Don't Avoid Steroid Use
Looking for:
Corticosteroids and glaucoma risk - StatPearls [Internet]. |
Steroid Induced Glaucoma - StatPearls - NCBI Bookshelf - Continuing Education Activity
The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.
Abstract Corticosteroids glucocorticoids , used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure IOP when administered exogenously topically, periocularly or systemically and in certain conditions of increased endogenous production e. Publication types Research Support, Non-U.
In this condition, there is increased production and decreased destruction of the extracellular matrix of the trabecular meshwork. There is increased deposition of glycosaminoglycans, fibronectin, elastin, and Type IV collagen and reduced activity of matrix metalloproteinases. Trabecular meshwork cells have glucocorticoid receptors, and steroids may act on them to alter cell migration and phagocytosis.
This reaction causes decreased cellularity of the trabecular meshwork and increased extracellular matrix deposition, thus increasing aqueous outflow resistance and a rise in IOP.
Glaucoma may develop if the IOP elevation is of sufficient magnitude and duration, thus leading to progressive damage to the optic nerve and visual field. Any form of steroid administration can cause glaucoma. It may occur after administration of topical steroids for a relatively trivial condition, after postoperative administration of steroids for refractive surgeries, or after prolonged systemic corticosteroid treatment for inflammatory conditions.
In severe cases, patients may complain of blurred vision or notice a visual field defect. Blurred vision may be due to corneal edema or steroid-induced posterior subcapsular cataract. An acute rise in IOP may sometimes cause a brow or eye ache. On examination, the eye is usually unremarkable. The IOP becomes elevated beyond the normal range of 10 mmHg to 22 mmHg, and upon soliciting a history of steroid use, the patient is said to be having steroid-induced hypertension.
Prolonged IOP rise may cause progression to steroid-induced glaucoma, with signs of glaucomatous optic neuropathy and the characteristic glaucomatous visual field defects. However, the clinical picture of steroid-induced glaucoma may be influenced by the age of the patient. Children may present with enlarged corneal diameters and buphthalmos similar to congenital glaucoma.
Elderly patients who have received steroid treatment and subsequently discontinued it may present as normal-tension glaucoma. It is critical to ask about a history of steroid use when presented with a patient with elevated IOP.
The history of the patient may give a clue to the underlying etiology of this condition. Patients with vernal conjunctivitis or another allergic conjunctivitis may be using steroid eye drops for a long time. Patients may be on topical steroid treatment for postsurgical conditions like PRK or may have an implanted depot steroid. Renal transplant patients are another group of likely candidates to develop this condition.
The evaluation includes recording visual acuity, thorough anterior and posterior segment examination, measurement of IOP tonometry , visual field testing, ocular coherence tomography OCT testing, and gonioscopy.
The first step in the management of steroid-induced glaucoma is the discontinuation of steroids. Removal of repository steroids is also indicated, if possible.
If it is difficult to discontinue steroids totally, the dose should be reduced, or a weaker steroid should be substituted for it. Antiglaucoma medications can be added to control the IOP. Elevated IOP can be caused by many things, even with concurrent steroid use.
Steroid-induced IOP is reversible on discontinuation. This differentiates it from glaucoma Below is a list of differential diagnoses:. Elevated IOP from steroid-induced glaucoma shares a similar prognosis to other types of glaucoma.
If the IOP is controlled, the likelihood of glaucoma developing is very low. Patients taking steroids should be educated on the risks of IOP elevation. While steroids will have a minimal effect on the IOP of most patients, there is a small population that will develop a large increase in IOP. Providers should inform patients that already have glaucoma that the risk of IOP elevation and glaucoma progression with steroids is greater than the general population.
This workup should include baseline IOP measurements, followed by checking IOP after two weeks, then every 4 to 6 weeks for about three months, and then six-monthly if the initial response is ruled out.
