American Journal of Ophthalmology
Sometimes improving alignment can come at an unexpected cost. Complete oculomotor nerve palsy (ONP) can cause severe exotropia due to loss of multiple extraocular muscle functions. Nasal transposition of the split lateral rectus muscle (NTSLR) is a surgical technique that redirects the lateral rectus nasally to improve alignment in patients with complete ONP. It offers meaningful cosmetic benefits, but can cause serous choroidal effusion or anterior segment ischemia, and until now, all such cases had retained some vision.
In this case, a 12-year-old girl with complete left ONP and ≥95 prism diopters of exotropia underwent NTSLR, achieving marked improvement in alignment. Within one week, she developed pain, eyelid swelling, and vision loss to no light perception. MRI demonstrated posterior displacement of the transposed lateral rectus toward the optic nerve. The authors proposed that posterior displacement of the transposed muscle may have compromised the central retinal artery and posterior ciliary circulation, producing combined arterial occlusion with choroidal ischemia, which is a mechanism distinct from the previously described vortex-vein compression that causes serous choroidal effusion. Decompression was offered but declined, and vision never recovered
This case highlights the potential for irreversible vision loss following NTSLR and the importance of recognizing postoperative pain, swelling, or visual decline as possible signs of vascular compression. Because even subtle variations in muscle traction or scleral fixation can compromise perineural circulation, close postoperative monitoring is essential, and early suture removal and decompression should be considered to reduce the risk of permanent vision loss.
A 73-year-old male with a PMHx of type 1 diabetes and CKD presents as a new patient with a chief complaint of intermittent blurry vision for the last 6 months. He denies flashes, floaters, pain, or any other visual symptoms. Visual acuity is 20/25 OU; the full exam is notable for pseudophakia, mild epiretinal membrane changes bilaterally, and a history of laser retinopexy OS for a retinal tear.
On dilated exam, an incidental finding is noted in the left eye: several deep, yellow-orange choroidal lesions scattered around the optic disc and extending toward the old laser retinopexy site, without signs of vitritis or intraocular inflammation. The right eye is unremarkable. FA shows minimal to no leakage from the lesions, while ICG angiography reveals extensive hypofluorescent spots. A broad uveitis workup, chest X-ray, and MRI of the brain return negative.
Given the imaging, the patient is started on an empiric oral steroid taper. Further chart review turns up outside records from seven years earlier, in which an outside ophthalmologist had identified similar choroidal lesions. Comparison of prior imaging indicates the lesions to be unchanged, with the patient never having received any immunosuppressive treatment in the interim.
What is the most likely diagnosis?
A. Birdshot chorioretinopathy
B. Multifocal choroiditis with panuveitis (MFCPU)
C. Primary vitreoretinal (CNS) lymphoma
D. Sarcoidosis or infectious uveitis (e.g., syphilis, tuberculosis)
E. Chorioretinal scarring from prior laser retinopexy
F. Indolent, nonprogressive multifocal choroidal lesions
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