Case #17 (07-06-2004)

[Andrew_Doan]

CC: 67 y.o. woman with a history of HTN and DM who complains of gradual vision loss OD and presents to the retina clinic for a second opinion in regards to her diabetic retinopathy.

HPI: She was told by another eye clinic that nothing else could be done for her diabetic retinopathy OD. The patient reports a gradual decline in vision OD. No complaints of pain, headache, or other problems. Her blood sugars range from the 80s to 130s which she "checks weekly".

PMH/FH/POH: DM treated with oral hypoglycemics and HTN treated with atenolol. History of focal laser treatments for diabetic macular edema OD and OS. No history of ocular trauma or additional intraocular surgery. FH non-contributory.

EXAM
Best corrected visual acuities: 20/250 OD and 20/25 OS.
Pupils: No RAPD.
Confrontational VF: constricted OD and OS.
EOM: Full OU.
IOP: 19 mmHg OD, 22 mmHg OS
Anterior segment: no iris neovascularization, 1-2+ NS cataracts OD and OS.
DFE: see photos below.

Fundus Montage - Right Eye

Photograph of the right fundus denoting: flame hemorrhages, dot-blot hemorrhages, macular exudates, marked macular edema, microaneurysms, and cotton wool spots. No neovascularization observed on exam.



Fundus Montage - Left Eye

Photograph of the left fundus denoting: flame hemorrhages, dot-blot hemorrhages, macular exudates, microaneurysms, cotton wool spots, and massive subhyaloid hemorrhage with blood layering out superiorly. No neovascularization observed on exam.


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?

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[Redhawk]

How about an FA? Some of the blood appears to be deep to the vessels (subretinal?)

She has DM which "may" be well controlled but no apparent evidence of neovascularization, though other changes are present.

How has her HTN been controlled? She has no HA or apparent papilledema but she does have other signs such as flame shaped hemorrhages and exudate. What's her BP now?

I'm not sure what that greenish "stuff" is in the macula. I can tell it's been almost a year since I finished my last ophtho rotation....

Any other bleeding/bruising problems? Recent CBC? HbA1c?

 

[eye4world]

can you give me blood pressure recordings ?
You have mentioned focal laser OD and OS i cant see any laser marks ?
For macular oedema OD we need a FA ( fluroscein Angiography ) and laser it if its not a iscahemic macular oedema.
as you have mentioned there is no nVD or NVE i cant get the cause of Vit Hage its not proliferative DR in that case maybe blood picture can help kindly give CBC and any other haematological investigations that have been preformed.

CC: 67 y.o. woman with a history of HTN and DM who complains of gradual vision loss OD and presents to the retina clinic for a second opinion in regards to her diabetic retinopathy.

HPI: She was told by another eye clinic that nothing else could be done for her diabetic retinopathy OD. The patient reports a gradual decline in vision OD. No complaints of pain, headache, or other problems. Her blood sugars range from the 80s to 130s which she "checks weekly".

PMH/FH/POH: DM treated with oral hypoglycemics and HTN treated with atenolol. History of focal laser treatments for diabetic macular edema OD and OS. No history of ocular trauma or additional intraocular surgery. FH non-contributory.

EXAM
Best corrected visual acuities: 20/250 OD and 20/25 OS.
Pupils: No RAPD.
Confrontational VF: constricted OD and OS.
EOM: Full OU.
IOP: 19 mmHg OD, 22 mmHg OS
Anterior segment: no iris neovascularization, 1-2+ NS cataracts OD and OS.
DFE: see photos below.

Fundus Montage - Right Eye

Photograph of the right fundus denoting: flame hemorrhages, dot-blot hemorrhages, macular exudates, marked macular edema, microaneurysms, and cotton wool spots. No neovascularization observed on exam.



Fundus Montage - Left Eye

Photograph of the left fundus denoting: flame hemorrhages, dot-blot hemorrhages, macular exudates, microaneurysms, cotton wool spots, and massive subhyaloid hemorrhage with blood layering out superiorly. No neovascularization observed on exam.


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?

 

[Richard_Hom]

CC: 67 y.o. woman with a history of HTN and DM who complains of gradual vision loss OD and presents to the retina clinic for a second opinion in regards to her diabetic retinopathy.

