By Kimberly Rueb, OD   |  PCLI—GREAT FALLS, MT

DLK After

SUMMER 2023       distributed quarterly to 2800 optometric physicians

Ami Halvorson, OD

 

PCLI—Portland, OR

From the EDITOR   If you care for LASIK patients, you likely have seen diffuse lamellar keratitis (DLK) cases. It is a potentially serious complication that occurs early in the post-op period but is relatively infrequent and usually responds well to prompt treatment. In this issue, my colleague Kimberly Rueb discusses DLK, associated risk factors, grading, and treatment.

Over the last twenty years,  LASIK surgery in the United States has grown exponentially. As with all refractive surgeries, patients have high expectations for their vision. Diffuse lamellar keratitis (DLK) is a rare but potentially serious post-op complication. When not diagnosed and treated correctly, it can negatively affect visual outcomes.

INTRODUCTION

DLK, also known as interface keratitis or Sands of the Sahara, is a non-infectious, sterile inflammatory response that occurs on average in about 4% of LASIK patients. Characterized by white, granular inflammation in the flap interface, DLK usually presents in a mild form at the one-day post-op exam. As the condition progresses, inflammatory cells can accumulate and develop a classic wave-like appearance. Without prompt treatment and close follow-up, permanent consequences can include scarring, opacification, flap striae, a hyperopic shift, and reduced BCVA.

CAUSES

Inflammation causes an accumulation of white blood cells in the interface. These produce cytokines and chemokines that further attract similar cells. Once in the interface, inflammatory cells are unimpeded by collagen or stromal cells and can move freely through the space. There are many hypothesized causes of DLK, with the etiology being multifactorial—including mechanical, chemical, and biological elements.

 Mechanical – tissue damage during the flap creation with a microkeratome or femtosecond laser.

 Chemical and biological – contaminants, including blood, meibomian oil secretions, interface debris, lubrication/foreign material/metallic fragments from the microkeratome, marking pens, surgical gloves, povidone-iodine solution, and bacterial endotoxins or other products of the sterilization process.

RISK FACTORS

Some ocular conditions increase the risk of DLK. These include atopic disease, ocular rosacea, and a history of seasonal allergies. Untreated atopic patients have a five-times increased risk of developing DLK than those pre-treated with oral antihistamines. Patients with pannus or peripheral neovascularization are also more at risk of DLK if the corneal blood vessels are transected during the procedure, resulting in a hemorrhage at the flap margin. Epithelial defects that occur during LASIK also increase the risk of DLK.

DLK GRADING

This four-stage grading system can be helpful when illustrating what you see in your exam and communicating that with the surgeon or LASIK facility.

TREATMENT

Treatment involves stopping the inflammatory cycle with medication or removing the causative agent. The maximum inflammatory response in DLK occurs between three and five days post-op.

Treatment in stages one and two includes high-dose topical corticosteroids—one drop every one to two hours. The patient should be seen every 24 to 48 hours until there is improvement. Some clinicians include corticosteroid ointment for overnight coverage. This dosing is continued until the inflammation peaks and begins to subside. Then start a slow steroid taper over a few weeks until complete resolution occurs.

If the severity of DLK progresses to stage three, additional intervention is required to prevent intrastromal scarring that occurs in stage four. This includes a course of oral corticosteroids, starting with 40mg-80mg per day until improvement is seen, then reducing to 20-30 mg/day and tapering off within ten days. An alternative treatment is re-lifting the flap to perform a washout of the interface.

SUMMARY

If not appropriately treated, DLK following uncomplicated LASIK can have detrimental effects on vision and flap integrity. It is essential to carefully view the flap interface at the one-day post-op exam for signs of mild inflammation. Once identified, determine the stage of inflammation and begin proper treatment. If the stage of DLK is difficult to determine, increase the dosage of topical corticosteroids to every one to two hours and follow the patient daily. If the condition worsens and visual acuity is affected, consult the surgeon and consider additional treatment—an oral corticosteroid or further surgical intervention. All LASIK patients with signs of inflammation should be seen every 24 to 48 hours until the inflammation improves. Prompt diagnosis, treatment, and frequent follow-up are the biggest factors in preventing permanent sequelae.

Stage 1

Inflammatory cells are outside the visual axis at the flap margin in the peripheral interface. They often present the day after LASIK, even in a mild form.

Stage 2

Inflammatory cells have crossed through the pupillary axis and can involve only the visual axis or be spread diffusely throughout the entire interface, peripherally and centrally.

Stage 3

Inflammatory cells aggregate more densely in the central visual axis and clump together with surrounding clear areas. At this time in the disease course, visual acuity declines objectively, subjectively, or both. The operating surgeon should be consulted, and additional treatment considered. Irrigation under the flap or oral steroids are common treatments.

Stage 4

Flap integrity is affected and has a mud-crack appearance. This stage is characterized by scarring and stromal melt causing tissue loss and a hyperopic shift in refractive error. It is questionable if this is a precursor or the same entity as central toxic keratopathy (CTK).

LASIK

Questions If you have questions, feel free to contact any of our optometric physicians. We’re always happy to help.

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ABOUT THE AUTHOR

Kimberly Rueb

 

PCLI GREAT FALLS, MT

Positive, friendly and attentive, Kim Rueb’s unassuming manner and natural affection for people show in her patient care and interaction with others. Born in Sycamore, Ohio, Kim grew up on a corn and wheat farm with a menagerie of 4-H animals. She enjoys being outdoors, golfing, kayaking, hiking and running. Kim and her husband, Lindy, a small business owner, live in Great Falls, Montana. They have a daughter and son—Maura and Jack.

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Prompt diagnosis, treatment, and

frequent follow-up are the biggest factors in preventing permanent sequelae.

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