Chapter 18 Trauma to the middle ear can present as an isolated injury or may be associated with severe trauma to the skull base with resultant neurologic sequelae. The cause of injury varies from motor vehicle collisions and industrial accidents to recreationally related mishaps, falls, and assault. In all cases the structures embedded in the temporal bone are at risk for significant injury. Temporal bone injuries can present with facial paralysis, conductive hearing loss, sensorineural hearing loss, vertigo, and/or cerebrospinal fluid (CSF) leak (otorrhea or rhinor-rhea). Middle ear injuries can occur with or without fracture of the temporal bone. When a fracture is present, however, its configuration may help predict the resultant injury. Temporal bone fractures have been classified as longitudinal or transverse. Long-itudinal fractures account for 70 to 90% of temporal bone fractures and usually result from direct blunt injury to the temporal region. The fracture line extends from the squamous portion of the temporal bone, bypassing the dense bone of the otic capsule, and travels toward the foramen lacerum and the jugular foramen. The middle ear space and the posterosuperior external auditory canal are often involved in the path of the fracture. As a result, the clinical presentation of longitudinal fractures often includes conductive hearing loss caused by hemotympanum, tympanic membrane perforation, or ossicular discontinuity. Sensorineural hearing loss, facial nerve injury, and CSF leak occur less frequently with this type of fracture, and are usually less severe. Transverse fractures account for 20 to 30% of temporal bone injuries. These fractures most frequently occur after a severe blow to the occipital or frontal region. The fracture line crosses the petrous apex, extending from the jugular foramen to the foramen lacerum or spinosum. The otic capsule often is violated, resulting in a sensorineural hearing loss. Vertigo often accompanies traumatic sensori-neural hearing loss. Immediate facial paralysis is common, occurring in up to 50% of these injuries. CSF leaks are relatively common, resulting in otor-rhea or, if the tympanic membrane is intact, rhinor-rhea. Although the classification of temporal bone fractures into longitudinal and transverse is a useful guide in delineating the clinical features and prognosis of patients presenting with these injuries, many patients present with a mixed fracture. In fact, as was shown by Ghorayeb and Yeakley,1 most fractures are oblique. The clinical findings in these patients are dependent on the path of the fracture line and the specific structures involved. Despite the myriad mechanisms leading to middle ear injury, generally four clinical presentations may require surgical intervention: facial paralysis, conductive hearing loss, CSF otorrhea or rhinorrhea, and (rarely) persistent vertigo. In all cases, prior to addressing issues dealing with the temporal bone, patients should be assessed for cervical spine, hemodynamic, and neurologic stability. Overall, temporal bone trauma results in facial nerve injury approximately 7% of the time.2 Posttraumatic facial paralysis may present immediately after the injury or may be delayed for several hours or days. Patients experiencing paralysis immediately after trauma are relatively more likely to have nerve transection, whereas those presenting in a delayed fashion do not have transection. Immediate paralysis is more common with transverse fractures of the temporal bone and is generally associated with more serious closed head injuries. Every effort should be made in the emergency room to determine facial nerve function. Painful stimuli to evoke a grimace should be sought of comatose patients prior to the use of a muscle relaxant. During the physical examination, the clinician should note if paralysis is complete and if all branches of the facial nerve are involved. This may be difficult if multiple facial injuries are present. Intratemporal facial nerve injuries usually affect the entire distribution of the facial nerve. Radiographic evidence of facial nerve injury, such as temporal bone comminution, transverse fracture of a temporal bone, or fracture through the geniculate area of the facial nerve, also can help determine the need for surgery. A high-resolution computed tomography (CT) scan of the temporal bone should be obtained. Although management of traumatic paralysis remains controversial, a systematic approach that accumulates all of the available clinical and electro-diagnostic data is best. The important issues that need to be considered include the following: 1. Which patients are most likely to recover facial nerve function spontaneously? 