HPI: She was told by another eye clinic that nothing else could be done for her diabetic retinopathy OD. The patient reports a gradual decline in vision OD. No complaints of pain, headache, or other problems. Her blood sugars range from the 80s to 130s which she "checks weekly".

PMH/FH/POH: DM treated with oral hypoglycemics and HTN treated with atenolol. History of focal laser treatments for diabetic macular edema OD and OS. No history of ocular trauma or additional intraocular surgery. FH non-contributory.

EXAM
Best corrected visual acuities: 20/250 OD and 20/25 OS.
Pupils: No RAPD.
Confrontational VF: constricted OD and OS.
EOM: Full OU.
IOP: 19 mmHg OD, 22 mmHg OS
Anterior segment: no iris neovascularization, 1-2+ NS cataracts OD and OS.
DFE: see photos below.

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?

Tests
1. FA and/or OCT to differentiate between macular edema and exudative macular degeneration.
2. Doppler of carotids for the possibility of venous occlusion (BRVO or CRVO)
3. VDRL and STD testing to r/o syphillis
4. Tests for parasitic infections
5. Hypercoagulation tests

DDx:
1. CRVO/BRVO
2. Parasitic neuroretinitis
3. AMD (exudative) and "wet"
4. Proliferative diabetic retinopathy

Richard_Hom

 

[Yogi Bear]

great picture! did u use ur little digicam to take it?

 

[Andrew_Doan]

great picture! did u use ur little digicam to take it?

I wish!

No, these photos and montages were taken and generated by the department's new digital photography system.

 

[Yogi Bear]

I wish!

No, these photos and montages were taken and generated by the department's new digital photography system.

lol! so does that partially negate the need for digicams? i.e. if there was a big fancy machine, i'd like to use it...hehe.

 

[Andrew_Doan]

lol! so does that partially negate the need for digicams? i.e. if there was a big fancy machine, i'd like to use it...hehe.

Of course not!

Each device serves a unique purpose. Not every practice/institution can afford a fancy digital imaging system, and not every slit lamp can be outfitted with a digital capture device.

 

[IdiotBoxen]

Tests:

1) Fluorescein angiogram.
2) Coag panel
3) B-scan us.
4) Blood glucose and complete urine.

Differentials:

Proliferative Diabetic Retinopathy
Diabetic Macular Edema
Haemoglobinopathies

I think parasitic is unlikely in this pt, however, it'd probably be worth doing blood work to cya.

Questions:

When was the diagnosis of DM made?
What was her BP?
How much did that cool camera cost??

 

[JJMD]

FA to exclude/confirm ischemic maculopathy OD--may benefit from IVK
Likely with NV you can't see OS

HbA1c that will be 13

BTW, it may be CRVO/BRVO, but carotid dopplers? since when was that in the work up for venous occlusive disease? Also, a 67 y/o hypertensive/diabetic, is an expensive coag panel a good idea with no history of systemic thrombi? Bilateral parastic disease?

 

[IdiotBoxen]

Ok, lemme explain my reasoning

I'd want to exclude sickle cell trait, sickle cell c, sickle-thallasemia.

It could be Eales disease... but the lack of neovascularisation counts against that. But BRVO can be seen in pts with Eales disease.

I'm not that sure about the carotid doppler either. I think CVA is unlikely in this case. Maybe it's because of the DM/HTN or just policy?

 

[Andrew_Doan]

Heme A1C = 6.5%
Blood Pressure = 270/110

You may look at the discussion of the case here: http://webeye.ophth.uiowa.edu/eyeforum/case17.htm

 

[cpw]

270/110... good lord !!!!

So, Andrew...did they put her on nifedipine to drop her pressures? And if so.. what are the percentage risks of her developing NAION after the pressure drop due to hypoperfusion ??

 

[Andrew_Doan]

270/110... good lord !!!!

So, Andrew...did they put her on nifedipine to drop her pressures? And if so.. what are the percentage risks of her developing NAION after the pressure drop due to hypoperfusion ??

There hasn't been any good studies to address this point. Her blood pressure was lowered gradually using amlodipine and HCTZ. End organ ischemia is another problem when dealing with lowering the BP.

From Dr. Hayreh's work, we know hypotension is a major risk factor for NAION:

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=11704035

Hayreh SS, Podhajsky PA, Zimmerman B.

