Ophthalmic complications associated with orthognathic surgery

CLINI AL ARTICLE J Oral Maxillofac Surg 51:480-494,1993

Ophthalmic Complications Associated With Orthognathic Surgery DENNIS T. LANIGAN, DMD, MD,* KEN ROMANCHUK, MD, FRCS(C),t AND CHARLES K. OLSON, DMD:f: Ophthalmic complications are rare following maxillary osteotomies. Potential complications include a decrease in visual acuity, extraocular muscle dysfunction, neuroparalytic keratitis, and nasolacrimal problems involving both an increase or a decrease in tearing. Ophthalmic injuries appear to be primarily mediated through indirect injuries to neurovascular structures occurring from traction, compression, or contrecoup injuries from forces transmitted during the pterygomaxillary dysjunction using an osteotome or from fractures extending to the base of the skull or orbit associated with the pterygomaxillary dysjunction or the maxillary downfracture. A review of the literature of previous ophthalmic complications as well as eight new cases are reported. The possible etiologic basis for these injuries is discussed in detail as well as treatment possibilities when appropriate.

any cases of nasolacrimal injury or obstruction following inferior turbinectomy and Le Fort I maxillary superior repositioning. Little et al? have discussed the possibility of transient epiphora following Le Fort I osteotomies due to surgical edema creating a functional obstruction ofHasner's valve of the distal lacrimal duct apparatus. The low incidence of permanent epiphora is influenced by the angulation of the bony nasolacrimal canal and the ability of the distal lacrimal complex to undergo deformation of the soft tissue within the bony framework while still maintaining its patency. The meatal opening of the nasolacrimal duct in the roof of the inferior concha of the nose also affords additional protection against permanent epiphora. You et al,!" in an experimental study, looked at the anatomy of the nasolacrimal canal with reference to high mid facial osteotomies. The inferior orifices of the nasolacrimal canal were found to be superior to the simulated high Le Fort I osteotomy cuts in all their specimens. Le Fort I osteotomies immediately inferior to the infraorbital foramen are thus relatively safe procedures for the nasolacrimal apparatus. In their specimens, the course of the nasolacrimal canal was found to be positioned within a 5.5-mm wide zone that extended between the lacrimal sac and the anterior attachment of the inferior turbinate on the anterior wall of the maxilla. Osteotomy cuts for modified Le Fort II or Le Fort III osteotomies should thus not be made in this area. Freihofer and Brouns!' reported an impairment in the function of the lacrimal system in 4% of all their high midface procedures. Keller and Sather'?

Although a great deal of information is available in the literature regarding the ophthalmic complications of maxillofacial trauma, little has been written regarding ophthalmic complications associated with orthognathic surgery."!" Tomasetti et all reported a lack of tearing in a 24-year-old woman following a Le Fort I osteotomy to correct maxillary retrusion. One month after surgery, it was noted that the patient was unable to tear from the left eye. The ophthalmologic consultant thought there had been damage to the parasympathetic fibers to the lacrimal gland. Limited tearing returned by 5 months postoperatively, and there was normal function of the lacrimal gland by the eighth postoperative month. Demas and Sotercanos' discussed the possibility of injury to the nasolacrimal duct system following Le Fort I osteotomies with superior repositioning as well as the risk to the canaliculi and lacrimal sac during the naso-orbital osteotomies associated with Le Fort II or Le Fort III osteotomies. They did not, however, report

.. Professor and Head, Division ofOral and Maxillofacial Surgery, University of Saskatchewan, Saskatoon, Canada. t Associate Professor, Department of Ophthalmology, University of Saskatchewan, Saskatoon, Canada. t In private practice, Portsmouth VA. Address correspondence and reprint requests to Dr Lanigan: Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Saskatchewan, Saskatoon, SK, Canada S7N OWO.

© 1993 American Association of Oral and Maxillofacial Surgeons 0278-2391/93/5105-0003$3.00/0

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LANIGAN, ROMANCHUK, AND OLSON

reported one patient who experienced nasolacrimal duct dysfunction in their series of 54 patients who had undergone a quadrangular Le Fort I osteotomy. Bilateral, mild, sporadic, increased tearing was noted postoperatively, which resolved spontaneously within the first year. Watts2 was the first to report extraocular muscle dysfunction following a Le Fort I osteotomy. An 18year-old woman with maxillary retrusion was treated with a Le Fort I osteotomy with advancement. On the first day postoperatively, the patient complained of diplopia, and a right abducent nerve palsy with a lack offunction ofthe right lateral rectus muscle was noted. After 7 weeks, the abducent nerve palsy had completely recovered. Carr and Gilbert' reported a case of an isolated partial oculomotor nerve palsy following a Le Fort I "Wake't-type osteotomy with advancement to correct a midfacial retrusion secondary to a bilateral cleft lip and palate deformity. Early on the first postoperative day, the patient developed a right-sided ptosis and divergent stabismus with diplopia. By the fourth day after surgery, the ptosis had improved, as had the range of extraocular muscle movements. By 8 weeks postoperatively, there was full restoration ofeye movement and complete resolution of the diplopia. Reiner and Willoughby4 reported a case of a right abducent nerve palsy following a Le Fort I maxillary osteotomy with advancement and superior repositioning in a 27-year-old woman with maxillary retrusion and mandibular prognathism. The patient complained of diplopia on the first day postoperatively, and the right eye was unable to move into right lateral gaze. Complete recovery occurred within 5 months postoperatively. Uttley et al5 reported one patient who developed a transient unilateral abducent nerve palsy following the use of a Le Fort I osteotomy to approach a midline skull base tumor. This palsy resolved completely within 3 days. 0'Ryan6 mentions one additional case ofa transient neuropraxia of the VI nerve following a Le Fort I osteotomy but gives no details regarding this complication. Four cases of carotid-cavernous sinus fistulae, with resulting ophthalmic complications, have been reported following orthognathic surgery.P:" As these cases have been reviewed in detail previously.v-" they are not discussed in this article. Sirikumora and Sugar" reported a case of a right-sided tonic pupil in isolation (Adie's pupil) following a Le Fort I osteotomy with advancement and drop-down in a 24-year-old woman with a maxillary retrusion and vertical deficiency. On the first postoperative morning, the patient was noted to have a markedly dilated right pupil with no direct , or consensual light reflex. There was no proptosis and, although the patient complained of blurred vision on extreme left gaze, there was no diplopia or impairment of extraocular muscle movement. Fundoscopy revealed

a normal-appearing disc with positive venous pulsations. The ophthalmologist who saw her in consultation thought the findings were consistent with a diagnosis of Adie's pupil. It was uncertain whether this problem was a genuine complication of her orthognathic surgery or purely a coincidence. By 18 months postoperatively, the right pupil had almost totally recovered in both size and function, with only limited reduction in accommodation.

Report of Cases In 1986, a questionnaire was sent to North American oral and maxillofacial surgeons requesting information about major vascular complications associated with orthognathic surgery. Included in the almost 800 replies received were two cases dealing with ophthalmic complications. Since that time, information has been obtained on an additional six cases.

Case 1 A 33-year-old woman was admitted for orthognathic surgical correction of her malocclusion. She had a long-standing history of facial pain and temporomandibular joint dysfunction, which was primarily muscular in origin, but that severely limited her masticatory function. Two years previously she had undergone a multiple segment Le Fort I osteotomy, bilateral sagittal mandibular ramus osteotomies, a genioplasty, and a bone graft from the iliac crest to correct an open-bite malocclusion and a complex facial asymmetry. During this surgery, the posterior maxilla was impacted and the maxilla was rotated medially. Corticocancellous bone grafts were placed along the entire lateral aspect of the maxilla and in the pterygomaxillary regions. The surgery was uneventful and initially the patient had some relief of her symptoms. The patient, however, experienced a recurrence of her severe masticatory dysfunction owing to persistent muscle spasms and severe incapacitating pain in the left temporomandibular joint region, which did not respond to conservative treatment. Some relapse of her malocclusion was noted. She retained some facial asymmetry, with noticeable canting of her occlusal plane. The patient was reoperated with a Le Fort I osteotomy with intrusion on the left-hand side, drop-down on the right with interpositional bank bone grafting, and bilateral sagittal ramus osteotomies of the mandible. The bony architecture and consistency of the bone in the posterior maxillary regions was thought to be significantly different from what the attending surgeon had noted at the initial surgery. A thin curved osteotome was used to achieve the pterygomaxillary dysjunction. The dysjunction itself appeared to be satisfactory and the maxillary downfracture was accomplished easily with minimal pressure. A minor area of bone that had not been separated about the posterior medial wall of the right maxillary sinus was freed with minimal effort and force. The remainder of the surgery was completed in a conventional manner. Initially after surgery, the patient did not complain of any visual problems, nor did the nurses note any pupillary abnormalities on routine postoperative status checks. The morning after surgery, however, the patient complained of no light perception vision in the right eye, and she was noted to have a fixed, dilated right pupil. A consensual pupillary response was noted in the right eye, although this was di-

