Other Indications

There are some other indications for vitrectomy besides a non-clearing vitreous hemorrhage, and most of these are fairly obvious. For instance, referral is mandatory if the patient appears to be developing progressive traction that is threatening the macula, or if the macula has just been yanked off. Sometimes, however, making this call is not as easy as one would think. The traction can build up very slowly, often simulating refractory macular edema as the retina is slowly thickened—like a peanut butter and jelly sandwich being pulled open. If you are not sure about the stability based on your clinical exam, an OCT can be very helpful assuming care is taken to maintain uniform fixation between tests.

Don't depend entirely on technology, though. You can always resort to ancient and primitive methods, such as actually talking to the patient about their symptoms. Slowly progressive traction can cause metamorphopsia or changes in peripheral vision that patients can detect, and you should take complaints along these lines very seriously, even if you cannot see any clinically apparent changes. Sometimes it helps to provide patients with an Amsler grid to help them monitor for progression. If there is any doubt, a referral is in order. This is because the results of surgery in this situation tend to be much better if the problem is fixed before the fovea pops off. (Of course, your retina person then has to weigh the risks of doing surgery that may snuff out vision versus losing vision from conservative observation — but that is why he or she did a fellowship in the first place.)

On the other hand, sometimes ominous-looking traction can be quite stable. In fact, the majority of patients with localized areas of traction do not progress. At times the retina can even look like a campground full of hammocks and pup-tents, yet the patient never needs surgery. A very creepy pattern can occasionally develop because many so-called diabetic traction retinal detachments are, in fact, areas of tractional retinoschisis—there is still an outer layer of retina stuck to the RPE. These eyes can sometimes get nasty-looking inner-layer holes that resemble Swiss cheese draped over clotheslines, leaving one wondering how on earth the retina is remaining attached at all. (It remains in place, of course, because there are no true full-thickness holes.) Monitoring, and especially lasering, eyes filled with traction can be a bit nuanced and usually such eyes are referred to specialists until they are known to be stable. If you are watching eyes like this, make sure the patients know when to call.

Retinas can become so atrophic, however, that they do develop full-thickness holes, and then patients get a rhegmatogenous detachment in addition to any traction that is present. The rather dramatic downturn in their vision and the floppy, bulbous appearance of the retina usually make the need for referral obvious. Putting an atrophic, lasered-out retina back on the RPE and getting it to stay there can be difficult, to say the least, and the visual outcomes—although better than nothing — do not tend to be great. Please don't pat such a patient on the back and say that they will be as good as new after surgery.

Another indication for vitrectomy is the presence of progressive rubeosis in the setting of a vitreous hemorrhage that precludes laser treatment. In the old days, people would try to put in panretinal cryotherapy without visualizing the retina, trying to kill off enough retina to stop the neovascularization and give the eye a chance to clear the hemorrhage. This approach may still be used if a patient is too sick for surgery or if you do not have access to a vitreoretinal specialist. If there is a chance of useful vision being obtained from the eye, however, it is best to do a vitrectomy rather than "blind" cryotherapy; cryo can really stir up pain, inflammation and scarring, and is more of a last-resort approach. Intravitreal anti-VEGF treatment can be invaluable in this situation, as well. Basically, patients who have progressive anterior segment neovascularization and a vitreous hemorrhage should receive a prompt referral.

Another less common reason for performing a vitrectomy is elevated intraocular pressure secondary to the presence of vitreous blood coming into the anterior chamber and clogging up the trabecular meshwork. This process can actually occur in three ways:

1. Fresh erythrocytes accumulating in the meshwork.

2. Hemolytic glaucoma, wherein hemosiderin-filled macrophages obstruct the meshwork.

3. Ghost cell glaucoma, wherein erythrocytes lose their hemoglobin and block the meshwork because they are less pliable than normal erythrocytes. Such cells are khaki-colored and are usually seen with old, yellowish vitreous blood.

Whatever the pathology, the pressure can get quite high, and if it does not respond to medical management a vitrectomy is required to wash the eye out.

