Cerebrospinal Fluid Otorrhea, Rhinorrhea, and Temporal Bone Fractures Todd Spock
Christopher P. Hogrefe
THE CLINICAL CHALLENGE
Recognition of cerebrospinal fluid (CSF) leaks from the anterior or lateral skull base requires a high level of suspicion and a thorough examination to prevent potentially life-threatening sequelae. Blunt skull trauma, which disrupts the dural integrity and allows for CSF fistulization, accounts for 80% to 90% of CSF leaks. Patients with persistent CSF leaks have a 10% to 37% risk of developing meningitis, which carries a mortality rate of nearly 10%.1 In cases of basilar skull fracture, epistaxis or hemotympanum may obscure the presence of clear fluid drainage from the nose or ear, making the diagnosis challenging. The temporal bone is involved in 18% to 40% of all skull fractures and may also contribute to a CSF leak.2,3 Despite this noteworthy incidence, concomitant injuries usually associated with this diagnosis may distract providers’ attention. A thorough examination to identify injuries to nearby neurovascular structures (eg, facial nerve, internal carotid artery, internal jugular vein) and potential CSF leak is critical. In addition to trauma, CSF leaks may occur iatrogenically from surgeries of the sinus, skull base, or ear. Finally, although less common in the emergency setting, approximately 10% of patients suffer nontraumatic etiologies of CSF leaks, including those resulting from increased intracranial hypertension or sinonasal neoplasms.
PATHOPHYSIOLOGY
Cerebrospinal Fluid
Approximately 400 to 600 mL of CSF is produced per day, allowing complete renewal three to five times per day. CSF is confined to the subarachnoid space by dura mater. At the interface with the nasal cavity, the dura is further bound by the bone of the ethmoid roof and the paranasal sinus mucosa.
Disruption of the barriers separating the subarachnoid space from the nasal cavity or middle ear space allows for bidirectional transmission of CSF, air (pneumocephalus), and microbes (meningitis). The magnitude or flow of CSF is a function of the location and size of dural disruption, as well as the pressure differential between the subarachnoid and extracranial spaces. When the efflux of CSF outpaces the rate of production, intracranial hypotension may result, leading to headaches, nausea, and vomiting.
In rare cases of dural disruption in conjunction with CSF leak, tension pneumocephalus can occur. In this scenario, air accumulates within the subdural space, leading to displacement of the
brain parenchyma by mass effect. Ball-valving obstruction of the subdural space or application of positive pressure ventilation often exacerbates the development of tension pneumocephalus. This may lead to altered mental status, focal neurologic deficits, and even cardiac arrest if not emergently addressed.
brain parenchyma by mass effect. Ball-valving obstruction of the subdural space or application of positive pressure ventilation often exacerbates the development of tension pneumocephalus. This may lead to altered mental status, focal neurologic deficits, and even cardiac arrest if not emergently addressed.
Elevated Intracranial Pressure (ICP) and Spontaneous CSF Leaks
Idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri, is a syndrome of elevated ICP without identifiable cause, such as hydrocephalus, cerebral venous sinus thrombosis, or intracranial masses.4 Clinical manifestations of IIH include headaches, visual disturbances (eg, papilledema, sixth cranial nerve palsy), and pulsatile tinnitus. The elevated ICP and constant pulsations from the dura may cause thinning of the skull base and eventual bony dehiscence, allowing encephaloceles and CSF fistulas to form. Locations of the skull base that are naturally thin, such as the lateral lamella of the cribriform plate, are particularly vulnerable. The resulting spontaneous CSF leakage often provides significant ICP diversion, which masks the common symptoms of IIH and inhibits the development of papilledema.5 Therefore, unilateral, clear rhinorrhea may be the only presenting symptom in patients with IIH and is often confused with allergic rhinitis.
The demographic common to patients with IIH and spontaneous CSF leaks is that of an overweight female of childbearing age. The rising epidemic of obesity in western culture has mirrored the increased incidence of IIH. Obesity is thought to increase intra-abdominal and intrapleural pressures, leading to decreased cardiac filling. As a result, decreased venous return from the brain leads to a sustained elevation of ICP and subsequent IIH. In addition to obesity, patients with obstructive sleep apnea (OSA) have 4.7 times greater odds of developing spontaneous CSF fistula because hypoxia and hypercapnia precipitate increased cerebral blood flow and elevated ICP.6
Traumatic CSF Leaks, Anterior Skull Base, and Temporal Bone Fractures
The anterior skull base and temporal bone are both sites that are highly susceptible to CSF leak with blunt trauma. The anterior skull case has thin bone at the ethmoid roof and tight adherence of the dura in this region; a defect in this area causes CSF rhinorrhea. Similarly thin bone exists at the roof of the middle cranial fossa formed by the temporal bone and greater wing of the sphenoid. Fractures along the tegmen of the temporal bone with CSF leak permit fluid to accumulate within the air cells of the mastoid and petrous bone or middle ear space. Fluid may transgress a ruptured tympanic membrane to produce otorrhea or travel through the eustachian tube to cause clear rhinorrhea or postnasal drip.
