This article presents an overview of endoscopic endonasal repair of cerebrospinal fluid (CSF) rhinorrhea. In recent years, endoscopic repair has become the standard of care for managing this condition, because it gradually replaces the traditional open transcranial approach. Discussion includes the etiologic classification of CSF rhinorrhea, management paradigm for each category, diagnosis algorithm, comprehensive description of the surgical technique, and an updated review of the literature regarding the safety and efficacy of this procedure. In addition, the authors present their experience, including 2 surgical videos demonstrating endoscopic repair of CSF rhinorrhea in 2 distinct clinical scenarios.
Key points
- •
Surgical repair is the mainstay of management in cases of persisting cerebrospinal fluid (CSF) rhinorrhea.
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The principal indication is prevention of the possible complications that include ascending meningitis, intracranial abscess, and pneumocephalus.
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Endoscopic endonasal repair is an effective and well-tolerated procedure for the vast majority of CSF rhinorrhea cases, with primary closure rates of greater than 90% in large series and systematic reviews.
- •
Compared with the traditional open approaches, endoscopic endonasal repair carries similar results with fewer complications.
Introduction
General
Cerebrospinal fluid (CSF) rhinorrhea is caused by an abnormal communication between the subarachnoid space and the nasal cavity. This condition most commonly occurs secondary to a predisposing event, such as accidental or iatrogenic trauma. Nevertheless, CSF rhinorrhea may also occur spontaneously, a condition associated with benign intracranial hypertension (BIH). Surgical repair of CSF rhinorrhea is recommended to prevent the potential serious sequelae that include ascending meningitis, intracranial abscess, and pneumocephalus.
The most common anatomic sites leading to CSF rhinorrhea are located in the anterior skull base (ASB), namely the ethmoid roof, the olfactory groove, the roof of the sphenoid sinus, and the posterior wall of the frontal sinus. Historically, these defects have been repaired via an external approach, including a frontal craniotomy, and pericranial flap closure. However, the development of endoscopic endonasal skull base approaches in the last 2 decades provides an alternative to the traditional open approaches and has gradually gained popularity.
Following a thorough review of the existing literature, this article discusses the pathophysiology, diagnosis, and management of spontaneous and traumatic CSF rhinorrhea and provides a comprehensive description of the endoscopic endonasal approach (EEA) for repairing ASB CSF leaks.
Anatomic Considerations
CSF rhinorrhea refers to CSF leakage into the nasal cavity. Most commonly, CSF enters the nasal cavity through defects in the ASB. Understanding the anatomy of the related components of the cranial base, nasal cavity, and paranasal sinuses is essential for successful management of this condition. This section focuses on the anatomic interface between the intracranial and sinonasal cavities, outlining the areas that are prone to injury.
The ASB is formed by the ethmoid, sphenoid, and frontal bones and is separated from the middle cranial base by the sphenoid ridge, joined medially by the chiasmic sulcus. Two parts form the medial part of the ASB: the crista galli and the cribriform plate of the ethmoid bone anteriorly, and posteriorly, the planum and the body of the sphenoid bone. The nasal cavity is bounded superiorly by the anterior cranial fossa above and is divided sagittally into 2 compartments by the nasal septum. The paranasal sinuses are 4 pairs of pneumatic cavities: namely, the frontal, ethmoid, sphenoid, and maxillary sinuses. Each paranasal sinus is named after the bone in which it is located, and they all communicate directly with the nasal cavity. Excluding the maxillary sinuses, all the paranasal sinuses are superiorly bounded by the cranium.
The frontal sinuses are housed in the frontal bone between the inner and outer tables. The inner table forms the posterior wall of the sinus, separating it from the anterior cranial fossa. Anatomically, it is much thinner than the outer table, and thus prone to injury. The frontal recess constitutes the frontal sinus outflow tract.
