Article

Don’t let DED mar a perfect eye lift

A careful dry eye screening can help surgeons to determine how to proceed with surgery.

The development of symptomatic dry eye disease (DED) after eyelid surgery, such as blepharoplasty, can be very disconcerting to both patient and surgeon. Patients may not appreciate even an exquisite aesthetic result if experiencing symptoms including ocular pain, tearing, light sensitivity, foreign-body sensation or reduced vision that have been precipitated or aggravated by aesthetic eyelid surgery.

In fact, exacerbation of existing and new onset DED are known complications of many oculoplastic procedures.1,2 Post-blepharoplasty DED has a reported prevalence of 10-26%.3,4 However, many of these patients have previously undiagnosed asymptomatic DED that becomes symptomatic postoperatively. A contributing factor: The demographics of patients choosing to have elective eyelid surgery are similar to those at risk for DED, including female sex and the aging population.5

Still, surgeons can reduce a patient’s chances of developing, or exacerbating, DED, so that nothing distracts from that stellar aesthetic result.

FIRST, CONSIDER THIS

Along with those listed above, factors associated with DED include exposure from eyelid laxity or scleral show, history of diabetes, menopause, hormonal therapy, allergies and previous refractive surgery. Postoperative onset and exacerbation of DED can occur because of meibomian gland dysfunction (MGD); exposure keratopathy; and suboptimal blink dynamics due to facial nerve weakness, decreased orbicularis contraction and lateral canthal tendon disinsertion.

DED and MGD are increasingly prevalent in the general population, partially due to the digital era in which we live today.6,7 Meibomian glands deliver oil into the tear film, but these glands become dysfunctional when inflamed or obstructed. This results in an unstable tear film, also known as evaporative dry eye. Factors that contribute to MGD include computer vision syndrome, blepharitis and poor blink dynamics, most notably from facial nerve palsy.

THE FACIAL NERVE PALSY CONNECTION

The association between facial nerve palsy and MGD is thought to result from decreased function of the muscle of Riolan, which regulates meibomian gland secretion. Studies show that the meibomian gland morphology is altered as quickly as one week to three months after onset of facial nerve palsy.8,9

When facial nerve palsy patients have a complete blink, they have significantly longer tear break-up time. Facial nerve palsy with an incomplete blink, however, results in significantly shorter tear break-up time, more superficial punctate keratopathy, vascular engorgement, increased eyelid margin irregularity and decreased secretion of meibum.8,10

The lessons learned from the causal relationship between facial nerve palsy and meibomian gland disease may likely be applied to other conditions that weaken the contraction of orbicularis muscle. These include some eyelid surgery, periocular botulinum toxin, eyelid laxity and lateral canthal tendon disinsertion.9

Figure 1. Keratitis sicca

ADDITIONAL CONTRIBUTORS

Multiple factors can adversely affect the meibomian glands and subsequently contribute to signs and/or symptoms of DED through exposure keratopathy or incomplete tear dispersion. These may include changes in the frequency or completeness of the blink from neurologic conditions such as facial nerve palsy, anatomic abnormalities such as lateral canthal tendon disinsertion, systemic conditions such as thyroid eye disease and post-surgical changes.

Dispersion of the tear film across the corneal surface is spread by blinking, mediated through the facial nerve and orbicularis muscle. Lateral canthal tendon disinsertion can result in a reduction in blink dynamics, lagophthalmos, pseudoretraction, lacrimal pump function and secondary DED.11

Furthermore, patients with a history of thyroid eye disease with exophthalmos and eyelid retraction have a higher incidence of exposure problems. Dry eye symptoms after eyelid procedures such as blepharoplasty can also result from lid retraction, lagophthalmos, lacrimal pump insufficiency or inflammation exacerbated by aggressive tissue dissection or resection.12

YOUR FIRST WEAPON: A THOROUGH SCREENING

The most important factor in reducing the incidence of DED in patients considering eyelid surgery such as blepharoplasty is carefully screening patients preoperatively for DED signs or symptoms. It’s often challenging to diagnose dry eye since signs and symptoms often do not correlate. Dry eye questionnaires are helpful in determining whether patients are symptomatic.

Current options in evaluating and diagnosing dry eye have changed dramatically over the last several years, with point of care testing with improved specificity and objectivity. The most common diagnostic tests we use in our offices to evaluate for dry eye include tear osmolarity, MMP-9 and meibography. Despite the value of these objective tests, they are no substitute for evaluating the patient. Examining the lids and lid margins, as well as the cornea for staining and assessing the quality of tear film, should be incorporated into every patient exam.

Figure 2. MGD atrophy: Severe (top), moderate (middle) and normal glands (bottom).

