Tame inflammation before vision correction

Underlying conditions must be controlled prior to surgery.

Many patients seek refractive surgery because they have underlying inflammatory conditions that make it difficult to wear contact lenses; dry eye, meibomian gland disease, anterior blepharitis and allergic conjunctivitis are among them. But as we know only too well, not only will refractive surgery not solve those problems, it will likely exacerbate them.

Numerous peer-reviewed publications document the need to control inflammation before laser vision correction.1-3 The patient will have a smoother recovery, better clinical outcome (better uncorrected and best-corrected vision, less residual refractive error and less chance of needing an enhancement) and less chance of postoperative infection.

As if we need further reasons to hunt for inflammatory conditions before surgery, here’s one that has been said many times: Telling patients before surgery about their ocular surface disease makes it their problem; telling them afterward makes it our problem. In the interest of preempting problems, here are our best practices for controlling inflammatory conditions.


First, any objective data that we can present to the patient are very helpful, such as tear osmolarity scores, matrix metalloproteinase-9 (MMP-9) results and meibography images. These data are valuable in guiding Dr. McDonald’s diagnosis and treatment plan, as well as in increasing patient compliance.

The most common causes of preoperative inflammation are dry eye and meibomian gland disease. Eighty-six to 92% of dry eye patients have meibomian gland disease as well, according to peer-reviewed publications by Michael Lemp, MD, and Kelly Nichols, OD.4-6 It is critical to diagnose these conditions preoperatively and to use an algorithm to guide treatment. The TFOS DEWS II and Meibomian Gland Workshop guidelines are excellent, straightforward ways to start.7,8 The charts can be posted in the office until the doctors and technicians have them memorized, which happens quickly.

Some older (often hyperopic) patients may also have exposure keratitis due to lagophthalmos, especially if they have undergone a blepharoplasty; this is treated with night-time bland ointments, available over the counter. Other patients may have epithelial basement membrane dystrophy (EBMD), also known as map-dot-fingerprint dystrophy, which make them better candidates for PRK than LASIK. PRK will have therapeutic as well as refractive value for EBMD. The only caveat: if the EBMD is central, it could lead to inaccurate preoperative measurements. In this case, the EBMD should be treated with mechanical debridement first; three months later, the preoperative evaluation for PRK can be performed accurately.

Many preoperative patients have a form of contact lens-related allergic conjunctivitis known as giant papillary conjunctivitis (GPC). This occurs when contacts become coated with protein and calcium from their tear film and become a new antigen to which they become allergic. Stated differently, GPC patients are “deposit formers” who soil their contacts faster than normal patients. With or without a diagnosis of GPC, ask spherical soft lens wearers to discontinue their contacts for three weeks before the preoperative exam; tell soft toric and gas permeable wearers to abstain for four weeks.

During this time, many GPC patients will have great improvement in their condition merely by discontinuing the lenses. Some will still be inflamed to the point where the preoperative exam must be cut short; we treat these patients with topical bepotastine and loteprednol for several weeks before we can complete the preoperative exam.


Don’t be afraid to cut the preoperative exam short when you diagnose clinically significant OSD. I have never — to my knowledge — lost a patient because I have terminated the exam early to begin treatment for a month. If the preoperative exam is completed before the doctor diagnoses the OSD, the patient will have to return to have many of the tests repeated, which is a waste of time for all concerned.

In Dr. McDonald’s practice, the technician knows to stop the exam and consult with her if the patients has a tear osmolarity score of 325 mOsmol/L or greater, or a topography image with significant tear film breakup on the placido ring image or the color map. Then, she enters the exam room, explains the situation and suggests treatment, usually for a month, before the final preoperative exam. Without fail, patients are grateful for my careful attention to detail.


Few patients — luckily very few — have such severe OSD that a combination of cyclosporine drops b.i.d., lifitegrast drops b.i.d., lid scrubs b.i.d., preservative-free artificial or serum tears every two hours while awake, night-time ointment (bland or antibiotic), omega-3 nutritional supplements, four punctal plugs, oral doxycycline, microblepharoexfoliation/thermal pulsation therapy, amniotic membrane treatments and twice-weekly Acthar injections (Mallinckrodt Pharmaceuticals) do not control the OSD. Often, such patients have Sjogren’s syndrome and/or other autoimmune conditions, or anatomical anomalies.

The patient’s tear osmolarity scores will stay high, and their MMP-9 test will remain markedly positive for inflammation. This is when a prudent surgeon might consider deferring corneal refractive surgery — at least until the next therapeutic breakthrough comes along. OM


  1. Garcia GA, Farid M. Management of ocular surface disease in cataract and refractive surgery patients. Ocul. Surf. 2018: 43-60.
  2. Albietz JM, McLennan SG, Lenton LM. Ocular surface management of photorefractive keratectomy and laser in situ keratomileusis. J Refract Surg. 2003;19:636-644.
  3. Ambrosio R, Jr., Tervo T, Wilson SE. LASIK-associated dry eye and neurotrophic epitheliopathy: pathophysiology and strategies for prevention and treatment. J Refract Surg. 2008;24:396-407.
  4. Lemp MA, Nichols KK. Blepharitis in the United States 2009: a survey-based perspective on prevalence and treatment. Ocul Surf. 2009;7(2 suppl):S1-S14.5.
  5. Lemp MA, et al. Distribution of aqueous-deficient and evaporative dry eye in a clinic-based patient cohort: a retrospective study. Cornea. 2012;31:472-478.
  6. Nichols KK, et al. The international workshop on meibomian gland dysfunction: executive summary. Invest Ophthalmol Vis Sci. 2011;52:1922-1929.
  7. Nelson JD, Craig JP, Akpek EK, et al. TFOS DEWS II REPORT. Ocul Surf. 2017;15: 269-650.
  8. Nichols KK, et al. The international workshop on meibomian gland dysfunction. Invest Ophthalmol Vis Sci. 2011;52:1917-2085.

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