The ethmoid sinuses are formed by 5 components: the crista galli, cribriform plate, perpendicular plate, and paired lateral ethmoidal labyrinths, which contain the ethmoid air cells. The ethmoid cells are divided by the basal lamella of the middle turbinate into anterior and posterior divisions, which drain into the middle meatus and the sphenoethmoidal recess, respectively. The roof of the ethmoid labyrinth, which separates the ethmoidal cells from the anterior cranial fossa, is formed by the relatively thick orbital plate of the frontal bone, called the fovea ethmoidalis. The fovea ethmoidalis attaches medially to the thinner lateral lamella of the cribriform plate (LLCP), completing the roof of the ethmoid air cells. Therefore, the ethmoid roof contains a transition from a thick bony part laterally to the thinner LLCP medially. The olfactory fossa is the region of depression of the horizontal cribriform plate below the level of the fovea ethmoidalis, and between the lateral lamellas. The vertical attachment of the middle turbinate divides the ASB into the cribriform plate medially and the fovea ethmoidalis laterally. Consequently, the anterior part of the nasal cavity’s roof between the vertical attachment of the middle turbinate and the nasal septum is located directly under the horizontal cribriform plate ( Fig. 1 ).
The sphenoid sinus originates in the sphenoid bone at the junction of the anterior and middle cranial fossa and separates the pituitary gland from the nasal cavity. The sphenoid bone has a central portion called the body, which contains the sphenoid sinus. Three pairs of extensions spread out of the sphenoid body to form the complete sphenoid bone: 2 lesser wings that spread outward from the superolateral part of the body, 2 greater wings that spread upward from the lower part, and 2 pterygoid processes that are directed downward. During embryogenesis, the sphenoid bone is formed from the ossification and fusion of 5 cartilaginous areas that subsequently fuse into a single bone. As first described in 1888 by Sternberg, incomplete fusion of the greater wing with the central cartilaginous precursors can result in a persistent lateral craniopharyngeal canal, called Sternberg canal.
Following a systematic literature review of endoscopic approaches for repairing CSF leaks, Psaltis and colleagues reported that the central part of the ASB is the most susceptible region to injury. Specifically, the ethmoid roof and cribriform region were found to be affected in more than half of the cases, independent of cause. This observation might be explained by several previously reported anatomic findings: first, the LLCP was found to be the thinnest, and therefore, the most vulnerable structure of the entire skull base. Second, it has been reported that the horizontal cribriform plate is a thin and fragile bone that is covered only by an arachnoid layer, and hence, missing the protection of a true dural investment. Moreover, it is located in the midline of the anterior fossa, and CSF may preferentially gravitate to this area. Finally, there is a firm adherence of the dura mater to the cribriform plate, ethmoidal roof, and the roof and lateral wall of sphenoid sinus. As a result, any pathologic process located in these structures can easily result in CSF rhinorrhea.
Psaltis and colleagues also identified the sphenoid sinus to be the second most common site of injury, affecting 30% of cases. Shetty and colleagues demonstrated that an overpneumatized sphenoid sinus, especially in the lateral recess, is a common site of CSF rhinorrhea. A proposed explanation includes extensive lateral pneumatization, leading to weakening of the bony sphenoid roof. According to another theory, persistence of Sternberg canal may act as a susceptible site for CSF fistula within the lateral sphenoid sinus.
Introduction
General
Cerebrospinal fluid (CSF) rhinorrhea is caused by an abnormal communication between the subarachnoid space and the nasal cavity. This condition most commonly occurs secondary to a predisposing event, such as accidental or iatrogenic trauma. Nevertheless, CSF rhinorrhea may also occur spontaneously, a condition associated with benign intracranial hypertension (BIH). Surgical repair of CSF rhinorrhea is recommended to prevent the potential serious sequelae that include ascending meningitis, intracranial abscess, and pneumocephalus.
The most common anatomic sites leading to CSF rhinorrhea are located in the anterior skull base (ASB), namely the ethmoid roof, the olfactory groove, the roof of the sphenoid sinus, and the posterior wall of the frontal sinus. Historically, these defects have been repaired via an external approach, including a frontal craniotomy, and pericranial flap closure. However, the development of endoscopic endonasal skull base approaches in the last 2 decades provides an alternative to the traditional open approaches and has gradually gained popularity.