DOES DED RULE OUT EYELID PROCEDURES?

Some surgeons consider preoperative DED a contraindication for blepharoplasty and other elective eyelid surgery for fear of worsening DED. The diagnosis of DED does not necessarily disqualify a patient from blepharoplasty or other eyelid procedures but may require that surgical procedures be modified to reduce or eliminate worsening of symptoms. A skin-only blepharoplasty with preservation of the orbicularis muscle and conservative skin resection is preferred in order to maintain proper blink dynamics.

Other potential modifications include not correcting eyebrow or eyelid ptosis when performing a blepharoplasty and supporting the lower lid and lateral canthus with a canthopexy or canthoplasty in the setting of lateral canthal tendon disinsertion to anchor the lids and enhance orbicularis contraction.

Patients with evidence of dry eye should be treated and counseled on the risk of exacerbation of their DED.

SURGICAL MODIFICATIONS

Peer review literature suggests that preserving the orbicularis muscle and its innervation with a skin-only blepharoplasty minimizes the changes in dynamics of eyelid closure, tear pumping and tear distribution, thereby reducing the risk of postoperative DED.12-14 Supporting the lower lid and lateral canthal anchor with a canthopexy or canthoplasty can also improve blink dynamics.11 Exacerbation or the development of DED after blepharoplasty can be minimized by leaving an adequate amount of skin for lid closure with a conservative blepharoplasty5 and treating pre-existing DED with liberal use of lubricating drops and ointment for the first few weeks after eyelid surgery.

CONCLUSION

The development or exacerbation of dry eye symptoms after aesthetic eyelid procedures can induce patient frustration and dissatisfaction — even if the aesthetic results are excellent. Proactively screening and treating for DED, managing MGD and making subtle modifications in surgery can help the surgeon achieve gratifying results while minimizing the patient’s ocular discomfort from DED. OM

REFERENCES

  1. Rees TD, LaTrenta G. The role of the Schirmer’s test and orbital morphology in predicting dry-eye syndrome after blepharoplasty. Plast Reconstr Surg. 1988;82:619-625.
  2. Mack W. Blepharoplasty complications. Facial plast Surg. 2012;28:273-287.
  3. Prischmann J, Sufyan A, Ting JY, et al. Dry eye symptoms and chemosis following blepharoplasty: A 10-year retrospective review of 892 cases in a single-surgeon series. JAMA Facial Plastic Surgery. 2013;15:39-46.
  4. Hamawy AH, Farkas JP, Fagien S, Rohrich RJ. Preventing and managing dry eyes after periorbital surgery: A retrospective review. Plast Reconstr Surg. 2009;123:353-359.
  5. Rees TD. The “dry eye” complication after blepharoplasty. Plast Reconstr Surg. 1975; 56:375-380.
  6. Benedetto S, Drai-Zerbib V, Pedrotti M, et al. E-readers and visual fatigue. PLoS One. 2013; 8:E83676. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083676 . Accessed Mar. 11, 2019.
  7. Cardona G, Garcia C, Seres C, et al. Blink rate, blink amplitude, and tear film integrity during dynamic visual display terminal tasks. Curr Eye Res. 2011;36:190-197.
  8. Wan T, Jin X, Lin L, Xu Y, Zhao Y. Incomplete blinking may attribute to the development of Meibomian Gland Dysfunction. Curr Eye Res. 2016;41:179-85.
  9. Call CB, Wise RJ, Hansen MR, Carter KD, Allen RC. In vivo examination of meibomian gland morphology in patients with facial nerve palsy using infrared meibography. Ophthal Plast Reconstr Surg. 2012 Nov;28:396-400.
  10. Takahashi Y, Kakizaki H. Meibomian Gland Dysfunction in Cranial Nerve VII Palsy. Ophthal Plast Reconstr Surg. 2015;31:179-181.
  11. Shriver EM, Erickson BP, Kossler AL et al. Lateral Canthal Tendon Disinsertion: Clinical Characteristics and Anatomical Correlates. Ophthal Plast Reconstr Surg. 2016;378-85.
  12. Farrand KF, Fridman M, Stillman IÖ, et al. Prevalence of diagnosed dry eye disease in the United States among adults aged 18 years and older. Am J Ophthalmol. 2017;182:90-98.
  13. Saadat D, Dresner SC. Safely of blepharoplasty in patients with preoperative dry eyes. Arch Facial Plast Surg. 2004 6:101-104.
  14. Kiang L, Deptula P, Mazhar M. Muscle-sparing blepharoplasty: A prospective left-right comparative study. Archives of Plastic Surgery. 2014;41:576-583.

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