A Case of Paralytic Lagophthalmos Following Melanoma Surgery Induced Seventh Nerve Palsy
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ABSTRACT
BACKGROUND
Post-surgical inflammation that causes a seventh cranial nerve palsy can lead to various ophthalmic complications. A significant finding is paralytic lagophthalmos, which can cause the following conditions: exposure keratopathy, entropion, dry eye syndrome, and corneal abrasion. Without treatment, additional complications can include severe corneal ulcerations or blindness. This case report discusses the pathophysiology of a facial nerve palsy and details a case of facial nerve paralysis after melanoma surgery and the ocular complications from a resultant paralytic lagophthalmos.
CASE REPORT
A 76-year-old Caucasian male presented with an acute onset unilateral left facial weakness after a wide local excision for a left facial lentigo maligna melanoma. He complained of moderate ocular irritation, ocular discomfort, and foreign body sensation in the left eye. The patient’s ocular history was significant for a corneal posterior polymorphous dystrophy, combined forms of age-related cataracts, moderate dry eye syndrome with meibomian gland dysfunction, anterior blepharitis, and posterior vitreous detachments in both eyes.
CONCLUSION
This complex case highlights the need for close monitoring and prompt intervention of post-surgical inflammation as a risk factor for facial palsy and ocular surface complications. It also highlights the importance of comprehensive post-operative care to minimize the risk of such complications. In the presence of severe corneal complications secondary to exposure keratopathy, patient comfort management improves their quality of life. Close observation is indicated until facial paralysis completely resolves.
Keywords: exposure keratopathy, post-surgical inflammation, paralytic lagophthalmos, cranial nerve 7 palsy, wide local excision of melanoma of cheek, exposure keratopathy, exposure keratitis, lagophthalmos, paralytic lagophthalmos
INTRODUCTION
The management of facial nerve palsy following wide local excision and linear closure for facial malignant melanoma can present a unique set of challenges. Wide excision near the left cheek area can result in irritation or trauma to the facial nerve,1 leading to paralytic lagophthalmos and the risk of severe ocular complications such as exposure keratopathy. Typically, complete eyelid closure and a normal blink reflex are essential to protect the ocular surface and maintain adequate ocular surface lubrication. Prolonged corneal exposure to air can lead to ocular complications that may induce corneal ulcerations or blindness without treatment.2,3 Paralytic lagophthalmos, therefore, can have a deleterious impact on a patient’s vision. This article discusses a case of melanoma surgery-induced facial nerve paralysis and the subsequent ocular complications that occurred. It also addresses current therapeutic options and the benefits of close observation to hasten recovery and improve the visual outcomes for affected patients during the postoperative period and beyond.
CASE REPORT
A 76-year-old male presented to the urgent care facility for wound care and dressing changes one day after undergoing a wide local excision of a left facial lentigo maligna melanoma (2 cm x 1 cm, excision size 7 cm x 4 cm with 1.2 cm circumferential margins). During the visit, the optometry clinic was consulted to assess the patient’s inability to blink his left eye. In addition, he reported a history of foreign body sensation and moderate irritation in the left eye since his procedure. These findings prompted a bedside ocular examination.
His ocular history was significant for a corneal posterior polymorphous dystrophy in both eyes, age-related cataracts in each eye, moderate dry eye syndrome with meibomian gland dysfunction (MGD), anterior blepharitis, and posterior vitreous detachments in both eyes.
His medical record included a history of left facial lentigo maligna melanoma with wide local excision, history of latent syphilis, major depression, post-traumatic stress disorder, bowel obstruction, cholangitis, hyperlipidemia, opioid dependence, thyroid disorder, osteoarthritis, and lumbar spondylosis. His medications included duloxetine, megestrol acetate, ondansetron, pregabalin, oxycodone, and cholestyramine. He disclosed a family medical history of malignant neoplasms. His family ocular history and social history were unremarkable.
Upon ocular examination and motor function testing bedside, there was weaker left facial muscle tone, mild asymmetry in muscle tone of the left eyelid and eyebrow, a 3 mm lagophthalmos with consistent incomplete blink and a widened palpebral aperture of the left eye. A 3 mm difference between interpalpebral aperture measurements created the appearance of a reverse ptosis in the right eye. The clinical findings were consistent with a lower motor neuron left seventh nerve palsy. The cranial nerve exam was conclusive for a suspected seventh nerve palsy by testing the following facial expressions:: smiling, closing the eyes, puffing the cheeks, frowning, raising eyebrows. His visual acuity was not checked during the bedside exam. The slit lamp exam revealed a linear area of epithelial opacification and staining of the lower third of the cornea. No other anterior segment pathology was detected.
Exposure keratitis precautions secondary to lagophthalmos were discussed and carboxymethylcellulose (CMC) 1% ophthalmic gel, one drop every two to four hours in the left eye was prescribed. To prevent interference with the facial wound and bandage, the treatment plan did not include eyelid taping to alleviate exposure. The patient was scheduled to follow up in one to two days for a comprehensive ocular exam.
