| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (WX) Class of 2024, Baylor College of Medicine, Houston, Texas |
| Transcript |
We're going to be talking a little bit about anemic retinopathy and the reason you need to know about this is because sometimes we're called for vision loss and it's not clear what the etiology is. And this can come to us either from an optic nerve standpoint or a retinal standpoint. So from an optic nerve standpoint versus retina, normally we can just look in the back of the eye and see what the problem is. In the optic neuropathy side, because the red blood cell is the cell carrying the oxygen, the most common optic neuropathy that we see is actually non-arteritic anterior ischemic optic neuropathy (NAION). Obviously in older patients you still have to worry about arteritic anterior ischemic optic neuropathy (A-AION).However in patients who are anemic you really have to correct the hematocrit before doing a sedimentation rate(ESR)and that correction formula we've talked about in a different video, and that is the Fabry equation. You should look that up. Otherwise, you end up biopsing a lot of these anemic retinopathies who have NAION when their sedimentation rate is really elevated just because they're anemic. The other problem with anemic retinopathy is it can be either primary or secondary, and so the most common anemia is that we see our iron deficiency anemia, but it can occur after blood loss or trauma or surgical procedures, and that ischemia is also an NAION. And the most common NAIONs that we see after surgical procedures are spine surgery and cardiac surgery and so it's important that those patients' hematocrit be maintained if possible, and that they be warned about the risk of the transfusion or have autologous blood ready. There are other risk factors in post-surgical NAION other than anemia but that's a treatable risk factor. We can get their iron up. We can give them erythropoietin. We can have autologous blood ready and also we can have a lower threshold for transfusing those patients, especially for spine surgery where the patients aren't really told usually that they could lose their vision, because the surgical field is very far away from the eye. The secondary anemias can occur from malignancy and the ones that you have to be very careful about is if the patient has leukemia. So in patients, for example, who have leukemia whether that's an acute form or a chronic form, whether it's the myeloid form or the lymphoblastic form. These types of leukemias cause shutdown in the bone marrow. So if you're making 283 thousand white cells, well you're really not going to have much bone marrow left to work on the platelets and the red cells. And so anemic retinopathy in the setting of leukemia can be confusing because you're trying to figure out, oh is this an optic nerve infiltrative process or sometimes this leukemia can become a lymphoma which is the Richter's transformation into diffuse large B-cell lymphoma. So it's kind of a high-stakes thing here that we have to first decide is it retina or optic nerve? And if it's optic nerve is it ischemic or is it infiltrative leukemic disease or compressive lesion from the Richter transformation lymphoma? So it's really critically important that we do a dilated fundus examination in every patient who has vision loss who has anemic retinopathy and leukemia because we would not radiate anemic retinopathy, but we're going to radiate leukemic infiltration of the Richter transformation. And the key and differentiating feature of the retinal anemic retinopathyis that the hemorrhages are different sizes, different locations, multifocal, four-quadrant, and different layers of the retina. So normally when we see retinal hemorrhages, the different pathogenesis of the hemorrhage tells us what layer we're in. So for example, if we're in the nerve fiber layer that produces a flame hemorrhage, and it looks like a flame to you because you're looking at it like this, and that's gonna run in the nerve fiber layer and so things that happen in the nerve fiber layer cause flame-shaped hemorrhages, like central retinal vein occlusions because the arteries in the vein is right under that layer, versus intra-retinal hemorrhages which are orientated like this. And so they look like to you as dots and blots of hemorrhages, even though the hemorrhage is actually accumulating between the cellular elements of the retina. So on face even though it really is this, what you see is the top of the column so you see a dot or a block of hemorrhage. These are intraretinal hemorrhages and the most common cause of that is a diabetic retinopathy because this is small vessel disease. So hypertension and vein occlusions are in the nerve fiber layer of flame hemorrhages and then we've got these intraretinal hemorrhages for diabetes. And then you've got hemorrhages that are under the retinal pigment epithelium or subretinal and then we've got hemorrhages that are preretinal. So the key and differentiating features in anemic retinopathy causing the vision loss is multi-focal hemorrhages, four quadrants, and in different levels. So I've got a preretinal hemorrhage, a subhyaloid hemorrhage, a flame shape hemorrhage, and intracranial hemorrhage and a subretinal hemorrhage. That tells us that the problem is not the blood vessel per se, but the blood itself. And so the combination of a very low hematocrit and thrombocytopenia can lead to a retinopathy which we call anemic retinopathy and sometimes those hemorrhages have white centers in them which we call the Roth spot. So the presence of the multifocal, four-quadrant, different level hemorrhages in a patient with leukemia should make you suspicious of anemic retinopathy more than leukemic infiltration retinopathy and steer you away from infectious inflammatory or infiltrative optic neuropathies. |
