Maxillofacial fractures are often associated with blunt head injuries, of which skull base trauma is a common component. However, most oral and maxillofacial surgeons do not provide definitive management of temporal bone fractures involving the skull base and their sequelae. Persistent cerebrospinal fluid (CSF) leakage that is refractory to conservative measures usually requires surgical closure to decrease the risk of meningitis. In general, reduction of the displaced fragment of the skull base in temporal bone fractures is not considered a priority. We describe an unusual case of craniomaxillofacial injury exhibiting CSF otorrhea because of a temporal bone fracture with a fragment that included the zygomatic arch. The persistent traumatic leakage was stopped after C-arm-guided reduction of the depressed zygomatic arch. This technique facilitated minimal and only necessary manipulation, without overcorrection, thereby avoiding additional damage to the surrounding tissues. The present case illustrates the definitive contribution of therapeutic measures based on maxillofacial surgery as part of an interdisciplinary approach to the management of the complications of severe head injuries; more invasive neurosurgery was thus avoided.
Maxillofacial fractures are often associated with blunt head injuries, of which skull base trauma is a common component. These require interdisciplinary management. Among the temporal bone injuries, fractures of the inferior squamous part of the temporomandibular joint (TMJ), such as the glenoid fossa or articular eminence, are handled by oral and maxillofacial surgeons . However, they do not provide definitive management of temporal bone fractures involving the skull base and their sequelae .
The common sequelae of these fractures are facial nerve paralysis, injury to the cochlear–vestibular apparatus, and cerebrospinal fluid (CSF) leakage . The latter is usually because of a tear in the dura and arachnoid and an abnormal bony gap at the tegmen tympani, which allows the tympanic cavity to communicate with the external auditory canal through the ruptured tympanic membrane. Although the incidence ranges from 11% to 45% , this leakage tends to recede spontaneously with the application of conservative measures, such as elevation of the head, bed rest, and stool softeners. Bell et al. described the uncomplicated resolution of this problem within 2–10 days in 85% of patients with CSF leakage. Brodie and Thompson reported that the risk of meningitis increased from 3% in cases with CSF leakage that was stopped within 7 days after trauma to 23% in cases in which it persisted beyond 7 days. Thus, surgical closure is indicated for leakage that lasts longer than 14 days . The surgical approach depends on the degree of remaining hearing function: a repair via middle fossa craniotomy and trans-mastoid approach, or obliteration of the tympanic cavity followed by fat grafting .
The displaced fragment that has possibly caused the CSF leakage, especially CSF rhinorrhea caused by an anterior skull base fracture, should be reduced early; this will stop the leakage without the need for further invasive treatments . However, research done on CSF leakage has not focused on cases with otorrhea , probably because the management of temporal bone fractures is generally aimed at restoring function rather than reducing and fixing bone fragments, which often involve highly invasive open approaches . The zygomatic process of the temporal bone can be used to achieve a closed reduction of temporal bone fractures that cause persistent CSF leakage; although this may not always be possible, this would be a realistically less invasive method to manage the sequelae.
Here we present a case of craniomaxillofacial injuries with CSF otorrhea because of a temporal bone fracture with a fragment that included the zygomatic process. The persistent CSF leakage was stopped after C-arm-guided reduction of the depressed fragment.
An 18-year-old male presented to the emergency department of our institution. While driving a motorbike, he had toppled sideways and had been run over by a car. Preliminary examinations revealed a patent airway, low respiratory rate with weak thoracic motion, and reduced lung sounds. He had a Glasgow Coma Scale (GCS) score of 3; the pupillary response was bilaterally reactive with anisocoria. He was subsequently intubated and ventilated. Chest radiography revealed a right pulmonary contusion. Further detailed examination revealed that his face was bilaterally and symmetrically swollen; facial nerve paralysis was not noticeable. He also had an intraoral open fracture of the anterior mandible.
Computed tomography (CT) revealed the presence of traumatic subarachnoid haemorrhage, cerebral contusion, and fractures of the cranial and facial bones. Intracranial pressure monitoring was initiated. The patient underwent a tracheotomy and fixation of the mandibular dental arch because of bleeding from the edge of the mandibular fracture. A follow-up head CT showed no signs of deterioration in the intracranial haemorrhage and cerebral oedema. Fluid from the external auditory canal displayed a ‘halo sign’ on the gauze, indicating CSF otorrhea due to a ruptured tympanic membrane. The patient was placed on bed rest with his head elevated to 30°.
The patient was referred to the department of oral and maxillofacial surgery for a consultation regarding his maxillofacial fractures. Facial CT revealed displaced fractures of the mandible in the parasymphysis and contralateral side of the angle region and the ipsilateral side of the zygomatic arch fracture. The fragment of the latter fracture stemmed from the lower squamous component of the temporal bones (i.e., the zygomatic process; Fig. 1 ). In the middle cranial fossa, the main fracture line was parallel to the long axis of the petrous bone (known as a longitudinal type of fracture) and involved the sella turcica. The otic capsule, orbital floor, mandibular condyle, and glenoid fossa were all intact.
On day 7, he had a fever. A lumbar puncture was performed but CSF examination revealed no evidence of meningitis. The CSF leakage persisted for more than 1 week. After consultation with the neurosurgery team of the emergency department, maxillofacial fracture repair surgery was done on day 10: the mandibular fractures were reduced and fixated with titanium miniplates (MatrixMANDIBLE 2.0; Synthes, Paoli, PA, USA). Under a C-arm system, OEC-9800 Plus (GE OEC Medical Systems, Salt Lake City, UT, USA), the depressed zygomatic arch was gently and carefully reduced, avoiding overcorrection, using a transcutaneously inserted J-shaped traction hook ( Fig. 1 ). No significant perioperative bleeding from the external auditory canal was detected.
On the day after the operation (i.e., day 11), no neurological deterioration or otorrhea was detected. A CT scan showed no signs of further intracranial injuries; there was substantial improvement in the displaced zygomatic arch and the tegmental defect ( Fig. 2 ). On day 12, sedation was completely stopped; the patient’s respiratory status was stable. However, he was unable to move the mandible to the occlusal position and his mandibular opening and closing was severely restricted. A hearing evaluation performed by an otolaryngologist revealed mixed hearing loss on the affected side because of the tympanic membrane rupture and possible labyrinth concussion. Facial nerve function was moderately reduced, with grade 3 on the House–Brackmann facial nerve injury scale. Although ophthalmological examinations detected incomplete oculomotor paralysis on the affected side, the patient’s optic nerve function was intact. He commenced jaw exercises 1 week after the operation, and the degree of mouth opening increased gradually to more than 40 mm while maintaining a stable occlusion. He was discharged from the hospital 1 month after the operation.