- Email: [email protected]
Management of postoperative complications of skull base surgery
Operative Techniques in Otolaryngology (2011) 22, 237-245
Management of postoperative complications of skull base surgery Ameet Singh, MD,a Anand V. Germanwala, MDb From the aDivision of Otolaryngology, George Washington University School of Medicine Rhinology and Skull Base Surgery, George Washington University Medical Center, Washington, DC; and the b Department of Neurosurgery, The University of North Carolina School of Medicine, Cerebrovascular and Skull Base Neurosurgery, The University of North Carolina Hospital, Chapel Hill, North Carolina. KEYWORDS Cerebrospinal fluid leak; Endoscopic skull base surgery; Vascular injuries; Cerebrovascular accidents; Meningitis
The limits of endoscopic skull base surgery have significantly expanded over the past decade. More complex and challenging skull base pathology continues to be treated using endoscopic approaches. The expanding role of endonasal skull base surgery has been possible by a concerted effort to prevent and manage postoperative complications such as cerebrospinal fluid leaks, vascular injuries, neurological deficits, cerebrovascular accidents, and infectious sequelae. © 2011 Elsevier Inc. All rights reserved.
Although complications are inherent in any surgical procedure, they are best prevented rather than treated. This is especially true when addressing the complex pathology of the skull base. Preventing, minimizing, and successfully managing complications with minimal morbidity and mortality remain paramount in endoscopic skull base surgery. This goal presents multidisciplinary surgical teams with an ongoing challenge because larger and more complex intraand extraaxial lesions continue to be treated endoscopically. The combination of successful management and, more importantly, prevention of complications is necessary to achieve excellent outcomes while minimizing morbidity in endoscopic skull base surgery.
Cerebrospinal fluid leak Separation of the intracranial and sinonasal cavities after skull base surgery is necessary to prevent cerebrospinal Address reprint requests and correspondence: Ameet Singh, MD, George Washington University Medical Center, Endoscopic Pituitary and Skull-Base Surgery, George Washington University Hospital, 2021 K Street, Suite 206, Washington, DC 20006. E-mail address: [email protected]. 1043-1810/$ -see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.otot.2011.09.007
fluid (CSF) leaks and to avoid the risks of meningitis and pneumocephalus. Postoperative CSF leaks have been coined the “Achilles heel” for the skull base surgeon, illustrating the challenge of successful skull base reconstruction. Initial reports of postoperative CSF leaks after expanded endoscopic procedures were as high as 40%.1 The introduction of closure techniques for extended skull base defects such as the vascularized nasoseptal flap,2 the “gasket seal,”3 and “bilayer button”4 have reduced overall postoperative CSF leak rates to well below 5%. Additional techniques such as the temporoparietal, turbinate,5 palatal,6 and pericranial7 flaps offer additional reconstructive options available for primary and revision endoscopic skull base procedures. Although these reconstructive options have significantly reduced postoperative CSF leaks, multilayered reconstruction remains the mainstay of any successful skull base reconstruction. A plethora of factors may play a role in postoperative CSF leaks. These include characteristics of the leak (high flow vs low flow), defect (size, location, dural and bony margins), type of lesion, extent of intracranial dissection (dead space volume, volume of leak), repair technique, and patient-related factors (previous radiation therapy, diabetes, renal failure, obesity).8,9 In a prospective, multiinstitutional
