Acute Management of the Effects of Facial Paralysis
Clinical management issues related to acute facial paralysis can be divided into three categories. The first involves management directed at underlying conditions causing facial paralysis (i.e., infection, tumor). The second is concerned with treating the dysfunctional facial nerve itself (i.e., neuritis, trauma) and its branches.1,2 The final category, and often the one associated with the greatest potential for positive intervention, includes management and prevention of the negative effects of acute facial paralysis. Examples of these include ophthalmic pathology such as corneal exposure injury,3,4 psychiatric effects such as anxiety or depression, and manifestations of oral sphincter incompetence. The focus of this chapter is on the practical clinical management of this latter category: the negative sequelae of facial paralysis in the acute and subacute settings. The first of these two categories as well as definitive management of the effects of facial paralysis in the chronic setting are dealt with in Chapters 21 through 26 of this book.
Management of the Eye
Orbicularis oculi palsy negatively impacts the eye in several ways. First, lagophthalmos (inability to close the eye) results in an increased duration of time during which the cornea is exposed to drying and irritating influences. Second, the loss of lower eyelid muscle tone in combination with other factors such as gravity, frequent wiping, and excess stretching often result in paralytic ectropion. This, too, results in increased corneal exposure as well as a disturbance of the normal tear flow mechanism via outward deflection of the lower eyelid and lacrimal punctum relative to the globe. It also results in impaired cosmesis and bothersome tearing to a degree that can be socially disruptive.
If orbicularis oculi palsy is encountered in the setting of concomitant trigeminal nerve loss, the absence of the usual protective influence of corneal sensation (i.e., loss of Bell phenomenon, absent blink reflex) also increases the risk of corneal exposure. Furthermore, it is possible that the site of lesion may have an impact on risk of corneal injury so far as it is possible for pregeniculate lesions to negatively affect lacrimal output via derangement in function of the greater superficial petrosal nerve.
The problems of increased corneal exposure and decreased lacrimation, especially with corneal anesthesia, may lead to the most dreaded ocular complication associated with facial palsy—namely, exposure-related corneal pathology causing decreased vision. Specifically, this includes a spectrum of scattered corneal punctate epithelial loss, epithelial erosions, and ulceration involving deeper layers. These may result in corneal vascularization or stromal scarring with associated visual deficits. If secondary infection occurs as well, corneal ulceration and scarring can be more severe.
The management of the eye in facial paralysis will be influenced by the expected prognosis and cause. Temporary facial paralysis (weeks or a few months) may be treated nonsurgically, but long-term facial paralysis requires more definitive, usually surgical, treatment of the eye. These include gold weight implantation,5,6 lower eyelid procedures, and all forms of facial reanimation.
Most patients in the early stages can be managed with the nonsurgical measures described here, but if corneal exposure persists, surgical measures such as gold weight implantation may be used in the early stages of facial paralysis. Gold weight implantation is aesthetically superior, reversible (if required), and preferred to tarsorrhaphy.
Drops/Ointment
Sterile artificial tears (ideally preservative-free) are recommended at a frequency of two drops every 1 to 2 hours while awake to combat corneal desiccation ( Table 19.1 ). The most commonly encountered artificial tear preparations contain a form of methylcellulose; however, numerous varieties exist. Bland ophthalmic ointment is applied just inside the lower eyelid prior to sleep for protection at night. Furthermore, it is recommended that the patient additionally apply ointment once every 4 hours during the waking hours if redness persists despite application of drops. Unfortunately, ointment can be somewhat messy and necessarily causes blurred vision for a moderate duration of time following application.
Eye Taping
If performed properly, eye taping can be useful in combination with ocular lubricants to treat lagophthalmos and paralytic ectropion. Variations in technique exist for waking hours and for bedtime. While awake, patients are recommended to place a crescent-shaped piece of tape (preferably a paper variety that is conducive to adhesion with the thin sensitive eyelid skin) over the upper eyelid and rectangular piece horizontally over the lower eyelid to lift the lower lid. While sleeping, the eyelids can be carefully taped in a closed position with a piece that spans vertically over the lateral aspect of the eye from the forehead, over both closed eyelids, and then onto the cheek ( Fig. 19.1 ).
Although a helpful adjuvant, eye taping has some potential associated pitfalls. Caution should be made to ensure that the tape is not in contact with the globe as this can cause contact abrasion, especially in cases where corneal sensation is impaired. Taping can be particularly difficult at night when concomitant application of ointment may render tape relatively nonadhesive; nighttime taping is often abandoned for this reason. Furthermore, placement of tape should not involve excessive stretching or shearing forces on the lower eyelid as this can exacerbate ectropion.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