The paired temporal bones articulate with the sphenoid bones anteriorly, occipital bones posteriorly, and parietal bones superiorly. The temporal bone is a complex structure housing numerous structures, including the internal carotid artery, posterior meningeal artery, internal jugular vein, greater petrosal nerve, and portions of cranial nerves VII through XI as well as the middle and inner ear components. Consequently, a great deal of potential pathology can arise from temporal bone injury. As the thickest bone in the body, it requires up to 1875 pounds (850 kg) of force to fracture the temporal bone. Such fractures are typically the result of lateral, high-energy force such as motor vehicle collisions, falls, and assaults. Approximately 90% of temporal bone fractures are accompanied by concomitant intracranial injuries, whereas 9% of the time a cervical spine injury will also be present.7
Although several classification systems exist to describe these fractures, the historically most utilized characterizes the fracture as longitudinal, transverse, or mixed in reference to the long axis of the petrous ridge of the temporal bone (Figure 21.1). Longitudinal fractures (paralleling the long axis of the petrous temporal bone) constitute approximately 80% of all temporal bone fractures and are more likely to result in CSF otorrhea, tympanic membrane perforation, and conductive hearing loss. Conversely, transverse temporal bone fractures are less common but more likely to result in violation of the otic capsule or injury to the facial nerve.3,8 The modern classification describes involvement or violation of the otic capsule, which is the dense bony labyrinth that contains the components of the inner ear (ie, cochlea, semicircular canals, and vestibule). Fractures that violate the otic capsule are more likely to result in hearing loss (both sensorineural and conductive), facial nerve weakness, and CSF leakage.9 Overall, most temporal bone fractures are unilateral, with only 8% to 29% occurring bilaterally.
 Figure 21.1: Axial CT of left temporal fractures (A) longitudinal fracture (white arrow) without violation of the otic capsule and (B) transverse fracture (white arrow) without violation of the otic capsule. |
APPROACH/THE FOCUSED EXAM
A meticulous history often provides the key to elucidating the diagnosis and etiology of a CSF leak. Commonly, a patient with a CSF leak describes unilateral, clear rhinorrhea that worsens with bending forward or straining. This fluid is often described as being watery rather than having the consistency of mucus. Salty or metallic tasting nasopharyngeal drainage often accompanies these symptoms and persists despite topical steroid management, differentiating a CSF leak from chronic rhinitis or sinus disease. Iatrogenic CSF leaks are a rare but well-documented complication of endoscopic sinus surgery caused by occult skull base injuries. Iatrogenic leaks may present in a delayed fashion, so any historical account of sinus surgery, skull base surgery, or septoplasty should be considered a risk factor. Recurrent epistaxis, nasal obstruction, or constitutional symptoms (eg, fevers, night sweats, weight loss) may suggest a neoplasm involving the skull base. IIH may be considered in patients with known risk factors (eg, overweight females of childbearing age) and should be screened for by inquiring about headaches or vision changes prior to the onset of rhinorrhea.
It is imperative to consider a temporal bone fracture in any trauma to the head, particularly those with significant force, such as direct blows to the head from motor vehicle collisions, falls, and/or assaults. Studies suggest an increased proportion of temporal bone fractures caused by assaults versus motor vehicle collisions.3,7 The force of the injury may be temporal or parietal (causing longitudinal fractures) versus frontal or occipital (resulting in transverse fractures). Hypacusis (total or significant hearing loss), tinnitus, balance problems, and vertigo are common complaints.10 In cases of blunt head trauma, altered patients may not be able to describe symptoms, which can lead to delay in the recognition of a CSF leak. In addition, epistaxis or hemotympanum from skull base fractures may obscure clear rhinorrhea or otorrhea (Table 21.1). In these instances, a high index of suspicion and radiographic imaging will be necessary to unmask a CSF fistula.
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