Intraoperative and Postoperative Complications of Laser In situ Keratomileusis

Jennifer G Bromley; Trent D Albright; Bhairavi Kharod-Dholakia; Joung Y Kim

Disclosures

Expert Rev Ophthalmol. 2012;7(1):25-31. 

In This Article

Early Postoperative Complications

Flap dislocation is displacement of the flap from the stromal bed. It typically occurs within the first 24 h postoperatively. It can occur later, secondary to trauma, but this is rare. The patient often has significant pain with severely reduced vision and urgent treatment is required. The flap, which is often edematous and rolled, should be lifted, flattened and repositioned. The bed should be cleaned and rid of debris and epithelial cells prior to repositioning the flap[21] and bandage contact lens should be placed to avoid recurrent dislocation. Femtosecond laser flap adhesion has been found to be significantly stronger than microkeratome adhesion strength in animal studies, which may decrease flap dislocation rates.[22]

Flap striae and microstriae occur much more commonly than frank dislocations. They are often asymptomatic; however, irregular astigmatism with visual aberrations may occur if they are located over the pupil. Striae may occur from misalignment of the flap, movement of the flap or 'tenting' of the flap over the ablated stromal bed. Striae become more difficult to remove over time so visually significant striae should be treated early. If the patient is symptomatic the flap should be lifted, hydrated and placed back into position.[23] Additional treatments such as suturing may be required for persistent striae.

Epithelial trauma at the time of surgery can result in epithelial proliferation and the advancement of epithelial cells into the space between the stromal bed and flap. This may result in epithelial ingrowth. Epithelial ingrowth is more common after an epithelial defect, flap slippage or following an enhancement, especially when lifting older flaps. Femtosecond laser is thought to reduce epithelial trauma and also allow for the creation of vertical and side cut flaps, serving as a more effective barrier in preventing epithelial ingrowth.[24] Although epithelial ingrowth is a relatively common complication occurring after LASIK, it may often be observed if it is not causing visually significant symptoms.[25] Occasionally, the epithelial cells can cause loss of best-corrected visual acuity (BCVA) by growing into the central visual axis or by causing irregular astigmatism. In extreme cases the epithelial cells may cause flap melt by blocking nutritional support for the overlying stroma.[26] Lifting and scraping the epithelium from the stromal bed as well as scraping the underside of the flap can remove the epithelial cells. Gluing the edges or suturing the flap may reduce the risk of recurrence.[27] In cases where the ingrowth is not progressing rapidly, the Nd:YAG laser has also been used to destroy epithelial cells and prevent their advancement.[28]

Infections are a rare but a devastating complication after LASIK. The incidence of infection ranges from 0–1.5%.[29] Most infections are acquired intraoperatively, however, some may also be caused by postoperative contamination. Many different causative agents have been identified. Infectious keratitis following LASIK may be divided into two groups: early onset (within 2 weeks of surgery) and late onset (2 weeks to 3 months after surgery). Common bacterial pathogens such as Staphylococcus and Streptococcus are found in the early onset group and opportunistic organisms such as fungi, Nocardia and atypical mycobacteria are included in the late-onset group.[29–31]

Bacterial keratitis following LASIK typically presents within 72 h after surgery. Clinically there will be a localized infiltrate on the surface of the flap or at the flap interface. It may increase in size like a corneal ulcer if left untreated.[30,31] Reactivation of herpes simplex and zoster have been reported after LASIK and appear in a similar manner as in non-LASIK corneas with corneal dendrites. Many surgeons therefore advise patients with a history of ocular HSV to avoid refractive surgery. If the patients elect to undergo laser vision correction, an oral antiviral prophylaxis is recommended.[32–34] A delayed exacerbation of subepithelial infiltrates caused by adenovial keratitis has been documented after LASIK. Early recognition and prompt treatment with topical corticosteroids will lead to a good visual outcome when this occurs.[35] Fungal infections typically have a delayed onset and may be related to prolonged topical steroid use.[36] The incidence of atypical mycobacterial infections may be decreasing due to the routine use of fourth-generation fluoroquinolones for antibiotic prophylaxis. Suspicious infiltrates should be managed immediately with a culture and prompt treatment. If the infiltrate is found at the flap edge or in the interface, the flap should be lifted, the infiltrate scraped and cultured, and the interface irrigated with antibiotics prior to replacing the flap. The initial treatment while awaiting culture results is typically a topical fourth-generation fluoroquinolone alternating with fortified cefazolin 50 mg/ml every 30 min in addition to the discontinuation or reduction of topical steroids. Close monitoring of the patient is necessary. Fortified vancomycin may be used in place of cefazolin if methicillin-resistant staphylococcus aureus is suspected. Topical amikacin 35 mg/ml and clarithromycin may be use for suspected atypical mycobacterial infections. The addition of doxycycline 100 mg twice daily may also be beneficial. Epithelial dendrites should be managed with topical or oral antiviral therapy.[30,31] Prompt identification and management of infectious keratitis is necessary in order to prevent scarring and a reduction in BCVA. It has been reported that a BCVA of 20/40 or better can be obtained in the majority of patients if managed properly.[31]

