Andrew_Doan

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CC: 48 y.o. AA woman with c/o of photophobia, tearing, and eye pain OU.

HPI: 48 y.o. AA HIV(+) woman with 1 month of gradual photophobia, tearing, and eye pain OU. She was started on anti-retroviral therapy 1 year ago when her CD4 count was <50. After starting antiretroviral therapy, her CD4 count has been above 250. She was doing well until one month ago when she c/o of increasing redness and eye pain OU. On presentation, she was photophobic.

No c/o of fevers, chills, or night sweats. No joint pains. No shortness of breath. No other complaints. No recent exposures to illnesses.

PMH: HIV(+) on antiretroviral therapy. TB test performed one year previous was negative, but the candida control was also negative. No previous ocular problems.

Exam:
Best corrected visual acuities: 20/50 OD and 20/40 OS.

Pupils: irregularly shaped (see photo), reactive, no RAPD.

EOM: full OU

VF: normal

IOP: normal

DFE: retina exam notable for normal macula, vessels, and periphery OU. No vitreous cells.

SLE: notable for marked conjunctival injection OU, ciliary flush OU, 2+ cell/flare OU, and large keratic precipitates on the corneal endothelium OU. There was central posterior synechia around the pupil margin OU.

SLE Photo of the right eye (left eye similar)
redeye_03042004.jpg


SLE Photo of the right eye denoting keratic precipitates (higher magnification)
redeye2_03042004.jpg



Feel free to discuss the following:

What tests should you order (I'll post labs when asked for them)?

What's the differential diagnosis?

What's the diagnosis?

What is the treatment of choice, surgically and/or medically?
 

Redhawk

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Here's a list of causes of anterior uveitis that I have found:
AIDS, HSV, Syphilis, TB, Zoster, Rubella, Rubeola, Toxoplasmosis, Toxocariasis, Ankylosing spondylitis, Behcet, heterochromic iridocyclitis, Reiter, Sarcoid, Lupus, VKH syndrome, Wegener.

Sarcoid?
I don't think this is necessarily more likely with HIV(?) but I would think of this in any AA presenting with uveitic symptoms. She also has appears to be anergic which is not uncommon. You also say that she had "large" KP. Would you characterize them with the buzzword "mutton fat" that tends to be associated with granulomatous inflammation?
CXR? ACE levels?

TB?
She had a negative ppd but she also appears to be anergic (neg Candida skin test). She also appears to lack many of the classic sx such as hemoptysis and night sweats.
From what I'm reading this can often cause uveitis w/o other systemic sx, however, and must be diagnosed as "presumed TB uveitis" after lack of response to other tx.
CXR? AFB sputum smear?

Drug-induced uveitis?
Perhaps this could explain the symmetric symptoms? It has been reported in patients treated with cidofovir or rifabutin. Does she take either of these drugs? Apparently if rifabutin is the cause you decrease the dose and tx with steroids, but if caused by other drugs, they should be stopped.

Neurosyphillis?
No palmar rash, right?
How about an RPR, though?

Toxo?
I think this typically causes a posterior uveitis as well. (wrong) I've since read that this does cause anterior uvieitis.

CMV, VZV, HSV?
It seems they would typically affect the retina as well.

Reiter's syndrome?
She apparently has no arthritic sx or urethritic sx.

Immune recovery uveitis with HAART therapy?
"The onset of IRU usually occurs within a few weeks to a few months after an increase in CD4 counts of 70 cells/mm3 or more; however, IRU may occasionally occur after much longer periods of time. Only eyes with CMV retinitis are affected..."
She doesn't appear to have any evidence of CMV retinitis, though.
http://www.hopkins-aids.edu/publications/report/nov01_4.html

Hell, maybe even just HIV itself? I wouldn't be shocked.
 
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Kalel

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So we'd like the following labs/studies (not from the top of my head, from emedicine and with some help from another forum ;) ):

CXR: check for sarcoid/TB
FTA-ABS: Syphillis
PPD: TB
ACE level: Sarcoid
Lyme serology
Toxoplasmosis ELISA
MRI to evaluate for intraocular lymphoma
CBC with diff (CD4 count would not be useful in this setting as the patient is "sick" and it could be acutely lowered).

Anyways, these optho cases are tough without being given a differential (even though I like it better without the diff, because it becomes too easy with a given diff). I like my IM cases much better; they are much more med student friendly ;).
 

Andrew_Doan

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Originally posted by Kalel

Anyways, these optho cases are tough without being given a differential (even though I like it better without the diff, because it becomes too easy with a given diff). I like my IM cases much better; they are much more med student friendly ;).

That's why you're going into IM! ;)

:p
 

Soccrtrela

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I'm not even in med school yet (will start this fall) let alone ready to specialize but I had a bad case of acute iritis a few years ago and that DEFINITELY looks like iritis....
 

Redhawk

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I think Kalel might have made a good point by rasing the possibility of intraocular lymphoma, especially with her age(?) and HIV status. From what I've read, this appears to be best diagnosed via vitrectomy so I'm assuming it would be done when other causes are ruled out.

