A previously happy 34-year-old LASIK patient presented in the spring of 2001 after having impaled his left eye with a torque screwdriver while installing a refrigerator door. Notably, the patient wore no eye protection and reported that he did not think his vision had significantly decreased. He had undergone uneventful LASIK 2 years prior with the Automated Corneal Shaper™ (Bausch & Lomb Surgical, Claremont, CA) and the S2 Excimer laser (VISX, Inc., Santa Clara, CA). His preoperative refraction was -6.75 + 0.5 X 090 OD, and -7.25 + 1.0 X 095 OS. One week prior to the trauma, his uncorrected acuity in the left eye was 20/30-, and his refraction was -0.5 + 0.5 X 073 for 20/25+ 2 best spectacle-corrected visual acuity (BSCVA).
The patient's evaluation on the day of trauma revealed an uncorrected visual acuity of 20/20 OD and 20/40 OS. Slit lamp examination of the left eye showed what appeared to be a dislodged flap fragment. Further inspection revealed that three quarters of the flap was completely intact, but its center had been perforated to the depth of the prior interface, which extended from the central position superonasally. While at the slit lamp, I used a forceps to elevate the quartile flap, which I found was “hinged” superonasally. In essence, the patient had created a “mini-me” flap (as I have affectionately coined this case) by perforating a section of the original LASIK flap. I elected to use a Barraquer wire speculum while I washed out the interface with sterile, buffered saline solution, and let the flap/interface air-dry for approximately 2 minutes. The “mini-me” flap remained in an excellent anatomic position without sutures or a contact lens. I prescribed Quixin™ prophylactic antibiotics (Santen, Inc., Napa, CA), and closely monitored the eye for diffuse interface keratitis. My hope for repositioning the flap was the chance that visual aberrations would not be too dramatic, and that this intervention might suffice.
Over the next 3 months, the wound edges began to form a mild to moderate amount of new collagen, as well as a few epithelial cysts in the vertical portion of the wound. In addition, topography mapping revealed irregular astigmatism. The patient's uncorrected vision was 20/50, and he reported double imagery. Retinoscopy revealed an irregular reflex. The patient's BSCVA was 20/40 +1 with a refraction of +0.25 + 0.75 X 013, and the use of a rigid contact lens did not significantly improve his visual acuity.
It became evident that the patient's posttraumatic healing had induced irregular astigmatism that was not improving. Surgical options at this time included flap removal, flap transplant, and full-thickness grafting. I opted to perform the flap transplant, and grafted donor tissue from the corneal scleral rim, using the Anterior Chamber Maintainer System and Automated Corneal Shaper (Bausch & Lomb Surgical) to harvest a tissue flap of comparable dimensions. I lifted and truncated the host flap with a No. 64 blade. The donor epithelium was poor, so I placed an 8-bite antitorque suture. At 5 days postoperatively, the flap had totally re-epithelialized. However, 1+ central diffuse interface keratitis was present. I prescribed topical corticosteroids (prednisolone acetate 1%) for 10 days, and the suture was removed at postoperative day 9.
Three months postoperatively, the patient's uncorrected vision in the left eye was 20/30. His manifest refraction was + 0.50 + 0.75 X 165 for 20/25 visual acuity. Performing corneal topography and WaveScan WavePrint™ Analysis (VISX, Inc.) revealed a slight central flattening of the corneal surface in the 1-mm optical zone. The patient did not subjectively note any doubling of vision. I plan to see the patient in 3 months to assess his refraction and BSCVA, as it has improved on serial exams following suture removal. If there is significant residual refractive error present at the 6-month visit, I may perform additional laser vision correction.
This case illustrates the role that lamellar transplantation can play in post-LASIK complications. It worked well for this patient because the bed surface was not disrupted and had not lost tissue. If bed tissue had been lost, conducting a lamellar transplant would have been like placing a clear window over a poor optic, which would not yield optimal results. I have performed flap transplants for several conditions, including flap perforation due to an iatrogenic cause, an anterior corneal reconstruction following PRK haze, and this case. If used in the proper situations, the technique can provide visual restoration and permits relatively easy laser vision refractive enhancement if it is needed after the reconstructive effort is complete and stabilized.
John F. Doane, MD, FACS, is in private practice with Discover Vision Centers in Kansas City, Missouri, and is Clinical Assistant Professor of the Department of Ophthalmology, Kansas University Medical Center. Dr. Doane may be reached at (816) 350-4539; jdoane@discovervision.com
