||Andrew G. Lee, MD, Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, TX; Professor of Ophthalmology, Weill Cornell Medicine; Anirudh Mukhopadhyay, Baylor College of Medicine Class of 2023
||A traumatic optic neuropathy is an optic neuropathy due to trauma. The most common trauma is forehead indirect trauma. And the reason that's the trauma that causes traumatic optic neuropathy is the eyeball is inside the orbit and the orbit is shaped like a triangle on its side and that's because the orbit is shaped like a cone of bone. That cone of bone is meant to protect the globe. But if the blow is indirect like in your forehead here, the force wave will be transmitted by this little ice cream cone right down to the canal. So, the optic nerve and the optic canal. In that bony canal, a little bit of edema will cause a lot of vision loss because a little bit of swelling in this compartment will cause a compartment syndrome leading to vision loss. So the key in differentiating features of a traumatic optic neuropathy are the history that's compatible with a forehead indirect injury (like a motor vehicle accident or you flipped over your bicycle and hit your head on your forehead or you were struck in the forehead by somebody with an assault case) the force wave is transmitted to the canal and so you get decreased visual acuity (and it can be any degree visual acuity loss, sometimes no light perception), a visual field defect that is typically an optic nerve type pattern argue (arcuate, central scotoma). Something like that. And we're going to have of course have a relative afferent pupillary defect if it's unilateral or if it's bilateral but asymmetric and usually these are unilateral cases. And the fundus is usually normal because it's a retrobulbar optic neuropathy but sometimes there's swelling of the optic disk (but usually the fundus is fine). So, if we have a trauma case with loss of acuity and RAPD and a normal fundus that's kind of the prototype for the diagnosis of traumatic optic neuropathy. And so, in the right clinical setting where we can do a CAT scan. CAT scans are better for bone, for fracture and will help us look for things that are surgical like Sheep hematoma, fracture in the canal, or there's a bone fragment poking the optic nerve, we would consider doing surgery for that. And if there's no lesion seen you could do an MRI scan, but the yield is low and most of the time CT is good enough in these trauma cases and then you have to decide on what treatment are going to give. Today, there's no evidence-based treatment that works for traumatic optic neuropathy. So, you really could do nothing, and there's plenty of cases where spontaneous improvement occurs in traumatic optic neuropathy, or you can give steroids and the dose, the route, and the duration have never been proven in a randomized trial to show any benefits. So, it's really up to you whether you want to give intravenous or oral, whether you want to get high dose or medium dose or low dose or industrial strength dose. Whatever dose you want to give. There initially was some evidence that very high doses of methylprednisolone might be helpful and that was extrapolated from the spinal cord injury studies, but those studies were not designed for traumatic optic neuropathy and had to be given within 8 hours of the injury. So, a lot of things about the spinal cord steroid trial remain unknown and international optic nerve trauma trial was started, but it couldn't recruit enough patients and so it converted into an observational study and what that study basically showed is the route, the dose, the duration, and the type of steroid that you choose made no difference in traumatic optic neuropathy. And so today there is no evidence-based recommendation that I can give to you about the treatment of traumatic optic neuropathy.I will tell you one last thing though, which is CRASH which is the corticosteroid randomization after significant head injury study. In the crash study, the study was looking at whether steroids would help head injury patients. And in CRASH what they found was not only did steroids not help, you were more likely to die if you receive corticosteroids in the CRASH study, especially if your Glasgow Coma score was 14 or less. So, if you have anything on your Glasgow Coma Scale and you have a traumatic optic neuropathy, you should think twice before giving steroids because the CRASH study says there's a risk of mortality from that treatment.So traumatic optic neuropathy - the clinical diagnosis: RAPD, loss of vision, normal fundus supported by an imaging study (CT/MRI) to make sure there's no surgical indication sheathing (ie. retrobulbar hematoma, canal fracture, bone fragment), and steroids - maybe, it's a practice option but the route, the dose, duration, and the type of steroid have never been proven to be a more effective than any other route, dose, or duration. The CRASH study - the study of head injury - showed that steroids actually could harm you and could cause an increased mortality and so I don't give it for patients with significant deficit of Glasgow Coma Scale less than 14. And that's really what you need to know about traumatic optic neuropathy.