The increasing number of LASIK surgeries for myopia has led to an awareness of the potential hazards and retinal complications of this procedure. Reported posterior segment complications include rhegmatogenous retinal detachment,1 choroidal infarction,2 macular, submacular, or premacular hemorrhage,13 macular hole,4 central or branch retinal vein occlusion,5 retinal nerve fiber layer defects,6 optic neuropathy,7 and cystoid macular edema.8
We report a 30-year-old woman who underwent bilateral myopic LASIK. Retinal phlebitis with cystoid macular edema developed in both eyes 8 weeks postoperatively. Visual acuity returned to normal after treatment with oral steroids.
A 30-year-old woman with an insignificant medical and ocular history underwent bilateral myopic LASIK. Before LASIK, refractive error was -7.50 -3.25 × 15° in the right eye and -8.00 -2.75 × 140° in the left eye. Best spectacle-corrected visual acuity (BSCVA) in both eyes was 20/20. Postoperative uncorrected visual acuity (UCVA) was 20/20 in both eyes.
Eight weeks after surgery, the patient experienced onset of blurred vision in the left eye. Three days later, the same symptom occurred in the right eye.
On initial evaluation, BSCVA was 20/100 in the right eye and 16/200 in the left eye. Anterior segment examination was unremarkable except for a well-healed LASIK flap and trace subepithelial haze in both eyes. Intraocular pressure (IOP) was normal. The vitreous was free of cells. Fundus examination showed several focal whitish patches in the parafoveal and juxtafoveal areas and lack of foveal reflex in both eyes (Fig IA). Fluorescein angiography revealed late staining of the dye in the wall of the dilated venules (the left eye more than the right eye) and mild cystoid macular edema bilaterally (Fig IB).
Visual field testing with Humphery Central 30-2 Threshold Test (Humphery Instruments, San Leandro, Calif) was normal in the right eye, but demonstrated a paracentral scotoma in the left eye. No other extraocular lesion was observed. Results of laboratory studies were normal. Therefore, diagnosis of retinal phlebitis in both eyes was made. The patient was treated with oral corticosteroids with tapering dose.
On subsequent examinations, visual acuity continued to improve. One month after treatment, UCVA was 20/30 in the right eye and 20/200 in the left eye. Best spectacle-corrected visual acuity improved to 20/20 in the right eye and 20/25 in the left eye. Whitish fundus patches decreased in number and size in both eyes. Fluorescein angiography demonstrated moderate resolution of cystoid macular edema and no venous dye staining in both eyes. Visual field in the left eye also returned to normal.
Two months after treatment, UCVA was 20/20 in the right eye and 20/30 in the left eye (BSCVA 20/20). Fundus examinations revealed faint whitish patches and normal foveal reflex in both eyes. On final examination 6.5 months after treatment, UCVA had returned to 20/20 in both eyes. Fundus examinations in both eyes were essentially unremarkable except for some mottling changes of retinal pigment epithelium at the posterior pole of the right eye (Fig 2A). Fluorescein angiography of both eyes revealed no venous dye staining or cystoid macular edema (Fig 2B).
Retinal vasculitis has posed a difficult diagnostic problem for ophthalmologists for many years. It is a sight-threatening inflammatory disease with an unknown etiology and pathogenesis. Retinal veins, capillaries, and arterioles may be involved and veins are most commonly affected. It may occur as a complication of infection, neoplasm, degenerative disorders, or be associated with systemic inflammatory diseases (eg, Behcet's syndrome, sarcoidosis, uveomeningitis, HLA-B-27 related arthritis) or isolated findings.9 In a study by Graham et al9 of 150 patients with idiopathic retinal vasculitis, 67 (45%) patients had isolated retinal vasculitis and 83 (55%) patients had retinal vasculitis associated with systemic inflammatory disease. In our patient, we found no evidence of associated systemic inflammatory disease, infection, or neoplasm. The patient's reduction in visual acuity was not caused by myopic subretinal neovascularization or hemorrhage but by cystoid macular edema. No previous ocular disease was reported that could have explained cystoid macular edema, and no events (trauma or other inflammation) other than LASIK occurred. Therefore, we believe this patient's retinal phlebitis with cystoid macular edema may be associated with LASIK.
The rise and decompression of IOP during suction and the acoustic shock waves created by the laser might have been responsible for the retinal phlebitis seen in our patient.1 An IOP of at least 65 mmHg is necessary to create a corneal flap with the microkeratome. During this time, the shape of the anterior segment may change rapidly and structures posterior to the suction ring are also compressed in sequence.1011 When the suction stops and the suction ring is released, ocular decompression leads to dynamic equatorial elongation and anterior-posterior contraction.10 This barotrauma is analogous to what happens in closed-eye injury1213 and can alter delicate retinal structures, especially small vessels, and induce vitreoretinal traction at the vitreous base and posterior pole.1014 Sudden elevation of IOP also disturbs the retinal circulation and increases venous pressure, which results in retinal ischemia. All of these conditions may aggravate the original impaired blood-retinal barrier in highly myopic eyes and increase vascular permeability,15 leading to the loss of integrity of tight junctions of endothelial cells.
Laser in situ keratomileusis-induced shock waves can generate up to 100 atm.16 Although the pressure decreases steadily to values below 10 bars toward the retina,1 we believe it may still cause mechanical stress to the retina, resulting in structural damage and intraocular inflammation. In addition, total energy and duration increase with higher refractive error and the effect of mechanical stress may be more severe in higher myopia, which has more liquefaction of the posterior vitreous gel.17
Of course, one case report does not prove a causeand-effect relationship between LASIK and retinal phlebitis. However, this report should alert ophthalmologists to the importance of determining the risk factors, performing echography of vitreous, indirect ophthalmoscopy with scleral depression, and possibly photography and fluorescein angiography of macula to determine whether the LASIK procedure itself might exacerbate the original pathologic changes of myopia.
Figure 1. Fundus photograph and fluorescein angiogram 8 weeks after LASIK. A) Fundus photographs showed several focal whitish patches in the parafoveal and juxtafoveal areas (arrows) and lack of foveal reflex in both eyes. B) Late phase of fluorescein angiography revealed staining of the dye in the wall of the dilated venules (small arrows, the left eye more than the right eye) and mild cystoid macular edema bilaterally (large arrows).
Figure 2. Fundus photograph and fluorescein angiogram 6.5 months after treatment. A) Fundus photographs in both eyes were essentially unremarkable except for some mottling retinal pigment epithelium at the posterior pole of the right eye (arrowhead). Normal foveal reflex was noted in the left eye (arrow). B) Fluorescein angiography revealed no venous dye staining or cystoid macular edema.
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