I'm still bettin' on sarcoid until the tests prove me wrong...;)
 

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This is a patient with HIV and an anergic TB skin test one year previous when her CD4 count was low. After starting ART, she was doing well until her granulomatous (mutton fat) uveitis developed. We know this process was long standing because of the central posterior synechiae (pupil being tacked down to the anterior lens capsule by inflammation). We repeated a TB skin test, and it was POSITIVE because now she had a reconstituted immune system to mount a skin response. We also worked her up for syphilis and sarcoid, which were negative. In an HIV patient, the uveitis can be a result of immune reconstitution syndrome (patients are usually much more ill) or from the original HIV infection. The latter is a diagnosis of exclusion.

We referred this patient to internal medicine/infectious disease for treatment. We started her on prednisolone drops (steroid for inflammation) and homatropine or scopolamine (dilation and cycloplegic to prevent further synechial formation and for comfort- it's best to use an intermediate cycloplegic so the pupil still can react to prevent peripheral anterior synechiae formation). We also tried to break the pupil synechiae with pilocarpine (causes pupil constriction) before starting the scopolamine.

Here is an article on e-medicine about granulomatous, anterior uveitis:
http://www.emedicine.com/oph/topic586.htm

The differential diagnoses include:

Sarcoidosis (low ACE)

Syphilis (negative titers)

Vogt-Koyanagi-Harada syndrome (associated with posterior retinal findings, poliosis, vitiligo, and sometime hypopyon)

Sympathetic ophthalmia (no history of eye trauma or surgery excludes this)

Multiple sclerosis (no eye pain with movement, atypical presentation)

Lyme disease (no history of tick bites or camping)

Tuberculosis

Herpes zoster (no associated skin rash)

Coccidioidomycosis (must consider in HIV)

Leprosy (no associated skin lesions)

Toxoplasmosis (usually associated with posterior uveitis: headlights, i.e. retinal lesions, in the fog)

Brucellosis (doesn?t fit the history: http://www.emedicine.com/emerg/topic883.htm)

Idiopathic (includes immune reconstitution syndrome and HIV uveitis)
 

Andrew_Doan

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Originally posted by Kalel
lymphoma

Good thought, but usually intraocular lymphoma presents with many cells but little flare (i.e., low protein in the aqueous). Patients are typically older than this one. Often, we find sub-retinal lesions on exam. Diagnosis can be confirmed with an anterior chamber tap to remove cells for FLOW cytometry and ECHO of the eye to look for choroidal infiltrates.
 

Redhawk

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So it seems the presumption was that the uveitis was caused by the TB due do a negative workup for everything else.

How exactly do you know when someone has posterior synechiae? Do they form close enough to the pupil to be visible or do you just infer their presence by when you see an irregular pupil in a person with uveitic sx?

How successful is pilocarpine in breaking them? What's the reason for for constricting the pupil to break them? Will they not break with dilation or will that cause damage?
 

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Originally posted by Redhawk
So it seems the presumption was that the uveitis was caused by the TB due do a negative workup for everything else.

How exactly do you know when someone has posterior synechiae? Do they form close enough to the pupil to be visible or do you just infer their presence by when you see an irregular pupil in a person with uveitic sx?

How successful is pilocarpine in breaking them? What's the reason for for constricting the pupil to break them? Will they not break with dilation or will that cause damage?

It is a presumption, and we typically don't like giving people more than one diagnosis. If the uveitis remains persistent after the treatment of TB, then the patient needs another work-up. This is why uveitis can be so difficult.

Central posterior synechiae is clear on slit lamp exam. When the light hits the pupil, you'll see that the pupil margins are tacked down on the anterior lens surface. Peripheral anterior synechiae occurs in the angle and peripheral cornea. This is best seen with gonioscopy.

The circular sphincter muscles are stronger than the dilator muscles of the pupil. One can break the synechiae with dilation too, but sometimes it requires something stronger, i.e. direct cholinergic stimulation with pilocarpine. Becareful giving pilocarpine in the setting of uveitis for the concern of causing worsening central posterior synechiae and pupil block glaucoma; thus, patients should be dilated immediately after trying pilocarpine.
 

Soccrtrela

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Originally posted by Andrew_Doan
It is a presumption, and we typically don't like giving people more than one diagnosis. If the uveitis remains persistent after the treatment of TB, then the patient needs another work-up. This is why uveitis can be so difficult.

Central posterior synechiae is clear on slit lamp exam. When the light hits the pupil, you'll see that the pupil margins are tacked down on the anterior lens surface. Peripheral anterior synechiae occurs in the angle and peripheral cornea. This is best seen with gonioscopy.

The circular sphincter muscles are stronger than the dilator muscles of the pupil. One can break the synechiae with dilation too, but sometimes it requires something stronger, i.e. direct cholinergic stimulation with pilocarpine. Becareful giving pilocarpine in the setting of uveitis for the concern of causing worsening central posterior synechiae and pupil block glaucoma; thus, patients should be dilated immediately after trying pilocarpine.

Andrew Doan (I was the one with the pics of Greece in the Lounge...):

Just as a side note... when I had a case of this, I had to keep my eyes dilated for a week to break the synechiae. I was also on prednisone (50mg for 2-3 days, then tapered down over the course of several weeks) because the prednisolone drops just weren't doin it for me.

The only thing I can link to my case is a bad virus I was fighting the week before the inflammation in the eye came on (this happened in october of 2002). My eye was also filled with white blood cells... did you see this in this patient as well?
 
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