Although steroid-induced glaucoma is a dangerous and potentially blinding condition, it is manageable by early detection and prompt initiation of anti-glaucoma treatment. Steroids are widely prescribed by healthcare workers, including the nurse practitioner, physician assistant, and physicians.
One of the most dangerous side effects of these drugs is an elevated IOP. When treating glaucoma, the prognosis is good. This book is distributed under the terms of the Creative Commons Attribution 4.
Turn recording back on. Help Accessibility Careers. StatPearls [Internet]. Search term. No matter how a steroid is used in the eye or in the body, it will get into your bloodstream. One of the consequences of this is that using a topical steroid in one eye can cause an IOP rise in the fellow untreated eye.
A normal trabecular meshwork cell nucleus contains both alpha and beta glucocorticoid receptors. The beta receptors are believed to inhibit the alpha receptors, whose job is to manufacture extracellular matrix, which can clog up your drainage system.
You can see this effect with other drugs as well; if you put an aqueous suppressant like timolol in one eye to lower the pressure, it gets into your bloodstream and the pressure in the other eye goes down a little bit.
Since steroids may cause a pressure increase, this unintended effect on the fellow eye is of more concern. People falling into this category include: — Glaucoma suspects, primary open-angle glaucoma patients and low-tension glaucoma patients. Armaly found that 95 percent of POAG patients have a significant rise in pressure when treated with steroids. Likewise, almost percent of low-tension glaucoma patients are steroid responders.
Even glaucoma suspects have a much higher risk of a pressure rise than the general population. They can have a significant pressure rise. This is especially likely in people with more than 5 D of myopia. The reason for this is not yet clear. Try prescribing a weaker steroid. For example, switch from Pred Forte to milder prednisolone acetate.
Reduce the frequency of administration. When you put a drop in your eye and blink, that pumps some of the drug into your nose; from there, some is absorbed into your bloodstream.
Simply keeping your eye closed for two or three minutes after putting in the drop prevents this from happening, increasing the absorption of the drug into your eye and decreasing the systemic absorption. Studies have shown that this can reduce systemic absorption by 60 percent. Also, studies have found that nasal lacrimal occlusion and eyelid closure have similar success in reducing the systemic level of topically applied eye drops. This almost certainly is the result of systemic absorption of the steroids used after surgery.
If a patient has this problem, you may want to have the patient try eyelid closure; this simple strategy may bring the pressure back down in the other eye. However, glaucoma patients who are already on several drops and then get a pressure rise in response to a steroid may need to have surgery in order to control the pressure.
As already noted, a steroid drop placed on the eye will be at least partly absorbed systemically. In addition to possibly causing the pressure to rise in the fellow eye, systemic absorption can cause problems such as gastrointestinal ulcers.
How much more pressure can it handle without further damage? In that situation, be especially conservative with your use of steroids and generous in your follow-up schedule. Minimally invasive glaucoma surgeries are getting a lot of attention these days. Most MIGS surgeries, such as a stent or some kind of trabecular bypass or trabeculotomy, are designed to get the trabecular meshwork to flow better.
If you use a lot of steroids in those people, the pressure can still go up. This may seem odd, but a recent study by Darryl R. Overby, PhD, may provide an explanation. We always used to think that steroids only clogged the upstream collector systems, like the trabecular meshwork.
This is particularly challenging with steroids. For this reason we have to be very careful when we give our patients steroids. Clearly we use them for specific positive purposes, but we have to make sure we find the best drug, the best concentration, the best frequency, the best route of delivery—which might be topical, peribulbar, intravitreal or systemic—and only have the patient use it as long as necessary.
We have to know which patients are at the greatest risk of suffering an adverse effect from the steroid.
❿Steroids for Glaucoma: Both Friend and Foe - Also By The Authors
Federal government websites often end in. Before sharing sensitive information, make sure you're on a federal government site. The site is secure. NCBI Bookshelf. Kaberi B. Feroze ; Leila Khazaeni. Authors Kaberi B. Feroze 1 ; Leila Khazaeni 2. Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions. Although they do have numerous benefits, steroid usage can cause many adverse effects as well.
