 And last but certainly not least, we have Dr. Michael Murray who's going to be discussing a case of unilateral blurry vision and headache. I'm sorry to interrupt but I just want everyone to know that he looks amazing this morning and that's despite being woken up by me at 6 a.m. in the call room when he was a little disoriented sitting up on the couch wondering what was happening. So you clean up well, Mike. You look good. Thank you so much. All right. So I'll be discussing a case of unilateral blurry vision and headache unlike other presenters. I don't have financial disclosures. Maybe I wish that I did at this point but I do not. So this was a patient who came in with a right eye blurry vision and headache, a 78-year-old male. I had a past medical history of polymyalgia, rheumatica, a cabbage in 2007 and then diabetes and presented to a rheumatology clinic with about a weak history of right eye blurry vision. It was described as blurry throughout the eye without flashes or floaters and then an associated headache described as unilateral at frontal with some mild-associated jaw pain. There was no recent illness or other systemic symptoms and past medical history and ocular history were pretty non-contributory other than stated here. He was on prednisone, 10 milligrams daily and aspirin, had a penicillin allergy and then a former smoky had a 50-packier history. So at this point in the rheumatology clinic, the differential was quite broad including vascular causes, GCA, NA, UN, infectious inflammatory causes is listed, neoplastic autoimmune. The point of this slide is that the differential was or should have been quite broad. The patient was told by the rheumatologist to increase his steroid dose to 30 milligrams per day and then was sent home. Then two days later came back to the emergency department, had a worsening headache and at this time he had a mild ptosis in that right eye and some right facial numbness and also severe right-sided facial and forehead and retroorbital pain and still had this blurry vision. Temporal artery biopsy was arranged at that time and taken and then he was told by the ED after consultation with rheumatology to increase the prednisone to 60 milligrams per day and sent home. And then two days after that, so four days after his initial presentation and almost two weeks after the symptoms started, he came back to the emergency department for progression of his symptoms and pain and meanwhile the biopsy for GCA has come back negative. Mike was he already on the 10 milligrams of prednisone before this? Chronically was on it for the polymyalty aromatic. So his visual acuity in that right eye was NLP at this time. He had an unreactive five millimeter pupil. He had an APD by reverse and then on extroocular movements he was fixed in the right eye and the left eye had an abduction deficit. Pressure was normal and his visual fields were normal in the left eye and then he didn't have vision in the right eye obviously. So on bedside exam, he had moderate proptosis in the right eye and a complete ptosis and mild fullness of the right upper and lower lids. He had a corneal epithelial defect without infiltrate. Otherwise, ACIRIS lens exam relatively normal and on his dilated exam, the optic nerve didn't show any signs of edema or pallor. There was no non-hemorrhageal ischemia visible. Craneal nerve exam kind of summed up. The only other thing besides the NLP vision and the ethylamplasia of the right eye was also a decreased sensation of V1 distribution of the right side. Otherwise, cranial nerves were normal. So this is a photograph of him just demonstrating that right eye ophthalmoplesia and the left eye abduction deficit here. So selected lab exams. He had an elevated white count. He had an LP performed that PCR came back for strep pneumo on his CMP and demonstrated metabolic anion gap acidosis. PT, PTT were within normal limits and his A1C was 14.5. So working differential at this point, obviously thinking about vascular causes septic emboli, cavernous sinus thrombosis, infectious causes. He has some bacterial meningitis, bacterial fungal invasive disease, neoplasic otomy, and obviously a little bit lower down at this point. And I just wanted to talk just a quick kind of learning point about temporal arthritis since this was kind of an anchor diagnosis in this case. Looking in the literature, it can exhibit multiple cranial nerve signs. It's pretty rare to have it be bilateral. And here's a couple of isolated cases, but they're kind of case reports. And especially seeing a facial nerve, or sorry, a V1 distribution sensory nerve and also abduction deficits, a little unusual. And then I liked this quote, it's Sherlock Holmes. He says, I make a point of never having any prejudices and of following dossily where a fact may lead me. And in an outside hospital, there was an astute ID doc, as this patient was admitted and being worked up for some meningitis concerns who thought that the facts might lead him to look here. So this is a photo that we actually obtained when the patient was transferred to us showing black discoloration of the right palate. And then here's some other imaging. So on the left-hand side, this is a MRI post-contrast T1 image showing that superior ophthalmic vein, and there's a thrombosis there. Also on the right image, there's evidence of occlusion of the right patrosal