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http://rosacea-support.org/ocular-rosacea-video-worth-a-watch
Heather Potter, MD – University of Wisconsin, Dept of Ophthalmology & Visual Sciences Grand Rounds ‘Ocular Rosacea’ - useful general summary video of some current thinking on ocular rosacea pathogenesis and treatment.
Warning: This is a doc’s eye view. Struggling to find someone informed and skilled enough to help us manage this, I’m not detached enough to find this disease so 'intellectually fascinating'. If you're the same on the first part, maybe skip to 05:00.
‘Rosacea is multifactoral vascular hyper-reactivity.’ (It's not just vascular, a dermatologist or immunologist would expand on this.)
‘Rosacea is a neural disease where normal vasodilation is greater and more persistent. It then has an autoimmune component where minute amounts of extravasated plasma induce a dermal inflammation. With repeated vasodilation, the telangiectasias form and the redness develops. With repeated bouts of inflammation, fibrosis and hypertrophic scar tissue is produced.’
’The eye disease is not related to the severity of the facial disease.’
Has anyone used Sodium sulfacetamide as a lid scrub? Interesting she uses tea tree shampoo in this way.
Explains well why the usual combination of anti-inflammatory and antibacterial topicals and subantimicrobial levels of oral antibiotic helps the meibomian glands and prevents damage on the eye surface. Some docs question why the ophth use antibiotics without apparent improvement in this way, with the risk of building bacterial resistance. It's to save people's corneas. This is why we need surface disease specialists. (Although some of us know all too well that oral isotretinoin is contraindicated with any meibomian gland dysfunction.)
‘Increased interleukin 1-a and promatrix metalloproteinase 9 within the tears...' [causes the ocular surface damage we see].
(Just for info, symptoms LM had for the side effect ‘pseudotumour cerebri’, which name the ophth use and the neurologists find hilarious, ie intracranial hypertension (definitely not benign from her point of view since it leads to optic nerve swelling and vision loss) were: persistent headache, peripheral vision wavering, camera-shutter transient visual obscurations, generally exhausted and unwell. Treat with diuretic and monitored, no lumbar puncture should be done without neuroophthalmologists. NB at puberty she was in a higher-risk group than someone older and the antibiotic we used had a higher risk profile than eg doxycycline, so shouldn't put you off if needed.)
What do you think? [Thanks to Dori and David Pascoe for posting this.]
Heather Potter, MD – University of Wisconsin, Dept of Ophthalmology & Visual Sciences Grand Rounds ‘Ocular Rosacea’ - useful general summary video of some current thinking on ocular rosacea pathogenesis and treatment.
Warning: This is a doc’s eye view. Struggling to find someone informed and skilled enough to help us manage this, I’m not detached enough to find this disease so 'intellectually fascinating'. If you're the same on the first part, maybe skip to 05:00.
‘Rosacea is multifactoral vascular hyper-reactivity.’ (It's not just vascular, a dermatologist or immunologist would expand on this.)
‘Rosacea is a neural disease where normal vasodilation is greater and more persistent. It then has an autoimmune component where minute amounts of extravasated plasma induce a dermal inflammation. With repeated vasodilation, the telangiectasias form and the redness develops. With repeated bouts of inflammation, fibrosis and hypertrophic scar tissue is produced.’
’The eye disease is not related to the severity of the facial disease.’
Has anyone used Sodium sulfacetamide as a lid scrub? Interesting she uses tea tree shampoo in this way.
Explains well why the usual combination of anti-inflammatory and antibacterial topicals and subantimicrobial levels of oral antibiotic helps the meibomian glands and prevents damage on the eye surface. Some docs question why the ophth use antibiotics without apparent improvement in this way, with the risk of building bacterial resistance. It's to save people's corneas. This is why we need surface disease specialists. (Although some of us know all too well that oral isotretinoin is contraindicated with any meibomian gland dysfunction.)
‘Increased interleukin 1-a and promatrix metalloproteinase 9 within the tears...' [causes the ocular surface damage we see].
(Just for info, symptoms LM had for the side effect ‘pseudotumour cerebri’, which name the ophth use and the neurologists find hilarious, ie intracranial hypertension (definitely not benign from her point of view since it leads to optic nerve swelling and vision loss) were: persistent headache, peripheral vision wavering, camera-shutter transient visual obscurations, generally exhausted and unwell. Treat with diuretic and monitored, no lumbar puncture should be done without neuroophthalmologists. NB at puberty she was in a higher-risk group than someone older and the antibiotic we used had a higher risk profile than eg doxycycline, so shouldn't put you off if needed.)
What do you think? [Thanks to Dori and David Pascoe for posting this.]