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Case report

Unusual cause of visual symptoms after bilateral laser in situ keratomileusis

Sandhu, Sukhpal S. MB ChB, MRCOphth; Gnanaraj, Lawrence MBBS, FRCS, FRCSEd; James, Andy MB ChB, MD, FRCP; Figueiredo, Francisco C. MD, PhD, FRCOphth

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Journal of Cataract & Refractive Surgery: February 2005 - Volume 31 - Issue 2 - p 446-449
doi: 10.1016/j.jcrs.2004.09.017
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Abstract

Laser in situ keratomileusis (LASIK) is increasingly requested by patients and chosen by surgeons to manage low and moderate myopia, hyperopia, and astigmatism.1–4 The procedure has unique postoperative challenges that must be identified and managed effectively. We present a serious systemic cause of visual symptoms in a patient following successful bilateral LASIK.

Case Report

Bilateral LASIK was performed in a healthy 51-year-old white woman at a private clinic in January 2002. The patient sought repeated consultation for unexplained visual symptoms soon after surgery. She was aware of a constant shadow in the left eye vision and was not happy with the corrected distance and near vision.

Preoperatively, the patient had moderate hyperopia (right eye, +4.50 +0.25 × 45; left eye, +3.75 +0.50 × 50) with a best corrected visual acuity (BCVA) of 6/9 in the right eye and 6/7.5 in the left eye. Ocular and general health and family history were unremarkable except for treated hypercholesteremia.

One month after bilateral LASIK, the BCVA was 6/9 in the right eye (−0.50 −0.25 × 25) and 6/12 in the left eye (+1.75 sphere). The patient reported variable vision postoperatively, which was still apparent 2 months later when the BCVA was 6/18 in both eyes (right eye, plano +1.75 × 100; left eye, +1.00 +1.50 × 90). Pachymetry was 472 μm in both eyes, which was considered adequate for possible retreatment by the referring ophthalmologist.

Two months later, the patient's vision was worse and she had problems driving. The BCVA was 6/18 in the right eye (+1.50 −1.25 × 50) and 6/36 in the left eye (+1.50 −1.25 × 140). Ocular examination was normal. The patient was referred to our service for a second opinion and possible enhancement surgery.

The patient came to our department 6 months after LASIK for initial assessment of reduced vision and shadows. She was well except for intermittent bifrontal headaches. The BCVA was 6/9 in the right eye (+0.50 −0.50 × 20) and 6/36 in the left eye (no improvement with lenses). Corneal topography was compatible with central hyperopic laser treatment, and the pupils were normal.

Color vision with Ishihara plates showed disparity, with 14/17 in the right eye and 1/17 in the left eye. No relative afferent pupil defect was present. On confrontation, the left eye had subjective desaturation of red color compared with the right eye. Anterior segment examination showed a LASIK flap in position with no evidence of complications; disc examination suggested a possible temporal pallor in both fundi.

Further investigations were initiated as it was apparent that the patient had unexplained reduced vision and visual field symptoms, suggesting possible optic neuropathy in the left eye. A visual field test (Humphrey Analyzer) showed upper bitemporal quadrantanopia defects (Figure 1). Visual evoked potentials in the left eye showed significant delayed responses, suggesting left optic nerve function impairment, and a normal right eye.

Figure 1.
Figure 1.:
Humphrey visual field plots at presentation. A: Left eye. B: Right eye.

A repeat Goldmann visual field test confirmed the defects were mainly in the bitemporal upper quadrants but also involved the upper medial visual fields (Figure 2). A magnetic resonance imaging (MRI) scan showed a large pituitary mass extended laterally into the cavernous sinuses and superiorly, causing elevation and compression of the optic chiasms with marked distortion of the anterior third ventricle. There was no hydrocephalus (Figure 3). Hormonal assay suggested adequate adrenal cortisol reserve (maximum cortisol during short synacthen test, 1224 nmol/L) with inappropriately low lutein hormone (<1.0 IU/L) and follicle stimulating hormone (1.5 IU/L) for a postmenopausal female not on hormone replacement therapy, suggesting partial hypopituitarism. Thyroid stimulating hormone was normal (1.78 mIu/L) and free thyroxine was low (9 pmol/L), indicative of central hypothyroidism. Prolactin was elevated (1334 μm/L), consistent with pituitary stalk compression.

Figure 2.
Figure 2.:
Goldmann visual field plots preoperatively. A: Left eye. B: Right eye.
Figure 3.
Figure 3.:
Magnetic resonance imaging scan. Left: Sagittal view. Right: Coronal view.

Transnasal and transsphenoidal excision of the patient's pituitary tumor was performed in November 2002. Histology revealed it to be a pituitary null cell adenoma.

The visual field defects resolved as a result of the decompression of the optic chiasm postoperatively. However, the patient is still aware of a shadow in the right eye, evident on the Goldmann visual field plot (Figure 4). The visual evoked potential and vision have improved.

Figure 4.
Figure 4.:
Goldmann visual field plots postoperatively. A: Left eye. B: Right eye.

Discussion

Laser in situ keratomileusis is the most widely performed procedure to correct refractive errors. Postoperative complications after LASIK occur in 1.8% to 3.1% of cases and are well documented.1–4 Early complications (ie, presenting within the first few days of surgery) include diffuse lamellar keratitis, interface debris, flap striae, infection, and a shifted and dislodged flap. Delayed complications (ie, weeks to months after surgery) include epithelial ingrowth, stromal melt, overcorrection, undercorrection, regression, haze, irregular astigmatism, decentration, central island, and keratectasia.

In our patient, no signs in the anterior segment explained the visual symptoms. Ancillary tests (refraction, corneal topography, and pupillometry) confirmed this. However, it was important to consider other causes for the patient's visual symptoms. Posterior segment pathology was suspected as there are reports of a 0.06% incidence of vitreoretinal conditions5 and optic neuropathy diagnosed after LASIK.6–10 These cases involved patients who had symptoms of visual disturbance with proven prechiasmal (optic nerve or nerve-fiber layer) visual field defects that were thoroughly investigated, including neurological imaging (MRI of head in most cases). In our case, a young woman with no history of glaucoma had visual field defects typical of chiasmal or postchiasmal pathology.11 Vital investigations were required to make a clinical diagnosis once the possible causes of the symptoms were recognized. The final surgical outcome was not compromised by the delay during investigation.

This case highlights the importance of preoperative and postoperative patient assessment. The symptoms in our patient would not have been correctable by further refractive laser surgery. We recommend all laser patients have a comprehensive ophthalmological examination and documentation with full investigation of preexisting abnormalities. This must remain a priority as there have been isolated reports of nonophthalmologists (eg, dermatologists and plastic surgeons) performing LASIK.6 Patients' symptoms and their reasons for requesting the surgical procedure should be established to ensure the safety of this now common procedure is optimal.

References

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2. Stulting RD, Carr JD, Thompson KP, et al. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999; 106:13-20
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© 2005 by Lippincott Williams & Wilkins, Inc.