Ipsilateral recurrence of nonarteritic anterior ischemic optic neuropathy.

PURPOSE: To report the prevalence of recurrence of nonarteritic anterior ischemic optic neuropathy (NA-AION) in the same eye and possible contributing risk factors. DESIGN: Cohort study. METHODS: Setting: Institutional. STUDY POPULATION: The study includes 594 consecutive patients (829 eyes) with a diagnosis of NA-AION and follow-up of at least two months after the onset of NA-AION, examined in the Ocular Vascular Clinic since 1973. Simple progression of visual loss during an episode of NA-AION was not considered a fresh episode. INTERVENTION OR OBSERVATION PROCEDURES: Every patient had ophthalmic evaluation, including visual acuity, visual fields with a Goldmann perimeter, intraocular pressure, and slit lamp and ophthalmoscopic evaluation at initial visit and at each follow-up visit. The patients also had systemic evaluation; some patients had echocardiography (166 patients) and 24-hour ambulatory blood pressure (BP) monitoring-the latter was investigated in 80 patients (17 with and 63 without recurrence of NA-AION) who consented to participate in this study which was started in 1989. While optic disk edema was present, the patients were followed every 2 to 3 weeks. Once the optic disk edema resolved, they were followed up after 3 months, 6 months, and then at yearly intervals unless they had some new visual complaint. MAIN OUTCOME MEASURES: Prevalence of a fresh episode of NA-AION in the same eye, and comparison of ocular and systemic risk factors between patients with and without recurrence of NA-AION in the same eye. RESULTS: Of the 594 patients (829 eyes) in the study, recurrence of NA-AION in the same eye occurred in 45 patients (53 eyes) with a median follow-up of 3.1 years (range 2 months to 30.5 years) from the first onset of NA-AION. The Kaplan-Meier survival curve showed cumulative percentage of recurrence of NA-AION from first episode to second episode at three months 1.0%+/-0.4%(SE), at 6 months 2.7%+/-0.7%, at one year 4.1%+/-0.9%, and 2 years 5.8%+/-1.1%. There was no significant association between recurrence of NA-AION and the systemic conditions that were examined, except for nocturnal arterial hypotension. Overall patients with a recurrence of NA-AION had a significantly lower mean nighttime minimum diastolic BP (P =.003) and greater mean percentage drop during sleep in diastolic BP (P =.011) than those with no recurrence of NA-AION; all other measures of nocturnal hypotension were not significantly predictive. CONCLUSIONS: Recurrence of NA-AION in the same eye is uncommon (6.4%). Our study indicates that nocturnal diastolic arterial hypotension may be a risk factor; however, since this is a multifactorial disease, other so far unknown risk factors may also play a role. The role of various risk factors which may contribute to the recurrence of NA-AION is discussed.

 

[Andrew_Doan]

In addition, because of her DM status, she was also started on ACE-inhibitors. ACE-inhibitors may be of some benefit to patients who suffer from NAION because endogenous vasoconstrictors may precipitate NAION events.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3500445

Hayreh SS.

Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis.

Ophthalmology. 1987 Nov;94(11):1488-502.

Visual disturbance after marked and/or recurrent blood loss has been known for at least 25 centuries, since Hippocrates; however, so far its clinical features have been controversial and its pathogenesis enigmatic. The author studied seven patients, four of whom were seen soon after the visual loss and followed prospectively. A detailed review of the extensive literature and analysis of the cases provide relevant information on the subject. The blood loss is usually from the gastrointestinal (GI) tract, less often from other sites. There is typically a time lag between the bleeding and the onset of visual loss--usually up to 10 days, less often even 2 to 3 weeks. The ocular findings are typically those of anterior ischemic optic neuropathy (AION) and are usually bilateral. Considerable evidence has accumulated that blood loss, with or without arterial hypotension, causes increase in release of renin and endogenous vasoconstrictor agents (e.g., angiotensin, epinephrine, and vasopressin) because of activation of the sympathoadrenergic system and vasomotor center. Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION. In view of all the evidence, it is postulated that in the production of AION after blood loss, release of endogenous vasoconstrictor agents is probably a very important factor, with arterial hypotension an additional factor; increased platelet aggregation may also play a role.