Ocular Allergy Medicine Profile

BRAND NAME	GENERIC NAME	MANUFACTURER	PEDIATRIC USE	BOTTLE SIZE(S)	DOSING
Acute Care Products
Acular LS	ketorolac tromethamine 0.4%	Allergan	> 3 years	5ml	q.i.d.
Alrex	loteprednol etabonate 0.2%	Bausch & Lomb	> 12 years	5ml, 10ml	q.i.d.
Elestat	epinastine HCI 0.05%	Allergan	> 3 years	5ml	b.i.d.
Emadine	emedastine difumarate 0.05%	Alcon	> 3 years	5ml	q.i.d.
Livostin	levocabastine hydrochloride 0.05%	Novartis	> 12 years	5ml, 10ml	q.i.d.
Optivar	azelastine hydrochloride 0.05%	Bausch & Lomb	> 3 years	3ml, 6ml	b.i.d.
Patanol	olopatadine hydrochloride 0.1% & 0.2%	Alcon	> 3 years	5ml	b.i.d./q.d.
Zaditor	ketotifen fumarate 0.025%	Novartis	> 3 years	5ml	b.i.d.
Chronic Care Products*
Alamast	pemirolast potassium 0.1%	Vistakon	> 3 years	10ml	q.i.d./b.i.d.
Alocril	nedocromil sodium 2%	Allergan	> 3 years	5ml	b.i.d.
Alomide	lodoxamide tromethamine 0.1%	Bausch & Lomb	> 2 years	10ml	q.i.d.
Crolom	cromolyn sodium 4%	Bausch & Lomb	> 4 years	10ml	q.i.d.
Opticrom	cromolyn sodium 4%	Allergan	> 4 years	10ml	q.i.d.
*Any eye drop instilled onto an "itchy-burny" eye will give some immediate relief of symptoms, however the full measure of mast cell stabilization does not occur for a few days.

 

 

Use steroids with caution when there is a significant corneal epithelial defect. In most cases, you want to achieve re-epithelialization prior to adding a steroid, if in fact one is needed. An exception to this rule is when there is significant underlying stromal inflammation that can impede epithelial healing. For example, it's common to see corneal stromal infiltration where the overlying epithelium is secondarily broken down and stains with fluorescein.

Conventional teaching says not to use a steroid. A better approach, however, calls for combination therapy such as TobraDex. The dexamethasone will suppress the cell-mediated inflammatory response, commonly a result of corneal hypoxia, while the tobramycin prophylaxes againstopportunistic bacterial infection. Only when the underlying stromal inflammation is controlled can epithelial integrity be restored in many cases.

This underscores an important clinical observation: It's often impossible for the epithelium to remain intact if the underlying stroma is sufficiently inflamed. In these cases a steroid must be instituted in order to facilitate corneal re-epithelialization, an approach which runs counter to what many of us have been taught.

In most cases of nodular episcleritis, the conjunctival epithelium overlying the inflammatory nodule is compromised to such a degree as to give positive fluorescein staining. Just as with corneal tissue, if there is sufficient episcleral inflammation present,overlying conjunctival epithelial function can be compromised, i.e. epithelial breakdown. How are these tissues restored to normal? By suppressing the inflammatory condition with a potent topical corticosteroid. Furthermore, for nodular episcleritis, we simply use a pure steroid, not a combination antibiotic-steroid. Were there a risk of opportunistic bacteria infection, the expert textbooks would recommend use of a combination drug; they don't, so we don't. Having been privileged to collectively treat hundreds of patients with episcleritis, we have found the textbooks to be true.

In rare circumstances, even following good anti-inflammatory therapy, an epithelial defect may linger. This could represent a local toxic effect to one of the components in the drug(s) being used, or its preservatives. In these circumstances, there can often be seen an increase in punctate epithelial staining. Solution: Reduce frequency of instillations, or stop the drug(s) if deemed clinically appropriate, and lubricate aggressively with a preservative-free artificial tear solution for several days.

 

 

 

Many clinicians retain an disproportionate concern about secondary increased IOP with steroid usage. A study of known steroid responders nicely addresses this issue.

In this study, a group of steroid responders was treated with four different steroids: rimexolone, fluorometholone, dexamethasone and prednisolone.1 The results showed that IOP didn't start to rise until after three weeks of treatment with prednisolone and dexamethasone, and five weeks with the relatively IOP-sparing rimexolone and fluorometholone.

The beauty of these findings is that in the worst of scenarios, there is about a three-week window of relative safety when treating with a topical ophthalmic corticosteroid. The great majority of inflammatory eye disorders are controlled well within this time frame, which explains why IOP increases are not a substantial concern in the medical management of eye disorders.

Interestingly, topical steroids may in some cases actually help lower IOP. When a patient presents with severe inflammation and concurrent increased intraocular pressure—indicating that inflammatory debris or trabecular inflammation itself has retarded aqueous outflow—steroids suppress the trabeculitis and the inflammation. This in turn helps reestablish normal outflow facility and reduces IOP. Examples of this are glaucomatocyclitic crisis and post-zoster uveitis.