He returned two days after the initial encounter reporting symptoms of a foreign body sensation and irritation despite admitting good compliance with the prescribed treatment.
Upon ocular examination, his best corrected visual acuity (BCVA) in the left eye was 20/30. Extraocular muscle ranges showed mild adduction limitation. Pupil testing and confrontational fields were normal. Overall, a paralytic left facial muscle tone, mild lagophthalmos in the left eye, and a widened palpebral aperture persisted in the left eye. Lower left facial muscle tones were difficult to assess given the large wound and edema of the left cheek. The slit lamp exam of the left eye revealed: moderate MGD, anterior blepharitis, moderate conjunctival injection, a 4 mm × 0.75 mm inferior corneal epithelial defect with adjacent subepithelial infiltrates (Figure 1), reduced tear break-up time and moderate superficial punctate keratitis in the left eye (Figure 2). All other anterior segment findings were unremarkable.
Figure 1. Inferior epithelial defect and opacification with areas of subepithelial infiltrates adjacent to the epithelial defect of the left cornea. This photo was taken after the instillation of Fluress.
Figure 2.Cobalt blue filter displaying moderate superficial punctate keratitis of the left eye.
New subepithelial infiltrates and minimal improvement to the epithelial defect suggested signs of staphylococcus-associated marginal keratitis. These clinical findings likely contributed to the patient’s symptoms of discomfort. Tobradex 0.3% ophthalmic suspension was prescribed, alternating it with the CMC 1% ophthalmic gel drops, each four times daily. A bland ocular lubrication ointment was added to the left eye at night. The patient was scheduled to follow up in one week.
Nine days after the initial visit and three days after the linear closure/skin graft placement of the open wound, his lagophthalmos remained unchanged. The patient reported improvement in his ocular symptoms in the left eye, and his BCVA in the left eye improved to 20/25.
His anterior segment findings remained unchanged from last visit with moderate conjunctival injection, and an area 4 mm horizontally x 0.75 mm vertically of inferior epithelial staining with mild to moderate superficial punctate keratitis (Figure 3). The subepithelial infiltrates and inferior peripheral corneal opacification had resolved with the Tobradex treatment (Figure 4).
Figure 3. Cobalt blue filter displaying mild to moderate signs of superficial punctate keratitis of the left eye.
Figure 4. Image showing mild to moderate signs of superficial punctate keratitis on the cornea with no signs of corneal edema or subepithelial infiltrates of the left eye.
Overall, the clinical findings and symptoms improved once his staphylococcal marginal keratitis resolved. There was no change in the left facial weakness. With improved corneal surface findings, the patient was advised to discontinue the Tobradex 0.3% ophthalmic suspension and continue CMC 1% ophthalmic gel drops four times a day along with lubricating ointment at night in the left eye. Warm compresses were initiated twice a day for a 10-minute duration after eyelid hygiene. A follow-up visit was scheduled in three months to monitor the recovery of his paralytic lagophthalmos. He was advised to return to the clinic if he had new symptoms.
Three months later, the patient reported an occasional intermittent foreign body sensation with overall improvement in his ocular symptoms. His BCVA improved to 20/20 in the left eye. He reported inconsistent compliance with the prescribed treatment regimen.
At this visit, the open wound on his left cheek was fully healed and the left facial paralysis was nearly fully resolved. There was a residual lagophthalmos of about 0.8 mm in the left eye with improved blinking ability and interpalpebral aperture measurement compared to previous measurements. There were signs of mild dry eye, exposure keratopathy, anterior blepharitis and his MGD persisted. Maintenance therapy with CMC 1% ophthalmic gel drops four times a day, lubrication ointment at night, warm compresses twice a day, and eyelid hygiene in both eyes was prescribed. The patient was advised to return annually and as needed for new symptoms.
DISCUSSION
Lentigo maligna melanoma physiology
Lentigo maligna melanomas (LMM) are the third most common melanoma subtype, accounting for 4-15% of all melanomas and 10-30% of those occurring on the head and neck.4 They are characterized by an atypical proliferation of melanocytes along the dermal-epidermal junction. Risk factors for LMM growth include high ultraviolet radiation exposure, fair skin, a history of severe sunburn, and an increased number of melanocytic nevi. Surgical excision with at least 1 cm margins is recommended by numerous studies for invasive melanomas, with meticulous preoperative planning to minimize impact on surrounding nerves.5
The patient’s melanoma was on the midface, where the superficial aspect of the facial nerve lies in close proximity to the maxillary branch of the trigeminal nerve. This makes both nerve branches susceptible to damage during facial surgery for lentigo maligna melanoma.