482 minished in amplitude. The right eye was approximately 20 diopters exotropic and 10 diopters hypotropic. Fundoscopic examination of the right eye revealed a normal-appearing disc and spontaneous venous pulsations. On general digital pressure, arterial pulsations were noted in the disc of the right eye. Vision, fundoscopic examination, and confrontation fields were grossly normal in the left eye. Extraocular movements were full in all directions with the exception of adduction of the right eye, which was incomplete but up to almost 75% of the normal range. She had obvious ptosis of the right eyelid and the margin ofthe right upper lid appeared swollen and red. The clinical impression was of a complete right optic nerve dysfunction and a partial right oculomotor (III) nerve palsy. A computed tomographic (CT) scan of the right orbit and head was done immediately to rule out pressure in the optic canal. The CT scans revealed multiple facial and basilar skull fractures. These fractures included the roof of the right maxillary sinus, the posterior wall of the right maxillary sinus, and the pterygoid plates. There appeared to be a fracture through the medial wall of the right orbit posteriorly. There were fractures ofthe sphenoid bone on the right side extending through the floor of the middle cranial fossa (Fig IA). A fracture through the lesser wing of the right sphenoid bone extended just lateral to the optic foramen. A small bony fragment, probably from the fracture of the roof of the right maxillary sinus, was in close proximity to, or in contact with, the right optic nerve in the region of the optic foramen near the superior orbital fissure (Fig IB). There was diffuse enlargement of the right optic nerve, probably related to edema, primarily distal to the optic foramen and proximal to its arrival at the optic disc. The optic nerve appeared intact and unaffected proximal to the optic foramen. The medial rectus muscle appeared swollen. No hematomas were noted in the orbit. Consultations were obtained from several experts in the fields of neuro-ophthalmology and orbital pathology. Treatment options suggested included high-dose intravenous steroids, as well as the possibility ofsurgical exploration to deroof the orbit to decompress the optic nerve. The consensus, however, was for high-dose dexamethasone sodium phosphate (Decadron, Merck, Sharp, and Dohme, Pointe-Claire, Quebec, Canada) therapy, and the patient also preferred to have no surgical intervention. The patient was advised that although the prognosis for the recovery ofthe oculomotor nerve function was good, the prognosis for recovery of optic nerve function was guarded and she would likely remain permanently blind in the right eye. The patient was initially treated with Decadron, 40 mg IV every 6 hours for five doses, and the dose was then lowered to 10 mg IV every 6 hours. The patient's third nerve palsy resolved quickly. By the time of her discharge, 5 days postoperatively, there was essentially complete resolution of the ptosis and the limitation of movement ofthe right medial rectus muscle. The pupil ofthe right eye remained a bit more dilated than the left. The patient did not regain any vision in the right eye and the blindness has persisted. The surgeon involved in this case thought that the influence of previous surgery and healing should be considered in the etiology ofthis complication. A comparison between the cephalometric radiograph taken before the first operation and the radiograph prior to the second operation revealed a noticeable increase in radiopacity in the posterior maxillary regions following the initial surgery. The posterior maxillary impaction and the bone grafting carried out in the pterygomaxillary area were believed to have resulted in partial obliteration of the naturally occurring pterygomaxillary fissure

OPHTHALMIC COMPLICATIONS: ORTHOGNATHIC SURGERY

FIGURE I. A. The short arrow points to a fracture of the right lesserwingof the sphenoidextendingthroughthe floorof the middle cranial fossa. The long arrow points toward a fracture of the left pterygoid plate. B. This CT scan cut demonstratesa fracture at the back of the rightorbit. The arrow points towarda small fragment of bone impingingon the optic nerve.

and a more robust buttress of bone in this region. The anatomic differences in the pterygomaxillary region, as compared with the first surgery, necessitated the surgeon having to position the curved osteotome used to achieve the pterygomaxillary dysjunction somewhat closer to the base of the skull. These factors may have contributed to the aberrant fractures that extended to the base of the skull and orbital regions despite an apparent relatively atraumatic and routine pterygomaxillary dysjunction and down fracture being noted at the time of surgery.

LANIGAN,

RO~IANCIIUK,

AND OLSON

Case 2 A 16-year-old girl with a rnidfacial retrusion was treated with a Le Fort I osteotomy with advancement. Numerous attempts at intubation through the left nostril were unsuccessful, resulting in bleeding, but the patient was subsequently intubated easily through the right nostril. The classic Le Fort I osteotomy sequence was then followed, with the ptcrygomaxillary dysjunction being carried out between the maxillary tuberosity and pterygoid plates. The maxilla was downfractured easily. No significant bleeding was encountered at that time, and both descending palatine arteries were noted to be intact . Infraorbital rim suspension wires, in addition to intraosseous wires, were used for stabilization. At the completion of the operation, the drapes were removed and the left eye was noted to be extremely proptotic and tense. An ophthalmology consultation was requested immediately, but no cr scan was done. The maxilla was redownfractured, and although minor mucosal bleeding was seen in the right antrum, no hematoma was noted in the antra, nor did there appear to be significant bleeding from the pterygornaxillary . regions. Copious blood was suctioned from the left nasal cavity, however, and following this the orbital swelling and proptosis decreased dramatically. At this point, the ophthalmologist examined the eye and confirmed the diagnosis ofa retrobulbar hemorrhage. As the intraocular pressure in the left eye was increased to 46 mm Hg, the ophthalmologist first performed a lateral canthotomy, including relaxing incisions of the superior and inferior cruxes of the lateral canthal ligaments to relieve orbital tension and try to prevent central retinal artery occlusion or optic neuropathy. An incision and drainage of the inferior medial region of the orbit was then performed through the lower lid and a 0.25·inch Penrose drain placed. The patient was also given 500 mg of acetazolamine (Diamox, Lederle Laboratories, Markam, Ontario, Canada) and 50 mL ofa 25% mannitol solution intravenously to reduce intraocular pressure by pharmacologic means. The intraocular pressure after 30 minutes decreased to 34 mm Hg. The patient was sent to the surgical intensive care unit (lCU) for observation. In the ICU, the ophthalmologist noted very slight blanching of the optic nerve on fundoscopic examination, but all the blood vessels appeared normal. The ophthalmologist placed the patient on timolol maleate opthalmic solution (Merck, Sharp, and Dohme) and pilocarpine in an effort to again reduce intraocular pressure. The patient's intraocular pressure quickly returned to normal values. She was discharged from hospital 4 days postoperatively. She has had no long-term problems with visual acuity.

Case 3 A 17-year-old girl with vertical maxillary excess and apertognathia was treated by a Le Fort I osteotomy with intrusion and a genioplasty. The surgery was carried out without incident. The operation lasted approximately 3 hours and was completed shortly after 3 PM. The patient was transferred to an intensive care unit for postoperative monitoring. She had been given 8 mg of Decadron IV preoperatively, another 4 mg at 8 PM, and was then to continue taking 4 rng three times a day during her hospital stay. At 9 PM on the day of surgery, the patient first complained to the nurses of being unable to see anything from her left eye. At that time, the left pupil appeared to react very slightly and slowly to light, constricting from 6 to 5 mm, and then back again. The right pupil was 5 mm in size and reacted briskly to light.