DLK is another entity seen in the early postoperative period following LASIK. It generally occurs within the first few days after surgery and is believed to be an interface inflammatory process. White blood cells infiltrate between the flap and stromal bed, which can lead to foreign body sensation and decreased visual acuity. The epidemiology of DLK is believed to be a nonspecific inflammatory response to multiple different stimuli. Sporadic and clustered occurrences have been reported. Meibomian gland secretions, microkeratome blade debris, povidone–iodine solution, bacterial endotoxin and intraoperative epithelial defects have all been referenced as possible causes of DLK.[37] DLK has been reported to occur in a higher incidence of patients after LASIK using a femtosecond laser than with a mechanical microkeratome.[38] There are some reports that the incidence of DLK decreases with higher frequency and lower energy settings and yet others indicate that higher frequency settings in fact do not decrease the incidence of DLK. More data need to be collected regarding this issue.[39]

Patients with DLK may be asymptomatic or have symptoms such as mild pain, photophobia and decreased vision. In a clinical setting, a fine, white, granular reaction in the interface is seen and is more prominent in the flap periphery. DLK is graded to be based on the severity and location of the clinical findings. The clinical presentation of grade 1 DLK is focal, white to gray, granular material in the interface with no other ocular inflammation or anterior chamber reaction. This is found outside of the visual axis and the vision is normal. Grade 2 is defined as diffuse, white to gray, granular material in the interface with no other ocular inflammation or anterior chamber reaction with normal visual acuity. Grade 3 is defined as diffuse interface material under the flap with slight conjunctival injection and no anterior chamber reaction, but with a reduced visual acuity. Grade 4 is defined as diffuse, confluent, white to gray, granular material under the flap with inflammation localized to a 2–4 mm area of intense central inflammation. There may be central interface striae, conjunctival injection with no associated anterior chamber reaction. Patients with grade 4 DLK have markedly reduced visual acuity. Prognosis and management is dependent on the DLK grade. Grade 1–2 patients are treated with topical steroids every 1–2 h along with a prophylactic topical antibiotic. If grade 2 DLK has not improved over several days, or if grade 3 is identified, the flap should be lifted and the interface irrigated with a balanced salt solution. Grade 4 DLK requires flap lift and irrigation as well, along with frequent topical steroids afterward.[40]

Central toxic keratopathy (CTK) is a noninflammatory process that occurs in the early postoperative period. It presents as a central corneal opacification with stromal tissue loss and striae. The cornea flattens, resulting in significant hyperopia. It was once believed to be in the same spectrum of disease as DLK, but is now believed to be a separate entity. CTK has been reported following both LASIK (performed with femtosecond laser or microkeratome) as well as photorefractive keratectomy. This suggests that the syndrome is not dependent on flap creation. CTK typically resolves within 18 months without treatment. Most experts agree that corticosteroids are not indicated due to the noninflammatory nature of CTK and elect to observe.[41] Additional laser ablation can be carried out to treat residual refractive error.

Transient light sensitivity syndrome is an unusual phenomenon of photosensitivity that develops 2–6 weeks after LASIK performed with a femtosecond laser. The etiology is felt to be related to the pulse energy used during flap creation. Typically visual acuity is unaffected and there are minimal slit lamp examination findings. Steroid therapy is effective at reducing the symptoms. Low-energy settings for flap creation and prompt treatment after diagnosis reduce the incidence of this complication. Topical cyclosporine A may also be beneficial.[42]

Steroid-induced intraocular pressure (IOP) rises following LASIK contributes to two related syndromes. Several reports of interface fluid syndrome associated with elevated IOP have been described.[43–45] Slit lamp examination of patients with this condition shows a clear zone between the stromal bed and flap representing a pocket of interface fluid. It can be clinically similar to DLK, but occurs beyond the immediate postoperative period that is typically associated with DLK. It is felt that elevated IOP causes a transudation of fluid into the interface. However, the IOP measures falsely low due to the pocket of fluid and the true nature of the condition may be masked for several months. Patients complain of decreased vision and the symptoms are unresponsive to topical steroids. Management includes medications to lower the IOP and discontinuing topical steroids. BCVA is regained after proper management. However, vision loss related to glaucomatous optic neuropathy has been described.[46] Belin and Nordlund described patients who developed a DLK-like picture 1 week postoperatively.[46,47] The IOP was elevated using pneumotonometry and by applanation. Interface haze identical to classic DLK, but without interface fluid, was described. The condition was exacerbated by frequent topical steroids and resolved with IOP-lowering treatment and discontinuation of steroids. This condition was termed pressure-induced stromal keratitis.[47]

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