2. Which patients should undergo facial nerve exploration and when should the intervention be carried out? 3. Which surgical approach should be used? 4. Which nerve repair should be carried out once the pathology is identified? As Turner3 demonstrated, 84% of patients presenting with facial nerve dysfunction resulting from temporal bone injury recover to full function spontaneously. With this in mind, the challenge is to identify the minority of patients who require surgery for nerve decompression or repair. Stratification based on clinical presentation and electroneurography (ENoG) helps determine prognosis and timing of surgery. Patients who present with delayed facial nerve paresis or paralysis have a 94 to 100% chance of spontaneous recovery to House-Brackmann (HB) grade 1 or 2 and therefore should be treated conservatively.2–4 Brodie and Thompson2 found that the latency to recovery could vary from 1 day to 1 year, but that 88% had recovered by 3 months. In general, patients presenting with immediate-onset complete facial paralysis are most likely to need surgery. Some authors argue that ENoG should be the primary method of determining which patients should be explored because it is more objective than historic information.5,6 Nosan et al5 found that all patients presenting with temporal bone trauma with facial paralysis who demonstrated ENoG >90% degeneration had significant facial nerve pathology at time of exploration, regardless of time of onset of paralysis. Fisch7 demonstrated the utility of ENoG in assessing facial nerve function and prognosticating likelihood of recovery. He noted that patients who had undergone deliberate facial nerve transection for tumors resulted in 100% degeneration on ENoG in 3 to 5 days. Fisch also presented three patients with delayed facial paralysis occurring 3 to 7 days after vestibular nerve section. ENoG showed progressive denervation that became complete after 14 to 21 days, and all three patients had nearly complete return of facial function. Therefore, if ENoG demonstrates >90% degeneration in the first 6 days, one can infer that significant facial nerve injury has occurred and surgical exploration should be carried out. On the other hand, if >90% degeneration does not occur until 14 days, then good recovery is expected without surgical intervention. The group of patients who obtain >90 to 95% degeneration between 6 and 14 days have various degrees of intermediate nerve injury. Facial nerve exploration in these patients can benefit those few who would otherwise have poor spontaneous recov-ery. Patients who present several months after the initial injury can be followed with electromyography (EMG) to detect subclinical return of facial nerve function. If no return of function is detected within 6 to 12 months, facial nerve exploration is warranted. Delayed exploration should be performed within 1 year, as nerve-grafting results tend to deteriorate after this interval. The surgical approach for facial nerve exploration depends on the site of the lesion and the status of hearing on the affected side. Several authors have observed that the perigeniculate region is the site of injury in 80 to 90% of traumatically induced facial nerve lesions.6,8 Furthermore, as Felix et al9 demonstrated, traumatic injury at the geniculum induces retrograde degeneration through the labyrinthine and distal meatal segments of the facial nerve. Therefore, the surgical approach to facial nerve exploration should provide access to these areas. In addition, the surgical field should be prepped for exposure of the entire facial nerve from the brainstem to the pes anserinus, and should include the neck for a great auricular nerve graft, even if more limited exposure and repair are likely. Initial exposure of the facial nerve is accomplished using a transmastoid approach. This allows for visualization of vertical and horizontal segments of the facial nerve, as well as the opportunity to repair ossicular discontinuity transcanal.10,11 If hearing is good, then the transmastoid approach is combined with a middle cranial fossa approach to allow visualization of the nerve proximally. If hearing is not useful, then a translabyrinthine dissection following a transmastoid approach provides adequate visualization of the facial nerve. Once the facial nerve has been exposed and the location, type, and severity of pathology have been discovered, surgical repair can be performed. Findings at the time of facial nerve exploration include intraneural hematoma or contusion, bony impingement, and nerve transection. If hematoma is found, then facial nerve decompression should be carried out along the path of the nerve above and below the site of injury. Bony impingement should be removed, again followed by decompression. Should the epineurium be incised following decompression? May,10 Fisch,12 and Yanagihara13 advocated opening the nerve sheath to allow the nerve fascicles to expand and relieve edema. However, animal experimental data by Greer et al14 and Boyle15
SURGERY FOR TRAUMATIC MIDDLE EAR CONDITIONS
CLASSIFICATION OF TEMPORAL BONE FRACTURES
FACIAL PARALYSIS
WHICH PATIENTS ARE MOST LIKELY TO RECOVER SPONTANEOUSLY?
WHICH PATIENTS SHOULD UNDERGO FACIAL NERVE EXPLORATION, AND WHEN?
WHICH SURGICAL APPROACH SHOULD BE USED?
WHICH NERVE REPAIR SHOULD BE CARRIED OUT ONCE THE PATHOLOGY IS IDENTIFIED?
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