Some of these effects are on the eye, the most important being steroid-induced glaucoma and cataracts. This activity describes steroid-induced glaucoma, its pathophysiology, and highlights the role of the interprofessional team in its prevention and treatment. Objectives: Describe the epidemiology of steroid-induced glaucoma. Review the presentation of a patient with steroid-induced glaucoma. Summarize the treatment options for steroid-induced glaucoma.
Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by steroid-induced glaucoma.
Access free multiple choice questions on this topic. Although it has numerous benefits, steroid usage can cause many adverse effects on the eye, the most important being steroid-induced glaucoma and cataract. Steroid-induced iatrogenic glaucoma was described for the first time in the s with the observation of glaucoma following the use of systemic adrenocorticotropic hormones and topical or systemic steroids.
Steroid-induced glaucoma or ocular hypertension can occur after steroid use in susceptible individuals. They are seen most commonly after topical, periocular, or intraocular administration. However, they can also occur after intranasal, inhalational, systemic use, and dermatological applications. Intraocular pressure IOP rise usually occurs 3 to 6 weeks following topical steroid use, however, may occur earlier. Corticosteroid injections may cause a rise in IOP after several months.
Individuals who develop an increase in IOP following steroid use are referred to as "steroid responders". Studies have shown that there are a number of risk factors for the development of high responsiveness such as history or family history of primary open-angle glaucoma, diabetes mellitus, high myopia, and connective tissue disorders such as rheumatoid arthritis.
The elderly population is more susceptible as are children less than 6 years of age. Based on the IOP response to topical administration of betamethasone and dexamethasone, Armaly and Becker suggested three categories:. Steroid-induced glaucoma is considered to be a type of secondary open-angle glaucoma, caused by increased resistance to the outflow of aqueous at the level of the trabecular meshwork.
In this condition, there is increased production and decreased destruction of the extracellular matrix of the trabecular meshwork.
There is increased deposition of glycosaminoglycans, fibronectin, elastin, and Type IV collagen and reduced activity of matrix metalloproteinases.
Trabecular meshwork cells have glucocorticoid receptors, and steroids may act on them to alter cell migration and phagocytosis. This reaction causes decreased cellularity of the trabecular meshwork and increased extracellular matrix deposition, thus increasing aqueous outflow resistance and a rise in IOP. Glaucoma may develop if the IOP elevation is of sufficient magnitude and duration, thus leading to progressive damage to the optic nerve and visual field.
Any form of steroid administration can cause glaucoma. It may occur after administration of topical steroids for a relatively trivial condition, after postoperative administration of steroids for refractive surgeries, or after prolonged systemic corticosteroid treatment for inflammatory conditions.
In severe cases, patients may complain of blurred vision or notice a visual field defect. Blurred vision may be due to corneal edema or steroid-induced posterior subcapsular cataract. An acute rise in IOP may sometimes cause a brow or eye ache.
On examination, the eye is usually unremarkable. The IOP becomes elevated beyond the normal range of 10 mmHg to 22 mmHg, and upon soliciting a history of steroid use, the patient is said to be having steroid-induced hypertension. Prolonged IOP rise may cause progression to steroid-induced glaucoma, with signs of glaucomatous optic neuropathy and the characteristic glaucomatous visual field defects.
However, the clinical picture of steroid-induced glaucoma may be influenced by the age of the patient. Children may present with enlarged corneal diameters and buphthalmos similar to congenital glaucoma. Elderly patients who have received steroid treatment and subsequently discontinued it may present as normal-tension glaucoma. It is critical to ask about a history of steroid use when presented with a patient with elevated IOP. The history of the patient may give a clue to the underlying etiology of this condition.
