Facial paralysis can result in serious ocular consequences. All patients with orbicularis oculi weakness in the setting of facial nerve injury should undergo a thorough ophthalmologic evaluation. The main goal of management in these patients is to protect the ocular surface and preserve visual function. Patients with expected recovery of facial nerve function may only require temporary and conservative measures to protect the ocular surface. Patients with prolonged or unlikely recovery of facial nerve function benefit from surgical rehabilitation of the periorbital complex. Current reconstructive procedures are most commonly intended to improve coverage of the eye but cannot restore blink.
Key points
- •
Facial nerve injury often results in orbicularis oculi weakness, which impairs eyelid closure and blink, causing potentially serious ocular consequences.
- •
Patients with inadequate Bell’s phenomenon, corneal anesthesia, and decreased tear production are at high risk for exposure keratopathy in the setting of orbicularis oculi weakness and require a thorough ophthalmologic evaluation.
- •
If the recovery of facial nerve function is likely, then temporary and conservative measures to provide corneal protection and increase ocular surface lubrication are the mainstays of therapy.
- •
If the recovery of facial nerve function is unlikely or expected to be prolonged, then surgical rehabilitation of the periocular complex should be considered.
- •
Current surgical reconstructive procedures are most commonly intended to improve coverage of the eye but cannot restore blink.
Introduction
Facial nerve injury is one of the most serious complications of parotid diseases and parotid surgery. Transient facial paralysis has been reported in as many as 65% of patients after parotidectomy, whereas permanent facial paralysis has been reported in up to 5% of patients. The temporal, zygomatic, and buccal branches of the facial nerve innervate the orbicularis oculi muscle, which is the main protractor of the eyelids. Up to 75% of patients with permanent facial nerve injury following parotidectomy also have orbicularis oculi weakness caused by disruption of its innervation.
Impaired function of the orbicularis oculi manifests as incomplete eyelid closure and reduced blink frequency and amplitude. Blink is essential to effective tear film distribution across the corneal surface. Inadequate blink leads to excessive evaporation of the tear film and desiccation of the cornea. Furthermore, in the setting of orbicularis oculi weakness, the action of the eyelid retractors (levator palpebrae superioris and Müller’s muscle for the upper eyelid, and inferior tarsal muscle for the lower eyelid) become more pronounced. This condition manifests as upper and lower eyelid retraction, and widening of the vertical palpebral fissure. Reduced orbicularis oculi tone also means less counteraction against the gravitational pull on the lower eyelid, which may result in paralytic ectropion. Together, these dynamic and static changes of the eyelids lead to increased exposure of the ocular surface. If not managed appropriately, patients may develop corneal epithelial defects, ulcers, perforations, and even endophthalmitis. These ocular complications may cause loss of vision and even loss of the eye. Therefore, it is of paramount importance that patients with facial nerve injury involving the periocular complex undergo a thorough ophthalmologic evaluation and, if indicated, periocular reconstruction.
Evaluation
A thorough history of the nature and time course of facial nerve injury should be elicited. The likelihood for recovery of facial nerve function should be determined. Patients with a history of facial nerve sacrifice during surgery, facial nerve malignancy, or facial nerve injury longer than 12 months are less likely to recover. The presence of ocular symptoms, including change in vision, eye irritation, pain, foreign body sensation, and tearing, should be documented. A past ophthalmologic medical and surgical history should be obtained. Patients with corneal conditions, including dry eye, have less reserve to withstand increased corneal exposure. Monocular patients with facial paralysis affecting the eye with vision must receive special attention.
Physical examination of the periocular complex should begin with observing the patient at repose with spontaneous blink and then with gentle and forced eyelid closure. The integrity of the main corneal protective mechanisms, including frequency and amplitude of blink, orbicularis oculi strength, Bell’s phenomenon, corneal sensation (trigeminal nerve), and tear production, must be assessed ( Table 1 ). Bell’s phenomenon, not to be confused with Bell’s palsy, is the spontaneous upward and outward movement of the eye when an individual attempts to close the eyes. This reflex is present in most patients and is a corneal protective feature for patients with facial paralysis. Visual acuity should be obtained. The ocular surface should be examined with fluorescein dye to identify any corneal epithelial defects or ulcers; conjunctival injection should also be noted because this is often a sign of ocular surface exposure ( Fig. 1 ). If one or more of the corneal protective mechanisms are impaired, or if the patient has ocular symptoms, decreased visual acuity, or any signs of ocular surface abnormalities, then an urgent ophthalmology consultation is warranted. An evaluation of the static changes of the periocular complex should also be performed to guide reconstructive management ( Fig. 2 , Table 2 ).
