| Transcript |
So we are going to be talking about what we're doing for hypercoagulable state workups in ophthalmology. Obviously, we're not going to cover the whole thing, but you should be thinking about hypercoagulable states in young patients or older patients who have no vasculopathic risk factors, who present with an ischemic event and, so for us, in neuro-ophthalmology, that's going to be a central retinal artery occlusion or a branch retinal artery occlusion in someone who has no hypertension or risk factor. It can also be on the venous side, that's recurrent or bilateral central retinal vein occlusion or branch retinal vein occlusion, that's on the venous side, or if you have a patient who has a homonymous hemianopsia or cortical visual impairment from stroke in the young, that's also going to be a person who's going to get the stroke workup, but part of that stroke workup is thinking about the hypercoagulable state including the hypercoagulable state of malignancy. So, when we're dealing with these stroke syndromes in the eye, and another one that you need to know is cerebral venous sinus thrombosis. So, we have a sagittal sinus thrombosis or a transverse sinus thrombosis, that's going to present with papilledema, and it might even look like IIH, that's another one of these worrying about hypercoagulable states. So, in the hypercoagulable state workup for ophthalmology, we'd like to chunk this, so that each section has a list of its own, so that you don't have to memorize the whole list, you can just memorize parts of the lists. So, we've got three kind of genetic things that we have to worry about, of course the most common inherited hypercoagulable problem is the factor V Leiden mutation, but the one that's paired with this is the prothrombin mutation, which is at position 20210,which is A to G substitution there. These two are probably the most common genetic mutations that we're thinking about in the hypercoagulable state. There's also abnormalities in the methylene tetrahydrofolate reductase gene, which is involved in the conversion of homocysteine to methionine, and that is of course a folate dependent pathway because the methylene donor is from the dihydrofolate to tetrahydrofolate, and that enzyme is methylene tetrahydrofolate reductase. We also have the deficiency states. There happens to be three of those as well, and so in the coagulation pathway that you memorize, the both the external, internal, meeting at a common pathway, the V, and then V,X, to II, that is the normal coagulation pathway, but deficiency states of the break-it pathway, protein C, protein Sand antithrombin III, if you have low numbers of these things, that can lead to the hypercoagulable state. And then we've got too much factors. The factor that we worry about is factor VIII, all the other factors we're really not worried as much about those factors because they usually cause hemophilia, not the hypercoagulable state. So, if you've got too much factor VIII, but all the other components of the blood have to be looked at as well, because it can be hypercoagulable from too much of stuff. So, if you have too many red cells, that's going to cause polycythemia, that's going to be a hyper-viscous state that could cause hypercoagulability. If you have too many white cells, that's leukocytosis, but usually it's going to require leukemia, one of the leukemias, or you could have too many platelets, or abnormal platelets, that's going to be thrombocytosis or essential thrombocytosis, which is the mildest plastic version of it. You could have too much protein, and that's why we're going to do the serum protein electrophoresis, we're going to be thinking about cryoglobulinemia, Waldenstrom's macroglobulinemia, monoclonal gammopathy, some various significance or not significant, and antibodies, and the antibody that we're thinking about here is antiphospholipid antibody, part of the anti-cardiolipin antiphospholipid syndrome, for which we are going to do the functional assays, and in our hospital we are using the dilute vessel venom viper time, but lupus anticoagulant, PT/PTT, the normal kind of functional assays, as well as the IgG and IgM for antiphospholipid antibodies and the anti-glycoprotein to be. And in those patients with the antiphospholipid syndrome, we have to ask females about spontaneous miscarriages and preeclampsia, eclampsia, and which week did they lose the fetus. So, those are additional GYN criteria for making the diagnosis antiphospholipid antibodies in there. So, you should bethinking about these hypercoagulable things in our stroke patients in the eye, when patients have recurrent thromboses elsewhere, like repeated deep venous thrombosis or pulmonary embolus, especially unprovoked thrombosis, where there's no real reason why they had a thrombosis. The other things that you have to think about in young people are the hypercoagulable state of malignancy, and also birth control pills in females. So, you should be thinking about doing a hypercoagulable workup in patients who have stroke in the eye, or stroke in the brain, but a stroke in the young, in patients that have what looks like pseudotumor cerebri, but it's really from a venous sinus thrombosis. You should bethinking about the genetic things, the deficiency states, and the excess states in the hypercoagulable state workup |