vein. These images are also MRI post-contrast T1 images showing an infiltrative disease involving the right orbit and then extending to the right cavernous sinus. And then here's a post-contrast T2 image showing also that involvement in the right cavernous sinus. So I wanted to talk a little bit about orbital apex syndrome and superior orbital fissure syndrome. Basically the biggest difference between this is how far back compression is occurring. So the orbital apex syndrome is involving cranial nerve 2. And I like this anatomical diagram here as a view looking towards the orbit. And then superior orbital fissure syndrome is a little bit more anterior. Spares the optic nerve and it's common trauma related. And then cavernous sinus. So the anatomy of it, it's a complex network of vein, lots of septations in there. And a 1 by 2 centimeter cavity drains blood from the superior and inferior ophthalmic veins as well as supraparital sinus and the superior and inferior cerebral veins. And the two sides are connected by an intro cavernous sinus. I like that lower depth diagram that shows the space that contains cranial nerve 3, 4, 5 and 6 and the internal carotid artery. And it also shows great proximity to the sphenoid sinuses in the roof of the pallet. So cavernous sinus syndrome first described by Richard Bright in 1831. He actually had two volume sets of renal disease and then cerebral vascular disease has these remarkable drawings. You can buy a first edition online for like $20,000 if you want. And there's three types that have then been described. And it's basically anatomically how far back the cavernous sinus is involved. Posterior being all branches of that trigeminal nerve. Whereas anterior is just V1 and middle is V1 and V2. Common causes continue to spread from nasal frunkel, the sphenoidal ethmoidal sinuses and dental disease and the pathogens are listed there. Staff and strep obviously common and then less common gram, negative rocks, fungal and u-core. There's also aseptic causes, trauma, malignancy, dehydration, anemia, granulomidus disease. So this is histology. This patient's palatal biopsy, a representative photo here showing this septated hyphae there and then also the staining on GMS. So I want to talk a little bit about mucomycosis. Described first actually in 1885 by Richard Ploff. He was a medical forensic professor in Prague and then actually didn't really get much attention to literature until about the 1940s. Vascular invasive is part of the zygomucosis family. Commonly rise spacer mucor and has affinity not just for the rhinoorbital tract but pulmonary and GI tracts as well. It's associated with diabetes, especially DKA, which our patient happened to have, as well as being immune to compromise either from medications or malignancy causing neutropenia, etc. And the initial presentation is similar to our patient with a headache sinusitis and then some visual changes. The cavernous sinus symptoms which can spread to the other eye and that's actually what was happening in this patient is that they were spread along that intra-cavernous sinus causing the left ABduction deficit. Treatments from mucomycosis, obviously you've got to stop the fire that's stoking the flame so getting rid of any immunomodulatory therapy as quick as you can taper it down, correcting the metabolic derangements, so DKA in this case. And then an IV antifungal, commonly anaphtericin B at 5 to 7.5 mix per kick per day and then the aggressive surgical debreement is just really paramount in causing the source control. Other therapies that are actually being looked at as adjunctive therapy and I'm sad that Dr. Patel couldn't be here today but he actually published a case report where they were able to save an eye from exeneration using interorbital irrigation of anaphtericin B in kind of concert with these other therapies. There's also a case report for retrobulber injections of amphotericin B. Hyperbaric oxygen has been shown also to be kind of another adjunct therapy that people have been interested in and then another therapy that people have looked at is iron chelation. Deferaserox was in this Defeat Meurek trial and unfortunately that didn't show any benefit. The difficulty in all of these therapies is really coming up with any meaningful amount of patients that you can get at a single center because meucomicosis is relatively rare. And so finding the end size to be able to power a study to show significance is difficult but there's more studies that need to be done. So the follow up for our patient the clinical course unfortunately after extensive consult with neurosurgery and ENT and ID this decision was made not to perform surgery. He had extensive involvement to the skull base and they didn't think that the morbidity of the surgery was able to justify doing surgery in his case and they'd be able to clear the affected tissue. So Palliative Care was consulted and the amphotericin B was actually continued but other comfort care measures were taken and the patient was transferred back to Montana for his end of life care. These are my references. Just wanted to thank Dr. Patel, Dr. Marx and Tina Manlis actually helped out with this case a bunch and as an ode to summer I'm sad that it's over. This is some of my favorite summer activities at Bear Lake and then I'm happy to take some any questions. It's a picture of the family.