Feb 14: Lessons with Dr.J ; April: asking questions

How do you react to patients with difficult prognosis?




Thyroid eye disease is a terrible thing.
So far I have learned that:

Hypothyroid : treats with either synthroid, dessicated thyroid, levothyroxine
Hyperthyroid: treats with tapazole or beta-blockers (especially those who are allergic to tapazole).

Never mind all that primary or secondary disorder because I don't remember.

I know that Hyperthyroid --> heat, eat more but wasted, sweaty and tired all the time --> thin
Hypothyroid --> usually overweight (doesn't eat much but easily gain weight)

Treated with either thyroidectomy or radioactive iodine, thyroid eye disease may develop in either.

To be specific, thyroid eye disease is different from the actual thyroid disorder (Grave's (hyper), or Hashimoto's, or hypo or hyper) as ALL can develop thyroid eye disease. Reasons as explained in another post: Here






A patient walks in with stylish sunglasses and begin to tell me about the episode she had last Saturday and that Dr. J already knew about this, as the resident made phone call to Dr.J at 7am in the morning on Sat.
She has never felt any intense pain in her eyes before.




She has used drugs that costs thousands and had injections twice.
Yet, when the problem should be stagnant, it keeps on developing and evolving into grimmer situation.
There's no answer.
She might tears.



What do I do? is what she asks
What should professionals do in this case?
I could feel tears coming up - putting myself into her shoes.
Having to live with that.
Doing everything and no real progress. Not even a stop to its development.



Radiation treatment 1/3 of what is used to treat cancer, he says. But later, he adds, after we try this.




Giving prescription to the lady, asking her to not to get into argument with her loved ones and sell or buy any big things like house, property or cars (side effect of prednisone)




We will get through this.
We need to stop that.

That's what he says.






We have to be the calm one, then I realized.




We have to be the professionals.









Update made in April 2013



Dexamethasone (swelling) vs. Prednisone (inflammation) in use for thyroid eye disease.
If dexamethasone is 6.6 times more potent than prednisone (when you calculate the dose required for every 10mg of dexamethasone, approx 66mg of prednisone is needed). I then wondered why use prednisone when you have rampant thyroid eye disease, wouldn't it be better to use low dose dexamethasone.

I asked Dr. J this one day and he was honest with me that he couldn't remember exactly but that dexamethasone is glucocorticoid and so is prednisone but mineralcorticoid action in prednisone is very minor. He also mentioned from the end of his memory that the efficacy, and potency differences as well.
I tried to find if there are any comprehensive guidelines that firmly says why prednisone might be better but I haven't found a good source yet.

For the third time I heard " (name ) if you read my brochure, you will realize that I don't say it definitely." 
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...

As the inflamed conjunctiva becomes hyperemic (red) and boggy, the eyes tear and discharge mucus. The patient reports a feeling of tightness (yes), irritation (yes), and intermittent blurring of vision (yes), much as one might experience with infectious conjunctivitis ("pink eye"). The lower eyelids become boggy, and palpation elicits a sense of rubbery induration that is only mildly tender.

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

Shape Mechanism Common Associated Conditions Dot Hemorrhage Rupture of deep capillaries Diabetes Flame Hemorrhage Rupture of superficial pre-capillary arterioles, small veins Systemic hypertension, leukemia, severe anemia, thrombocytopenia, retinal vein occlusion, trauma Boat Hemorrhage Rupture of large superficial retinal veins into the space between the retina and vitreous; sometimes these bleeds break into the vitreous cavity Sudden increase in intracranial pressure, anemia, thrombocytopenia, trauma Submacular Hemorrhage Rupture of choroidal vessels under the fovea Age-related macular degeneration Vitreous Hemorrhage Rupture of superficial retinal vessels or vessels on a fibrovascular stalk extending into the vitreous Proliferative diabetic retinopathy, hypertension, trauma