Following a thorough review of the existing literature, this article discusses the pathophysiology, diagnosis, and management of spontaneous and traumatic CSF rhinorrhea and provides a comprehensive description of the endoscopic endonasal approach (EEA) for repairing ASB CSF leaks.
Anatomic Considerations
CSF rhinorrhea refers to CSF leakage into the nasal cavity. Most commonly, CSF enters the nasal cavity through defects in the ASB. Understanding the anatomy of the related components of the cranial base, nasal cavity, and paranasal sinuses is essential for successful management of this condition. This section focuses on the anatomic interface between the intracranial and sinonasal cavities, outlining the areas that are prone to injury.
The ASB is formed by the ethmoid, sphenoid, and frontal bones and is separated from the middle cranial base by the sphenoid ridge, joined medially by the chiasmic sulcus. Two parts form the medial part of the ASB: the crista galli and the cribriform plate of the ethmoid bone anteriorly, and posteriorly, the planum and the body of the sphenoid bone. The nasal cavity is bounded superiorly by the anterior cranial fossa above and is divided sagittally into 2 compartments by the nasal septum. The paranasal sinuses are 4 pairs of pneumatic cavities: namely, the frontal, ethmoid, sphenoid, and maxillary sinuses. Each paranasal sinus is named after the bone in which it is located, and they all communicate directly with the nasal cavity. Excluding the maxillary sinuses, all the paranasal sinuses are superiorly bounded by the cranium.
The frontal sinuses are housed in the frontal bone between the inner and outer tables. The inner table forms the posterior wall of the sinus, separating it from the anterior cranial fossa. Anatomically, it is much thinner than the outer table, and thus prone to injury. The frontal recess constitutes the frontal sinus outflow tract.
The ethmoid sinuses are formed by 5 components: the crista galli, cribriform plate, perpendicular plate, and paired lateral ethmoidal labyrinths, which contain the ethmoid air cells. The ethmoid cells are divided by the basal lamella of the middle turbinate into anterior and posterior divisions, which drain into the middle meatus and the sphenoethmoidal recess, respectively. The roof of the ethmoid labyrinth, which separates the ethmoidal cells from the anterior cranial fossa, is formed by the relatively thick orbital plate of the frontal bone, called the fovea ethmoidalis. The fovea ethmoidalis attaches medially to the thinner lateral lamella of the cribriform plate (LLCP), completing the roof of the ethmoid air cells. Therefore, the ethmoid roof contains a transition from a thick bony part laterally to the thinner LLCP medially. The olfactory fossa is the region of depression of the horizontal cribriform plate below the level of the fovea ethmoidalis, and between the lateral lamellas. The vertical attachment of the middle turbinate divides the ASB into the cribriform plate medially and the fovea ethmoidalis laterally. Consequently, the anterior part of the nasal cavity’s roof between the vertical attachment of the middle turbinate and the nasal septum is located directly under the horizontal cribriform plate ( Fig. 1 ).
The sphenoid sinus originates in the sphenoid bone at the junction of the anterior and middle cranial fossa and separates the pituitary gland from the nasal cavity. The sphenoid bone has a central portion called the body, which contains the sphenoid sinus. Three pairs of extensions spread out of the sphenoid body to form the complete sphenoid bone: 2 lesser wings that spread outward from the superolateral part of the body, 2 greater wings that spread upward from the lower part, and 2 pterygoid processes that are directed downward. During embryogenesis, the sphenoid bone is formed from the ossification and fusion of 5 cartilaginous areas that subsequently fuse into a single bone. As first described in 1888 by Sternberg, incomplete fusion of the greater wing with the central cartilaginous precursors can result in a persistent lateral craniopharyngeal canal, called Sternberg canal.
