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Photodynamic therapy for corneal neovascularisation and lipid degeneration
  1. B J Brooks,
  2. B K Ambati,
  3. D M Marcus,
  4. A Ratanasit
  1. Department of Ophthalmology, Medical College of Georgia, Augusta, GA, USA
  1. Correspondence to: Bonnie J Brooks MD Department of Ophthalmology, Medical College of Georgia, Augusta, GA 30912, USA, bbrooksmail.mcg.edu

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Corneal neovascularisation, and subsequent lipid keratopathy is a potential complication of penetrating keratoplasty, corneal trauma, and corneal ulceration. Corneal neovascularisation increases the risk of corneal opacification and graft rejection. Photodynamic therapy (PDT) using systemically or topically administered photosensitisers to occlude corneal vessels has successfully produced microvascular thrombosis without causing overt damage to surrounding tissues in animal models.1,2 The efficacy of PDT is achieved through the generation of reactive oxygen species from the interaction of light, oxygen, and photosensitisers such as verteporfin,3 commonly used to treat choroidal neovascularisation. Although animal models have demonstrated treatment parameters for corneal PDT,1 there have been no human studies to date. We present a case of lipid keratopathy secondary to corneal neovascularisation that was successfully treated with corneal PDT.

Case report

Our patient is a 36 year old white man who underwent penetrating keratoplasty in 1999 secondary to keratoconus complicated by acute hydrops. He presented in May 2003 with decreased vision due to lipid keratopathy secondary to corneal neovascularisation. The affected area was approximately 2.7 mm×2.7 mm at the inferonasal margin of the corneal graft (fig 1). Best corrected visual acuity (BCVA) in the affected eye was 20/200. After reviewing treatment options at length with the patient, the decision was made to pursue PDT in an attempt to occlude the corneal vessels. Lipid formulated verteporfin was administered intravenously at a dose of 3.64 mg/m2 of body surface area. Ten minutes after the infusion, light was delivered using a 689 nm non-thermal laser light for 300 seconds over a 3 mm×3 mm spot size. A total light dose of 4.5 J/cm2 was given. At the 2 week follow up, the corneal opacity was significantly reduced in size, and significant regression of corneal neovascularisation was noted (fig 2A); BCVA was 20/50. At 6 weeks after treatment continued regression was realised (fig 2B) and BCVA was 20/30.

Figure 1

Lipid keratopathy secondary to corneal neovascularisation after penetrating keratoplasty.

Figure 2

(A) Two weeks after photodynamic therapy (PDT). (B) Significant regression of neovascularisation and lipid deposits 6 weeks after PDT. Visual acuity improved to 20/30.

Comment

While the cost of photosensitisers may be limiting,3 PDT offers a minimally invasive alternative treatment of corneal neovascularisation. Rapid elimination of photosensitisers from the body with minimal local and systemic side effects2 make PDT an attractive alternative to repeat corneal grafting. The most common adverse reactions associated with verteporfin include visual disturbances, injection site reactions, and photosensitivity reactions.3 Because there is little or no damage to the surrounding tissues, PDT is a viable option for patients with decreased vision due to lipid keratopathy secondary to corneal neovascularisation.4 Additionally, because of the safety of PDT, multiple treatment sessions for recurrent or resistant neovascularisation are possible.

References

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