The ocular surface is a delicate and complex anatomic and physiologic system that maintains the health of the cornea and, therefore, vision. Primary and accessory lacrimal glands produce the 3 layers of the tear film. The eyelids, through a complex and delicate blink mechanism, spread the tear film evenly across the cornea and modulate the evaporation of tears. Blepharoplasty can impact the anatomy and physiology of the ocular surface through a variety of mechanisms. Some of the perturbations are mild and transient, but extreme iatrogenic disruption of ocular surface protective mechanisms can lead to disabling effects on comfort or vision. Potential mechanisms of ocular-surface disruption associated with blepharoplasty are lacrimal gland or lacrimal nerve injury, anterior lamellar shortening, middle lamellar shortening (full-thickness eyelid scar), orbicularis paralysis with inadequate blink, and conjunctival injury or inflammation.

It is not possible to eliminate the risk of ocular surface injury in blepharoplasty. An element of unpredictability is inherent in surgery, and even expertly performed blepharoplasty occasionally results in ocular surface problems. However, there are measures that minimize the risk of postoperative ocular surface problems.

Patient selection

I cannot predict with certainty which patients will experience symptomatic dry eye after blepharoplasty, but some factors clearly increase the risk. Patients with a history of symptomatic dry eye, laser-assisted in situ keratomileusis (LASIK) surgery, blepharoplasty, or facial palsy are at increased risk. The Schirmer test is not adequately sensitive or specific, in my experience, to significantly add to the patient’s history and examination findings, and I do not routinely perform it. During the initial patient evaluation, I pay attention to orbicularis weakness, tight eyelids, or other causes of incomplete blink.

The relatively proptotic eye places the eyelid at mechanical disadvantage; patients with this characteristic frequently demonstrate preoperative scleral show. Repositioning of the globe, relative to its bony support, may be appropriate before or in conjunction with blepharoplasty. A rapid blink rate can sometimes indicate a borderline-compensated ocular surface and, of course, obvious conjunctivitis, blepharitis, or keratitis may indicate chronic ocular surface problems. These risk factors do not eliminate the possibility that surgery can be safely performed, but they should provoke a thorough patient analysis.

Treatment of the skin and orbicularis

We require about 20 mm of upper eyelid skin to close our eyelids comfortably (Figure 1). If the eyebrow is surgically elevated, the requirement for eyelid skin may be even greater. I try to be as conservative as possible when excising skin. Much upper eyelid aesthetic improvement results from forehead lift and from improved skin quality; excellent aesthetic results can be achieved without extensive skin resection.

Lagophthalmos resulting from inadequate anterior lamella after upper blepharoplasty. Only 14 mm of skin remained from the eyelid margin to the eyebrow. (Courtesy of the Regents of the University of California. Copyright © 2003; used by permission.)

Another risk of extensive upper eyelid surgery is orbicularis weakness. Risk is heightened when additional insult to the orbicularis or its nerve supply occurs during canthoplasty or transcutaneous midface lift. Subtle orbicularis weakness often occurs after blepharoplasty; it is underdiagnosed and acts synergistically with anterior lamellar inadequacy to impair eyelid closure and blink mechanism (Figure 2).

Upper eyelid orbicularis weakness after blepharoplasty, combined with anterior lamellar inadequacy, causing impaired blink. Note the spontaneous eversion of the upper eyelid margin with forced closure. (Courtesy of the Regents of the University of California. Copyright © 2003; used by permission.)