Patients with vernal conjunctivitis or another allergic conjunctivitis may be using steroid eye drops for a long time. Patients may be on topical steroid treatment for postsurgical conditions like PRK or may have an implanted depot steroid. Renal transplant patients are another group of likely candidates to develop this condition. The evaluation includes recording visual acuity, thorough anterior and posterior segment examination, measurement of IOP tonometryvisual field testing, ocular coherence tomography OCT testing, and gonioscopy.
The first step in the management of steroid-induced glaucoma is the discontinuation of steroids. Removal of repository steroids is also indicated, if possible. If it is difficult to discontinue steroids totally, the dose should be reduced, or a weaker steroid should be substituted for it. Antiglaucoma medications can be added to control the IOP. Elevated IOP can be caused by many things, even with concurrent steroid use.
Steroid-induced IOP is reversible on discontinuation. This differentiates it from glaucoma Below is a list of differential diagnoses:. Elevated IOP from steroid-induced glaucoma shares a similar prognosis to other types of glaucoma. If the IOP is controlled, the likelihood of glaucoma developing is very low.
Patients taking steroids should be educated on the risks of IOP elevation. While steroids will have a minimal effect on the IOP of most patients, there is a small population that will develop a large increase in IOP. Providers should inform patients that already have glaucoma that the risk of IOP elevation and glaucoma progression with steroids is greater than the general population.
This workup should include baseline IOP measurements, followed by checking IOP after two weeks, then every 4 to 6 weeks for about three months, and then six-monthly if the initial response is ruled out.
Although steroid-induced glaucoma is a dangerous and potentially blinding condition, it is manageable by early detection and prompt initiation of anti-glaucoma treatment.
Steroids are widely prescribed by healthcare workers, including the nurse practitioner, physician assistant, and physicians.
One of the most dangerous side effects of these drugs is an elevated IOP. When treating glaucoma, the prognosis is good.
This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on. Help Accessibility Careers. StatPearls [Internet].
Search term. Steroid Induced Glaucoma Kaberi B. Author Information Authors Kaberi B. Affiliations 1 King Faisal University. Continuing Education Activity Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions. Introduction Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions.
Etiology Steroid-induced glaucoma or ocular hypertension can occur after steroid use in susceptible individuals. Epidemiology Individuals who develop an increase in IOP following steroid use are referred to as "steroid responders".
Pathophysiology Steroid-induced glaucoma is considered to be a type of secondary open-angle glaucoma, caused by increased resistance to the outflow of aqueous at the level of the trabecular meshwork. History and Physical Any form of steroid administration can cause glaucoma. Evaluation The history of the patient may give a clue to the underlying etiology of this condition. The agents which may be used include beta-blockers, alpha-2 agonists, and carbonic anhydrase inhibitors.
Beta-blockers are the first-line agents in this condition. Prostaglandin analogs are relatively contraindicated in cases of steroid-induced glaucoma following uveitis treatment. Laser trabeculoplasty- may be considered if medical management is unsuccessful, and there is a threat of impending optic nerve damage.
It may also be considered in patients experiencing undesirable side effects with antiglaucoma drugs. Surgical management- surgery is indicated in those patients who fail to respond to medical and laser therapies. It may also be indicated in those patients who may be expected to have further exposure to steroids. The most commonly employed surgical procedure is trabeculectomy; other options include tube shunt surgeries or cyclodestructive procedures.
This differentiates it from glaucoma Below is a list of differential diagnoses: Angle-closure glaucoma. Prognosis Elevated IOP from steroid-induced glaucoma shares a similar prognosis to other types of glaucoma. Enhancing Healthcare Team Outcomes Steroids are widely prescribed by healthcare workers, including the nurse practitioner, physician assistant, and physicians.
Review Questions Access free multiple choice questions on this topic. Comment on this article. References 1. Steroid-induced glaucoma and childhood blindness. Br J Ophthalmol.
❾-50%}Prednisolone glaucoma.Corticosteroids and glaucoma risk
While steroids will have a minimal effect on the IOP of most patients, there is a small population that will develop a large increase in IOP. Providers should inform patients that already have glaucoma that the risk of IOP elevation and glaucoma progression with steroids is greater than the general population.
