Management of cerebrospinal fluid leak following lateral skull base trauma

Introduction

Leakage of cerebrospinal fluid (CSF) can occur when a defect of the skull base and dura results in an abnormal communication between the subarachnoid space and nasal or middle ear cavities. ^, This pathologic entity was first reported by St Clair Thompson in 1899 and can occur in the nose (CSF rhinorrhea) or the ear (CSF otorrhea). CSF leaks are further classified into traumatic and nontraumatic. Traumatic cases account for 80% to 90% of CSF leaks and more commonly present with rhinorrhea (80%) than with otorrhea (20%) in adult patients. ^, Most traumatic CSF leaks are clinically evident within the first 2 days of injury and almost all within the first 3 months. ^,

CSF leaks that occur secondary to skull base fractures account for 2%–3% of all closed head injuries. The most common fractures associated with posttraumatic CSF leakage involve the anterior skull base, including the frontal sinus and lateral lamella of the cribriform plate. ^, Approximately 12%–30% of patients with anterior skull base fractures develop a CSF leak, which include those with a mild head injury as rated by the Glasgow Coma Scale. Therefore, all closed head injuries should be evaluated for CSF leak. In addition, the incidence of anterior skull base CSF leaks is five to six times higher compared with that of the lateral skull base. ^, This is attributed to the firmer attachment of the dura to the anterior skull base, which may increase the likelihood of dural lacerations.

In the setting of a lateral skull base trauma, CSF leakage typically courses through the middle cranial fossa (tegmen tympani and mastoideum) and into the epitympanic recess, antrum, and mastoid air cell tract. Temporal bone fractures along the petrous bone and middle ear associated with dural defects may lead to CSF otorrhea if there is a perforation within the tympanic membrane, or CSF rhinorrhea via the Eustachian tube if the tympanic membrane is intact. In a retrospective study of 1773 patients with posttraumatic CSF leaks from the Taiwan Traumatic Brain Injury Registry System, the temporal bone was the most common fracture site (40.3%) for those with CSF otorrhea. The mortality rate in patients with CSF otorrhea was 8.5%, and CSF rhinorrhea was 10.9% (33/302). These patients also had a higher rate of intracranial hemorrhage (64.7%) compared with those without CSF leakage (28.8%, P < .001). Furthermore, in a study of 13,861 pediatric patients admitted to the hospital with skull fractures, 1.46% of patients developed CSF leaks, of whom 58.4% presented with CSF otorrhea and 41.6% presented with rhinorrhea. Notably, patients with CSF leaks were more likely to have longer average hospitalizations (9.6 vs. 3.7 days, P < .0001) and higher rates of neurologic deficits (5.0% vs. 0.7%, P < .0001), meningitis (5.5 vs. 0.3%, P < .0001), and hospital readmission (24.7% vs. 8.5%, P < .0001) at 90 days. Taken together, these studies elucidate the importance of diagnosing and managing skull base CSF leaks following traumatic injury.

Lateral skull base CSF leaks tend to have a higher likelihood of spontaneous resolution than anterior skull base CSF leaks. ^, In a review of 81 cases of posttraumatic CSF leaks, 17/28 (60.7%) of lateral skull base CSF leaks resolved spontaneously, compared with only 14/53 (26.4%) of anterior skull base leaks. Similarly, in a retrospective study of 699 patients with 820 temporal bone fractures and 122 CSF leaks, 95/122 (77.9%) CSF leaks resolved spontaneously in less than 1 week, 21/122 (17.2%) in less than 2 weeks, and only 5/122 (4.1%) persisted. Despite the higher rates of spontaneous resolution, lateral skull base CSF leak following traumatic injury must be appropriately evaluated and managed to reduce the risk of meningitis and other complications.

Spontaneous CSF leaks represent cases that present without distinct etiologies for the leak, such as trauma, surgery, and congenital anomalies. Recent studies have noted an increase in the incidence of spontaneous CSF leaks, exploring associations with rising obesity rates, obstructive sleep apnea, idiopathic intracranial hypertension, and superior semicircular canal dehiscence. Unlike traumatic or intraoperative CSF leaks, spontaneous CSF leaks can have a more insidious presentation with nonspecific symptoms of otorrhea, hearing loss, and aural fullness. The etiology underlying spontaneous lateral CSF leaks is not entirely well elucidated, but one theory posits that arachnoid granulations within the temporal bone respond to CSF pulsations, causing erosion of the skull base over time.