Treatment of Nerve Injuries
By Babak Azizzadeh MD, Grigoriy Mashkevich, MD
Nerves at Risk in Facial Cosmetic Surgery: Anatomy and Sites of Injury
The facial nerve, upon its exit from the stylomastoid foramen, penetrates the substance of the parotid gland, by which it is well protected in the pre-auricular region. Within the gland, it divides into five major branches, which exit the periphery of the gland deep to the superficial muscular aponeurotic system (SMAS). Anterior to the parotid gland, distal facial nerve branches (zygomatic and buccal) are situated evendeeper - under the masseteric fascia. This anatomic relationship creates a surgical plane between SMAS and the masseteric fascia, allowing for a sub-SMAS (or "deep plane") dissection anterior to the parotid gland.As zygomatic and buccal nerves course to innervate their target midfacial muscles from underneath (zygomaticus major and minor, levator labii, and superioris alaeque nasi), a sub-SMAS plane of dissection can be followed until the first midfacial muscle is encountered (zygomaticus major), at which point the dissection must proceed superficial to this muscle (and SMAS).
Dissection in this area places zygomatic and buccal branches at risk for injury, due to their close proximity. Similarly, a subperiosteal midface dissection (when performed for a midface lift) makes these deep branches vulnerable while lifting the periosteum from the anterior surface of the maxilla. Great care must be taken if such surgical approachesare undertaken, and the use of cautery and forceful retraction should be avoided. Fortunately, anterior facial nerve branches substantiallyintercommunicate and innervate midfacial musculature with some redundancy. As such, single branch injuries are unlikely to cause significant dysfunction of the midface.
The temporal branch of the facial nerve exits the superior aspect of the parotid gland, deep to SMAS, and crosses the zygomatic arch at the junction of anterior one third and posterior two thirds. Additional surface landmarks may be utilized to approximate the course of the temporal branch. Pitanguy\'s line runs from 0.5 cm inferior to the tragus to 1.5 cm above the lateral eyebrow. This may be somewhat variable since the lateral aspect of the eyebrow is not always a precise landmark in some patients. A more consistent approximation is the line that begins at the inferior aspect of the ear lobule and bisects another line connecting the tragus and the lateral canthus (Fig 1). Above the zygoma, the temporal branch enters a more superficial layer of the temporoparietal fascia and courses to innervate the superior orbicularis and frontalis muscles. Secondary to this anatomical transition, surgical lifting of the forehead, temple, and the midface must be performed in a plane deep to the temporoparietal fascia. However, a face lift dissection carried over the zygoma must be in the subcutaneous plane, which is superficial to SMAS (where the temporal branch is transitioning to the temporoparietal fascia).
treatment of nerve injuries The marginal branch of the facial nerve exits from the inferior aspect of the parotid gland, at the angle of the mandible, and descends up to 2 cm inferior to the body of the mandible before returning to innervate the mentalis and depressor anguli oris muscles. As these muscles are superficial to the platysma, the marginal nerve penetrates through the platysma in this region, and becomes susceptible to injury in superficial procedures such as liposuction of the jowl region. During face and neck lifting, dissection deep to platysma in the neck, or sub-SMAS dissection inferior to the border of the mandible places the marginal nerve at risk for injury.
The spinal accessory nerve (cranial nerve XI) may be encountered during a neck lift if dissection is carried sufficiently inferior along the sternocleidomastoid (SCM) muscle. This nerve crosses the SCM approximately 1 cm superior to Erb\'s point (location along the posterior border of SCM at which the greater auricular nerve becomes superficial). Deep dissection over the SCM should be avoided as it can lead to spinal accessory nerve palsy. Clinically, this injury manifests as a potentially debilitating shoulder dysfunction, trapezius wasting, and dull pain in the shoulder region.
Several sensory nerves are consistently encountered during commonly performed cosmetic procedures of the face and neck. These include the greater auricular, lesser occipital, infra-orbital, mental, zygomatico-temporal, and zygomatico-facial nerves.