Following a systematic literature review of endoscopic approaches for repairing CSF leaks, Psaltis and colleagues reported that the central part of the ASB is the most susceptible region to injury. Specifically, the ethmoid roof and cribriform region were found to be affected in more than half of the cases, independent of cause. This observation might be explained by several previously reported anatomic findings: first, the LLCP was found to be the thinnest, and therefore, the most vulnerable structure of the entire skull base. Second, it has been reported that the horizontal cribriform plate is a thin and fragile bone that is covered only by an arachnoid layer, and hence, missing the protection of a true dural investment. Moreover, it is located in the midline of the anterior fossa, and CSF may preferentially gravitate to this area. Finally, there is a firm adherence of the dura mater to the cribriform plate, ethmoidal roof, and the roof and lateral wall of sphenoid sinus. As a result, any pathologic process located in these structures can easily result in CSF rhinorrhea.
Psaltis and colleagues also identified the sphenoid sinus to be the second most common site of injury, affecting 30% of cases. Shetty and colleagues demonstrated that an overpneumatized sphenoid sinus, especially in the lateral recess, is a common site of CSF rhinorrhea. A proposed explanation includes extensive lateral pneumatization, leading to weakening of the bony sphenoid roof. According to another theory, persistence of Sternberg canal may act as a susceptible site for CSF fistula within the lateral sphenoid sinus.
Diagnosis and preoperative considerations
Establishing the diagnosis of CSF rhinorrhea in cases with suggestive clinical scenarios (ie, clear nasal discharge, recurrent meningitis) is crucial for prompt and successful management of this condition. The following 3 steps, completed in a stepwise fashion, are essential to establishing the diagnosis:
- 1.
Cause-based classification: to develop a clinical suspicion by obtaining an accurate history
- 2.
Confirmation of CSF leak: to verify the presence of CSF in the nasal discharge
- 3.
Localization of the leak site: to preoperatively identify the site of the leak.
Cause-based Classification
Discussions about CSF rhinorrhea usually use a cause-based classification system. This breakdown is important because the specific cause may significantly alter the course of the disease and its management. Specifically, each cause requires a different management paradigm because of differences in rates of spontaneous closure, risk of ascending meningitis, size and location of the bony defect, and the long-term success rates of surgical repair.
The most commonly used cause-based classification of CSF rhinorrhea is the one presented by Schlosser and Bolger, who described 5 categories: accidental trauma, surgical trauma, tumor-related, congenital, and spontaneous rhinorrhea. Tumor-related leaks are usually operatively addressed following primary tumor resection. Likewise, congenital encephaloceles and CSF rhinorrhea are rarely encountered and constitute a separate entity. These 2 categories are beyond the scope of this review, and consequently, this discussion is devoted to spontaneous and traumatic rhinorrhea. Table 1 summarizes the different features of these categories.
| Features | Accidental Trauma | Surgical Trauma | Spontaneous |
|---|---|---|---|
| Most common site locations | Cribriform plate and frontal sinus | Sphenoid sinus and ethmoid roof | Cribriform plate, ethmoid roof, and lateral recess of sphenoid sinus |
| Approximate nonsurgical resolution rates | Up to 85% | 20% with lumbar drainage | Not relevant |
| Approximate overall risk of ascending meningitis (in unrepaired fistulae) | 30% | 20% | 10% |
| Management paradigm |
|
| Surgical repair (consider postoperative CSF pressure measurement to identify the need for subsequent VPS) |
Accidental traumatic cerebrospinal fluid leaks
Accidental traumatic CSF leaks, which were found to complicate up to 30% of nonpenetrating head injuries, present in either an acute or a delayed fashion. Most begin in the first 48 hours following the injury; however, up to 70% present within the first week. It is extremely uncommon for CSF leaks to present later than 3 months in this etiologic category.
Despite slight variations between different studies, the most common sites of accidental traumatic CSF leaks are the cribriform plate and frontal sinus. There are several important considerations when selecting a management strategy for these patients. On one hand, the vast majority of these cases resolve spontaneously or with conservative treatment, such as bed rest and external CSF diversion (40% resolution after 3 days and 85% after 7 days). On the other hand, the incidence of ascending meningitis in accidental posttraumatic leaks is relatively high, with an approximate 30% risk overall in unrepaired fistulae and a weekly risk of 7.5% during the first month after the injury. Importantly, CSF rhinorrhea secondary to temporal bone trauma is more likely to resolve with conservative management, compared with ASB defects.
