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Vitrectomy and autologous thrombocyte adhesion of an accidental macular hole caused by Nd:YAG laser
  1. S POTTHÖFER,
  2. M H FOERSTER
  1. Freie Universität Berlin, Universitätsklinikum Benjamin Franklin
  2. Augenklinik und Poliklinik, Berlin, Germany
  1. S Potthöfer.

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Editor,—A 30-year-old physics scientist looked accidently with his left eye directly into the path of a 1.064 nm Nd:YAG laser beam. The laser variables were not known. He experienced a dramatic decrease in vision in this eye. Upon examination at the local hospital, the patient’s corrected vision was 0.16 for the left eye, the intraocular pressure (IOP) was within normal range, and the cornea and lens were unremarkable. On funduscopy, an obvious retinal defect, partially covered with blood, was observed in the region of the fovea. Vitreal bleeding could be seen above the temporal inferior vessel arcade. The ophthalmic examination of the right eye was unremarkable.

Initially, the patient was treated with high dose corticosteroids and acetazolamide. Ten days after the accident, he was transferred to our department for evaluation. At this time the corrected vision in the patient’s left eye with eccentric fixation was 0.2. A well defined circular macular hole (approximate diameter 300 nm) with upright edges was observed; its centre corresponded exactly with the foveola (Fig 1). The vitreal haemorrhage had decreased considerably.

Figure 1

Large macular hole with upright edges 6 weeks after Nd-YAG laser accident. The visual acuity was 0.2.

Over the following 4 weeks, no further treatment was given. As there was no change in the size of the foramen or an improvement in the patient’s vision 6 weeks after the accident, a vitrectomy of the left eye was undertaken. It included removal of the posterior vitreous membrane, particularly in the area of the edges of the hole. To aid its closure, an autologous thrombocyte concentrate (ATC) was placed over the retinal hole. The vitreous chamber was subsequently filled with 30% SF6 gas and the patient lay on his back for 6 hours, followed by a strict programme of prone position for 7 days. The postoperative course was uncomplicated.

During the follow up investigations in the first, second, third, sixth, and ninth postoperative months, a gradual increase in the patient’s vision to 0.6 was observed. The patient had lost his metamorphopsia and the size of the central scotoma remarkably decreased. There was no development of a nuclear cataract following gas vitreal replacement. In the first postoperative months, the edges of the former retinal hole were smoothly reattached and the foramen itself could only be seen with difficulty. From the fourth postoperative month onward, increasing pigmentation in the region of the hole could be observed (Fig 2); this corresponded with a further increase in the patient’s vision.

Figure 2

Posterior pole 9 month after vitrectomy and thrombocyte adhesion. The edges of the hole are reattached, centrally an retinal pigment epithelium hypertrophy developed. The visual acuity was 0.6.

COMMENT

Laser beam accidents occur mainly in those professionally involved with lasers.1-4 The majority of the ocular accidents involve the Nd:YAG laser, which is used in medicine for diagnostic and therapeutic purposes as well as in many areas of research.2 The mechanism of injury differs from the thermal retinal injuries caused by argon, krypton, diode, or colour lasers23 and involves the photomechanical and thermal tearing of the retinal tissue.3

Nd:YAG lasers use very short laser pulses of 1 μs or shorter. They produce mechanical side effects like expansive microexplosions by plasma formation. With the Q-switched operation mode pulse durations of a few nanoseconds to a few microseconds can be created. As the energy is delivered in short time spans, very high peak powers up to hundreds of megawatts can be emitted, which lead to tissue disruption.3

In milder injuries retinal or vitreal haemorrhages only are observed. The visual prognosis in the more severe injuries with tissue disruption is dependent on the distance of the retinal hole from the fovea. The usual conservatively treated patient experiences a severe and permanent decrease in vision.4

Thach et al reported five cases of Nd:YAG laser beam injuries whereby the patients were treated conservatively.4 In two of these five patients, the resulting retinal holes included the fovea and 1 year later, the visual acuity remained at 0.3 and 0.05, respectively. In one of the patients with a centrally situated hole, a spontaneous closure occurred within 3 weeks following the accident. This corresponded with an increase in the patient’s visual acuity. The two remaining patients had parafoveolar holes and the visual acuity was not severely affected by the accident.

In our patient, the retinal hole was large with involvement of the fovea and a severe decrease in visual acuity to 0.16. As there was no sign of a possible spontaneous closure 6 weeks after the accident, a similar operative procedure to that performed in older patients with idiopathic macular holes was performed.5 Idiopathic holes are thought to be caused by a tangential traction of the posterior vitreous or an epiretinal membrane resulting in a foveolar dehiscence and enlargement of the retinal hole. The rationale in performing a vitrectomy is to relieve the traction on the rims of the hole by vitreous cortical peeling and to achieve reattachment of the retina and recovery of the sensory function of the reattached photoreceptors. Chorioretinal adhesion around the region of the foramen edges has been aided by several adjuvants. Our experience with ATC in patients with idiopathic macular holes suggests that the closure rate is higher when this adhesive is combined with the gas tamponade instead of the latter procedure alone; this is supported by the results of Gaudric et al in their pilot study.6 The preparation of the autologous thrombocyte concentrate followed the technique described by Gaudric et al6 and was performed just before vitrectomy.

References

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