Therefore, great care must be taken to remainsuperficial in order to avoid the greater auricular nerve injury. Another pitfall lies in the placement of sutures for suspension of SMAS to the mastoid periosteum. If placed sufficiently inferior or under undue tension, this may result in a compressive injury of the greater auricular nerve and loss of sensation over the inferior aspect of the auricle.
The lesser occipital nerve runs parallel and approximately 1 cm posterior to the greater auricular nerve, providing sensation to the superior and posterior aspects of the ear. This nerve is vulnerable to injury for the same reasons as the greater auricular nerve.
Trigeminal nerve branches (infraorbital and mental) exit through respective foramina in the maxilla and mandible, and typically become susceptible to injury during subperiosteal dissection of the midface (midface lift, implant placement) or mandible (chin implant pocket creation). These nerves, while large in caliber, are susceptible to stretch injury or transection during a subperiosteal dissection.
Zygomatico-facial and zygomatico-temporal penetrate through the lateral surface of the zygomatic arch and innervate the lateral cheek and temple. Subperiosteal dissection over the zygomatic arch, as performed during the midface lift, may damage these sensory nerves and lead to a sensory deficit in the area of their distribution.
Cosmetic Facial Procedures and Associated Nerve Injuries
Rates of Nerve Injury in Facial Cosmetic Surgery
During rhytidectomy, the greater auricular nerve is the most commonly injured sensory structure (1-7%), while motor nerve injury reaches 2.6 % . Depending on the series, either the marginal or temporal branches of the facial nerve appear to sustain the highest rate of motor injury. This has been in part explained by the lack of anastomotic and intercommunicating branches, which are present in zygomatic and buccal nerves.
Several large rhytidectomy series focusing on complications and outcomes have been reported in the literature and are briefly reviewed here. For the endoscopic brow lift, Jones reported a single case of frontal branch paresis in 538 patients (0.19%), while Sabini found eight cases of paresis in 350 patients undergoing a combined endoscopic forehead and midface lifts (2.29%). For face lifts, Kamer presented a series of 100 deep plane rhytidectomies, with no reported events of paresis or paralysis (0%). In SMAS-platysma lifts, Daane documented cervical branch injuries in 34 of 2002 cases (1.7%). This injury was labeled as "pseudoparalysis of the marginal mandibular nerve" and full recovery in all cases occurred within 6 months. Tanna reported no cases of nerve injury in "short scar rhytidectomy with SMAS suspension" in one thousand cases (0%). In another SMAS series of 96 patients, Sullivan documented temporary facial nerve weakness in 3%, and permanent ear numbness in 1% of cases. While these large series document the overall low rate of nerve injuries during rhytidectomy, Baker noted that while the facial nerve injury occurs in "less than one percent of the cases," about 20% of such injuries fail to undergo spontaneous return of function.
The spinal accessory nerve injury has also been documented to occur during rhytidectomy . While this represents a highly unusual occurrence in cosmetic surgery of the neck, one should be cognizant of the nerve\'s location if such operation is undertaken.
Peripheral Nerve Anatomy and Classification of Injury
In 1968, Sunderland published a classification system for peripheral nerve injury based on the severity of nerve disruption (Table II). In this system, the most benign form of injury is neuropraxia (Grade I), in which a local conduction block is present (from nerve compression or ischemia) without disruption of axoplasmic continuity. Such nerves may continue to transmit the electrical signal beyond the site of the block and completely recover their function once the block is removed. This is the only type of nerve injury in which distal Wallerian degeneration does not occur.
In more significant nerve injuries, axoplasmic (axonotmesis, Grade II) or a neural tubule (neurotmesis, Grade III) disruption leads to a Wallerian degeneration of the nerve distal to the site of injury. Axonotmesis undergoes excellent functional recovery, secondary to axonal regeneration through intact neural tubules. In contrast, neural tubule disruption promotes aberrant regeneration of nerve fibers within fascicles, potentially resulting in synkinesis.
