Case report

A healthy 22-year-old man with prognathism underwent a modified SSO using the Hunsuck modification and genioplasty. A reciprocating air-driven saw was used to perform the osteotomies. Small, thin chisels and a splinter were used to split the mandible. The split was uneventful. After the osteotomy, a prefabricated splint was applied, the segment was pushed back the predetermined distance (6 mm) and intermaxillary fixation (IMF) applied. The segments were then fixed in place using 2.0 mm titanium plates and 7 mm screws. After releasing the IMF, the occlusion was found to be acceptable. A 5 mm advancement genioplasty was performed with no complications.

The intraoperative course was uneventful and ice packs were applied during the first 24 h postoperatively. The day after the operation, oedema was mild and there was no evidence of neurologic injury, including the inferior alveolar nerve. On the third postoperative day, the patient had moderate facial oedema and complete right facial nerve palsy. The patient was unable to wrinkle his forehead and a severe asymmetric smile was present. Stapedial reflexes and taste functions were normal. He had no signs of viral infection. Panorax and lateral oblique X-rays were taken. No signs of unfavourable splits were noticed (including the styloid process).

The patient was started with parenteral steroids (dexamethasone 8 mg) four times daily for day one and thereafter a tapering dose of oral prednisone 5 mg (4 times daily for 3 days, 3 times daily for 3 days, twice a day for 3 days, and a single oral dose for the last 3 days). An eye patch, ointment for the right eye, lubrication and concomitant active physiotherapy were started. Vitamins were prescribed similar to previous reports : B1 75 mg, B6 75 mg, and B12 0.75 mg per day for 2 months. Two months after surgery, a gradual recovery of all right-sided facial muscle movement was noted. The authors ordered electromyography to rule out neurotmesis at 4 months, following C hoi et al. , because the clinical signs of recovery (Tinel’s sign or muscle movement) indicated slow progress or less progress than would be expected from a neuropraxia or axonotmesis injury. No failure of spontaneous eye closure was present, so no ophthalmic consultation was necessary. A complete recovery after 6 months was seen without residual asymmetry ( Fig. 1 ).

Photographs of the patient (A, C, and E) 3 days after SSO and (B, D, and F) 6 months after surgery, showing complete resolution of facial palsy.

Discussion

In general, the incidence of facial nerve palsy after orthognathic surgery is 0.17–0.75% . Most authors report it as a rare complication. Facial nerve compression is the most likely aetiology perhaps due to the relationship between the posterior border of the mandibular ramus and the facial nerve in the open-mouth position adopted for SSO (usually less than 1 cm) . All other factors that can lead to facial nerve injury include the manipulation of instruments too far behind the mandibular ramus, unfavourable fractures, pressure packing, injection of vasoconstricting agents deep in the perimandibular region , haematoma or oedema, and variation in the anatomic course of the facial nerve. An unprotected osteotome can cause a partial or complete transection of the facial nerve trunk, in which case, early surgical exploration is indicated. Surgical exploration is not usually necessary, even if the palsy occurs some time later . If complete facial palsy occurs immediately after primary surgery, restoration of the nerve is indicated.

Timing of initiation of steroid therapy plays an important role in enhancing nerve regeneration . A significantly better improvement can be expected when steroid treatment is begun early . Multiple oral dosage regimens of oral steroids and the vitamin therapy are available. The use of electrical stimulation has been linked to positive outcomes , and the type should depend on the pathology of the facial nerve. Biofeedback, ultrasound therapy, acupuncture and magnets have been used in combination with physiotherapy, but their specific efficacy requires further investigation .

Distinguishing central types of facial palsy from the peripheral type is important. The central type produces facial palsy in the lower facial muscles contralateral to the site of injury. Peripheral paralysis is subdivided into intrapetrosal and extrapetrosal types. A lesion in the intrapetrosal region usually produces deficient taste sensitivity and hyperacusia . The degree or level of nerve injury has important implications for recovery . Most facial palsies caused by compression or traction of the facial nerve are neuropraxia and axonotmesis, with complete recovery expected within weeks or months . In the case described, the most likely cause was oedema.

The assumption that postoperative facial nerve palsy always disappears is incorrect and the course of treatment should be handled with extreme care. There is evidence of facial nerve palsy following bimaxillary surgery and mandibular advancement . A high association between patients with cleft lip and palate and facial palsy after orthognathic surgery was observed by C hoi et al. . All efforts must be applied to reducing the patient’s postoperative psychological stress, to reassure the patient and document the incident to prevent future litigation. The decision to include this complication in the informed consent should be made by the consultant, considering that postoperative facial palsy is one of the most serious complications for a patient requiring correction of a dentofacial deformity, because their quality of life and social interaction are significantly reduced.