There is another group of patients that would likely benefit from early referral: the ones who respond poorly to PRP—even if a hemorrhage has not yet occurred. These tend to be younger Type 1 diabetics with a history of non-compliance, and it is hard to specify the exact level of disease that merits referral. Like the line about knowing the difference between art and pornography, however, you will recognize such patients when you see them. Anytime vascular fronds fail to respond to a solid PRP, you can assume you are dealing with an eye that is hellbent on destroying itself and you generally do not want your name to be the last one on the chart.

One option for these patients is to keep hammering in laser from the arcade to the ora, but this may just destroy peripheral visual field without controlling the problem—recall that the vessels are locked onto the vitreous and supping on the vasoproliferative substances that reside there because the eye is diffusely ischemic. The decision whether to operate on such patients is complicated; they tend to have relatively preserved vision, and the risks are not small. The point is that if your laser is not slowing down the growth of new vessels, it is better to get an early consult than to wait for multiple lasers to not work and then refer in a patient with big vessels, traction detachments and a totally atrophic peripheral retina, all of which carry a more guarded prognosis with surgery.

Refractory macular edema due to traction is another indication that may respond to a vitrectomy. Obvious cases usually have an epiretinal membrane that is gently tugging on the fovea and keeping the retina swollen. Sometimes the cortical vitreous can remain diffusely attached to the entire posterior pole, causing edema as it contracts without the presence of a distinct epiretinal membrane. This can sometimes appear as glistening sheen on the surface of the retina. OCT has really helped to identify situations where traction is contributing to the edema—this is also discussed in Chapter 10.

Figure 1. OCT

demonstrating very subtle traction contributing to cystoid macular edema.

Figure 1. OCT

demonstrating very subtle traction contributing to cystoid macular edema.

The role of vitrectomy for macular edema is less defined if there is no obvious epiretinal membrane or vitreous traction. There does not seem to be a lot of evidence that performing a vitrectomy in this setting is consistently effective, although there may be some patients who benefit from it. Studies are under way to try to define the role of vitrectomy in this situation, so hopefully there will be specific guidelines soon.

However, given all the potential treatments—including intravitreal therapy— anyone with bad macular edema should be referred whether it is for a vitrectomy or not. Remember that you can make two people happy with cataract surgery in the time it takes to explain treatments for refractory macular edema to one patient. Your unfixable problem is the retina person's reason for being, and retina specialists actually like doing it.

A more obscure reason to consider vitrectomy is the presence of vitreopapil-lary traction.1 Sometimes the vitreous can be freed from the posterior pole but can still exert traction at the nerve. This is a fairly common configuration; many diabetics with burned-out proliferative disease will have sclerotic vascular fronds that emanate from the nerve and are tugged up into the vitreous. Occasionally, there is actually enough traction that the nerve fiber layer is slowly choked and vision is lost. These patients have progressive visual field defects and worsening central vision without any obvious cause such as a hemorrhage or direct foveal traction. This problem is relatively uncommon, but it should at least be kept in mind when treating patients who have a lot of traction yanking on the nerve.

Figure 2. Schematic drawing of how traction at the nerve can damage the axons. Not a very common cause at all, but a good reminder of all the ways things can go wrong inside an eye. (Kroll P, Wiegand W, Schmidt J. Vitreopapiiiary traction in proliferative diabetic vitreoretinopathy. Br J Ophthalmol 1999;83:261-4.)

Figure 2. Schematic drawing of how traction at the nerve can damage the axons. Not a very common cause at all, but a good reminder of all the ways things can go wrong inside an eye. (Kroll P, Wiegand W, Schmidt J. Vitreopapiiiary traction in proliferative diabetic vitreoretinopathy. Br J Ophthalmol 1999;83:261-4.)

Finally, when it comes to performing a vitrectomy, whether for proliferative disease or macular edema, the path taken by the patient's fellow eye may help decide the issue. For instance, one would be much more inclined to do a vitrectomy if the fellow eye developed vision loss because a vitrectomy was not done soon enough. Conversely, a failed vitrectomy in one eye will make a patient very reluctant to have any surgery in the remaining eye—although this is usually the retina specialist's problem and not yours. Your job is to get the patient's disease as controlled as you can, and if things are not looking good then get them to a retina specialist at the appropriate time, and ideally a bit sooner, so that surgery can be considered when it can do the most good.

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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