483 The next morning, arrangements were made for an immediate cr scan and for consultation with a ncuro-ophthalmologist. The cr scan was performed with thin sections through the maxilla, orbits, optic canals, and the region of the sella. The results of the cr scan were basically negative, with no evidence of unusual fractures causing any mechanical disturbance around the optic nerve or of hemorrhage into the orbit or optic canal. The ncuro-ophthalmologist noted the visual acuity to be normal in the right eye, but there was no reaction to illumination of the left eye, and the patient was completely blind . The pupils both reacted to light shone on the right eye, but there was no reaction to illumination of the left pup il. There was a 4+ left relative afferent pupillary defect. Visual fields were normal in the right eye on confrontation. Extraocular movements were full and the eyes appeared aligned in all positions of gaze. There was a subconjunctional hemorrhage laterally over the temporal aspect of the sclera of the right globe and slight swelling of the upper and lower lids on the right. The examination of the external eyes and anterior segments was otherwise unremarkable. Fundoscopic examination revealed normal optic discs that were sharp and pinkish in color. The vessels,nerve fiber layer, and maculae appeared normal. There was no evidence of vascular occlusion, retinal infarction, or retinal hemorrhage. The ocular media were clear. Based on his clinical exam ination and the cr scan findings, the neuro-ophthalmologist thought the visual loss in the left eye was due to a retrobulbar lesion of the left optic nerve, either of the optic canal or intracranial portion. He was uncertain as to the etiology of the condition, although there did not appear to be a mechanical disturbance in or around the optic nerve. He recommended the patient be maintained on a short course of oral steroids. By the second day postoperati vely, the nurses noted that the pupil of the left eye was not quite as widely dilated, and by the third day, the left pupil was beginning to react very sluggishly and minimally to light. The nurses recorded in their notes that the patient seemed to know when the flashlight was shone in the left eye and that she appeared to be seeing some shadows briefly with the left eye when the light was flashed into it. On the fourth day postoperatively, the patient was again seen by the neuroophthalmologist and by another ophthalmologist for a seeond opinion. They thought the left eye had no light perception vision even with the bright light of the indirect ophthalmoscope. A marked left relative afferent pupillary defect was still present and the left pupil was completely nonreactive to direct illumination. The globes appeared normal and there was no proptosis. The fundi were virtually symmetric and identical. Ophthalmodynarnometry revealed no discrepancy in diastolic pressure measurements in the two eyes. The ophthalmologists suggested the patient be kept on steroids and ordered 80 mg prednisone daily. The patient was reviewed by the neuro-opthalmologist 6 da ys later. He noted that she now definitely had a pupillary reaction to light and the dilation ofthe left pupil had decreased markedly. The patient's vision in the left eye had improved somewhat and she was able to see hand movements in the inferior portion of her left visual field. On fundoscopic examination, there was still no evidence of any retrograde degenerative changes in the opt ic nerve head or nerve fiber layer. The patient was reviewed I week later; ie, 17 days postoperatively. The left pupil reacted to bright light, but the patient still had a 3+ Icft relative afferent pupillary defect. She could see hand movements and count fingers only in the inferior portion of her visual field and along the inferior temporal margin. On fundoscopic examination, there was now some early evidence of nerve fiber layer atrophy in the inferior

484 portion of the nerve, although the optic disc was still normal in appearance. The ophthalmologist began to taper the prednisone levels at this time. When the patient was seen next, 2 weeks later, her visual field in the left eye had expanded somewhat and she could now sec over two thirds of the inferior hemifield. Her vision was still limited to counting fingers as her field, as yet, did not extend to fixation. On fundoscopic examination, there was progression to mild optic atrophy in the left optic disc. There was some nerve fiber layer bundle defects noted in the arcuate regions, more so inferiorly than superiorly. When the patient was reviewed 6 weeks later, her examination had not changed significantly. She could sec well enough inferiorly in her left visual field to count fingers at about 3 to 5 ft. At the tangent screen, she could detect a 10mm white object in the inferior portion of her visual field, but she' could not detect any hand movements superiorly. Dilated fundoscopic examination demonstrated optic atrophy, with marked attenuation of the nerve fiber layer, more so inferiorly than superiorly. The findings on fundoscopic examination were consistent with the degree of visual field loss. The patient's visual condition had basically stabilized at this stage and she was left long term with some visual function in her inferotemporal field in the left eye, but the superior field of vision did not return. The surgeon involved in this case thought the problem was a complication related to hypotensive anesthesia rather than to the orthognathic surgery. The systolic blood pressure, as measured by a sphygmomanometer on the arm, had been maintained at 60 to 70 mm Hg for approximately a 3-hour period, with the patient in a 15° reverse Trendelenburg position. This indirect measurement of blood pressure may not have been sufficiently accurate to assess such low arterial pressures. lIer preoperative blood pressure values had been measured between 98/62 and 120/80.

Case 4 A 42-year-old woman with severe apertognathia was treated with a multisegmental Le Fort I osteotomy with superior repositioning. The pterygomaxillary dysjunction was achieved with a small, curved chisel placed in the pterygornaxillary fissures. The maxilla was down fractured without difficulty. No problems were encountered at the time of surgery or in the immediate postoperative period. Five days postoperatively, the patient did not complain of any eye symptoms when seen for her first postoperative visit. Eight days postoperatively, the patient telephoned her oral and maxillofacial surgeon to say that her left eye felt dry and itchy, with a sensation like "sand in her eyes." These sensations had begun during her drive to her home state, which has a drier climate. It was suggested that the patient sec an ophthalmologist, which she did immediately. The ophthalmologist found she had dry eyes and blepharitis. She was treated with combination dexamethasone, neomycin, polymyxin B (Maxitrol, Alcon, Mississauga, Ontario, Canada), an anti-inflammatory antibiotic ophthalmic solution three times a day, and combination dextran 70 and dyroxypropyl methylcellulose (Tears Naturale, Alcon), an artificial tears eye lubricant, every 3 hours while awake. The patient returned I week later complaining that her eyes were no better. She was again found to have dry eyes and blepharitis, with the left side being much worse than the right. Marked superficial epithelial changes and erosions were noted in the left eye. The Maxitrol solution was discontinued and the patient was taught to do lid scrubs twice a day. She was told to put copious amounts ofmethylcellulose on the eyes.

OPHTHALMIC CO:\IPLlCATIONS: ORTHOGNATHIC SURGERY

When reviewed 3 days later, the patient complained of blurred vision and a burning sensation of the left eye. She was still found to have a moderate amount ofcentral punctate erosions in the left cornea but had improved from the last appointment. The patient also was noted to have anesthesia of her left cornea, likely due to an injury to fibers from the nasociliary branch of the first division of the trigeminal nerve resulting in ncuroparalytic keratitis. lIer vision at that time, without correction, had dropped from 20/20 before her orthognathic surgery to 20/100 in the left eye; her vision in the right eye remained at 20/20. The patient was told to tape the left eye elosed at night and to usc copious amounts ofmethylcellulose lubricant during the day. Three days later, 25 days postoperatively, the patient was reexamined by the ophthalmologist. He found no moisture in the left eye except for the drops that the patient was using. The vision in the left eye had deteriorated further to 20/200. Marked punctate changes of the cornea were again noted centrally. The methylcellulose drops were discontinued and the patient was started on a preservative-free polyvinyl alcohol ocular lubricant drops (Refresh; Allergan, Markam, Ontario, Canada), every 2 to 3 hours, and petrolatum-mineral oil compound ocular lubricant ointment (Lacrilube; Allergan), three to four times during the day. No improvement was noted in tearing when the patient was seen 2 days later, but there was some improvement in the surface of the left cornea and her vision in the left eye had improved to 20/70. Five days later, 34 days postoperatively, the patient was rechecked. Her eyes were still dry, but she was complaining of less burning and itching. There was essentially no change in her cornea. When the patient was seen 2 weeks later, she said her left eye felt somewhat better when it was kept well lubricated, although the eye still burned and felt irritated and her vision was somewhat blurred. The ophthalmologist noted, much improvement in the left cornea, with only a small amount of punctate changes and improved visual acuity in the left eye to 20/25-2. The patient was started on vitamin A ophthalmic solution in an effort to heal some of the epithelial changes in the cornea. Two weeks later, 9 weeks postoperatively, further improvement was noted on examination of the cornea, although the left eye remained dry. A Schirmer's test under anesthesia, showed secretion of tears in both eyes to be minimal. The ophthalmologist had noted that the patient tended to have borderline dry eyes even before the orthognathic surgery, but this situation had definitely worsened postoperatively. A CT scan was done to look for a possible etiology for the patient's dry eye. The CT scan was reported as basically normal except for postsurgical fractures of the pterygoid plates and posterior lateral wall of the right maxillary sinus. When the patient was reviewed by the ophthalmologist 10 weeks postoperatively, vision had improved to 20/20 in the left eye and a small pool of lubricant was noted in the lacrimal lake ofthe left eye. The condition ofthe cornea had improved. At a visit 13 weeks postoperatively, the vision in the left eye remained normal, although no new lubrication had developed. The patient's eye felt normal unless she forgot to use the lubricant. She was now using the lubrication only once every 3 hours, whereas initially, she was using it every 20 minutes. At 15 weeks postoperatively, a trial using a hydroxypropyl cellulose insert (Lacrisert; Merck, Sharp, and Dohme) was begun to sec if this would improve the dry eye condition. Initially, with the Lacrisert, the eye felt more irritated and by the afternoon her vision was more blurred than when using the ointment and drops. By 20 weeks postoperatively, she felt comfortable using the Lacrisert and her tearing had

LANIGAN, ROMANCHUK. AND OLSON

improved but was still subnormal. A repeated Schirmer's test showed normal lacrimation in the right eye, but lacrimation in the left eye was still markedly decreased. The cornea was clear and her vision remained at 20/20 in the left eye. The cornea still had no sensation. By I year postoperatively, there had been no noticeable further increase in tearing. The patient was continuing to use artificial tears four to five times a day and a lubricating ointment at night. By 2 years postoperatively, the patient subjectively felt that her symptoms of a dry eye had decreased significantly.She continued, however, to use the artificial tears in the left eye three times a day. A Schirmer's test showed equal tear production in both eyes and her vision remained at 20/20. She had increasing return of sensation of the left cornea, although sensation to the superior one third was still lessthan on the right. The patient did not find her ophthalmic problems a particular inconvenience because they did not interfere with her usual lifestyle. She was sufficiently happy with the results of her orthognathic surgery to state she would have the surgery again without hesitation even if meant enduring the eye problems.

