Skull-base fractures involve one or more of the cribriform plate of the ethmoid bone, orbital plate of the frontal bone, sphenoid bone, occipital bone, and petrous or temporal bone. Although the fractures themselves only require reduction and reconstruction when the skull base is severely comminuted and altered, even small fractures and the traumatic shear forces can create tears in the meninges and thus predispose to cerebrospinal fluid leaks. This article explores the preoperative, intraoperative, and postoperative management of skull-base fractures, which most commonly involves resolution of the cerebrospinal fluid leak and the prevention of future leaks or meningoencephaloceles.
Key points
- •
Although conservative management may be appropriate for some skull-base injuries, prompt and judicious surgical management can improve morbidity and reduce the risk of meningitis.
- •
Management of the skull-base fracture depends largely on the type of injury, the location of injury, and the presence or absence of a cerebrospinal fluid (CSF) leak. The presence of a persistent leak is the most common indication for surgical intervention.
- •
Preoperative studies should include computed tomography with image-guidance navigation and with axial, coronal, and sagittal reconstructions for surgical planning. Other ancillary studies to confirm or locate a CSF leak may be used.
- •
Preoperative studies to rule out injury to the carotid artery and the need for preoperative endovascular treatment is crucial.
- •
The anatomy and location of trauma dictates the approach and surgical treatment needed. The high success rate of endoscopic management has greatly reduced the morbidity of skull-base reconstruction and has increased the otolaryngologist’s involvement in these interventions.
- •
Massive tissue loss with multiple comminuted fractures or severe derangements to the skull base may require intracranial repair. Loss of adjacent tissue such as the orbit or skin may require microvascular free-tissue transfer for the best results.
Introduction
Skull-base fractures (or basilar skull fractures) are potentially devastating fractures of the craniofacial skeleton. These fractures involve 1 or more of the following bones: cribriform plate of the ethmoid bone, orbital plate of the frontal bone, sphenoid bone, occipital bone, or petrous or squamous temporal bone. Although the fracture themselves only require reduction and reconstruction when the skull base is severely comminuted and altered, even small fractures are associated with shear forces which can create tears in the meninges and thus predispose to cerebrospinal fluid (CSF) leaks. In addition, encephaloceles or meningoencephaloceles can form in these skull-base defects, potentially leading to a surgical emergency.
Introduction
Skull-base fractures (or basilar skull fractures) are potentially devastating fractures of the craniofacial skeleton. These fractures involve 1 or more of the following bones: cribriform plate of the ethmoid bone, orbital plate of the frontal bone, sphenoid bone, occipital bone, or petrous or squamous temporal bone. Although the fracture themselves only require reduction and reconstruction when the skull base is severely comminuted and altered, even small fractures are associated with shear forces which can create tears in the meninges and thus predispose to cerebrospinal fluid (CSF) leaks. In addition, encephaloceles or meningoencephaloceles can form in these skull-base defects, potentially leading to a surgical emergency.
Signs and symptoms
Signs and symptoms of skull-base fractures include epistaxis, CSF rhinorrhea, clear otorrhea, periorbital ecchymosis (raccoon eyes), hemotympanum, and ecchymosis of the mastoid process or postauricular area (Battle sign). Other signs are manifestations of cranial nerve or sensory deficits such as ophthalmoplegia, deafness, nystagmus, or other cranial nerve palsies. The first, third, fifth and seventh cranial nerves are the most common to present with palsies.
CSF Leak
The diagnosis of a CSF leak may be obvious, such as the patient with profuse clear drainage that is reproducible with positioning. However, more often the diagnosis is confounded by the similar appearance of nasal secretions and a more intermittent leak.
Described signs of CSF leak include the reservoir sign or flexing of the head to elicit CSF, and the target sign or a bull’s-eye stain, with blood in the center when drainage is collected on gauze or a napkin. This sign is caused by a further migration of CSF than blood, but is unreliable because nasal secretions can create the same pattern. Both of these signs have unknown, but not particularly high sensitivities or specificities.
CSF leak with possible resultant meningitis is the major complication of skull-base trauma, and results from even minor tears in the dura during impact. Head injuries associated with craniofacial fractures are the cause of 80% of CSF leaks, and CSF leaks develop in 11% to 45% of skull fractures. CSF leaks resulting from trauma usually begin within 48 hours of injury and are apparent within 3 months 95% of the time. More than 70% of these leaks cease with conservative nonsurgical treatment, which includes bed rest and CSF diversion. The mechanism of the resolution of the leak is unknown but is thought to be due to regeneration of the nasal mucosa or fibrous tissue. The location of the trauma may dictate whether a CSF leak is likely to close spontaneously with conservative measures. For example, the geometry of the skull base at the cribriform plate is unfavorable for spontaneous resolution of a leak. In other areas, mild herniation of the brain can create a seal to close the leak, but this is difficult to achieve at the cribriform plate.
