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Diagnostic Challenges in Optic Disc Edema 73 Year-Old Diabetic Male Presents for Examination with Unilateral Optic Nerve Head Edema and Unique Macular Changes

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Diagnostic Challenges in Optic Disc Edema 73 Year-Old Diabetic Male Presents for Examination with Unilateral Optic Nerve Head Edema and Unique Macular Changes Shilpi Ratra O.D., Resident Gregory S. Wolfe O.D., Attending Diagnostic Challenges in Optic Disc Edema 73 year-old diabetic male presents for examination with unilateral optic nerve head edema and unique macular changes. OCT findings reveal vitreal-retinal traction at the disc and macula, acting as a masquerader of the underlying etiology. I. Case History 1. Chief Complaint: a. Hispanic 73 year old Male b. Sudden, painless, loss of central vision, right eye only, started 6 days ago. No temporal pain, no trouble chewing, no headaches 2. Ocular History a. Mild Non-Proliferative diabetic retinopathy without clinically significant macular edema OU b. Optic Atrophy OS 2’ to NAION c. Mild hypertensive retinopathy OU 3. Medical History a. Neutropenia, tinea, joint shoulder pain, allergic rhinitis, lumbago, Essential hypertension, Diabetes type II since 1998 b. Last HbA1c: 8.5, Last BS ~156 4. Medications: a. Topical Ketoconazole cream, Topical Fluorouracil cream, Lispro insulin, Losartan, Metformin, Omeprazole, Simvastatin 5. Other information a. LEE 6 days prior: VA OD 20/25, OS 20/70- with EV b. DFE findings: OD: C/D 0.15 round healthy disc, no signs of edema, elevation or hemes. Scattered dot hemes and micro aneurysms inferior retina. OS: 0.25 disc with 2+ temporal pallor c. OCT Stratus OD: normal, foveal contour intact, OS general depression/thinning of fovea d. OCT Stratus: RNFL OD: avg thickness 85.59, WNL 360 OS 83.03, temporal thinning. II. Pertinent findings: 1. BCVA OD 20/50+1, OS 20/80 w EF PHNI (decrease VA OD by 4 lines since 6 days ago) 2. Pupils: PERRL-APD, pupils briskly reactive, no APD OS 3. Color vision HRR test: OD 6/14, OS 10/14, Ishiahara test: OD 14/14, OS 11/14 4. No pain or tenderness along temporal scalp upon palpitation 5. DFE findings: OD C/D 0.15 round, sectoral disc edema superior temporally, no hemes or NVD; scattered dot hemes around macula and ONH, 1 blot hemes inferior to ONH, (+) retinal elevation at macula; 2/3 AV ratio, Mild venous tortuousity, No NVE, No retinal breaks, tears 360 in periphery OS unchanged from previous evaluation 6. OCT Cirrus Optic Disc Cube: OD Avg thickness: 155, NFL edema superior and temporal; OS Avg thickness 85, temporal thinning, all other quadrants WNL 7. OCT Cirrus Mac cube 512 x 128: OD (+) Significant vitreo-macular traction with cystic edema, central thickness 399; OS Central thickness 203, normal foveal contour 8. HVF 24-2 Sita Fast OD: Reliable showing superior defects and inferior para-central defects; OS: Unreliable general reduction in sensitivity and enlarged blind spot LABS: HbA1C: 7.0, ESR (Westergren): 26, CRP (sensitive): >0.50, CRP (non-sensitive): 6.6, Fibrinogen: 375 (250-425), Platelets 99 (150- 400), reduced since 2006. 9. MRI of brain with and without contrast: No abnormality of the orbits, chronic infractions of left thalamus and right cerebellum. 10. IVFA: OD: Optic disc edema with some associated hemorrhages, leakage around the entire optic nerve, mostly temporally and inferiorly. No diffuse leakage in the macula, multiple pinpoint leakages in the macula and the periphery, consistent with microaneurysms. III. Differential Diagnosis: 1. Non-Arteritic AION a. Patient presented with atypical presentation, no color vision loss, and not significant vision loss 2. Arteritic AION: Giant cell arteritis a. Patient did not present any constitutional signs or symptoms of GCA, and no APD. 3. Optic Nerve head drusen a. Optic nerve presentation was acute; and not present at prior exam 6 days ago. 4. Optic nerve Papillitis a. Atypical presentation, no pain on eye movements, no color vision loss, no APD 5. Optic nerve neuritis a. Atypical presentation, no pain on eye movements, no color vision loss, no APD 6. Malignant hypertensive papilledema a. BP historically controlled on meds, last BP 123/71 b. Unilateral in presentation. 