I have read the brochure about 4 times but because of that, am reading again.
what's the brochure's name? Dr.J's handwritten brochure about Thyroid eye disease ~*
Proptosis, lid retraction, diplopia, optic nerve compression, strabismus, thy name is Thyroid/Grave's disease. |
Thyroid eye disease is interesting. These are so far, things I have observed and maybe noticed traits of patients with this pathology. (perhaps because I was told that the patient is often by my much experienced predecessors)
- talkative (have to cut them in middle of conversation while I'm screening, or else I will fall behind...)
- may not be pleasant.
- sometimes aggressive/paranoid
However, although I might have met paranoid person, luckily I have not had any extensive unpleasant experience... actually I can only recall seeing friendly thyroid patients who might have been more talkative than other patients.
*side note: what I do when I see thyroid patients. I write the code 0906A.
What's weird is that Thyroid eye disease (or thyroid orbitopathy, Grave's disease, Grave's orbitopathy etc) is an autoimmune disease that occurs in people 'with a history of thyroid problems...[but]...occur before or decades after the development of thyroid gland disease.' Another curious thing is that it can manifest even after the thyroidectomy. WHY?!?!? you don't have thyroid, so shouldn't you be free from these problems?
Actually I just found out through U of M website, that ophthalmic manifestation is divided into 2 groups.
Hypermetabolic and infiltrative
(http://www.kellogg.umich.edu/theeyeshaveit/acquired/graves-disease.html)
Hypermetabolic: excess thyroid hormone --> sympathetic pathway activation --> retraction of lids
= the "stare sign" -- when the patient is to look downward, the upper eyelids remain elevated or begin moving downward only after a delay -- a sign called "lid lag"
Infiltrative: lymphocytic infiltration of the orbital soft tissue, NO RELATIONSHIP to the LEVELS of the THYROID hormone.
so that's why Mr.K, even after thyroidectomy had this problem. back to it being an autoimmune disease...
When the extraocular muscles and orbital fat become inflamed, the eyes are displaced forward in the orbit (proptosis, exophthalmos), and the movements of the eyes may be limited. At first, the impaired eye movements are due to swollen, inefficient extraocular muscles. If the inflammation persists beyond a year, the muscles scar in a contracted, noncompliant state. Typically, some extraocular muscles are affected more than others, driving the eyes out of alignment in some fields of gaze, and causing the patient to experience double vision.
As the muscles swell, they may compress the optic nerve in the posterior orbit, where they are packed in a tight space. If the compression is not relieved, axoplasmic flow within the nerve comes to a halt, and vision fails. This compressive optic neuropathy is the most dreaded ophthalmic consequence of Graves' disease.
Another outcome of marked swelling of extraocular muscles and orbital fat is massive proptosis which interferes with the protective function of the eyelids and results in drying of the cornea. This "exposure keratopathy" is the second most feared ophthalmic manifestation of Graves' disease.
The combination of hypermetabolic and infiltrative ophthalmic signs gives away the diagnosis of Graves' disease.
But when the hypermetabolic component is absent and infiltrative signs are mild, the condition is often misdiagnosed as infectious or allergic conjunctivitis.
When one side is relatively spared, the physician may incorrectly diagnose an orbital tumor.
And when inflammation relatively spares the most visible tissues—the conjunctiva and eyelids—the physician may fail to consider Graves' disease as the explanation for diplopia or visual loss.
But Mr.K had other problem. and that is what prompted me to write this post. He developed a Retinal Hemorrhage (bleeding behind retina) so he has to get injection in his eye with a needle ever 3 weeks in addition to chronic predinisolone drops.
"What were you injected with", I asked.
" Oh, I'm not sure..."
"Is it the steroid?"
"Oh, I use that drop everyday, but it's not that."
Dr.J must know. surely.
So I asked Dr. J and he answered "anti-VEGF"
Vascular endothelial growth factor.
as VEGF encourage the development of new blood vessel so in order to stop the evolution of bleeding. You use this. The most commonly marketed drug for this. LUCENTIS.
I asked if this anti-VEGF is must be used for cancer and he said yes..
Turned out the drug named AVASTIN is used to treat colorectal, lung, breast and brain cancer. The difference is that LUCENTIS is used specifically for the eyes and therefore smaller molecule.
It amazed me that this procedure was just implemented 3 years ago.
Before it was all corticosteroid.
side note:
Retinal Hemorrhages
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