Accordingly, Prosser and colleagues suggested a graduated management paradigm for accidental traumatic leaks. The first stage should be a trial of conservative treatment, followed by a second stage in which CSF diversion is used in persistent cases. Surgical repair should be reserved for cases that do not resolve after these 2 stages. Considering the different probability for nonsurgical resolution, each of these stages should be pursued over a different time period, depending on the site of the defect. The threshold for surgical repair of ASB leaks is lower, and 3 days for each stage is sufficient. Conversely, with temporal bone leaks, a week for each stage seems more appropriate, given the lower rate of meningitis and the higher rate of spontaneous closure.
Surgical traumatic cerebrospinal fluid leaks
Surgical traumatic CSF leaks most frequently occur secondary to either functional endoscopic sinus surgery (FESS) or neurosurgical procedures. Overall, the most common sites of surgical traumatic CSF leaks are the ethmoid roof and the sphenoid sinus.
Expectedly, the most common site of traumatic CSF leaks following neurosurgical procedures is the sphenoid sinus, Which is due to the increased use of EEA for various skull base pathologic conditions, predominantly pituitary adenomas. Kassam and colleagues reported that CSF leaks represented the most common postoperative complication in 800 cases using EEA approaches, with an overall rate of 15.9%. Of these, 23.6% were treated with short-term CSF drainage through a lumbar drain. The remaining 76.4% required endoscopic endonasal reconstruction. Only one of these failed, requiring a transcranial repair. Recent reports show that postoperative leak rates have declined significantly, occurring in less than 3% of cases in experienced centers, likely due to improved closure techniques and increased surgeon experience. Several factors are associated with a higher risk of CSF leaks following EEAs. These factors include expanded EEAs, certain pathologic conditions (ie, craniopharyngioma), postoperative adjuvant therapies, idiopathic intracranial hypertension, and transplanum approaches with exposure of the third ventricle. Similarly, although the incidence of postoperative CSF leaks following resection of even large pituitary adenomas is less than 10%, EEAs for ventral skull base meningiomas are associated with a considerably higher incidence (more than 30% for olfactory groove and more than 20% for tuberculum sellae meningiomas). CSF leaks following FESS are most commonly associated with injury to the ethmoid roof or the LLCP. The overall risk of ascending meningitis in unrepaired cases of surgical traumatic leaks is approximately 20%.
In addition to the different features already discussed, surgical leaks are distinct from accidental ones because they tend to be much larger and associated with a higher volume of flow. Furthermore, the later the CSF leak presents following the surgery, the lower the likelihood of achieving durable repair with nonsurgical measures. Accordingly, the management paradigm suggested by Prosser and colleagues for surgical traumatic leaks differs from accidental leaks, encouraging a more aggressive approach. The management of select, recently operated, iatrogenic leaks may include short-term conservative measures limited to no longer than 1 week. All other cases, as well as all cases failing conservative measures, require surgical repair.
Spontaneous cerebrospinal fluid leaks
Spontaneous CSF leaks are classified by a lack of any identifiable cause and represent a diagnostic and therapeutic challenge. Despite being commonly referred to as idiopathic, there is growing evidence suggesting a strong association between spontaneous leaks and BIH. Schlosser and his group published several studies providing evidence of a link between spontaneous CSF leaks and BIH. Both disorders share common clinical and radiographic features, including a high prevalence in women, patients with obesity, and individuals with radiographic evidence of empty sellae. Furthermore, mildly elevated intracranial pressure (ICP) was frequently encountered when evaluating patients with spontaneous leaks by lumbar puncture. Finally, more than 70% of patients with spontaneous CSF satisfy the modified Dandy criteria that are commonly used for diagnosing BIH. The association between spontaneous CSF leaks and high-pressure hydrocephalus contributes to the high risk for recurrence in these patients, despite attempts at surgical repair.
