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LASIK induced choroidal infarcts
  1. R B Jain1,
  2. A Chopdar2
  1. 1RBM Eye Institute, Delhi - 110 085, India
  2. 2East Surrey Hospital, Redhill, Surrey RH1 5RH, UK
  1. Correspondence to: Dr R B Jain; drrbjain{at}bol.net.in

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Laser in situ keratomileusis (LASIK) is now commonly used for correction of refractive error. Anterior segment complications relating to flap occurs occasionally.1,2 However, posterior segment complications are rare.3–10 Choroidal infarct following LASIK, to our knowledge, has never been reported. Here we report a case of bilateral choroidal infarct following a routine LASIK procedure.

Case report

A 23 years old woman underwent a LASIK excimer procedure to both eyes for correction of hypermetropia. Her preoperative refractive errors were right eye +5.00 and left eye +3.75, improving vision to 6/6 in the right eye and 6/5 in the left eye. However, the axial length was not measured. She had no other ocular pathology. The anterior segments and the fundi were normal. She was generally healthy and her blood pressure was 120/76 mm Hg. Her routine blood tests and chest x ray were within normal limits. She did not have any history of thromboembolic phenomenon, therefore a routine thrombophilia screening test was not performed.

An uncomplicated routine LASIK procedure was performed on 31 August 2001 in both eyes. The keratome used was Hansatome. Postoperatively, she complained of reduced and wavy vision, with floaters in both eyes. However, 2 months later (3 November 2001) she had been referred to one us (RBJ). On examination now her vision was 6/18 with +1.0 D sph/+1.75D cyl @ 75° and 6/18, with −1.25 D sph/+1.50 D cyl @ 70° in right and left eye respectively. There were normal LASIK scars and no corneal staining. The intraocular pressure (IOP) was 20 mm Hg in both eyes. The anterior chambers were quiet and pupils reacted normally. The retinal examination showed multiple yellow-grey deep retinal lesions at posterior poles in both eyes. In each eye, there was at least one larger triangular shaped lesion measuring approximately 2 × 3 disc diameters in size temporal to the macula. There were several smaller satellite lesions around the macula, which were somewhat polygonal in shape. These lesions had sharp, well defined borders with a mild degree of retinal oedema. It should be noted that the lesions were almost symmetrical in each eye. The discs and blood vessels appeared normal. Fluorescein angiography showed normal transit of dye through the discs and blood vessels. The arteriovenous phase in each eye showed two typical triangular hyperfluorescent areas with apex pointing posteriorly. The smaller polygonal lesions showed punctate hyperfluorescence. The intensity of hyperfluorescence increased with the concentration of circulating dye during the transit and faded away towards the later phases of the angiography. The lesions were situated at a deeper level in comparison with the retinal blood vessels. The late phase in both eyes showed generalised staining of all lesions (Fig 1).

Figure 1

(A) The arteriovenous phase of the fluorescein angiogram of the right eye shows two punctate hyperfluorescent triangular lesions with apex pointing towards the posterior pole on the temporal side of the macula. There are several smaller lesions above and below the macula. (B) The late venous phase of the fluorescein angiogram of the left eye done at the same session shows a large palquoid lesion on the temporal side of the macula with increased hyperfluorescence due to staining of the lesion.

The patient was treated with 60 mg of oral prednisolone in two divided dosage for 3 weeks which was then reduced to 20 mg twice daily. She was reviewed fortnightly. She was also given flurbiprofen sodium 0.03% as local anti-inflammatory drops to both eyes three times daily for 4 weeks.

After 6 weeks the retinal oedema settled with visible fine peppery pigmentation over the lesions. Fluorescein angiography was repeated which showed increasing hyperfluorescence of all lesions during the transit with minimal staining towards the late phase.

On her final review her visual acuities were right eye 6/9 with +1.0 D sph/+0.50 D cyl @ 180° and in left eye 6/6 with −1.0 D sph/−0.50 D cyl @ 180°. The IOP was 18 mm Hg in each eye. The anterior chambers were quiet. The fundi showed well defined fine pigmented lesions with well defined borders. There were no fresh lesions or change in size of earlier lesions.

Comment

Flap related complications following LASIK surgery are well documented.1,2 Posterior segment complications such as bilateral macular haemorrhage,3 premacular subhyaloid haemorrhage,4 anterior ischaemic optic neuropathy (AION),5,6 retinal detachment,7,8 field defects,9 and macular hole10 have also been reported but to the best of our knowledge this is first case report of choroidal infarcts occurring after LASIK.

During the flap making stage of LASIK, application of suction may increase the IOP to as much as 60 mm Hg or even more. This increase in IOP can result in poor perfusion leading to circulatory imbalance of the retina and the choroid. Alteration of perfusion pressure in susceptible individuals may precipitate clinical features of AION or choroidal infarct. In our case the increase in IOP might have reached much higher or be sustained for a much longer period. This might have been the basis of infarction of choriocapillaris lobules. The smaller lobules coalesce to form larger lesions. Subsequent pigment changes seen were due to changes in the overlying retinal pigment epithelium.

Bilateral almost symmetrical lesions indicate that it could not have occurred exclusively as a result of raised IOP during LASIK. Therefore it is possible that this patient must have had other risk factors and she was susceptible to the effect of raised IOP. The refractive surgeons must be aware of the general physical status of a patient’s health while considering keratorefractive surgery where a rise of IOP may be an associated factor.

References

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