This workup should include baseline IOP measurements, followed by checking IOP after two weeks, then every 4 to 6 weeks for about three months, and then six-monthly if the initial response is ruled out.
Although steroid-induced glaucoma is a dangerous and potentially blinding condition, it is manageable by early detection and prompt initiation of anti-glaucoma treatment. Steroids are widely prescribed by healthcare workers, including the nurse practitioner, physician assistant, and physicians. One of the most dangerous side effects of these drugs is an elevated IOP. When treating glaucoma, the prognosis is good. This book is distributed under the terms of the Creative Commons Attribution 4.
Turn recording back on. Help Accessibility Careers. StatPearls [Internet]. Search term. Steroid Induced Glaucoma Kaberi B. Author Information Authors Kaberi B. Affiliations 1 King Faisal University. Continuing Education Activity Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions. Introduction Steroids are one of the most commonly prescribed drugs, used mainly in the treatment of various autoimmune and inflammatory conditions.
Etiology Steroid-induced glaucoma or ocular hypertension can occur after steroid use in susceptible individuals. Epidemiology Individuals who develop an increase in IOP following steroid use are referred to as "steroid responders".
Pathophysiology Steroid-induced glaucoma is considered to be a type of secondary open-angle glaucoma, caused by increased resistance to the outflow of aqueous at the level of the trabecular meshwork.
History and Physical Any form of steroid administration can cause glaucoma. Evaluation The history of the patient may give a clue to the underlying etiology of this condition. The agents which may be used include beta-blockers, alpha-2 agonists, and carbonic anhydrase inhibitors.
Beta-blockers are the first-line agents in this condition. Prostaglandin analogs are relatively contraindicated in cases of steroid-induced glaucoma following uveitis treatment. Laser trabeculoplasty- may be considered if medical management is unsuccessful, and there is a threat of impending optic nerve damage. It may also be considered in patients experiencing undesirable side effects with antiglaucoma drugs.
Surgical management- surgery is indicated in those patients who fail to respond to medical and laser therapies.
It may also be indicated in those patients who may be expected to have further exposure to steroids. The most commonly employed surgical procedure is trabeculectomy; other options include tube shunt surgeries or cyclodestructive procedures. This differentiates it from glaucoma Below is a list of differential diagnoses: Angle-closure glaucoma.
Prognosis Elevated IOP from steroid-induced glaucoma shares a similar prognosis to other types of glaucoma. Enhancing Healthcare Team Outcomes Steroids are widely prescribed by healthcare workers, including the nurse practitioner, physician assistant, and physicians. Review Questions Access free multiple choice questions on this topic. Comment on this article. References 1. Steroid-induced glaucoma and childhood blindness. Br J Ophthalmol. Corticosteroids and open-angle glaucoma in the elderly: a population-based cohort study.
Drugs Aging. Steroid-induced iatrogenic glaucoma. Ophthalmic Res. Prospective, long-term evaluation of steroid-induced glaucoma. Eye Lond. Case series of children with steroid-Induced glaucoma.
Malays Fam Physician. The effect of inhaled steroids on the intraocular pressure. Digit J Ophthalmol. Orv Hetil. J Curr Glaucoma Pract. Steroid-induced glaucoma in the pediatric population. Steroid Induced Glaucoma. In: StatPearls [Internet].
In this Page. Bulk Download. Related information. Similar articles in PubMed. Epub Aug 5. Do systemic steroids increase the risk of ocular complication in uveitis patients? Focus on a Italian referral center. Clin Rheumatol. Epub Jun 6. Ned Tijdschr Geneeskd. Steroid induced glaucoma and cataract. Mohan R, Muralidharan AR. Indian J Ophthalmol.