7. Central retinal vein occlusion a. Vascular tree without impingement, A/V ratio 2/3 8. Clinically significant macular edema a. Macular edema cystic in nature, no signs of exudates or hemes 9. Central serous choroidal retinopathy a. Serous detachment more nasal rather than central in fovea 10. Cystoid Macular Edema a. No history of Niacin use, recent cataract extraction or use of prostaglandins 11. Diabetic Papillopathy with macular edema 12. Peripapillary vitreoretinal traction syndrome with vitreo-macular traction IV. Diagnosis and Discussion: Diabetic papillopathy is a condition that has been undergoing continual research due to its scantily understood etiology. Many arguments have been made of whether to label diabetic papillopathy as a condition in it’s own entity or as part of a spectrum of AION secondary to vascular event. According to Slagle et al. diabetic papillopathy has different course of sequelae that can be distinguished from NAION. Both processes are diagnosis of exclusion, therefore all testing including Lab work: ESR, CRP, CBC, imaging: MRI with and with out contrast should be performed to rule out any major sight and life threatening pathologies. In diabetic papillopathy there is a micro vascular pathology consisting of capillary venostasis leading to an imbalance in the reabsorption of fluid causing edema and leakage at the optic nerve head. Symptoms can vary but are much less severe compared to AION. There is minimal or gradual vision loss, mild to no afferent pupil defect, unilateral or bilateral optic disc swelling, edematous nerve with telangectatic engorged vessels and hyperfluoresence on fluorescein angiography (FA). According to Slagle et al. FA is a very important test to perform to understand the etiology of the optic nerve edema. With diabetic papillopathy FA will show late stage leakage confirming the presence of venous stasis at the capillary beds. This is a much different finding when compared to FA performed on NAION patients. In NAION there is a hypo perfusion vascular event causing ischemia to the optic nerve therefore showing a hypofluorescence of the affected areas in the optic nerve. In this unique patient an OCT was initially used to help understand the condition, but may have revealed a masquerader of the underlying etiology. Elevation of the optic nerve head was noted on the Disc cube analysis. Concurrent with the optic nerve head elevation, adhesion of the vitreous to the retina was seen upon OCT scans of the macula and optic nerve head. Cystic changes of the foveal region with a sensory detachment extending from the fovea nasally to the optic nerve head was seen on OCT. Due to the macular changes the posterior vitreous should be taken into consideration for possible peripapillary vitreomacular traction with impending posterior vitreal detachment. Peripapillary vitreomacular traction is clinically observed in the process of posterior vitreous detachments (PVD). PVD’s occur very commonly among patients in their early 60’s. Most symptomatic patients complain about floaters in their line of sight that move with eye movements, flashes of light or even cloudy vision. The vitreous has the strongest adhesion to three locations in the retinal interface, the midperipheral retina at the vitreous base, foveal region and optic nerve head. Impending PVD’s can cause more damage at times as there is a constant pull on the retina at the posterior vitreal interface. Most impending PVD’s can be under diagnosed, as it is difficult to see clinical signs of this condition other than synerisis in the vitreous. A helpful tool that can be used is the OCT. The OCT of either the macula or optic nerve head can show the details of the interface and adhesion between the retina and vitreous. It can also portray the amount of damage or elevation caused by the vitreal adhesion. With help of the OCT it was interesting to see a strong adhesion of the posterior vitreous to the retinal interface that could possibly be causing the optic nerve head elevation and macular changes. V. Treatment and Management: 1. Monitor with dilated fundus exams 2. Patient Education 3. Continual care with primary care provider for control of diabetes and glycemic controls. VI. Conclusion: Diabetic papillopathy and peripapillary vitreal traction are diagnosis of exclusion. By ruling out other causes of disc edema with lab work, imaging, and flourescein angiography we can narrow down the differential diagnosis. In both pathologies, patients present with unilateral disc edema, no APD, and minimal visual function loss. For peripapillary vitreal traction, an impending PVD must be diagnosed usually with the help of OCT imaging. In this case the patient presented clinical signs and symptoms of both conditions. Also with both conditions, the treatment plans are very similar, it is best to monitor the patient with dilated fundus exams for any changes and have the patient on glucose control. Due to the past history of the fellow eye with temporal pallor disc secondary to NAION from diabetes, it is more likely that the patient is having a second diabetic event affecting the optic nerve head. VII. Bibliography Slagle, William Scott, Angela N. Musick, and Daniel R. Eckermann. "Diabetic Papillopathy and its relation to Optic Nerve Ischemia." Optometry and Vision Science 86.4 (2009): E395-E403. Print. Wisotsky, Burton J., Carmelina B. Magat-Gordon, and James E. Puklin. "Vitreopapillary Traction as a Cause of Elevated Optic Nerve Head." American Journal Ophthalmology 126.1 (1997): 137-139. Print. Zerrin, Bayraktar, Alacali Nilay, and Bayraktar Sukru. "Diabetic papillopathy in the type II Diabetic patients." Retina 22.6 (2002): 752-758. Print. .
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