Lagophthalmos Evaluation and Treatment

This article is from April 2008 and may contain outdated material.

Proper eyelid closure and a normal blink reflex are essential to maintaining a stable tear film and a healthy corneal surface. Patients affected with lagophthalmos are unable to fully close their eyelids, and they may describe symptoms of dry and irritated eyes. Common morbidities of lagophthalmos are corneal exposure and subsequent keratopathy, which may progress to corneal ulceration and infectious keratitis. It is important to recognize lagophthalmos early in the patient’s course and begin treatment as soon as possible. The choice of therapy requires an understanding of both the etiology and expected duration of the lagophthalmos.

Initial Evaluation

Taking the history. A careful history should seek to determine the etiology of the lagophthalmos. Any recent trauma or surgery involving the head, face or eyelids should be documented. Past infections should be reviewed, with particular attention to any history of herpes zoster infection. It is also important to document any past symptoms suggestive of thyroid disease or obstructive sleep apnea.

Testing the lids and globe. Ask the patient to look down and gently close both eyes. Lagophthalmos is present when a space remains between the upper and lower eyelid margins in extreme downgaze. Document the degree of lagophthalmos by measuring this space, in millimeters, with a ruler. Also, record the blink rate as well as the completeness of the blink. Carefully test cranial nerve function, paying particular attention to ocular motility and the strength of the orbicularis oculi muscle. The latter can be assessed by evaluating the force generated on attempted eyelid closure. Also, the presence and quality of the Bell’s phenomenon should be noted, as the cornea is better protected when the eye rolls upward on attempted closure of the eyelids.

Testing the cornea. Next, test corneal sensitivity by applying soft cotton to the unanesthetized cornea and comparing the blink reaction with that of the fellow eye. Conduct a slit-lamp exam that focuses on the presence of punctate epithelial erosions or abrasions highlighted with fluorescein staining, and pay particular attention to the inferior cornea where lid excursion ends. Also, record the tear breakup time. Any epithelial defects or corneal ulcers should be carefully documented. 

Etiology

Facial nerve. The facial nerve (seventh cranial nerve) innervates both the frontalis muscle, which raises the eyebrow, and the orbicularis oculi muscle, which closes the eyelids. Loss of function of the facial nerve inhibits eyelid closure as well as the blink reflex and the lacrimal pumping mechanism. In addition, the facial nerve innervates the muscles of facial expression including the zygomaticus muscles, which elevate the cheeks as well as the corrugator supercilii and procerus muscles, which depress the eyebrow. These muscles play an important role in maintaining facial symmetry. Facial nerve weakness may result from a host of causes:

• Trauma. The facial nerve is susceptible to blunt trauma or laceration along its bony course. Fractures to the skull base (petrous portion of the temporal bone) or mandible can damage the nerve or one of its branches. Neurosurgical procedures present additional risk.
• Cerebrovascular accidents. The facial nerve receives its blood supply from the anterior inferior cerebellar artery. It is most susceptible to ischemic damage just proximal to the geniculate ganglion.
• Bell’s palsy. This is an idiopathic facial nerve palsy that is thought to be associated with an acute viral infection or reactivation of herpes simplex virus.
• Tumors. Acoustic neuromas in the cerebellopontine angle and metastatic lesions are most commonly associated with lagophthalmos. MRI with gadolinium best characterizes the mass.
• Infectious, immune-mediated causes. Less common causes of lagophthalmos include Lyme disease, chickenpox, mumps, polio, Guillain-Barré syndrome, leprosy, diphtheria and botulism.
• Möbius’ syndrome. This rare, congenital condition is characterized by cranial nerve palsies (especially sixth and seventh cranial nerve palsies), motility disturbances, limb anomalies and orofacial defects.

Eyelids. The upper and lower eyelids contain seven structural layers. Beginning anteriorly, these comprise 1) skin and subcutaneous tissue, 2) orbicularis oculi muscle, 3) orbital septum, 4) orbital fat, 5) muscles of retraction, 6) tarsus and 7) conjunctiva. Damage to or degeneration of any of these tissues may inhibit good eyelid closure. Related causes of lagophthalmos include:

• Cicatrices. Chemical or thermal burns, ocular cicatricial pemphigoid, Stevens-Johnson syndrome or mechanical trauma may cause scarring of the soft tissues or retractor muscles.
• Eyelid surgery. Excessive removal of eyelid skin or muscle (e.g., blepharoplasty, tumor excision) can lead to lagophthalmos of the upper eyelids or retraction of the lower eyelids. Overcorrection in ptosis repair has also been implicated.
• Proptosis. Exophthalmos of one or both globes may inhibit eyelid closure. Also, retraction of the upper and lower eyelids is a common feature of thyroid ophthalmopathy that may increase the degree of lagophthalmos.
• Enophthalmos. Posterior displacement of the eye may affect eyelid apposition and closure. Acquired causes include socket contracture (orbital blowout fractures); orbital fat atrophy (trauma, infection, inflammation, aging or a wasting disease such as linear scleroderma or HIV-AIDS); a phthisical or prephthisical eye; or scirrhous carcinomas leading to contraction of orbital fat.
• Floppy eyelid syndrome. This condition is the result of severe laxity and flexibility of the superior and inferior tarsal plates, and it may be associated with obstructive sleep apnea.

