Acute onset bilateral blurry vision after LASIK surgery
The patient’s symptoms began approximately 24 hours after undergoing LASIK.
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A 29-year-old woman noticed decreased vision for 1 week in both eyes. The right eye was worse than the left eye, and both distance and near vision were affected. She denied significant eye pain, except for some mild foreign body sensation.
History
The symptoms began approximately 24 hours after undergoing LASIK surgery from an outside ophthalmologist.
She had no other past ocular history except for moderate myopia. She was not taking any medications. Her past medical, surgical and family histories were noncontributory. The patient drank alcohol occasionally, and she denied smoking or illicit drug use.
Examination
The patient’s uncorrected visual acuity was 20/30+2 in the right eye and 20/25 in the left eye. Her best corrected visual acuity was 20/20 in both eyes. Pupillary responses were normal in both eyes and IOP was 11 mm Hg in both eyes. Confrontation visual field testing was full, and extraocular movements were within normal limits.
Upon anterior segment examination, left greater than right, diffuse, white, granular, subepithelial infiltrates were noted, most prominently at the LASIK flap interface. In the left eye, moderate cellular infiltrates with some clumping were present from the 1 o’clock to 9 o’clock positions around the flap (Figure 1a). Some interface debris was also noted halfway between the 4 o’clock and 5 o’clock positions in the left eye. In the right eye, mild cellular infiltrates without clumping were noted around the flap interface from the 3 o’clock to the 11 o’clock positions (Figure 1b).
There was no conjunctival injection or anterior chamber reaction in either eye. Posterior segment exam was unremarkable bilaterally.
Image: Ho J, Wu H
What is your diagnosis?
Bilateral blurry vision
Differential diagnosis for these corneal findings includes diffuse lamellar keratitis (DLK), central toxic keratopathy (CTK), pressure-induced stromal keratopathy (PISK), infectious keratitis — atypical mycobacterial, fungal, bacterial or viral — interface debris and epithelial ingrowth.
Potential diagnoses
DLK is a condition marked by sterile white inflammatory corneal infiltrates, occurring soon after LASIK surgery. Patients usually complain of a mild decrease in vision along with a hyperopic shift. In extreme cases, vision loss may be severe. Upon examination, diffuse subepithelial white granular infiltrates are present, most notably at the LASIK flap interface. The appearance of the infiltrates is responsible for its nickname, the “sands of the Sahara.” There is typically no anterior chamber reaction or conjunctival injection. The diagnosis is clinical, although imaging, including confocal microscopy and optical coherence tomography, may be helpful.
CTK is similar to DLK in that it also presents with increased corneal opacity within several days after LASIK surgery. Patients also have an associated hyperopic shift, as in DLK, although with CTK, there is stromal tissue loss and often corneal striae. Neither condition typically presents with conjunctival injection or anterior chamber reaction.
Although the infiltrates are close to the flap interface in DLK, with CTK they are typically centrally located and extend proximally and distally from the interface. The onset tends to be more acute rather than gradual for CTK. In certain patients, CTK may be confused for advanced stages of DLK or for disciform herpetic keratitis.
The etiology of CTK appears unclear; however, the laser photoactivation of various substances such as talc within the flap interface has been suggested as a potential cause. The management of CTK is conservative, and steroids and flap lifting are often times not required because CTK is not considered to be an inflammatory disorder.
PISK is a condition associated with diffuse stromal haze in the setting of elevated IOP occurring 1 to 2 weeks after surgery. In most cases, the elevated pressures are thought to be secondary to steroid responses; however, other possible mechanisms have been suggested. When evaluating a patient for PISK, it is important to note that IOP from the central cornea may be falsely low given the stromal interface fluid. Thus, pressure measurements should be taken more peripherally. Management includes tapering steroids and starting pressure-lowering medications.
Infectious keratitis
Infectious keratitis is a potentially vision-threatening LASIK-associated complication. Along with corneal infiltration, conjunctival injection and anterior chamber reaction are often evident on examination. Patients typically complain of significant ocular discomfort. The most common causative organisms include bacteria, viruses, fungus and atypical mycobacteria.
Clinically, infectious keratitis is divided into early and late onset. The most common organisms responsible for early onset infections, defined as occurring in the first 2 week postoperative period, include Staphylococcus aureus and Streptococcus species. Late onset infections, defined as occurring from about 2 weeks to 3 months postoperatively, most commonly involve atypical mycobacteria and fungal etiologies. In the past, atypical mycobacteria were the most common cause of infectious keratitis after LASIK; however, with increasing use of fluoroquinolones, S. aureus infections, especially methicillin-resistant strains, have become more common early in the postoperative course. Viral etiologies include adenovirus, which is relatively benign, and herpes simplex virus, which often leads to permanently decreased visual acuity.