CaseS A 39-year-old woman with vertical maxillary excess, mandibular retrognathia, and facial asymmetry was treated by u Le Fort I osteotomy with intrusion, bilateral sagittal mandibular ramus osteotomies with advancement and rotation, and a genioplasty. The pterygomaxillary dysjunction was carried out utilizing a curved osteotome and the downfracture was accomplished easily. The patient's initial postoperative course was uneventful. Eight weeks postoperatively, however, she saw her optometrist in consultation because she was experiencing difficulty in wearing contact lenses owing to a continual complaint of dryness in the right eye. She also noted decreased lacrimation after crying and complained of slight photophobia in the right eye. These problems had first been noted about I month following surgery. The optometrist noted her pupils to be equal, round, and responsive to light. No afferent pupillary defect was noted. Extraocular muscle mobility and external ocular examination were within normal limits. Her refractive status showed normal 20/20 vision at distance and near. The cornea appeared normal, with no punctate lesions. A dilated fundoscopic examination revealed a normal optic disc, macula, and peripheral retina. Biomicroscopy revealed a one third decrease in the lacrimal lake of the right eye as compared with that of the left eye. The optometrist thought that the patient's inability to wear contact lenses was due to poor wetting from the decrease in the lacrimallake in the right eye. He suggested that she stop wearing contact lenses and prescribed new eyeglasses. The problem with dryness and slight photophobia has persisted, although it is subjectively somewhat better 14 months postoperatively. She notices more tearing when crying. The dryness has resulted in no significant sequelae except with the difficulty in wearing contact lenses. There have been no ocular complications. On a repeated examination, there was no superficial staining of the cornea, no superficial punctate keratitis, and no redness or discomfort of the eye.

Case 6 A 20-year-old woman with vertical maxillary excess and . mandibular retrognathia was scheduled for a Le Fort I osteotomy with intrusion and a mandibular advancement. An abnormal sagittal split of the left mandibular ramus forced abandonment of the mandibular advancement procedure.

485 However, the Le Fort I osteotomy with intrusion was completed successfully. The pterygomaxillary dysjunction was achieved using a curved osteotome. The right descending palatine neurovascular bundle had to be cut and ligated to anow for sufficient bone removal in the region of the right pterygoid plate. There was no mention in the operative report of whether the right pterygoid plate was intact or whether it was fractured and/or detached from the skull base. The patient's initial postoperative course was uneventful. At a follow-up examination 3 months following her surgery, however, she complained of a burning sensation in the right eye at nighttime. She was referred to an ophthalmologist, who saw her 2 months later. The ophthalmologist diagnosed a punctate keratopathy in the right eye and treated her with topical ocular lubricants. A formal evaluation of tear production was not performed until I month later, 6 months after her surgery. The examination revealed a marked relative reduction in tear production in the right eye. Visual acuity and corneal sensation were normal in both eyes. A cr scan of the head was reported as normal, with no evidence of an intracranial mass lesion as a cause of the patient's unilateral "dry eye." Thirteen months after her orthognathic surgery, the patient was referred to a neuro-ophthalmologist for a second opinion regarding her dry eye. The patient stated that her symptoms had remained stable over the past year. She had noted blurring in the right eye toward evening, irritation in the right eye in the morning, occasional redness in the right eye, decreased sensation over her right cheek bone, and a "cool" sensation in her right nasal passage when she inspired. She was using Hypotears (polyvinyl alcohol artificial tears, lolab, Peterborough, Ontario, Canada) three to four times a day and Lacrilube, an ocular lubricating ointment, at bedtime. On examination, her uncorrected visual acuity was 20/15 bilaterally. The patient's extraocular muscle movements were normal and her confrontation visual fields were full. Both pupils reacted briskly to light, from 6 to 3 mm, with no afferent pupillary defect. Dilated examination of the fundi revealed normal discs, retinal vessels, and maculae. There was mild hypesthesia to light touch over the right malar area in the distribution of the zygomaticofacial nerve. Slit-lamp examination was positive for mild blepharitis. The cornea and conjunctiva of the right eye showed mild to moderate punctate staining in the interpalpebral zone. The remainder of the anterior segment of the right eye was unremarkable. A tear meniscus was present on the right. A Schirmer's test revealed0 mm of wetting in the right eye and normal wetting, greater than 20 mm in 5 minutes, in the left eye. The ophthalmologist thought that the findings of keratitis sicca in the right eye, combined with ipsilateral malar hypesthesia and dryness of the turbinates, was highly characteristic of damage to the pterygopalatine ganglion. He thought that there were two possible indirect mechanisms that could have resulted in damage to the ganglion. The first involved contiguous spread ofa postoperative inflammatory response into the region of the pterygopalatine fossa, with resultant damage to the tissues there. The second mechanism could involve interruption of the vascular supply to the ganglion through damage to the descending palatine or maxillary arteries. The ophthalmologist did not consider the possibility of extension of untoward fractures into the pterygopalatine fossa damaging the ganglion either directly or indirectly via compression from edema or hematoma formation. He thought it unlikely that the patient's level of tear production would change significantly with time. The ophthalmologist recommended the patient increase the frequency of artificial tears in the right eye to every hour while awake and suggested

486 she switch to Refresh, artificial tears without preservati ves, to decrease the likelihood of developing an allergic response. He also suggested the patient apply warm compresses each day because the concomitant blepharitis interferes with the lipid layer of the tear film and leads to increased tear evaporation. The ophthalmologist thought that this regimen might clear the patient's mild keratopathy, but if corneal changes persisted, she might be a candidate for punctal occlusion . The patient has continued to function well, however, solely with the use of Lacrilube ophthalmic ointment at bedtime and the use of artificial tears as needed during the day. Punctate occlusion has not been needed , although the patient did undergo a temporary trial of dissolvable lacrimal plugs. The plugs did subjectively seem to result in increased watering in her right eye, but the patient did not think it was necessary to continue this treatment.

Case 7 A 15-year-old girl with a midfacial retrusion and anterior mandibular vertical excess was treated by a Le Fort I osteotomy with advancement and a genioplasty. The Le Fort I osteoiomy was carried out in a conventional fashion and the pterygoid plates were separated from the posterior aspect of the maxillary tuberosities with a curved osteotome. The maxilla was downfractured using Tessier spreaders. Following adequate mobilization and segmentalization into two segments, the maxilla was fixed into its new position using interosseous wires in the zygomatic buttress areas bilaterally. No problems were encountered at the time of surgery and the patient's initial postoperative course was uneventful. At a visit 5 months postoperati vely, the patient complained of excessive tearing from the right eye since her surgery. Initially, this was minor, but the problem had become progressively worse. The patient was subsequently referred to an ophthalmologist to see whether the epiphora was related to an alteration in the nasolacrimal duct as a result of her maxillary surgery. The ophthalmologist noted that the patient had a very full, watery tear lake on the right side. The lids and puncta were in normal position and she had a good blink mechanism. An enlarged, nontender tear sac was palpable. The valve at the junction of the common canaliculus with the lacrimal sac was competent, but there was obstruction of the patient's nasolacrimal duct. Ten months postoperatively, the patient underwent a dacryocystorhinostomy (OCR) and a good anastamosis was created . Silicone tubes were placed through the nasolacrimal system and through the anastamosis in the nose. These tubes were removed 5 months later. The patient has been asymptomatic since the DCR.