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study of 412 patients, there were 18 postoperative CSF leaks, 12 of which were managed nonoperatively, and 6 were returned to the operating room. Five of the failures included technical problems with multilayered closure (inadequate dead space elimination, dural-graft approximation, graft-bone approximation, and graft stabilization) or the pedicled flap (inadequate size, rotation, and excessive tension). Only one failure was directly attributable to patient comorbidities.10 Most postoperative CSF leaks are diagnosed clinically without any imaging or laboratory testing. CSF leaks usually present as clear rhinnorhea, exacerbated by head movement (reservoir sign). However, they may present with subtle nonspecific signs such as positional headaches, a “salty” taste in the mouth, and/or clear postnasal discharge. Meningeal signs, or unresolving pneumocephalus on imaging, may also portend a CSF leak. Subtle leaks may be diagnosed by leaning the patient’s torso and head forward, while asking the patient to perform a gentle valsalva. In addition, clinical improvement of a headache in a reclined position may also suggest the presence of a small postoperative CSF leak. Suspicion of a CSF leak without obvious clinical signs may require biochemical testing of nasal secretions for markers like -2-transferrin, or imaging studies such as a computed tomography (CT) cisternogram and/or radionucleotide study. Intrathecal fluorescein may also be used to diagnose and localize subtle leaks.11 Fluorescein is a green fluorescent dye introduced into the intrathecal space to help endoscopically identify small leaks in the skull base. Although initial reports warned of a risk of seizures with its use, subsequent studies have established its safety and efficacy.12,13
A noncontrast CT scan of the head is necessary to evaluate for clinically significant pneumocephalus in any postoperative CSF leak. Small CSF leaks with minimal or stable pneumocephalus may be treated with a combination of nonoperative measures such as lumbar drainage, bed rest, and stool softeners for a limited period. If this strategy is employed, serial CT scans or skull x-rays and frequent neurological monitoring are essential to monitor for any sign of expanding pneumocephalus.8 Expanding pneumocephalus, essentially a mass lesion, requires repeat urgent operative intervention to diagnose and fix the site of the leak (Figure 1A, 1B). The presence of a neurological deficit, including lethargy under such circumstances, requires immediate exploration, irrigation of the pneumocephalus cavity, identification of the leak, and repair through the above described techniques. Many surgeons prefer to return immediately to the operating room to revise the skull base reconstruction regardless of the leak characteristics. Large CSF leaks with or without clinically significant pneumocephalus are unlikely to seal without operative intervention and are best treated expeditiously to reduce the risk of bacterial meningitis, and increasing pneumocephalus.14 The use of the lumbar drainage as an adjunct in skull base reconstruction is controversial given the conflicting literature and lack of randomized studies. The advantages of lumbar drainage include temporary CSF diversion to facilitate healing of the skull base and potentially reduce the risk of postoperative meningitis.15 Once the patient exits the operating room, a routine CT scan of the head is performed to ensure the presence of only minimal pneumocephaly in the immediate postoperative state, prior to opening the lum-
Figure 1 Noncontrast axial CT demonstrating large intraparenchymal and intraventricular (A) and subarachnoid (B) pneumocephaly in a patient with sinonasal undifferentiated carcinoma of the skull base who developed osteoradionecrosis of the skull base and a CSF leak. Despite several attempts to fix the leak endoscopically, this patient ultimately went underwent a coronal incision and craniotomy for placement of a pedicled pericranial flap.
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bar drain. The disadvantages of this adjunct include increasing pneumocephalus, infection, herniation, nausea, and headaches. Many authors rarely use lumbar drainage without any increase in postoperative CSF rhinnorhea.16 Most surgical teams use lumbar drainage selectively, namely with large skull base defects, high flow leaks, preoperative CSF leaks, specific tumor pathologies, and patients with increased intracranial pressures, and limit drainage to 5 to 10 mL/h. CSF analysis is performed periodically to evaluate for infection.
