Steroids seem to be the ultimate "Radiator Stop Leak" for perifoveal capillaries. People initially went berserk when it became apparent that this drug could have a dramatic effect on reversing central cystic diabetic macular edema—something for which laser alone is often frustratingly ineffective. However, with time, it has become apparent that for many patients the initial positive response seems to gradually weaken, and the long-term results are less stunning. A recent study even suggested that laser is still better than triamcinolone alone for many patients.1 When you add in the inevitable cataract and risk of glaucoma, one begins to realize that this is not the miracle drug everyone at first thought it to be.
On the other hand, if used judiciously, it can be very effective in controlling central edema in selected patients.2 Unfortunately, there is no good way to figure out which patients will benefit the most, and there are no long-term controlled trials that provide specific guidelines. There is, therefore, absolutely no consensus about how this drug fits into the management of macular edema. If you are in a situation where triamcinolone is unavailable, then you have to work with lasers. If it is available, then you really need to talk to your local specialists about how they feel it fits in. You don't want to turn into some sort of renegade outlier from either overuse or underuse. The trick is to decide which patients seem to do best with the drug, and then hope that the risk of cataract and glaucoma does not offset any apparent gains.
It is agreed that mild macular edema, especially if it is away from the fovea, should simply be treated with laser. Once the edema starts to build up in the fovea, there is a sense that, somewhere, a clock begins to start ticking; it seems that leaving a lot of edema in the fovea for an extended period of time decreases the ultimate visual recovery. How much time is too much time? No one knows. Perhaps a reasonable guess is three to six months, but that is total speculation, so if you find someone who feels differently, please feel free to scratch out the above numbers and write in your own.
The point is that if you try a laser or two and there is persistent edema in the fovea, then you do not want to keep lasering and waiting and lasering and waiting. It is best to get the patient to someone who can do intravitreal therapy before there is more and more permanent microarchitectural damage. You also need to factor in the rate of change in terms of how fast you refer. If the fovea is mildly thickened and the vision is OK, then time is on your side. If the fovea is a bubbly mess with hard exudates streaming in like Leeroy Jenkins, then you should send the patient sooner (Figure 1). There is definitely a sense that the magic drugs work better on fresh edema than on old chronic disease.
Figure 1. This patient presented with central cystic macular edema and a vision of 20/400 in the right eye and 20/80 in the left eye. The worrisome thing about this case is that the hard exudates are just starting to build up into the fovea. You can see that the right fovea will soon be swamped, and the left fovea has a very scary "sugar dusting" of exudates that means that it will soon follow. This pattern does not tend to do well with laser alone, so it is not a good idea to put in some laser and wait three to four months to see what happens— permanent damage can occur. This is the kind of patient who will likely need intravitreal therapy, if available.
Here is an example of one approach: If there is fairly significant foveal thickening (say, greater than 300 microns on OCT testing), and if the vision is starting to deteriorate (say 20/30 to 20/40), you might consider intravitreal therapy in order to jumpstart the eye and get the edema reversed as you are adding the laser. (There is a sense that the laser creates long-term control once the intravitreal treatment has produced transient improvement.) Note, however, that these acuities are definitely not absolute. For instance, older, retired patients may not want to take the risk of intravitreal treatment until they are 20/80, whereas younger, wired types may want a full-court press to stay 20/20. If the patient does want an injection, some doctors feel it may be better to inject first and then do the laser a week or two later. This is because once the retina is thinner, it is easier to treat without getting the large burns caused by scattering of the laser beam through thickened retina. If you adopt this approach, you also want to be sure you remember where the pathology is. Once you flatten the retina with a drug, it can be hard to tell where you needed to treat.
The one thing you must never do is to give a patient an injection just because you can. Please do not be seduced by the intense immediate gratification that occurs when you bring your first patient back for a pressure check and the edema is gone (and the patient is actually happy and smiling at you like, well, a Lasik patient). This experience creates powerful positive reinforcement that is not really justified. The long-term reality of intravitreal therapy is never as good as your "first time." Try to remember that by using this medication you are embarking on a process that may end up being very frustrating for you and the patient as the edema keeps coming back and the vision slowly slips away (and the cataract gets worse, and then you have to do cataract surgery on an eye with a weepy macula and elevated pressure). Also, remember that the pressure can rise insidiously, and this may show up well after the drug should have worn off.3 If there is a concern about the pressure, it is reasonable to check the IOP periodically for perhaps a year or two after an injection. As a comprehensive ophthalmologist, this is particularly important to remember because your retina specialist may forget about this.
In many ways, the use of intravitreal triamcinolone involves a search for those patients who seem to gain long-term benefit from the treatment. If you or your retina specialist tries the drug and the fovea dries up, but the vision doesn't improve, then such a patient is not an ideal candidate for continued therapy (especially if the pressure goes up). If the vision improves and the effect seems to be
By the way, although this chapter emphasizes the side effects that are particular to each drug, don't forget that the patient also has to accept the risks of the intravitreal injection itself. These risks include infection, sterile uveitis, vitreous hemorrhage, retinal detachment, and some really embarrassing things like intralenticular injection, suprachoroidal injection and wound rupture (i.e., if the patient had recent cataract surgery, corneal transplant or a thin filtering bleb). Although these complications are unlikely, the risk can add up since most patients need multiple treatments. As a wise retinal specialist once put it: "These aren't flu shots we're giving here."
long-lasting, then such a patient may benefit greatly from intermittent injections combined with appropriate laser. If the results are somewhere in between—as is usually the case—then it comes down to the patient's wishes versus your sense of the long-term risk of chronic intravitreal steroid treatment.
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