Review Steroid-induced glaucoma: Epidemiology, pathophysiology, and clinical management. Cushing's syndrome. Patients over 40 years of age and with certain systemic diseases e. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma racial origins, hypertension, migraine, vasospasm is likely but not fully established.
The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene.
Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners.
Corticosteroids glucocorticoidsused frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure IOP when administered exogenously topically, periocularly or systemically and in certain conditions of increased endogenous production e.
Cushing's syndrome. Patients over 40 years of age and with certain systemic diseases e. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma racial origins, hypertension, migraine, vasospasm is likely but not fully established.
The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene.
Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.
Abstract Corticosteroids glucocorticoidsused frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure IOP when administered exogenously topically, periocularly or systemically and in certain conditions of increased endogenous production e. Publication types Research Support, Non-U. Gov't Research Support, U. Gov't, P. Substances Glucocorticoids.
Any form of steroid administration can cause glaucoma. It may occur after administration of topical steroids for a relatively trivial. Corticosteroids (glucocorticoids), used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure. rise in intraocular pressure that can result from using ophthalmic steroids, A hallmark of steroid-induced glaucoma is deposition of. The side effects of corticosteroid use and the risk of increased IOP in glaucoma patients should not deter us from using corticosteroids. When. Any form of steroid administration can cause glaucoma. It may occur after administration of topical steroids for a relatively trivial. Gov't Research Support, U. Ophthalmic Res.Toggle navigation Leadership in clinical care. In jected steroid use has become more common for ODs. The management of ocular disease becomes far more complicated when the individual exhibits one or more concomitant conditions. This predicament is no more apparent than when a patient presents with significant inflammation in the presence of open-angle glaucoma.
We stress this fact so often that young practitioners are apprehensive about using corticosteroids effectively. When prescribed responsibly, corticosteroids continue to be a valuable component of our pharmaceutical armamentarium against inflammation in our glaucoma patients.
Basic Pharmacology of Corticosteroids Inflammation involves the activation and proliferation of many types of chemical messengers and immune cells, including cytokines, macrophages and prostaglandins. Corticosteroids penetrate cell membranes and bind to receptors in the cytoplasm, yielding a conformational change in the receptor and facilitating transportation of the receptor-steroid complex into the cell nucleus, where it binds to specific sequences on DNA.
Additionally, they reduce the expression of cyclooxygenase-2, which leads to a further decrease in prostaglandin synthesis. Tissue and metabolic changes, such as facial swelling, fat redistribution, increased hair growth, weight gain and muscle weakness, have all been shown in patients on long-term corticosteroid treatment. Other changes include hyperglycemia, glucose intolerance, high blood pressure and osteoporosis. Of greater interest to optometrists, however, is the potential for posterior subcapsular cataracts and increased IOP.
It has also been shown that corticosteroids may cause a reversible crosslinking of actin fibers within TM cells, further contributing to increased outflow resistance. Francois, MD, published the first case report on corticosteroid-induced glaucoma in Palmberg, MD, PhD, and associates documented that IOP increase secondary to corticosteroid dosing was consistent and repeatable on the same patient over different periods of time.
Weinreb, MD, and associates showed that the IOP response is significantly more rapid in patients with previously diagnosed glaucoma than in those with a normal IOP. Considering these study data, it appears that glaucoma patients on corticosteroid thrapy are much more likely to experience an IOP increase than the rest of our patients.
Thus, we must remain extremely cautious when choosing an anti-inflammatory therapy for these individuals. Numerous forms of conjunctivitis, as well as episcleritis, scleritis, anterior uveitis and other anterior segment diseases, respond well to topical therapy. Becker showed that topical corticosteroids produced an IOP response similar to that associated their systemic counterparts, and that the response also was greater in patients with glaucoma than in those with normal IOP measurements.
It should be no surprise that treatment with systemic corticosteroids increases IOP in some patients; however, it is somewhat unusual that the response often is less significant—or takes longer to manifest—than that seen in patients on topical therapy.