Interface debris is common after LASIK. Metallic particles, in particular, occur when a microkeratome is used to create the flap. The particles may be of high or low reflectivity, with a lower density of particles found in flaps made with the femtosecond laser. The particles typically do not incite an inflammatory reaction and may remain inert for years.
Epithelial ingrowth is a condition that typically develops 2 weeks or later after LASIK surgery. It is marked by peripheral focal opacities at the edge of the flap, often times with finger-like projections. If mild, and if the visual axis is not involved, it may be observed. However, in more advanced cases, flap lifting, scraping and irrigation may be considered. The prognosis is usually good, with low rates of recurrence when managed properly.
Management of DLK
The appearance of this patient’s exam and clinical course were most consistent with moderate DLK, worse in the left eye than in the right eye. Thus, she was promptly started on hourly prednisolone acetate 1% eye drops. She was also started on oral prednisone 60 mg daily.
Upon follow-up 2 days later, the patient’s symptoms and exam were unchanged. A flap lift was performed on the left eye, and steroid therapy was continued. Two days after the flap lift, the patient reported subjective visual improvement in her left eye. Uncorrected visual acuity improved to 20/25+2 in the left eye, and decreased clumping of cells in the stromal infiltrates was appreciated. The vision and corneal appearance were unchanged in the right eye. Cultures from the flap interface were negative for bacteria, viral and fungal etiologies. At this point, oral prednisone and topical prednisolone acetate were tapered.
Upon subsequent follow-up, the patient reported minimal improvement in vision in the right eye despite the course of oral and topical steroids. Thus, about 2 weeks after initial presentation, her right eye underwent flap lift and irrigation. One day later, the patient’s visual acuity in her right eye improved to 20/20. The right eye opacities were noted to be about 75% improved. The left eye opacities were noted to be 95% improved.
At present, the patient only has minimal peripheral cellular infiltrates in both eyes and is off all steroid medications. Her vision remains at 20/20 with only mild complaints of glare while looking at computer monitors.
Discussion
DLK is a rare, but potentially vision-threatening condition that occurs soon after LASIK surgery. The incidence is approximately 1 in 5,000 cases. In 75% of cases, the involvement is bilateral on presentation, marked by diffuse white cell infiltration between the flap and the stromal bed.
The etiology of the condition is unclear, but bacterial endotoxins, meibomian secretions, oil, wax, povidone-iodine and atopy have all been suggested as causative agents. There is also a noted association between epithelial defects before LASIK and the development of DLK. In the present case, the patient underwent a “makeover” days before her LASIK procedure. Despite aggressive lid cleaning, makeup material was found in the tear lake postoperatively. Thus, this interface debris may have been a potential nidus.
The severity of DLK is classified by the Linebarger grading system. Stage 1, which is the most common, occurs in approximately one out of every 50 cases of DLK and accounts for 75% of the cases on presentation. It is typically discovered very early in the postoperative course; 85% of the cases were noted on postoperative day 1. The infiltrates are peripheral, without clumping or aggregation. Vision is usually unaffected, and close observation or topical steroids may be offered.
Stage 2 DLK occurs in about one out of every 200 cases. It is marked by migration of the peripheral cells into the paracentral cornea. Vision at this stage may be mildly affected, and flap lift, irrigation and cultures may be considered if there is no response to conservative treatment, or if there is progression to stage 3.
In stage 3 DLK, inflammation involves the central cornea with clumping and aggregation. This stage is also known as “threshold disease,” in that, generally, this is where the vision is affected and flap lift and irrigation is warranted. Despite the current treatment paradigm recommending early flap lift for moderate stages of DLK, some cornea specialists recommend conservative management over flap lift, even in the presence of stage 3 DLK.
Hoffman et al, conducted a retrospective study examining 4,000 eyes that underwent LASIK. He found that 4% of eyes developed DLK. Patients with stages 1 to 3 disease were started on a combination of oral and topical steroids without flap lift. No patients developed stage 4 DLK with conservative management. Additionally, no permanent loss of BCVA was noted.
Stage 4 is marked by corneal opacification, central corneal necrosis and scarring by the release of collagenases by white blood cells. It has the appearance of central toxic keratopathy. Some ophthalmologists believe that stage 4 DLK represents an entirely different disease from DLK stages 1 to 3. Most cornea specialists recommend aggressive oral and topical steroids for treatment at this stage. Flap lift and irrigation is controversial, because the presence of stromal melting may make the procedure difficult and lifting may lead to more tissue loss.
Our patient presented with stage 3 DLK in the left eye and stage 2 in the right eye. After left eye flap lift and irrigation, along with topical and oral steroids, that eye gradually improved to stage 1 (Figures 1c and 1d). In her right eye, the infiltrates initially remained fairly stable but improved to grade 1 about 1 month after flap lift and a course of steroids.