Traditional thinking holds that increased IOP is a major pitfall in steroid therapy. This, plus a fear of causing posterior subcapsular cataracts, makes many clinicians gun-shy when it comes to prescribing topical steroids.

The truth is that these side effects are extremely rare when steroids are used short term—that is, three weeks or less. If longer suppressive therapy is needed, then consider a relative IOP-sparing steroid such as loteprednol 0.5%. Steroids are extremely useful in managing most acute eye presentations, and are by far the most common acute care drugs we prescribe.
1. Leibowitz HM, Bartlett JD, Rich R, McQuirter H, Stewart R, Assil K. Intraocular pressure-raising potential of 1.0% rimexolone in patients responding to corticosteroids. Arch Ophthalmol 1996 Aug;114(8):933-7.

 

 

When prescribing topical steroids, choose the drug, dosage and frequency of administration based on the severity of the inflammation. Acute inflammatory conditions, most notably anterior chamber inflammatory reactions, are best managed aggressively (one drop every waking hour) until the inflammation is under control.

 

Don't automatically fall into the four-times-a-day routine, since in most cases this can leave the condition undertreated. As with any treatment, tailor the dosage to the specific presentation at hand.

Accurate diagnosis is crucial before prescribing any drug, but it's particularly important with steroids. There are three instances in which we would NOT consider using steroids by themselves, although it may be appropriate to use a steroid-antibiotic combination:

1. Avoid steroids when treating an acute bacterial or fungal infection, mainly because steroids do not possess antimicrobial properties. Steroids can also mask the infection, making the eye look white and feel better but doing nothing to address the underlying infection. An exception is a case where there is concurrent secondary inflammation. Here, a combination product like TobraDex will eradicate the bacteria and concurrently quiet the inflammatory expression.
   
   
2. Steroids are contraindicated when there is a significant corneal epithelial defect. The corneal epithelium is a critical barrier to bacterial invasion, so it's usually best to wait until the epithelium is intact before starting steroid therapy. Steroids may initially mute epithelial healing and invite secondary bacterial infection. An exception to this rule is when there is significant inflammation of the epithelial or stromal tissues. Then, use of a combination antibiotic/steroid drug may be helpful—perhaps even essential—in achieving tissue healing.
   
   
3. Steroids are contraindicated when you're unsure of the diagnosis. Since some inflammatory conditions are "non-specific," it's better to prescribe a steroid-antibiotic combination in these cases. If the slit lamp picture defies precise diagnosis—and you've ruled out herpes simplex keratitis, bacterial infection or a large epithelial defect—it's generally OK to treat with a steroid. In such cases, use a combination drug such as TobraDex.

One of the greatest problems we see among doctors is undertreatment with steroids. Remember, your goal is to restore normal tissue integrity as quickly as possible. Use steroids aggressively for the first few days until the inflammation is brought under control. Then, and only then, should you begin the tapering process. High doses of steroids over a short term of several days are almost always safe and effective. It is generally in protracted care (beyond three to four weeks of intensive therapy) where the risk of complications increases.

If steroids are used for a week or less, it is not absolutely necessary to taper them. But in general, when we prescribe steroids, we will taper them even if used for less than a week. After a few weeks of therapy (which is rarely indicated), tapering gives the body time to adjust its mechanism for producing the natural steroids hydrocortisone and corticosterone.

Tapering also avoids the inflammatory rebound effect that can result when you discontinue steroids abruptly. A good rule of thumb is to taper the dosage frequency by half for each given time interval once the inflammation is controlled. For example: q1h for 2 days , qid for 3 days, bid for 3 days.

Be especially aggressive when treating iritis. For a moderate to severe iridocyclitis, for example, initiate Pred Forte 1%, one drop q1h usually for 2 to 5 days or until the anterior chamber reaction is well controlled, then start the tapering process.

While treating a patient with steroids, it's also important to monitor the intraocular pressure for the rare side effect of ocular hypertension. The truth is that side effects are extremely uncommon when steroids are used short term, for two weeks or less. Fortunately, almost all primary care conditions respond in less than two weeks, and often less than one. Also, bear in mind that post-PRK patients may use steroids for one to three or more months with no reported steroid-induced side effects.

In general, any time a patient uses a steroid for more than a week or two, be sure to monitor the IOP frequently. Pressure increase is due to decreased outflow through the trabecular meshwork. If the pressure is high enough long enough, optic nerve head damage can develop. However, it is also important to remember that healthy optic nerves can endure pressures into the high 20s or low 30s for a few weeks without any measurable damage to structure or function.

If IOP does rise to a level of concern during the course of therapy, there are three easy approaches:

1. If inflammation is under control and the tapering process has begun, the IOP will usually self-limit as less steroid is instilled. In most cases, proper tapering is all that is required.
   
   
2. If inflammation is improving, yet requires therapy for several more days, switch to loteprednol etabonate 0.5% for the remainder of the therapy.
   
   
3. Add a glaucoma drug such as a beta-blocker, an alpha adrenergic agonist or topical CAI until the IOP level is acceptable.