||So today we're going to be talking about hypertension and especially as it relates to neuro-ophthalmology and optic property. As you know the staging system dates back decades, and we basically have four stages of hypertensive retinopathy. Stage one is "arteriolar narrowing", and that occurs because chronic hypertension leads to thickening of the wall in response to the high pressure, and so because we see the lumen of the red cell column and not actually the blood vessel itself, it looks narrow, but really it's narrow because it's thickened, and that's arterial sclerosis and hyalinization of the wall. The second stage is "AV nicking", and because of that arteriolar thickening at the crossing point where the vein and the artery cross, the vein will appear to be nicked because the vein is collapsible, and so when the arteriolar caliber increases, it presses on the vein on that location, and that's important because that's how hypertension and arterial disease can cause venous side disease like a central vein occlusion. So the most common causes of central retinal vein occlusion is actually hypertension even though hypertension is an arterial side disease. The artery thickens presses on the vein and leads to the vein occlusion at the shared common adventitial sheath of the artery of the vein. So those are the retina kind of findings, and that's not really neuropathy. Once you start getting to grade three hypertensive retinopathy, that is evidence of end organ dysfunction. But the end organ dysfunction is the brain, so it is the retina but not the photoreceptors and the retinal pigment epithelium. The nerve fiber layer and the optic nerve, these are the two that determine that we have hypertensive retinopathy of a sufficient grade to count as an organ dysfunction, and that is what defines hypertensive emergency and differentiates hypertensive urgency. So if we have grades one or two hypertensive retinopathy and our blood pressure is markedly elevated, that is the hypertensive urgency but does not require hospitalization. But once you start to get the grade three or grade four, and this is defined by the hemorrhages, the exudate, and the cotton wool patches, and then once you start to see swelling of the disc, optic disc edema, this is great for hypertensive retinopathy. So grade four is the disc edema, grade three is the bad retinopathy, and the line for admission between urgency and emergency is grade three/four. So an ophthalmologist needs to be able to look at the fundus in a patient whose blood pressure is high and determine what grade are we dealing with, and if you're in the grade four hypertensive retinopathy, you still have to work that up for the other causes of bilateral disc edema including papilledema. So this person is going to get the standard workup MRI plus contrast MR venogram, and we probably would include the orbit with fat suppression views to make sure there's no enhancement of the optic nerve. We're gonna ask the medicine service to admit the patient to the hospital, and we're gonna follow the current hypertensive guidelines on the slow reduction in the blood pressure over the first eight hours the first twenty-four hours, and normally we would not want to reduce more than twenty-five percent in that time period, and that means a titratable agent has to be used with a short half-life, in our hospital that's usually intravenous labetalol. But an ophthalmologist really doesn't need to know that. What you need to know is admit to the hospital hypertensive retinopathy grade three or grade four. We're gonna do an MRI. We're gonna check the lumbar puncture and make sure that it's not elevated intracranial pressure, but if it's negative then we're back to elevated intravascular pressure, the blood pressure, and not the ICP, the intracranial pressure, is the cause for the bilateral disc edema. In addition, chronic hypertension leads to the development of ischemic events, and that can be both in the anterior visual pathway, the posterior pathway, or on the efferent side, and so when we have hypertension, that's a risk factor for garden-variety conditions like non-arteritic anterior ischemic optic neuropathy, which produces optic disc edema in only one eye. So in grade four hypertensive retinopathy, we have to have the disc edema in both eyes. So if you just have one eye it's more likely to be NAION. We do not admit that to the hospital. We treat that as an outpatient. However if they have other evidence of end organ dysfunction, you would admit that, and that's also not your job. That's the heart and the kidney. So the three organs that we're assessing are brain, kidney, and heart. Brain is gonna be like transient ischemic attack, hemispheric TIA, stroke. Heart is gonna be like CHF, myocardial infarction, and kidney obviously is acute kidney dysfunction. So for hypertension in the posterior visual pathway, we're gonna be talking about homonymous hemianopsias and cortical visual impairment. Sometimes they have bilateral vision loss from cortical impairment from hypertension, and that's a whole different topic called PRES, and you can watch the video on that. That's a posterior reversible encephalopathy syndrome from vasogenic edema secondary to acute hypertension, and on the efferent side it can produce ischemic cranial neuropathies third, fourth and sixth, INOs, etc. So in summary, an ophthalmologist needs to measure the blood pressure, determine the grade of hypertension, determine whether we are grade three or four that is hypertensive emergency because it's an organ dysfunction. You need to be assessing the heart, kidney, and the brain at the same time, and any evidence of end organ dysfunction means admission. We're going to lower the blood pressure slowly with a titratable short half-life agent. We're still gonna work up the optic disc edema for the other causes because hypertensive grade four retinopathy optic disc edema in this setting is a diagnosis of exclusion, and you're going to think about the ischemic lesions both in the afferent and the efferent pathway anterior and posterior.