Subconjunctival preparations of corticosteroids have been made available for use in patients who do not respond well to topical treatments or those who are unable to apply topical medications i. Intraocular pressure response to injected steroids typically is lengthier and more pronounced than that caused by topical corticosteroid use.
So how, then, are we to manage external or internal ocular inflammation in this population? The key is to make responsible decisions in corticosteroid selection and then follow the patient diligently so that consequent IOP increase can managed properly. Corticosteroids differ in their ability to produce an IOP response. In general, the more potent the drug, the greater the hypertensive effect. Unfortunately, it has also been shown to produce a greater IOP response over a shorter period when compared to prednisolone.
The structural replacement of a ketone with an ester makes it possible for loteprednol to be metabolized by esterases—thus limiting the potential side effects of this medication. Then, if neither agent proves effective, I will switch to prednisolone or difluprednate—but only in doses small enough to produce a therapeutic effect.
A baseline measurement should be taken before therapy is initiated, as well as two to three weeks after. IOP should then be measured every three to four weeks while the corticosteroid therapy is ongoing. If your patient is undergoing intravitreal corticosteroid treatment, IOP should be monitored every two to three weeks for several months following the injection. In most instances, IOP returns to baseline within one to four weeks after treatment discontinuation. The IOP responds to treatment with most of our widely used topical anti-glaucoma medications, including beta-blockers, prostaglandin analogues, alpha agonists, carbonic anhydrase inhibitors and miotics.
Latanoprost has been shown to be effective in lowering IOP in patients with corticosteroid-induced glaucoma. Therefore, the prostaglandin analogues might not be the best first choice to add to a patient who is undergoing treatment for uveitis. The side effects of corticosteroid use and the risk of increased IOP in glaucoma patients should not deter us from using corticosteroids.
No matter which medication is selected, IOP must be monitored every few weeks while the patient remains on the medication or for a few months after intravitreal injection. Prudent use, not avoidance, is the key to effective treatment of inflammation in glaucoma patients.
Ensor is an assistant professor at the Southern College of Optometry in Memphis. He has no industry disclosures or direct financial interest in any of the products mentioned. Barnes PJ. How corticosteroids control inflammation: Quintiles prize lecture Br J Pharmacol.
New York: McGraw-Hill; Philadelphia: Elsevier; Corticosteroid-induced glaucoma: a review of the literature.
Eye Lond. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics: II. The effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol. Glucocorticoid-induced formation of cross-linked actin networks in cultured human traecular meshwork cells. Invest Ophthalmol Vis Sci. Francois J. Corticosteroid glaucoma. Ann Ophthalmol.
Becker B, Mills D. Corticosteroids and intraocular pressure. The reproducibility of the intraocular pressure response to dexamethasone. Am J Ophthalmol. Acute effects of dexamethasone on intraocular pressure in glaucoma. Dinning WJ. Steroids and the eye — indications and complications.
Postgrad Med J. Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol. Cubey RB. Glaucoma following the application of corticosteroid to the skin of the eyelids. Br J Dermatol. Inhaled and nasal glucocorticoids and the risks of ocular hypertension or open-angle glaucoma.
Bernstein H, Schwartz B. Effects of long-term systemic steroids on ocular pressure and tonographic values. Kalina RE. Increased intraocular pressure following subconjunctival corticosteroid administration. Intravitreal triamcinolone acetonide and intraocular pressure. Comparison of in vitro potency of corticosteroids with ability to raise intraocular pressure. Intraocular pressure elevation from topical difluprednate use.
Amon M, Busin M. Loteprednol etabonate ophthalmic suspension 0. Int Ophthalmol. Epub Jun Scherer W, Hauber F. Effect of latanoprost on intraocular pressure in steroid-induced glaucoma. J Glaucoma. Anterior uveitis as a side effect of topical brimonidine. Current Issue. All rights reserved. Reproduction in whole or in part without permission is prohibited.
Comments
Post a Comment