Vascular complications Meticulous intraoperative hemostasis is important to prevent postoperative vascular complications. Detailed study of neurovascular anatomy on preoperative imaging [CT, magnetic resonance imaging (MRI), and CT angiography] and using tools such as image guidance and Doppler are important to prevent catastrophic intraoperative vascular injuries. Bleeding may be classified by vessel type (capillary, venous, arterial), volume of bleed, and bleeding location (extra- or intracranial). The spectrum of bleeding includes minor nasal mucosal bleeding, troublesome venous oozing from a tumor bed, brisk venous bleeding from the cavernous sinus, pulsatile arterial bleeding from a moderate sized vessel (eg, sphenopalatine artery), or devastating bleeding from the internal carotid artery. Several surgical techniques have evolved to manage intraoperative bleeding and prevent postoperative hemorrhage.17 Nasal mucosal bleeding can be managed with topical thrombin with epinephrine, monopolar cautery, warm water irrigation (110°F), and/or a variety of hemostatic agents. Sinonasal arterial bleeding is usually controlled by monopolar cautery or clipping. Bony bleeding can be stopped with warm water irrigation, diamond drilling, or bone wax. Venous bleeding from the cavernous sinus or basilar plexus is best managed with direct application of hemostatic agents such as FloSeal fibular gelfoam with gentle pressure. Arterial bleeding from small intracranial vessels is challenging because sacrifice of the vessel may result in ischemia. Direct cautery to “weld” the vessel is ideal, although application of hemostatic agents or warm water irrigation may work in some circumstances. Sacrifice of an intracranial bleeding artery is considered a last resort. Although rare, injury to the internal carotid artery can lead to massive arterial bleeding and pseudoaneurysm or carotid-cavernous fistula formation (Figure 2A-2E). Good communication between the anesthesiology and surgical team, and immediate hemostasis, often achieved by multiple rounds of compressive packing, are paramount. Once hemodynamic stability has been maintained, emergent angiography is warranted to assess the vascular injury and intracranial circulation. Aneurysm clips with single shaft appliers, which can be applied endonasally, should be present in the operating room if hemostasis is unable to be achieved with compressive packing. Options for endovascular intervention include embolization with coils and/or
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balloon placement,18 carotid artery sacrifice, and stent placement, which requires strong antiplatelet therapy,19 and should be considered carefully in the setting of possible future surgery. Long-term follow-up imaging should also be performed to assess for pseudoaneurysm recurrence, delayed fistula formation, coil compaction, or in-stent stenosis. Minor immediate postoperative bleeding requires a nasal drip pad and humidification to prevent vestibular crusting. Endoscopic visualization of moderate or severe bleeding is recommended for expedient hemostatic control and preventing damage to the skull base reconstruction. If the patient is cooperative, local anesthesia and various hemostatic measures (hemostatic matrix, electrocautery, packing) can be applied under endoscopic guidance to control the bleeding. These measures, however, may be impractical if the bleeding occurs in the immediate postoperative period. Furthermore, if the bleeding is brisk, the source is not clearly visualized, or compressive packing cannot be used, controlling the hemorrhage in the operating room is recommended. This is particularly critical in the immediate postoperative period given the risk of displacing the skull base reconstruction.20 Finally, if an intracranial source of bleeding is suspected, emergent angiography is indicated.
Neurologic complications The limits of intracranial endoscopic surgery continue to be pushed, with resection of large intra- and extraaxial tumors being performed with increasing frequency at multiple institutions. Recent reports have noted the treatment of intracranial complex vascular lesions with these techniques.21 With increasingly complex surgeries, surrounding neurovascular structures are at risk. With sellar lesions such as Rathke’s cleft cysts and pituitary adenomas, attention must be paid to the neural structures within the cavernous sinuses. The medial wall can be readily identified; however, inadvertent cavernous sinus entry, particularly in cases with tumor infiltration or repeat endonasal surgery, can lead to injury of structures within the sinus. The abducens nerve, the most medial parasellar cranial nerve, can be temporarily or permanently injured, leading to a lateral gaze palsy. Intraoperative electrophysiological monitoring, including free running electromyography, can be a useful adjunct in these situations.22 Although visual disturbances are rare following endoscopic endonasal approaches, they can lead to significant morbidity for patients. With intracranial approaches and resections, the location of the optic nerves/chiasm and their blood supply must be respected. Thermal injury during high-speed drilling can lead to vision loss; therefore, periodic irrigation is recommended during bony work. Drilling immediately over the optic nerves is avoided for this reason. Ischemic injury can occur by stripping the visual apparatus of its blood supply; hence, perforating vessels of the nerves and chiasm are rarely cauterized. Also, manipulation of the nerves can lead to vision loss and so direct retraction is
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Figure 2 Sagittal (A) and axial (B) contrasted preoperative MRI demonstrating large planar meningioma. Note proximity to the anterior cerebral arteries. Intraoperatively, during the resection, arterial blood was visualized from the A2 branch of the right anterior cerebral artery. This was controlled with multiple rounds of packing. The remainder of the resection was aborted. The patient was taken to the interventional suite where an arteriogram revealed a small 2-mm pseudoaneurysm arising from this vessel (C). This was embolized. The patient did not develop any neurological deficits. Postoperative imaging reveals a small amount of residual tumor and a vascularized nasoseptal flap for dural reconstruction (D, E).