Spontaneous leaks most commonly originate from cribriform plate defects. The lateral sphenoid recess is also a relatively common location, especially in patients with an extensively pneumatized lateral sphenoid sinus. Another important observation regarding spontaneous leaks is the frequent presence of multiple leak sites, occurring in approximately 35% of the cases. The overall risk of ascending meningitis in cases of unrepaired spontaneous leaks is approximately 10%.
When analyzed by subtype, spontaneous CSF leaks have the highest recurrence rate after surgical repair. Difficulty in achieving durable repair of spontaneous leaks is attributed to several reasons: occult elevated ICP, multiple skull base defects, and a high rate of meningoencephalocele formation.
Appropriate management of spontaneous leaks includes surgical repair. Nevertheless, there is an ongoing debate about the management of these cases, specifically regarding the use of transient lumbar drainage or a ventriculoperitoneal shunt (VPS). One hypothesis is that surgical repair may further increase the CSF pressure postoperatively, resulting in an increased risk of leak recurrence. Carrau and colleagues reported that 6 of 18 patients with spontaneous CSF leaks were found to have high-pressure CSF when evaluated postoperatively. All 6 subsequently underwent ventriculoperitoneal shunting, with no recurrences observed at long-term follow-up. Accordingly, the investigators suggest that CSF pressure be routinely measured postoperatively through a lumbar puncture in patients with spontaneous leaks. This approach has yet to gain wide acceptance, because of the possible complications associated with postoperative lumbar drainage, and the contradictory reports in the literature.
Confirmation of Cerebrospinal Fluid Leak
Definitive confirmation of active CSF rhinorrhea in suspected cases is done noninvasively by analysis of the nasal discharge for the presence of CSF biomarkers. In light of this, every effort should be made to obtain nasal secretions and perform chemical analysis before other diagnostic methods, especially invasive ones. Moreover, Zapalac and colleagues encourage repeated collection of rhinorrhea for CSF biomarker analysis before pursuing invasive diagnostic methods.
Since it was introduced in 1979, β2-transferrin is the most commonly used CSF biomarker, with high sensitivity and specificity (approaching 97% and 99%, respectively). Another protein that is used for this purpose is β-trace protein. Although the latter carries similar advantages as the former, including even higher sensitivity and specificity (both approaching 100%), it is not widely used, mainly because its utility is limited in cases of bacterial meningitis or reduced glomerular filtration.
Radionuclide cisternography, which is a nonlocalizing invasive modality involving lumbar puncture and radiation exposure, is rarely used for confirmation of CSF rhinorrhea and should be reserved for highly suggestive cases in which confirmation could not be obtained with CSF biomarkers.
Localization of the Leak Site
Following definitive confirmation of CSF rhinorrhea, accurate localization of the leak site is the next imperative step for establishing the diagnosis.
Coronal, sagittal, and axial high-resolution thin-cut (1-mm) computed tomography scan (HRCT) with bone algorithm is considered by most groups to be the best modality for depicting any bony defects, as exemplified in Fig. 2 . MRI may also be a valuable localization modality, primarily T2-weighted sequences. Although the sensitivity of each of these modalities for detecting the leak site approaches 90%, combining both increases the sensitivity to almost 97%.
Nowadays, computed tomography (CT) cisternography is rarely used because of its invasiveness and low sensitivity (40%) in detecting inactive leaks. If additional localization is required, some investigators advocate for specific MRI techniques for CSF leak detection, which uses a fast spin-echo sequence with fat suppression and image reversal. This modality has a reported sensitivity and specificity of 92% and 100%, respectively. However, the combination of a suggestive clinical history, confirmation by positive β2-transferrin, and approximate localization with HRCT and routine MRI is usually sufficient to establish the diagnosis.