Symptoms

Lagophthalmos patients commonly complain of foreign body sensation and increased tearing. Pain may be worse in the morning due to increased corneal exposure and dryness during sleep. Patients often note blurry vision, which results from unstable tear film. In cases of advanced keratopathy and corneal ulceration, the symptoms and presentation may be severe.

Workup and Treatment

A stepwise approach based on the severity and expected duration of the lagophthalmos is recommended. Most important is close follow-up with frequent examination of the cornea.

Medical treatment and supportive care for corneal exposure. Nonpreserved artificial tears should be administered frequently (at least four times per day) in order to supplement the patient’s tear film. Ointments can be applied to the cornea once at bedtime or throughout the day in cases of severe corneal exposure. Moisture goggles also may be used. As the corneal surface normalizes, ointments may be replaced with 0.5 percent or 1 percent methylcellulose formulations. When choosing a lubricant, the patient’s ability to accept visual blurring caused by the viscosity of the lubricant should be considered. Infectious corneal ulcers should be treated with appropriate antibiotic therapy. Also, the surgeon may elect to patch the eye closed or place a Frost suture for temporary protection of the cornea.

Tarsorrhaphy. When recovery of the eyelid closure is expected within a few weeks, a temporary tarsorrhaphy achieves narrowing of the interpalpebral fissure. In most cases, the cornea can be protected adequately by suturing the lateral one-third of the eyelids together. Ideally, a small opening remains so that the patient can retain useful vision, the health of the cornea may be assessed and lubrication or antibiotic therapy can be applied to the eye.

When a protracted clinical course is evident, a permanent tarsorrhaphy may be performed by abrading the eyelid margins at the site of the sutures to create intermarginal adhesions. The sutures are removed in 10 to 14 days. If the patient regains useful function of the orbicularis oculi muscle, the adhesions can be lysed.

A limitation of tarsorrhaphy is that loosening of the sutures may occur, resulting in inadequate lid coverage of the cornea. Trichiasis and poor cosmetic appearance represent additional risks.

Gold weight implantation. Gold weights can be implanted into the upper eyelid to treat paralytic lagophthalmos. This procedure enhances eyelid closure in a gravity-dependent fashion. Gold has been considered an ideal substance because it is inert and tends to not show through the thin skin of the eyelid. In cases of allergy, platinum may be used.

Gold weights range from 0.6 to 1.6 g and come in 0.2-g increments. The appropriate weight is chosen preoperatively by taping weights of varying sizes onto the external lid above the tarsus and observing the closing and opening of the lids. Properly chosen, the ideal weight will allow full closing and opening of the lids, while avoiding ptosis in primary gaze. Gold weight implantation is usually well-tolerated. However, astigmatic shift as well as migration and/or extrusion of the gold weight may occur.

Upper eyelid retraction and levator recession. Recession of the upper eyelid retractors (levator and Müller’s muscles) is a useful procedure in patients with lagophthalmos related to upper eyelid retraction from thyroid ophthalmopathy. Also, a combination of full-thickness skin grafts, advancement flaps, tarsal-sharing procedures and release of scar bands can be performed on patients with lagophthalmos from cicatricial or postsurgical lid shortening.

Lower eyelid tightening and elevation. Laxity of the lower eyelid may occur in conditions such as facial nerve palsy and floppy eyelid syndrome. A tightening procedure such as a lateral tarsal strip will improve apposition of the lower eyelid to the globe and decrease tearing.

Patients who continue to have exposure of the cornea despite medical therapy and upper eyelid restructuring may also benefit from lower eyelid elevation. Here, the lower eyelid retractor muscles may be recessed from their insertion on the inferior tarsal border. An additional spacing graft may be sutured in the lid to achieve further elevation. Autologous ear cartilage, nasal cartilage or hard palate grafts are often used. In cases with a cicatricial component, a full-thickness skin graft and/or collagen or mucous membrane graft may be needed.

Ancillary surgical procedures. In cases of severe lagophthalmos related to facial nerve palsy, elevation of the midface may be achieved using a variety of materials including autogenous fascia slings and/or Coapt Endotine Midface implants. Facial reanimation procedures include temporalis muscle transposition/ transfer, nerve grafts and anastomoses, palpebral springs, soft tissue repositioning and suborbicularis oculi fat lifts. Each approach has been used effectively in patients with facial nerve palsy.

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Dr. Lawrence is an ophthalmology resident at the University of Tennessee in Memphis. Dr. Morris is doing an ASOPRS fellowship in oculoplastics at the University of Tennessee and Vanderbilt University.