avoided. Avoidance of any significant pressure on the optic apparatus is a must to avoid postoperative vision loss, and care must be taken to preserve perforating vessels. Cerebral
arteries located in the subarachnoid space in this area include the ophthalmic and superior hypophyseal arteries as well as chiasmatic perforators. Good knowledge of the neu-
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rovascular anatomy is vital to help prevent inadvertent injury. Inadvertent breaches through the lamina papyracea can injure the medial rectus muscle,23 leading to weakness of ipsilateral medial gaze and diplopia. Intentional approaches through the lamina papyracea for orbital lesions can lead to the development of orbital/retroorbital hematoma, injury to the extraocular muscles, and blindness from injury to the optic nerve or ophthalmic/central retinal artery in the orbit. At the conclusion of surgery, care must be exercised to ensure that no compression of the visual apparatus from the orbit to the intracranial portion of the visual apparatus occurs from intranasal packing. Immediate postoperative visual disturbances should be emergently explored with removal of packing and endoscopic exploration for the etiology. Orbital hematomas can be evacuated endonasally, accompanied with a lateral and/or medial canthotomy. A negative exploration mandates emergent noninvasive imaging and an ophthalmology consultation. Extradural transcribriform approaches can lead to injuring olfactory filaments, while intradural exposures in this region pose risk to the olfactory bulb/nerve, which can lead to permanent anosmia. Patients need to be counseled about the potential for loss of smell and subsequent taste in the preoperative setting. Most patients with pathology in this region likely have a preexisting component of anosmia. Such testing should be part of the comprehensive physical examination. Intradural transclival approaches permit access to the ventral posterior fossa. The location of the vasculature must be noted to prevent the initial dural opening from being immediately over the basilar artery. Intraoperative Doppler can be used to identify underlying such vascular structures. The location of underlying cranial nerves must also be identified. The abducens nerve, often found exiting the brainstem at the vertebrobasilar junction and traveling superolaterally, can easily be injured with wide dural exposures, and free running electromyography should be available. The cisternal segment of the oculomotor nerve can be seen coursing between the posterior cerebral and superior cerebellar arteries before it enters the cavernous sinus and care must be taken to avoid excessive manipulation. Injuring either of these nerves will lead to postoperative extraocular movement difficulties and diplopia, which may or may not improve over the course of several months. The use of bipolar cautery must be kept at a minimum in these areas. The vestibulocochlear complex, exiting the caudal pons, can be visualized with angled scopes prior to entry in to the porous. Pending the location of the lesion, the potential need for facial nerve monitoring and brainstem auditory evoked responses must be kept in mind. A significant amount of time should also be spent on dural reconstruction in this region. A combination of free abdominal fat grafting with a superimposed vascularized nasoseptal flap and several days of lumbar drainage are useful tools to help minimize the risk of postoperative CSF leak. Transpterygoid approaches pose a risk to the nerves of the pterygopalatine fossa, the small inverted space located
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behind the posteriomedial wall of the maxillary sinus. The maxillary division of the trigeminal nerve exits the middle fossa via the foramen rotundum and enters the perygopalatine fossa. Injury to this nerve leads to numbness of the cheek and infraorbital anesthesia. Just inferior and medial to the foramen rotundum lies the vidian canal, which transmits the vidian nerve and a small branch of the internal maxillary artery. Injury to the vidian nerve can lead to decreased emotional tearing and a dry eye. Recognition of the location of these nerves and the surrounding bony anatomy is important to avoid injury; however, tumors in this area often present with these neurological deficits preoperatively and a detailed preoperative examination is important.
