Epithelial Healing and Visual Outcomes Using Omega-3 Therapy Before and After Photorefractive Keratectomy (PRK) Surgery

Dry eye and persistent epithelial defects (PEDS) following LASIK and PRK are one of the most
common conditions encountered by refractive surgeons and their patient's today.¹⁻⁴ They are
associated with significant clinical morbidity in patients resulting in minor problems such
as discomfort, to extreme debilitation such as visual loss. There is no accepted definition
of persistent epithelial defect (PED) that includes a time period of recovery. We favor the
definition given in one text "… when the epithelium fails to re-grow over a defect within
the expected time course.⁵ The causes of PED are diverse, with several definite etiologies'
including dry eyes, limbal stem cell deficiency, diabetes mellitus and neurotrophic
problems. A variety of treatment modalities have been described for PED. The elimination of
predisposing associated risk remains a key factor in the management process. Therefore, to
prevent and manage this common disorder it is important to have an understanding of the
pathophysiology of dry eye after LASIK and PRK. This includes and understanding of the
relationship and interaction between inflammation, sensory denervation and essential fatty
acid pathways. Reports of clinical efficacy of anti-inflammatory therapies for treatment of
dry eye disease provide direct proof of the principle that inflammation is involved in the
etiology of dry eye disease. Research has shown that the omega-3 polyunsaturated fatty acids
are some of the most effective natural anti inflammatory agents available. The active
ingredients in omega 3, EPA ( Eicosapentanoic acid ) which is a 20 carbon omega 3-fatty acid
with 5 double-bonds , and DHA ( docosahexanoic acid )which is 22 carbon omega-3 fatty acid
with 6 double bond, both found in certain fish oils enhance the conversion of COX (
cyclooxygenase) to prostaglandin E3. A natural anti inflammatory agent, prostaglandin E3
competitively inhibits the effects of the arachidonic acid conversion to prostaglandin E2, a
highly inflammatory substance. Prostaglandin E3 also inhibits the synthesis of TNFα and
IL-1β, both of which are inflammatory leukotrienes, also by competitive inhibition.⁶ʹ⁷ By
decreasing inflammation and stimulating aqueous tear production in rabbits cAMP has been
shown to stimulate aqueous tear secretion in dry eye. Furthermore, by decreasing
inflammation and augmenting oil and water layers of the tear film, omega-3 supplementation
with fish oil rich in EPA may improve both the lipid and aqueous component of the tear film.
This may improve surgical outcomes by stabilizing the tear film, reducing epithelial defects
and promoting wound healing

Inclusion Criteria:

- Male or female candidate for PRK with refractive error of -1.00 to -6.00

- Male or female 18- 28 (may consider increasing this range) years old and >60 years
old post cataract surgery for enhancement.

- Patients without history of diabetes.

- Patients without history of hemorrhagic stroke.

- Patient without history of blood dyscrasia.

- Patient without history of diarrhea, abdominal bloating, and indigestion.

- Patient without history of peptic ulcer disease, gastroesophageal reflux and
gastroesophageal reflux disease.

Exclusion Criteria:

- Male or female < 18 years old for PRK.

- Male or female with a refractive error < -1.00 or >-6.00

- Patient with history of diabetes.

- Patient with history of hemorrhagic stroke.

- Patient with history of Blood dyscrasia.

- Patient with history of peptic ulcer disease, gastroesophageal reflux and
gastroesophageal reflux disease.

- Patient with history of diarrhea, abdominal bloating and indigestion.

- Pregnant women and women that are lactating (nursing mothers)