| Examination Component | Details |
|---|---|
| Blink | Frequency, amplitude, and completeness of involuntary and voluntary blink |
| Strength of orbicularis oculi | Amount of resistance needed to overcome eyelid closure (the less resistance needed, the weaker the orbicularis oculi) |
| Bell’s phenomenon | Upward rotation of the globe on attempted eyelid closure (minimal or no corneal show on attempted eyelid closure indicates intact Bell’s phenomenon) |
| Corneal sensation | Subjective sensation and reflexive blink in response to touching the cornea with a wisp from a cotton tip applicator |
| Tear production | Schirmer I test (without anesthesia) measures total tear secretion (basal and reflex): <10 mm is abnormally low |
| Examination Component | Details |
|---|---|
| MRD1 | Distance between pupillary light reflex to the upper eyelid margin. Upper eyelid normally rests 1 mm below the superior limbus. A high MRD1 reflects upper eyelid retraction, and a low MRD1 reflects blepharoptosis |
| MRD2 | Distance between the pupillary light reflex to the lower eyelid margin. Lower eyelid normally rests at or just above the inferior limbus. A high MRD2 reflects lower eyelid retraction |
| Lower eyelid laxity | Distraction test: the greater the distance the lower eyelid can be pulled away from the globe, the more laxity is present |
| Snap-back test: if the eyelid cannot snap back to oppose the globe without blink, then laxity is present | |
| Medial and lateral canthal tendon laxity | Medial and lateral distraction test: the greater the displacement of the medial and lateral canthi, the more laxity of the tendons |
| Lower eyelid malposition | Lower eyelid ectropion or punctal ectropion should be noted |
| Brow position | Brow ptosis can contribute to decreased superior visual field. Contralateral brow hyperelevation should be noted |
| Midface ptosis and/or negative vector | Midface ptosis and/or negative vector can exacerbate lower eyelid retraction |
Management
The goal of management of the periocular complex in patients with facial paralysis is primarily to protect the ocular surface and preserve visual function and secondarily to restore facial symmetry. A variety of temporary and long-term measures exist. An individualized approach to management should be implemented based on the duration of facial paralysis, the prognosis of recovery, the extent of dynamic and static dysfunction, the integrity of the corneal protective mechanisms, and the state of the ocular surface.
Temporary Measures
The first line of management for all patients with facial paralysis involving the periocular complex is aggressive ocular surface lubrication. Patients should use preservative-free artificial tears frequently throughout the day, and lubricating ointment before sleep. For patients with mild ocular surface exposure and expected recovery of facial nerve function, such as in the setting of neurapraxia following parotid surgery, lubrication alone in combination with taping of eyes during sleep may be sufficient. If there is moderate to severe ocular surface exposure caused by lagophthalmos, moisture chamber goggles or plastic wrap over the eye should be used during sleep to protect the cornea from desiccation and mechanical trauma. A nighttime humidifier may also be beneficial. Contact lenses, such as the prosthetic replacement of the ocular surface ecosystem (PROSE) device, have been shown to be effective in providing protection and constant hydration of the cornea. Patients with low tear production may also benefit from punctal occlusion with plugs or cauterization.
If conservative measures to increase lubrication are insufficient at maintaining the health of the ocular surface, then temporary interventional measures should be implemented. These measures are particularly beneficial for patients in whom the recovery of the facial nerve is expected, or for patients who are poor surgical candidates for other reconstructive measures. Chemodenervation of the levator palpebrae superioris with botulinum toxin-A can induce temporary ptosis for 8 to 12 weeks and effectively reduce upper eyelid retraction and lagophthalmos. Care should be taken to avoid inadvertently chemodenervating the superior rectus muscle, which would lead to diplopia and impairment of the protective Bell’s phenomenon ( Table 3 ). Alternatively, injectable hyaluronic acid filler can be used as temporary upper lid weight, and effectively reduces lagophthalmos and ocular surface exposure (see Table 3 ). Similarly, appropriately placed lower eyelid hyaluronic acid filler can three-dimensionally expand, elevate, and support the lower eyelid to reduce lower eyelid malposition and ocular exposure (see Table 3 ).