Case 8 A 42-year-old woman was admitted for treatment of maxillary hypoplasia and mandibular prognathism. She had a long-standing history of difficulty in breathing through her right nostril because of a deviated nasal septum and of right maxillary sinusitis. The patient had been taking antihistamines before her orthognathic surgery. She was treated with a multisegmental Le Fort I osteotomy, bilateral sagittal mandibular ramus osteotomies, a genioplasty, a submental Iipeetomy, and a right malar Proplast II (Vitek Inc, Houston, TX) implant augmentation. At the time of the maxillary downfracture, the right maxillary sinus was noted to have 'boggy' mucous membranes suggestive of a chronic sinusitis. The mucous membranes of the left maxillary sinus were normal.

OPHTHALMIC COMPLICATIONS: ORTHOGNATHIC SURGERY

A right turbinate reduction, in conjunction with an outfracture of the right inferior turbinate, was performed in an attempt to open the right nasal airway. The patient was discharged on the third day postoperati vely. Discharge medications includ ed oxyrnetazoline hydrochloride (Afrin; Schering , Kenilworth, NJ) 0.05% nasal spray, two sprays in each nostril every 12 hours as requir ed for nasal congestion and phenylpropanolamine syrup 2 tsp four times a day. On her second postoperative visit, which was the II th day postoperatively, the patient told her oral and maxillofacial surgeon that she was exp eriencing significant tearing from the right eye. Seven weeks postoperatively, the tearing in the right eye increased, became purulent in nature, and the eye became painful. The mucous membranes of her right nose were noted to be swollen to the extent that the patient could not breathe at all through her right nostril. She was given a prescription for cefadroxil, 500 mg, twice a day for I week, and gentamicin ophthalmic solution (Genoptic; Allergan), two drops to the right eye three to four times a 'day, Three days later, the patient was reexamined and the drainage from the right eye was found to be decreased and less purulent. An unsuccessful attempt was made to infracture the right inferior turbinate under intravenous sedation and local anesthesia. The patient was instructed to take pseudoephedrine hydrochloride (Actifed; Burroughs Wellcome, Inc, Kirkland, Quebec, Canada) tablets and to use nasal spray once a day. One week later , the patient still found it difficult to breathe through the right nostril , but found that taking the Actifed tablets on a regular basis every 4 to 6 hours did help to control the watering from her right eye. Fourteen weeks postoperatively, the patient saw an ear, nose, and throat (ENT) surgeon in consultation. The right nasal cavity was examined with a rhinoscope and found to be completely occluded by a severely deviated nasal septum. The deviat ion began just past the caudal end of the septum. An attempt was made to examine the nose with a fiberoptic scope, but even following decongestion of the nose with Afrin spray and topical 3% cocaine, the only visible opening was inferior and too narrow for a fiberoptic scope to be passed. No palpable swelling of the nasolacrimal duct was noted. The ENT surgeon thought it was possible that the patient's epiphora could be eliminated by performing a septoplasty because the fact that her increased tearing improved with Actifed suggested that mucosal edema rather than occlusion ofthe nasal opening ofthe nasolacrimal duct might be playing a role in its etiology. He advised that if the epiphora persisted, an ophthalmology consultation would obviously be indicated to have the nasolacrimal duct cannulated to ascertain the location of the obstruction. Seven months postoperatively, the patient underwent a scptoplasty and a right partial turbin ectomy with infracturing of the right inferior turbinate. The maxillary internal fixation plate around the right piriform fossa was removed at the same time. Following surgery, the excessive tearing stopped and the patient's nasal breathing became excellent for the first time she could remember. Very occasionally, however, when she blows her nose, the patient feels a sensation as if air were coming out of her right tear duct.

Discussion

Because so little information is available regarding ophthalmic complications following orthognathic surgery, the literature regarding ophthalmic injuries associated with facial fractures was reviewed to see what pertinent information could be gained. The highest in-

LANIGAN, ROMANCHUK, AND OLSON

cidence of serious ophthalmic injuries occurs in conjunction with midfacial or frontal bone fractures.19 The midfacial fractures most apt to be associated with ocular complications are comminuted zygomatic fractures, orbital floor fractures, and Le Fort II or Le Fort III fractures rather than isolated Le Fort I fractures. 2Q-25 In view of the paucity of reports of ophthalmic complications following Le Fort I fractures, where injuries occur in an uncontrolled fashion, it is not surprising that so few cases have been reported following orthognathic surgery specifically related to the operation itself. Injuries to the cornea could occur, of course, from contact with alcohol-based or detergent skin preparations, incomplete eyelid closure, or from an accidental injury during retraction. Based on previous reports in the literature, and the cases presented in this report, it appears that potential ophthalmic complications following Le Fort I osteotomies fall into four main categories: I) a decrease in visual acuity, 2) extraocular muscle dysfunction, 3) neuroparalytic keratitis, and 4) lacrimal apparatus problems, including both epiphora and keratitis sicca. Ophthalmic injuries after orthognathic surgery appear to be mediated primarily through damage to nerves or vascular supply. Because direct injuries to the optic nerve, cranial nerves III, IV, and VI supplying the extraocular muscles, the nerves supplying the nasolacrimal apparatus, and the first division of the trigeminal nerve are unlikely to occur from the osteotomies associated with the Le Fort I procedure, indirect injuries to the involved neurovascular structures must have occurred. Indirect injuries could result from traction, compression, or contrecoup injuries to neurovascular structures from forces transmitted during the pterygomaxillary dysjunction using an osteotome or from damage sustained by fractures extending to the base of the skull or orbit. Fine fissure fractures, which can be noted at surgery or autopsy, cannot always be detected on ordinary radiographs" or even on CT scans. These untoward fractures are most apt to occur during pterygomaxillary dysjunction with an osteotome or during the maxillary down fracture, particularly if a traumatic separation occurs between the maxillary tuberosity and the pterygoid plates or a difficult downfracture is encountered. It is interesting to note that the vast majority of ophthalmic complications that have been reported following Le Fort I osteotomies have involved right-sided structures. Although this may have occurred purely by chance, it could perhaps be related to surgical technique or to subtle anatomic differences between the right and left sides. Because the majority of surgeons are right .handed, there also may be differences in how the pterygomaxillary dysjunction and maxillary down fracture is achieved between the two sides. Wikkeling and Koppendraaier.P Robinson and

487 Hendy," and Lanigan and Guest." in their investigations of the pterygomaxillary dysjunction using a curved osteotome, have described high fractures of the pterygoid plates with subsequent disruption of the pterygopalatine fossa and with possible fractures extending to the base of the skull. Renick and Symington," using postoperative CT scans to assess the pterygomaxillary region following a Le Fort I osteotomy, found a similar pattern of pterygoid plate fractures to that described in Robinson and Hendy's" experimental study. In many cases, pterygoid plates assessed to be intact clinically were not found to be intact on a CT scan. This suggeststhat pterygoid plate fractures cannot be excluded as a contributing factor in unexplained postoperative complications even if they were thought to be intact at surgery." . Ifuntoward fractures extend to the base ofthe middle cranial fossa in areas such as the foramen lacerum or carotid canal, as has been reported,14,17,18,32 then injuries to the internal carotid artery can result, including carotid-cavernous sinus fistula or stroke. Anatomic variations, such as bony defects or incomplete ossification, can occur at the base of the skull,32,33,34 and abnormally thick posterior walls of the maxilla and pterygoid plates also can occur," which put patients at increased risk during the pterygomaxillary dysjunction or maxillary down fracture. Anatomic abnormalities may be more common in patients with craniofacial malformations 17,32,35,36 or following previous maxillofacial trauma or orthognathic surgery (case I). Variations in the anatomy of the sella tursica, sphenoid sinus, and sphenoid bone may be of particular importance in terms of increased risk for ophthalmic complications following orthognathic surgery.P Fujii et al37 studied the optic canal/sphenoid relationship in cadavers and found that 9% of optic nerves were devoid of medial osseous cover and 78% were covered by 0.5 mm or less of bone. The middle cranial fossa is the smallest and structurally most complicated of the three cranial fossae and is the most vulnerable part of the skull base to injuries either following facial trauma or orthognathic surgery. Lines offracture tend to continue in the axis ofthe striking force," so it is not surprisingly that occasionally untoward fractures occur toward the base of the skull or orbit in association with the pterygomaxillary dysjunction, especially if the osteotome is positioned incorrectly" or ifthere are associated unfavorable anatomic variants. Nerve or vascular damage can occur if fracture lines extend to foramina containing neurovascular structures. The longer the intracranial course of the nerve, the more vulnerable it is to such damage." This is why the abducent (VI) nerve is particularly vulnerable to injury following trauma or craniofacial surgery. Evidence to support the conjecture that ophthalmic complications of orthognathic surgery are related to