Facial nerve physiology      Â
There can be a significant risk for damage when surgery is performed near the facial nerve. The facial nerve branches traverse the cheek in a superficial plane making them vulnerable during surgical procedures in this region (Figure 5). The most critical branches include the temporal branch (innervates the frontalis, upper part of the face and orbicularis oculi orbital portion), zygomatic branch (innervates the orbicularis palpebral portion), buccal branch (innervates the buccinator and other midface muscles), marginal mandibular branch (controls the lower part of the face/lower lip) and the cervical branch (innervates muscles below the chin). Preserving these nerves is critical to avoid functional deficits such as facial asymmetry or difficulty with facial expressions.6
Figure 5. A diagram that demonstrates the distribution of facial nerves branches (in yellow) from the facial nerve nucleus located in the brainstem. This diagram also illustrates the proximity of the trigeminal nerve (in orange) to the facial nerve.
In the management of malignant melanoma on the midface, wide local excision followed by linear closure is a standard therapeutic approach aimed to help with complete tumor removal and prevent recurrence of the condition.7 However, this method can lead to compression of the facial nerve from residual post-surgical edema. In some instances, facial nerve palsy can manifest either immediately or with a delay after surgery, as documented in the literature with cases of vestibular neurectomies.8 The timing of onset is an important consideration in the management of the condition. Immediate onset facial paralysis usually suggests potential facial nerve transection, while delayed onset facial palsy suggests ongoing inflammation and swelling that can compress the facial nerve up to two weeks post-surgery.9 Many cases of delayed onset facial paralysis are reported after vestibular neurectomy, temporal bone fracture, vestibular schwannoma surgeries, acoustic neuroma surgery, or other ear surgeries.8-10 One case report discussed a delayed onset facial nerve palsy after Mohs surgery of a recurrent basal cell carcinoma of the left lateral malar cheek.11
Anterior segment complications and treatments
Paralytic lagophthalmos from a facial nerve palsy can result from the disruption of the facial nerve branches during surgical excision or with postoperative edema near the facial nerve. This can lead to paralysis of the orbicularis oculi muscle, preventing it from contracting.12 There are various etiologies for facial nerve palsy including infection, trauma, tumor, metabolic, toxic iatrogenic, neurological, congenital, and idiopathic.13 In this case, the patient’s melanoma excision led to a facial palsy, resulting in a paralytic lagophthalmos of the left eye. Paralytic lagophthalmos secondary to delayed facial palsy has a good prognosis, and there is optimistic support for spontaneous recovery.10 In most cases, patients can recover within a two-to-four-month period.9 However, during the recovery there is a risk for exposure keratopathy that can lead to severe corneal ulcerations or blindness without treatment.3,4 Therefore, identifying and addressing paralytic lagophthalmos in the postoperative period is crucial.
Depending on the severity, ocular surface complications resulting from paralytic lagophthalmos can be managed with non-surgical or surgical approaches. Palliative care may include artificial tears, lid taping, moisture chamber goggles, and lubrication ointment to decrease the incidence of exposure keratopathy.13 Although lid taping and moisture chamber goggles are recommended to mitigate risk, their use was not considered for this patient because of his healing wide local excision. As observed in this patient, his ocular surface revealed signs of subepithelial infiltrates along with exposure keratitis that suggested a component of staphylococcal-associated marginal keratitis. He was treated with steroids in conjunction with lubrication to treat the ensuing ocular inflammation. Chronic corneal exposure can induce severe conditions such as band keratopathy, corneal ulcerations, microbial keratitis and corneal scarring.13
Asymmetry of facial movements can be treated with botulinum toxin; it may also be useful in treating synkinesis, which can occur after facial paralysis.14 Paralytic lagophthalmos secondary to delayed facial palsy post-surgery is a self-limiting condition. In cases where resolution does not occur, temporary eyelid weight placements or oculoplastic surgical options to restore the upper and lower eyelid positions can be considered. Some of these procedures include tarsorrhaphy, upper eyelid weight implantation, neuroplastic surgery, and muscle transposition.13,15 The management of paralytic lagophthalmos following a wide local excision for malignant melanoma on the left face demands a multidisciplinary approach between the surgeon and eye care providers to monitor the resolution and need for secondary surgical interventions.
CONCLUSION
While the primary goal of facial melanoma removal is the complete removal of malignant tissue to control local disease, it is essential to closely monitor the onset of facial paralysis development during post-operative care. Close observation and timely intervention can prevent ocular surface disease complications and exacerbations of ocular symptoms from paralytic lagophthalmos.
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I graduated from the New England College of Optometry in 2023 and completed a residency in ocular disease at the VA Boston health care system, Brockton campus in 2024. I have a strong interest in anterior segment disease, retinal disorders, glaucoma and clinical education. Currently I am a primary care optometrist at Atrius Health where I enjoy sharing my expertise and helping patients with their visual needs.
Anne Bertolet graduated from the New England College of Optometry in 2017. She completed her residency and research fellowship at the VA Boston Healthcare System. She now works as an attending optometrist at the Brockton campus where she is the residency co-director of the VA Boston Healthcare System ocular disease residency program. Her interests include neurological manifestations on OCT imaging, glaucoma, and systemic manifestations of ocular disease.
