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Abstract
This case demonstrates the importance of an ophthalmic consultation on all patients
admitted with a diagnosis of optic neuritis. VKH can easily be mistaken for other
pathologies leading to treatments that risk the patient’s vision. Early diagnosis and
appropriate treatment are necessary to reduce the risk of permanent vision loss.
I. Case History
- Patient admitted to hospital for dizziness and decreased vision
- Tentative diagnosis of MS despite negative MRI (Neurology Dept)
- Quick steroid taper leading to return of symptoms
- Patient managed as atypical MS
- Internal medicine attending concerned about bilateral red eyes and decreased vision
- Ophthalmic consult ordered
Patient demographics
- Traditional patient is more pigmented (tends to be female)
- Increasing number of Hispanics diagnosed with VKH
Chief complaint
- Deceased vision (bilateral)
- Dizziness, fever, nausea (viral like)
Ocular, medical history
- none
Medications
- BCP and albuterol inhaler upon admission
- Upon consultation
o Solu-Medrol 1 g IV q. day
o Lovenox 40 mg subcu daily
o Atenolol 50 mg p.o. daily
o Lisinopril 10 mg p.o. daily
o Acetaminophen 500 mg q. 8h
Other salient information
II. Pertinent findings
Clinical
- bilateral red eyes with decreased VA
- bilateral panuveitis/choroiditis
- bilateral serous retinal detachments (photos)
- mild vitritis OU
Physical
- no vitiligo
- no poliosis
Laboratory studies
- blood work results
- lumbar puncture results
Radiology studies
- Negative MRI (x2)
Others
- Fluorescein angiography results
-multiple areas of placoid leakage and subretinal accumulation of dye
- OCT
-serous retinal detachments OU
- EEG
-results
III. Differential diagnosis
Primary/leading
-Vogt-Koyanagi-Harada Disease
Others
-sympathetic ophthalmia
-uveal effusion syndrome
-posterior scleritis
-sarcoidosis
-acute posterior multifocal placoid pigment epitheliopathy (APMPPE)
-primary intraocular B-cell lymphoma
IV. Diagnosis and discussion
-definition
-Stages
-prodromal, acute uveitic chronic, chronic recurrent
-Complete VKH vs Incomplete VKH vs Probable VKH
-high prevalence of probable VKH diagnosis
-blood work, OCT, fluorescein angiography, lumbar puncture, MRI
Uniqueness of VKH
-bilateral serous retinal detachments are a key factor
- bilateral pan-uveitis
V. Treatment, management
Treatment and response to treatment
-high dose oral steroids with extremely slow taper
- Results of patient abruptly discontinuing treatment
-extreme exacerbation of symptoms and inflammation
-OCT and Photos
-immediate initiation of high dose steroids
-quick resolution of symptoms (photo and OCT)
-6 month tapers are common
-need for close interaction with internal medicine doctor to manage steroid complications
-necessity for long term treatment
-varying the course of disease with early treatment
-oral vs intravenous vs intravitreal steroids
-role of immunosuppressants
-complications
-prognosis
Bibliography
1. Rajendram R, Evans M, Rao N. Vogt-Koyanagi-Harada Disease. Int Ophthalmol Clin.
2005;45(2):115-134.
2. Beniz J, Forster DJ, Lean JS, et al. Variations in clinical features of the Vogt-KoyanagiHarada syndrome. Retina. 1991;11:275-280.
3. Maruyama Y, Kishi S. Tomographic features of serous retinal detachment in VogtKoyanagi-Harada syndrome. Ophthalmic Surg Lasers Imaging. 2004;35:239-242.
4. Andrade RE, Muccioli C, Farah ME, et al. Intavitreal triamcinolone in the treatment of
serous retinal detachment in Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol.
2004;137:572-574.
VI. Conclusion
Clinical pearls
- An ophthalmic consult is needed on all optic neuritis patients, especially atypical
presentations
-
VKH must be treated aggressively and a slow steroid taper is necessary to decrease
the risk of re-inflammation