Grades IV (perineurium disruption, nerve sheath continuity preserved) and V (epineurium, or complete nerve transection) carry the worst prognosis for functional recovery, as neural regeneration is severely hampered by intra-neural scarring and aberrant pathway selection. Theoretically, Grade V injuries do not recover any function without anatomic re-approximation of the cut ends of the nerve.
Most cases of post-operative nerve dysfunction occur in a setting where little doubt exists about nerve integrity. These typically recover well with conservative management alone. Patients must be counseled that recovery is anticipated, but that it may take some time. In the immediate post-operative period, it is not uncommon to observe motor branch paralysis secondary to local anesthesia, which wears off within several hours and warrants no additional intervention. For nerves that sustain direct injury (such as from traction, cautery, etc), a typical time frame for recovery may be anywhere from several weeks to 6 months. This is consistent with the time required to undergo complete Wallerian degeneration and re-growth of nerve fibers at a rate of approximately 1mm per day.
While intriguing from the anti-inflammatory standpoint, the role of steroids in hastening the functional recovery of nerves remains unclear. To our knowledge, there are no studies of steroid administration in a setting of cosmetic facial surgery. However, steroids have been evaluated in other clinical scenarios involving the facial nerve. Unfortunately, these reports offer conflicting recommendations. The strongest evidence to date against the use of post-operative steroids for facial nerve dysfunction stems from a prospective randomized trial of patients undergoing parotid surgery . The study group receiving perioperative dexamethasone derived no benefit and, in fact, displayed a median time of 150 days to recovery, compared to only 60 days in the control group. This finding is in contrast to studies documenting a beneficial impact of steroids in patients with Bell\'s palsy.
Nerve Transection Injuries
If nerve injury is confirmed intraoperatively, immediate repair should be attempted with direct anastomosis of the cut ends. Tensionless technique represents a critical aspect of any nerve repair; otherwise, regeneration of fibers may be compromised through the site of nerve coaptation. Both ends of the nerve should be freshly cut and three to four epineurial 9-0 nylon stitches should be placed circumferentially in order to achieve an effective anastomosis (Fig 3).
Nerve grafting may be required in cases where tensionless closure is not possible or in those where nerve transection spans a segment. For facial nerve grafting, it is not unreasonable to sacrifice a regional sensory nerve, such as the greater auricular. Sural and lateral antebrachial cutaneous nerves represent alternative sources for nerve grafting (Fig 4).
Post-operative Management of Poorly Recovered or Paralytic Facial Nerve Branches
Several motor and sensory nerves are at risk during facial rejuvenation surgery. A thorough understanding of nerve anatomy is critical in avoiding neurologic injury, which may be severely debilitating for the patient. In the event of injury, its management depends on the degree of nerve disruption and may range from simple observation to exploration and grafting. Meticulous dissection technique, guided by knowledge of facial anatomy, should prevent most neurological sequelae during facial cosmetic surgery.
Table I: Facial cosmetic procedures, associated nerves at risk, and clinical manifestations of nerve injury.
Table II: Sunderland classification of nerve injuries and anticipated clinical recovery.
Fig 2. Peripheral nerve anatomy. The endoneurium envelopes individual nerve fibers, perineurium wraps around multiple nerve fibers (creating nerve fascicles), and epineurium covers the entire nerve bundle.
Fig 3. Nerve anastomosis performed with a 9-0 nylon suture (fine black strand in the photograph) spanning the epineurial layer of cut ends. Typically, 3-4 sutures are necessary to achieve stable closure. Nerve approximation must be performed under microscope magnification and without tension.
Fig 4. Sural nerve graft. A External marking on the left lower extremity prior to nerve harvest. The incision is placed approximately 2 cm posterior to the lateral malleolus of the fibula, and taken superiorly as necessary to obtain sufficient graft length. This nerve can also be harvested through a stab incision with a nerve stripper. B Internal anatomy (A - Achilles tendon, * - lesser saphenous vein, Arrow - sural nerve). Note the close relationship of the nerve to the vein, and a distal branching pattern, suitable in caliber to peripheral facial nerve branches.
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