488 untoward fractures or to compression, traction, or contrecoup injuries occurring in association with the pterygomaxillary dysjunction or maxillary downfracture is to this point limited. Hiranuma et al,38 in an experimental study, looked at strain distribution during separation of the pterygomaxillary suture by osteotomes. Although their study was not completely analogous to a clinical situation because it was performed on dry skulls, it did measure a large tensile and com pressive strain at the medial pterygoid plate on the side of osteotome application. The strain on the medial pterygoid plate was increased if the pterygomaxillary osteotome was not angulated correctly to avoid posterior-superior compression of the pterygoid process. Although their strain gauges showed the intensity of the strain distribution to be highest at the ipsilateral medial pterygoid plate area during the pterygomaxillary dysjunction, the strain was widely distributed within the skull. This could perhaps result in compression, traction, or contrecoup injuries to neurovascular structures. It is certainly not unusual to note fractures ofthe pterygoid plates clinically, similar to those noted experimentally, following the pterygomaxillary dysjunction and maxillary downfracture. Pterygoid plate fractures, however, are fortunately not routinely associated with complications such as hemorrhage.l? the development of arteriovenous fistulas l 6 •39 or false aneurysms," or neurologic" or ophthalmic problems. . This is because it is not necessarily the presence of pterygoid plate fractures per se but the underlying mechanism that caused them in the first place that may be responsible for these rare complications. In a very small percentage of patients, certainly much less than I %, clinical evidence of an ophthalmic complication is noted. If one looks at the reported cases of ophthalmic complications following orthognathic surgery in the literature and in this report, what evidence exists to suggest that problems encountered with the pterygomaxillary separation or maxillary downfracture may have contributed to these complications? The most obvious examples are the case presented by Reiner and Willoughby" of an abducent nerve palsy following a Le Fort I osteotomy and case I in this report. In Reiner and Willoughby's case, a postoperative CT scan demonstrated a comminuted fracture through the body of the sphenoid bone passing through the sella tursica, with lateral displacement of a bony fragment onto the medial surface of the right cavernous sinus. A comminuted fracture of a portion of the greater wing of the sphenoid bone in the middle cranial fossa, just lateral to the foramen rotundum, also was noted. There was medial displacement of some of the fragments leading to a narrowing of the foramen rotundum, and there was slight effacement of the inferior aspect of the

OPHTHALMIC COMPLICATIONS: ORTHOGNATHIC SURGERY

right cavernous sinus. The neuropraxia of the abducent nerve in this case most likely occurred in the cavernous sinus owing to the sphenoid bone fracture, with displacement ofa fracture fragment through the sella tursica onto the medial surface of the cavernous sinus. Because the abducent nerve is more medial than any other cranial nerves that enter the cavernous sinus, it is the one most likely to be involved, although the relati ve position ofthe cranial nerves varies from posterior to anterior within the cavernous sinus. In view of the extensive nature of the fractures, it was fortunate that other cranial nerves, including the optic nerve, or the carotid or ophthalmic arteries also were not involved. In case I of this report, a postoperative CT scan showed multiple fractures extending to the base of the skull and orbit. The fractures involved the roof of the right maxillary sinus and extended through the medial wall of the right orbit posteriorly, with fractures of the right sphenoid bone extending through the floor of the middle cranial fossa. A fracture through the right lesser wing of the sphenoid bone extended just lateral to the optic foramen. The fracture of the roof of the right maxillary sinus posteriorly appeared to be the source of the small bone fragment that was noted in close proximity or touching the optic nerve in the region of the right optic foramen and superior orbital fissure. The optic foramen lies between the two roots of the lesser wing of the sphenoid bone, whereas the superior orbital fissure is situated between the lesser and greater wings ofsphenoid bone (Fig 2). Whether the optic nerve was injured directly by impingement of the small bone fragment or more indirectly is uncertain. The fact that blindness was delayed in onset, however, suggests an indirect cause. The oculomotor nerve was likely damaged as it traverses the superior orbital fissure. Both the superior and inferior divisions appeared to be involved because the patient presented with ptosis, mydriasis, and dysfunction of the medial rectus muscle,

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notch.loramen 1r.I..u1l'-Y ptOCMol o' Irontal bone Ponerk)r and an»rior ethmokSforemen

_bene

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LANIGAN, ROMANCHUK, AND OLSON

although function of the muscle also may have been affected by swellingof the muscle itself. As they emerge from the superior orbital fissure, the superior division of the III nerve passes above the optic nerve, whereas the inferior division passes below the optic nerve. The remainder of the neurovascular structures in the superior orbital fissure were spared. In the case reported by Carr and Gilbert? ofa partial third nerve palsy following a Le Fort I "Wake"-type osteotomy, it may be purely coincidental that the patient had a bilateral cleft lip and palate deformity and that the oculomotor nerve problem happened on the same side as the more severe cleft. It is quite possible, however, that the altered anatomy in this patient may have put him at higher risk of sustaining an untoward fracture(s) extending to the base of the skull. The partial third nerve palsy in this case was delayed in onset, and the patient had completely recovered by 8 weeks. Carr and Gilbert thought it was likely caused by a neuropraxia induced either through forces directly transmitted to the nerve during separation of the pterygoid plates or perhaps through delayed, ascending edema and hematoma formation. Although a partial oculomotor palsy of this type may have been caused by a lesion involving both rami of the third nerve, at or about the superior orbital fissure, no fractures extending to the superior orbital fissure were noted on conventional radiography or on a CT scan, nor was there any evidence ofa retrobulbar hematoma. It also is unusual that the abducent nerve was spared because it is normally more vulnerable to damage than most structures running through the superior orbital fissure owing to its location in the most inferolateral aspect of the fissure.' Anatomic anomalies in a patient with a bilateral cleft lip and palate deformity may perhaps have led to the rami of the oculomotor nerve being located more inferiorly than normal, leading to their involvement, while sparing the more predictable abducent nerve injury.' The presence of clefts also may have directed edema and hematoma formation superiorly to the inferior and superior orbital fissure areas. A case of blindness and total ophthalmoplegia, where the damage to the involved cranial nerves was speculated to have occurred from pressure generated by postoperative swelling transmitted to the superior orbital fissure and optic foramen from the pterygopalatine fossa, has been reported previously." In the case of a transient unilateral abducent nerve palsy presented by Watts.' the pterygomaxillary dysjunction was more difficult to achieve than normal. The normal osteotome used for this purpose was unavailable so a larger, curved osteotome had to be used, .which was more difficult to position. The right pterygoid plate was separated first. Watts speculated that the most likely explanation for the abducent nerve palsy

489 was either displaced bone spicules from a fracture that extended upward to the inferolateral margin of the right superior orbital fissure causing injury to the abducent nerve from compression ofthe nerve from hemorrhage, or a neuropraxia from transmitted forces from the use of the osteotome. Watts thought the last explanation was the more likely in view ofthe fact that tomography did not show any obvious extension of fractures to the superior orbital fissure and because of the rapid recovery of the nerve palsy. The transient bilateral increased tearing reported by Keller and Sather'? following a high "quadrangular" Le Fort I osteotomy is not unexpected. Early transient epiphora following a Le Fort I osteotomy is usually secondary to edema that leads to a functional blockage of drainage of tears rather than from any neurologic damage. The damage to the nasolacrimal duct leading to obstruction reported in Case 7 of this report is more difficult to explain. The patient was treated with a conventional Le Fort I osteotomy, and only interosseous wires in the zygomatic buttress areas were used for fixation, so it is difficult to postulate direct damage from the orthognathic surgery to nasolacrimal structures unless unusual extension offracture lines occurred superiorly during the downfracture using the Tessier spreaders. In performing maxillofacial surgery, two areas of the nasolacrimal system are particularly vulnerable to inadvertent injury-the distal orifice ofthe lacrimal duct and the anterior wall of the nasolacrimal sac. The increased tearing reported in case 8 appears to be due to obstruction of the distal orifice of the nasolacrimal duct by mucosal swelling. A decreased right nasal airway occurred from an increase in deviation of an already deviated nasal septum and the outfracturing of the right inferior turbinate carried out in conjunction with the maxillary orthognathic surgery. We also received information about two additional cases of postoperative epiphora but complete records unfortunately were no longer available. Both cases involved 15-year-old girls, who underwent Le Fort I osteotomy and superior repositioning of the maxilla in the mid 1970s. It was this surgeon's customary practice at that time not to perform a complete osteotomy of the lateral wall of the nose. Once all the osteotomies were completed, the maxilla was down fractured with Rowe disimpaction forceps. In both cases,a rather large lateral nasal wall osseous spur fractured off near the root of the inferior nasal turbinate. In the postoperative period, both patients complained of epiphora, although one case resolved within 3 months. In the second case, the epiphora persisted for 9 months and was then successfully resolved by a dacryocystorhinostomy. The lack of tearing after Le Fort I osteotomies, first reported by Tomasetti et all and subsequently in this