Assessment
Laboratory Studies
The β2-transferrin test is the most popular chemical test for CSF leaks, as β2-transferrin is a protein that is found only in CSF, perilymph, and aqueous humor. The presence of β2-transferrin in nasal secretions is accurate for diagnosing CSF leaks, with 99% sensitivity and 97% specificity. However, there are often errors in interpretation and there is a lag time in the results, as the assays take 1 to 2 days to perform. Although only 0.5 mL is needed, this can be difficult to obtain in small intermittent leaks. Alternatives to β2-transferrin testing are using comparison testing of glucose, electrolytes, and protein with the serum and the use of β-trace protein (BTP). Testing of glucose, electrolytes, and protein is easy and rapid, but there can be many confounding factors. BTP is not readily available at many institutions but constitutes a faster test than β2-transferrin. BTP is not as accurate as β2-transferrin because it is not as specific for CSF.
Intrathecal Injection
Intrathecal fluorescein can be used for an accuracy of 96% when wide skull-base exposure has already been obtained or will be obtained. However, although rare, the complications of fluorescein can range from tinnitus, headaches, nausea, and vomiting to pulmonary edema, confusion, seizures, coma, and even death. Therefore, its use requires a thorough informed consent with explanation of the risks to the patient. Intrathecal fluorescein has not been approved by the Food and Drug Administration. Complications from intrathecal fluorescein mainly result from an error in the administration, as many studies have shown reliable safety in the small dose that is adequate for a preoperative examination. Schlosser and Bolger found no complications when using 0.1 mL of 10% fluorescein diluted in 10 mL of the patient’s CSF and a slow injection over 10 to 15 minutes. Similarly, other investigators have reported other formulations and dilutions of fluorescein that have produced no complications.
Imaging
High-resolution computed tomography (HRCT) with axial, coronal, and sagittal reconstruction is an important study in preoperative planning for the definition of bony details needed to plan the optimal approach. It also has 87% accuracy in predicting traumatic CSF leaks, but cannot always define its exact location. Coronal cuts may be able to provide the most information regarding the location ( Fig. 1 ).
Carotid angiography is an important preoperative examination in skull-base trauma, because of the possibility of carotid pseudoaneurysms and carotid-cavernous fistulas. These entities should be ruled out before a surgical approach is attempted.
Pseudoaneurysms and fistulas may be treated in an endovascular fashion before surgical intervention. Computed tomography (CT) cisternography can be useful in identifying the location of a leak in a specific circumstance, although it is more invasive than conventional imaging. Cisternography is currently rarely used, owing to the high quality of information obtained from HRCT. Cisternography requires an active leak at the time of intrathecal contrast injection or a reproducible leak by Valsalva, and is most accurate in the frontal and sphenoid sinuses because these sinuses can collect and retain the contrast material for a longer period of time to allow capture in the imaging. Radioisotopes can be used in low-flow leaks with the placement of intranasal pledgets typically at the cribriform plate, the middle meatus, and sphenoethmoidal recess, as the pledgets can be left in place for hours. However, this method cannot determine the location of the leak, and can have low sensitivity and high false-positive rates.
Magnetic resonance imaging (MRI) is a technique that uses the hyperintensity of CSF on T2-weighted imaging, and provides helpful additional information regarding the anatomy of the fracture. MRI with fast spin-echo sequence, fat suppression, and image reversal can have accuracy up to 89%. MRI can be similar to CT cisternography, but has the advantage of being noninvasive and also has the ability to differentiate brain parenchyma from CSF ; however, high false-positive rates have also been reported.
Nonsurgical management of skull-base fractures
Although the focus of this review is the surgical management of skull-base fractures, determining the need for surgery is a salient and well-debated topic. Investigators agree that a good proportion of fractures do not need surgical treatment, and many CSF leaks resolve with conservative management. Fifty percent to 85% of posttraumatic CSF leaks close spontaneously within 1 week. Nonsurgical management entails bed rest with head-of-bed elevation, carbonic anhydrase inhibitors, and strict precautions against CSF leak such as prevention of straining, nose blowing, use of straws, Valsalva maneuvers, and incentive spirometers. If noninterventional techniques fail, CSF diversion with lumbar drain puncture or a ventriculostomy tube is another useful tool. Although a large portion of posttraumatic CSF leaks resolve with nonoperative management, this does not indicate that the dura has sealed, and these patients should be counseled and followed for recurrent CSF leaks or late meningoencephaloceles. Delayed CSF leaks require operative management, as the chance of spontaneous cessation is low and these patients have a high risk of meningitis.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
