JM, Acott TS. The effect of dexamethasone on glycosaminoglycans of human trabecular meshwork in perfusion organ culture. Invest Ophthalmol Vis Sci. 1990;31(12):2568-2571.
  3. Steely HT, Bowder SL, Julian MB, et al. The effects of dexamethasone on fibronectin expression in cultured human trabecular meshwork cells. Invest Ophthalmol Vis Sci.1992;33(7): 2242-2250.
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