490 report, is a more difficult problem to explain. This is . particularly so when a true dry eye (keratitis sicca) is combined with corneal anesthesia (neuroparalytic keratitis), as in case 4, which leaves the cornea particularly vulnerable. Tomasetti et all thought that lack oftearing in their case was related to an extension of fractures associated with the left pterygoid plate fracture they noted at surgery. They did not specifically mention where the fractures extended, but consideration should be given to their extending to the base of the skull to involve the foramen lacerum or pterygoid canal, to the inferior orb ital fissure, or to a disruption involving the pterygopalatine fossa itself. They considered several etiologic possibilities for damage to the nerves invol ved with lacrimation, including that the pterygopalatine ganglion itself was injured, that the postganglionic parasympathetic fibers running with the maxillary nerve in the pterygopalatine fossa were injured," or that the zygomatic branch of the maxillary nerve was injured either by a bony spicule or by entrapment in a "crack" fracture. They largely discounted the first two possibilities because of a lack of concurrent paresthesia over the course of the maxillary nerve. Patients generally exhibit at least transient numbness over the distribution of the infraorbital branch of the maxillary nerve after Le Fort I osteotomies, but involvement of the zygomatic branch, such as was noted in case 6, is most unusual. Tomasetti et all did not consider more proximal damage invol ving the greater petrosal ner ve or the vidian nerve, although this is also a possibility. It should be borne in mind that the postganglionic parasympathetic fibers involved with lacrimation are all non myelinated and, as such, are more susceptible to injury than are myelinated fibers. I It is therefore possible for an injury to involve a nerve trunk and only result in enough damage to selectively injure the more vulnerable non myelinated fibers while sparing the less susceptible myelinated fibers. The surgeons involved in cases 4 and 5 were unable to speculate as to the etiology of the dry eye that occurred following orthognathic surgery. The patient in case 5 never underwent any additional diagnostic investigations, such as a cr scan , postoperatively, whereas the patient in case 6 had a CF scan done 9 weeks postoperatively. The CT scan showed fractures of both pterygoid plates and the posterolateral wall of the right maxilIary sinus. It is possible that additional fractures extending to the pterygopalatine fossa or base of the skull resulted in damage to the nerve(s) invol ved with lacrimation. The fact that the patient in case 4 had borderline dry eyes even before the orthognathic surgery and lived in a very dry climate may have con tributed to her problems. This patient also had anesthesia of the left cornea from damage to the nasociliary branch of the first division of the trigeminal nerve. This

OPHTHALr.IIC COMPLICATIONS: ORTIlOGNATIIIC SURGERY

suggests that the nerve damage may have occurred quite proximally unless one postulates different injuries resulting in nerve damage at multiple sites. The damage to nerves concerned with lacrimation in case 6 appears to have occurred in the pterygopalatine fossa, possibly involving the pterygopalatine ganglion. Decreased visual acuity or blindness has been reported following craniofacial surgery? but not previously following orthognathic surgery. One additional case of blindness following a Le Fort I osteotomy was reported in addition to the three cases presented in this report, but it was not possible to obtain details of this case from the surgeon involved. There is no doubt that fractures extending toward the base of the skull in the middle cranial fossa, or toward the orbit, have the potential to lead to this complication. Posttraumatic cases of blindness have been reported, however, where no obvious fractures could be visualized even on a CT scan. Although CT scans are useful in the delineation of fractures of the orbit and in the optic canal regions, a fracture could be missed if the thickness of the cut (ic, 5 mm rather than 2 mm) and the plane of ori entation are not appropriate." A fracture of the optic canal is certainly not necessary for damage to the optic nerve to occur, and its presence is merely an indication of the excessive energy delivered to the region of the optic canal and subsequently transmitted to the optic nerve." Hairline fractures may occur that are too small to be visualized radiographically, or other mechanism(s) may be involved, likely associated with the pterygomaxilIary dysjunction, that result in compression, traction , or contrecoup injuries to neurovascular structures supplying the orbit. Hiranuma et al 38 have shown that the pterygomaxillary dysjunction creates strains that are widely distributed within the craniomaxillofacial complex. These strains may be intensified if the correct technique is not used or unusual anatomic features are present. Dutton and Al-Quruiny" have discussed the effects of injuries to the globe resulting from distortion and concussion secondary to maxillofacial trauma. A traumatic optic neuropathy is the most common cause of permanent visual loss following blunt midfacial traurna.P An injury to the optic nerve is rarely the result of direct injury by osseous compression, laceration, or hemorrhage into the nerve itself. The most common mechanism appears to be indirectly via hemorrhage into the optic nerve sheath or contusion of the nerve with resulting edema and compression leading to a secondary compromise of the vascular supply and nerve infarction.P Although injuries to the optic nerve can occur anywhere along its length, the most common traumatic optic neuropathy occurs from canalicular optic nerve damage. The orbital portion of the optic nerve is somewhat loose and so is able to stretch with

491

LANIGAN, ROMANCHUK, AND OLSON

eye movements or eyeball compression and can thus withstand fairly strong shearing forces." The canalicular portion of the nerve is more vulnerable, however, because it is encased in a tight bony canal where it is partially adherent to the periosteum of the sphenoid bone. Although a fracture is not necessary to cause damage to the optic nerve, a fracture through the optic canal could result in a direct compression or contusion of the nerve or could have a shearing effect on the meningeal layers of the optic nerve or on the nerve itself. A close anatomic relationship exists between the optic canal, the lesser and greater wings of the sphenoid bone, and the sphenoid and ethmoid sinuses." This should be borne in mind if a fracture extends to the base of the middle cranial fossa following a Le Fort I osteotomy (case I). Manfredi et al 26 used CT scans to study facial fractures associated with blindness and found the most significant findings in the demonstration of indirect injury to the optic nerve were a lesser sphenoid wing fracture or a subdural hematoma in the optic nerve sheath. Evidence of sphenoethmoidal sinus hemorrhage on conventional radiographs should make one suspicious of the possibility of an optic canal fracture with associated optic nerve injury. Anderson et al 46 think that indirect optic nerve injury is secondary to the stretching, tearing, torison, or contusion ofthe optic nerve and its blood supply, which is caused not just from the momentum of the eyeball and orbital contents being absorbed by the fixed canalicular portion of the optic nerve but also by skeletal distortion caused by forces remote from the initial impact. This impact could occur during the pterygomaxillary dysjunction. Babajews" reported that there appears to be no direct correlation between the severity of the maxillofacial injury and visual disturbance, so there is a possibility that this complication could occur following Le Fort I osteotomies. The moment at which loss of vision occurs appears to be ofsignificant importance in establishing prognosis and therapeutic intervention. Ifblindness is immediate and complete, the prognosis is poor despite treatment. Ifvisualloss is delayed, progressive, or incomplete, then it may be ameliorated by massive doses of steroids or surgical decompression of the optic nerve. 26,48 Surgery should be considered if hematoma or bony fragments are impinging on theoptic nerve and steroids are unsuccessful in improving vision. Optic nerve decompression is most effective if done early, closer to the time of injury,"? Retrobulbar hemorrhage has been reported as a rare complication offacial fractures, usually malar or orbital floor fractures, but no cases following reduction of Le . Fort I maxillary fractures or following orthognathic surgery have been reported previously.P'!' The source

of the bleeding following malar or orbital floor fractures can be subperiosteal from the infraorbital artery or extracoronally from perforating branches of the infraorbital artery.50,51 With arterial bleeding, there can be a substantial rise in intraorbital pressure, followed by a rise in intraocular pressure. The blood supply to the retina is primarily via a branch of the ophthalmic artery, the central retinal artery (Fig 3). Although central retinal artery occlusion is possible, it is a rare cause of visual loss because the anatomic location of the central retinal artery within the optic nerve tends to protect it. The long and short posterior ciliary arteries lie within the extraocular muscle cone and enter the eye around the optic nerve to supply the uveal tract and anterior optic nerve (Fig 3). An injury within the confines of the extraocular muscles or penetration by bone spicule's from the orbital floor or elsewhere into the intraconal space may result in rupture of vessels posterior to the globe, particularly the short posterior ciliary arteries. The intraconal space is almost completely closed except for a small posterolateral communication with the extracoronal peripheral space. A retrobulbar hemorrhage into the muscle cone leads to increased pressure that could compress and eventually occlude the posterior ciliary arteries and lead to anterior optic nerve head ischemia and visual loss.P:" Intraocular pressure can increase to the extent that it only compromises the circulation of the optic disc without affecting the central retinal circulation." The etiology of the retrobulbar hemorrhage reported in case 2 is uncertain. The most likely arterial vessels involved with hemorrhage following a Le Fort I osteotomy are the descending palatine and sphenopalatine branches of the maxillary artery." It is highly unlikely that the descending palatine arteries were involved because they were noted to be intact intraoperatively, and no significant hemorrhage was encountered when the maxilla was redownfractured. Involvement of the . . .,_---Supr~orbi1al Artery