Endoscopic endonasal repair of cerebrospinal fluid rhinorrhea
Perioperative Adjunctive Modalities
Lumbar drain
The use of lumbar drainage following surgical repair of CSF leak remains controversial. Some groups oppose routine use of lumbar drainage in these cases, for 2 main reasons: first, the fear of drainage-related complications (mainly pneumocephalus), and second, because there is no solid evidence that it improves closure rates. In this regard, according to recent systematic review of the literature, the benefit of lumbar drains in CSF leak repair could not be supported by the available data. Nevertheless, most investigators report using it selectively, and 67% of otolaryngologists that were recently surveyed use lumbar drains routinely as part of their management of CSF fistulae. Commonly cited indications for perioperative lumbar drainage include all the high-risk factors for repair failure: large defects, coexistent meningoencepahloceles, associated high ICP, body mass index greater than 30, radiographic empty sella syndrome, and previous CSF fistula repair.
In the authors’ institution, they use lumbar drainage selectively. As described by other groups, the drain is placed in the supine position before or immediately after the operation, and it is opened at a low rate of approximately 5 mL/h. The drain is usually removed 24 to 48 hours after the operation. During this period, any neurologic deterioration prompts an immediate closure of the drain, followed by urgent CT scan to exclude expanding pneumocephalus.
Intrathecal fluorescein
Fluorescein is a green fluorescent dye that alters the color of CSF when introduced intrathecally, thus making it more easily visible, especially in a surgical field. Intrathecal injection of fluorescein is a useful adjuvant method in endoscopic endonasal repair of CSF leak. By enhancing the visualization of CSF, fluorescein facilitates the identification of the leak, especially in cases of multiple leak sites, and helps to verify a watertight closure of the repair at the end of the procedure. Intrathecal administration of fluorescein was reported to be neurotoxic, with potential complications including transient paraparesis, numbness, opisthotonus, and cranial nerve deficits. Despite these major safety concerns, its use remains common practice. Keerl and colleagues reported an acceptable safety profile of intrathecal fluorescein at low doses in a large series of 420 administrations. The most significant complications were seen in 2 patients who experienced grand mal seizures on the day of the intrathecal injection. In another recent case series, Seth and colleagues demonstrated that intrathecal fluorescein has a sensitivity of 73.8% and a specificity of 100% in detecting the intraoperative CSF leak site, along with a false-negative rate of 26.2%.
Placantonakis and colleagues established an administration protocol that includes intravenous administration of 10 mg of dexamethasone and 50 mg of diphenhydramine after intubation, performing a lumbar puncture and withdrawal of 10 mL of CSF, mixing this with 0.25 mL of 10% fluorescein solution, and slow intrathecal injection of the solution for about an hour before its visualization. In the authors’ institution, they use a similar protocol, with a few modifications: the lumbar drain is placed preoperatively while the patient is awake, so any possible side effects, such as epileptic seizures, can be recognized. The patient is then kept in the recovery area for at least 2 hours in a slight Trendelenburg position to allow for the fluorescein to enter the cranial cavity and mix with the intracranial CSF.
Image-guidance system
Despite considered by many to be an invaluable adjunctive tool in endoscopic endonasal skull base surgeries, the role of image-guidance systems using multiple planar CT or MRI information has not, to date, been widely studied. Tabaee and colleagues retrospectively analyzed the possible correlation between successful endoscopic endonasal repair of CSF rhinorrhea and use of computer-assisted surgery. Although the study failed to establish clear correlation, the investigators concluded that the use of computer assistance may improve the confidence of the surgeon and is a valuable adjunct in this procedure. In the authors’ institution, image-guidance systems are used routinely in every endoscopic endonasal skull base surgeries.
Surgical Technique
The objectives of surgical repair of CSF leaks include reconstruction of the tissue barriers separating the cranial cavity from the sinonasal tract, while preserving neurovascular as well as sinonasal function. Despite slight variations, most groups uniformly advocate the following basic principles of endoscopic repair of CSF rhinorrhea to achieve the above objectives ( Box 1 ).
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Endoscopic Endonasal Approach for Removal of Tuberculum Sellae Meningiomas
Endoscopic Endonasal Approach to Ventral Posterior Fossa Meningiomas
Endoscopic Endonasal Odontoidectomy
Chordomas
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