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Clinicopathologic Reports, Case Reports, and Small Case Series
Octomber 2007

Laser In Situ Keratomileusis Flap Necrosis After Trigeminal Nerve Palsy

Arch Ophthalmol. 2007;125(10):1423-1425. doi:10.1001/archopht.125.10.1423

Laser in situ keratomileusis (LASIK) surgery can induce changes in the corneal epithelium owing to a neurotrophic phenomenon as a consequence of the sectioning of nerves during flap cutting.1 More profound alterations have been reported with a superior hinge, compared with a nasal hinge, and the associated effects tend to normalize over approximately 6 months,2 although it is possible that complete reinnervation and recovery of the basal state may not occur.3 Epithelial damage has also been associated with a reduced blinking rate, which favors corneal exposition.4

To date, various cases of post-LASIK neurotrophic epitheliopathy have been reported, characterized by symptoms and signs of dry eye and a spotted distribution of rose bengal dye. Recommended treatments include artificial tears, tear plug, and autologous serum,5 among others. Herein, we report a case of severe corneal flap necrosis that occurred after formation of a trigeminal nerve lesion of vascular origin. The patient was successfully treated with autologous plasma rich in growth factors (PRGF).6

Report of a Case

A male patient, 48 years old and a smoker, underwent LASIK surgery of both eyes in 2000 for myopia (−5.00 OD and −6.00 OS). A microkeratome (Hansatome; Bausch & Lomb, Rochester, New York) was used to produce a cut with a diameter of 8.5 mm and a depth of 160 μm. Postoperative evolution was without incident, and the patient demonstrated satisfactory visual and clinical recuperation.

In December 2003, the patient arrived at the accident and emergency service of a local general hospital with what appeared to be a left-sided cerebrovascular injury, which was confirmed on brain computed tomographic scan. The same scan revealed several areas of small lacunar infarctions, one of them affecting the deep area of the right medial cerebral artery, for which the patient was asymptomatic. He was hospitalized for 5 days.

In May 2004, as a result of visual loss in his left eye in the absence of pain, the patient consulted his ophthalmologist, who observed flap necrosis at the inferior edge (Figure 1). Lubricant treatment was initiated, and because of poor evolution, the patient was referred to our center for further treatment. At that stage, he had necrosis of the temporal half of the flap associated with anesthesia of the left trigeminal region. The patient was treated successively during the following weeks with artificial tears without preservatives, tear plug, autologous plasma, cyanoacrylate adhesive, amniotic membrane patch, and a bandage contact lens. Two months later, epithelialization was achieved, leaving as a consequence an anterior stromal opacity and notable topographic irregularity (Figure 2), which only permitted a best-corrected visual acuity of less than 20/200, as measured with eyeglasses.

Figure 1.
Flap necrosis at the inferior edge of the laser in situ keratomileusis flap.

Flap necrosis at the inferior edge of the laser in situ keratomileusis flap.

Figure 2.
Orbscan (Bausch & Lomb, Rochester, New York) showing the corneal irregularity after partial flap necrosis.

Orbscan (Bausch & Lomb, Rochester, New York) showing the corneal irregularity after partial flap necrosis.

To improve corneal irregularity, we proceeded in October 2005 to extirpate the flap remnant and apply temporal tarsorrhaphy together with 3 layers of amniotic membrane to increase the permanence period, together with temporal tarsorrhaphy. Despite this procedure, an extensive epithelial defect in the resected zone persisted 1 month later (Figure 3). Consequently, in December 2005 and with the informed consent of the patient, we decided to commence treatment with PRGF (GAC Medical, Vitoria, Spain). Initially, approximately 20 μL (1 drop) was administered every 2 hours, progressively reducing the frequency of administration in accord with the observed improvement. During the following 6 weeks, progressive epithelial closure was observed (Figure 4), although long-term irregularity of the epithelium and opacity of the underlying stroma persisted. The final best-corrected visual acuity was 20/200.

Figure 3.
Epithelial defect after the amniotic membrane dissolution (lissamine green).

Epithelial defect after the amniotic membrane dissolution (lissamine green).

Figure 4.
Improvement of the epithelial defect after treatment with autologous plasma rich in growth factors.

Improvement of the epithelial defect after treatment with autologous plasma rich in growth factors.


This case presents 2 particularly salient aspects. First, we report flap necrosis due to a trigeminal nerve lesion more than 3 years after LASIK surgery. Second, we describe a novel method for the successful treatment of neurotrophic ulcers.

The first aspect raises doubts about the capacity of a LASIK-operated on eye to respond to certain situations that involve aggression to the ocular surface. Without ruling out the possibility that the trigeminal lesion may have caused a corneal ulcer, this patient demonstrated flap necrosis with minimum repercussion in the deep corneal layers. On removal of the flap remains and despite measures to favor reepithelialization, signs of wound healing were not apparent. In light of this poor response and the risk of corneal melting, treatment with PRGF was initiated. This treatment has been used previously in maxillofacial and orthopedic surgery. Treatment with PRGF involves obtaining platelet and plasma proteins from the patient. The extract contains a high concentration of growth factors that can enhance the mechanisms of repair and regeneration in distinct tissues.6 It is prepared by centrifuging a sample of the patient's blood and obtaining a plasma fraction enriched in platelets from which growth factors are released with the addition of calcium chloride. This treatment is being used in other patients with different forms of neurotrophic keratitis and is being subjected to further evaluation to characterize its efficacy.

Correspondence: Dr Durán, Instituto Clínico-Quirúrgico de Oftalmología, Virgen de Begoña 34, 48006 Bilbao, Spain (duran@icqo.org).

Financial Disclosure: None reported.

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