supratrochIHr_;;;~:::::~~_-J.~ Artery

Anterior Ethmoldal-----iT~\L. Artory

I-++f-- Anterior Cmlry Artory Long Posterior

Posterior Ethmoidal

Artory

-----.l;~WJt-".~l\ltli.r~I-f;...-hffT- Clliory Artory •

ShortPOSl.rior _ _----'r---T--'~ cmory Artery

I t+liiiii-if-----

Anterior Clinoid

Process

1-T7'---locrimal Artory

------

Optic N e r v e - - - _ .

Centr.1 Retinal Artery

Ophlholmic Artory

ri-----

Inl.rna'Carotid Artory

FIGURE 3.

The arterial supply to the orbit and globe.

492 sphenopalatine artery is a possibility because the patient was obviously having significant left-sided epistaxis, which might have been secondary to sphenopalatine arterial damage. Sphenopalatine arterial hemorrhage could lead to bleeding into the orbital cavity via a connection from the pterygopalatine fossa through the inferior orbital fissure. The etiology of the left-sided epistaxis is somewhat uncertain, however, and it may have been due to the traumatic intubation attempts through the left nostril. Injury to the anterior ethmoidal artery is possible from a traumatic intubation but for such an injury to result in retrobulbar hemorrhage one would have to postulate a disruption into the ethmoid sinuses, with a subsequent slow ooze of blood between the medial wall ofthe orbit and the orbital tissues. This is a possibility in this case. If the patient had a significant deviation of her nasal septum, combined with multiple traumatic intubation attempts, this could have resulted in a disruption into the ethmoidal sinuses. The fact that the orbital swelling and proptosis decreased dramatically following suctioning of copious amounts of blood from the left nasal cavity would tend to support the conjecture that there was a direct communication between the nasal cavity and orbit via a fractured lamina papyracea. A third possibility for the cause of the retrobulbar hemorrhage is that shearing or traction forces at the time of the pterygomaxillary dysjunction disrupted a vessel in the orbit. A fourth option is possible damage to the infraorbital artery or a tributory when placing the infraorbital suspension wire. No significant hemorrhage was noted from this area at the time of the wire replacement, although this does not preclude subsequent persistent minor bleeding inside the orbit from this source . The surgeon involved in case 3, in which a patient had a permanent decrease in visual acuity in the left eye following a Le Fort I osteotomy, thought this was a complication related to hypotensive anesthesia. Central retinal artery occlusion could have occurred if the systolic blood pressure was maintained below 60 mm Hg over an extended period , but this would be an unusual complication in a young, healthy woman. Moreover, the early typical fundoscopic appearance of central retinal artery occlusion following hypotensive anesthesia, an edematous retina with a cherry-red spot at the macula, was lacking. No swelling of the optic nerve was seen on the CT scan, which is a common accompaniment of optic neuropathy due to systemic hypotension. Although the CT scan of the orbits and optic canals were reported as normal, this does not necessarily rule out traumatic damage to the optic nerve in its intracanalicular portion. There does not appear to be sufficient evidence, however, to support positively one diagnosis over the other. Unilateral blindness has been reported following

OPHTHALMIC COMPLICATIONS: ORTHOGNATHIC SURGERY

anesthesia using hypotensive techniques to reduce hernorrhage.P:" Little" reported three cases of " retinal thrombosis" in 27,930 cases of controlled hypotensive general anesthetics. Most of the reported cases of blindness associated with general anesthesia, however, have been related to compression of the eye during surgery from, eg, a face mask , head rest, or sheet roll, 57· 60 although systemic hypotension does appear to be a factor in some of the reported cases. One case of vitreous hemorrhage leading to a decrease in visual acuity following hypotensive anesthesia, in which there was no pressure on the eyes at any time, has been reported." Optic neuropathy can thus occur in conjunction with systemic hypotension even if intraocular pressure is normal. It is more likely to occur, however, when there is preexisting optic nerve disease, such as nerve damage from open-angle glaucoma, or if there is systemic vascular disease such as preexisting hypertension, arteriosclerosis, carotid insufficiency, or diabetes. Retinal ischemia can occur from unilateral central retinal artery occlusion and choroidal ischemia from posterior ciliary artery occlusion, both related to ocular compression with or without systemic hypotension during general anesthesia/" Blood flow to the eye occurs against the pressure of the intraocular tension, an equilibrium that can be upset by increased intraocular tension or systemic hypotension." Progressively increasing levels of intraocular pressure, elevated well above diastolic and probably even temporarily above systolic blood pressure for a critical period of time, will cause a shutdown of perfusion of blood to the choroid and retina.f As the retinal arteries are end arteries, occlusion of these vessels produces blindness of the portion of the retina supplied. Occlusion of the central retinal and posterior ciliary arteries produces a characteristic fundoscopic appearance that, in the early stages, may include retinal edema, a cherry-red spot in the macula, dilated retinal arterioles, and edema of the optic disc. Arteriolar narrowing, optic atrophy, and focal retinal hypopigmentation or hyperpigmentation may be noted later. 62 When ischemia affects all intraocular tissues, including the layers of the retina, the outer retina suffers more than the inner retina, and the damage seen is similar to that seen in choroidal infarction. 63 · Paresis of extraocular muscles is an uncommon complication following Le Fort I osteotomies. Because these muscles are fixed posteriorly to a tendinous ring, the annulus of Zinn/" they will be put on a stretch, together with their accompanying neurovacular structures, if the orbital contents are subjected to traction, compression, or contrecoup forces during the pterygomaxillary dysjunction. The oculomotor and abducens nerves are situated within the common tendinous ring, whereas the trochlear nerve is situated outside

493

LANIGAN, ROMANCHUK, AND OLSON

specific ophthalmologic surgical intervention, although this may be indicated at times. Opt ic nerve

---;;'--i-f-

Ophthalmic

-nn"=:iU

Acknowledgment

artery

Inferior oph thalmic \lein

The authors would like to thank those oral and maxillofacial surgeons and their ophthalmologic colleagues who mad e details of their cases availabl e to us. and Dr LA. Al-Qurainy for his helpful suggestion s.

References FIGURE 4. . The location of the cranial nerves within the orbit.

(Fig 4). fractures of the base of the skull have been shown to result in cranial nerve injuries leading to ophthalmoplegia (case 1):t.27 Injuries to the nerves could result from direct compression of the involved nerve or indirectly from pressure from edema and hematoma. Ascending edema and hematoma formation from the pterygopalatine fossa also could result in ophthalmoplegia,"? Six cases of extraocular muscle palsy following orthognathic surgery have been reported (case 1).2.6 Abducent nerve palsies have been reported following craniofacial surgery.42.65 One case of superior oblique tendon sheath (Brown's) syndrome has been reported following craniofacial surgery in a 21-year-old man with congenital hypertelorisrn." This syndrome results in a restrictive ocular motility disorder secondary to impairment of free movement of the superior oblique tendon through the trochlea.

Summary Ophthalmic complications associated with Le Fort I osteotomies appear primarily to occur indirectly through injuries to neurovascular structures from traction, compression, or contrecoup forces transmitted during the pterygomaxillary dysjunction or from fractures extending to the base of the skull or orbit during the pterygomaxillary dysjunction or maxillary downfracture. Ophthalmic complications should be borne in mind and patients should be monitored for evidence of such problems in the postoperative period. Any visual complaints or clinical evidence of an ophthalmic problem warrants an immediate referral to an ophthalmologist. A patient with a decrease in visual acuity should have an emergency CT scan of the orbit and base of the skull. A decrease in visual acuity may respond to appropriate treatment, but frequently a patient can be left with either partial or complete permanent visual loss. Cases of ophthalmoplegia, epiphora, corneal dryness, and corneal anesthesia may improve spontaneously with time without the need for

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