Cerebrovascular accidents Cerebrovascular accidents can occur in skull base surgery regardless of the approach. Vascular injuries with resultant ischemia, emboli, venous sacrifice, and hypotension are some of the most common causes for cerebrovascular accidents. A thorough knowledge of the vascular anatomy and meticulous tumor dissection is critical to avoid cerebrovascular complications. The treatment of suprasellar lesions or sellar lesions with suprasellar extension, such as large or giant pituitary adenomas, craniopharyngiomas, and epidermoid tumors, requires a thorough knowledge of the circle of Willis and perforating vessels. Clear visualization must be obtained at all times through the endoscope. Resection of these tumors requires sharp dissection and transection of arachnoid adhesions tethering the vasculature with traction/ countertraction, principles of microsurgery. Identifying the location of the anterior and posterior cerebral arteries, recurrent arteries of Heubner, and anterior/posterior communicating arteries are of prime importance (Figure 3A-3C). Electrophysiological monitoring, including somatosensory evoked potentials and electroencephalogram, are required if manipulation of the cerebral vasculature is a possibility during tumor resection. Arterial bleeding from the circle of Willis vessels can be disastrous and must be dealt with in a similar fashion as described above.
Endocrinological complications Diabetes insipidus (DI) is one of the more frequently encountered complications in transsphenoidal pituitary and craniopharyngioma surgery. Disturbance of the posterior pituitary, pituitary stalk, and neurons from the hypothalmus may lead to temporary or permanent imbalance of antidiuretic hormone-regulated water homeostasis. The overall incidence of transient and permanent postoperative DI in transsphenoidal pituitary surgery has been reported to range from 4% to 20% (transient) and 0% to 5% (permanent)24 but may be as high as 68% for transsphenoidal resections of craniopharyngioma.25 Recent literature has shown that patients with tumors, including macroadenomas, craniopharyngiomas, and rathke’s cleft cysts, with an associated intra-
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Figure 3 Sagittal (A) contrasted preoperative MRI demonstrating large cystic and solid mass. Intraoperative pathology revealed pituitary adenoma. Although the patient did not develop any symptoms, postoperative diffusion-weighted imaging revealed a small stroke involving the right caudate head (B), likely because of ischemic injury from the recurrent artery of Heubner. Sagittal contrasted MRI after resection demonstrated near total resection (C).
operative CSF leak may have an increased incidence of postoperative DI; such a finding may be explained by having a higher incidence of gland injury and concomitant CSF leak with more aggressive dissections. Also, reoperation can increase the risk of hypopituitarism because of increased scar, difficult dissection, and the challenge of identifying the normal gland. The fluid status and serum chemistries of patients need to be monitored postoperatively. Urine specific gravity and serum sodium should be measured when urinary output exceeds 300 mL/h. The combination of serum sodium ⬎145, urine specific gravity ⬍1.005, and such increased urinary output over consecutive hours should alert the treating physician to the administration of vasopressin. The immediate postoperative development of DI often remains permanent, while DI developing 1 to 2 days following surgery may be reversible. Following transphenoidal surgery, patients should be maintained on a small dose of steroids (often dexamethasone, 2 mg by mouth two times per day) in the setting of possible hypocortisolemia. The evening dose is typically held on postoperative day 1 and a morning serum cortisol is checked on postoperative day 2. A cortisol level less than 10 g/dL indicates adrenal insufficiency and the need for maintenance steroid therapy. This issue can be reevaluated weeks later to determine the potential need for long-term therapy.
Craniopharyngiomas and other lesions, including granular cell tumors that invade and infiltrate the infundibulum, often require transection of the infundibulum to achieve a cure (Figure 4). Depending on the goal of surgery, treating surgeons must decide on the aggressiveness of the resection. Patients need to be counseled preoperatively about the possibility of developing panhypopituitarism, which impacts fertility and requires lifelong medication.
Infection Despite the theoretic risk of infection by introducing sinonasal flora into the subarachnoid space with direct communication and passage of instruments, the overall infection rates are low and rival those of traditional craniotomy.26 Antibiotic prophylaxis is given preoperatively and is continued until removal of nasal packing. Frequent irrigation during surgery and good skull base reconstruction techniques help keep infection rates low. Patients presenting with symptoms of infection (fevers, elevated white blood cell count) and meningeal signs (headache, nuchal rigidity, mental status changes) warrant immediate evaluation with a CT scan followed by lumbar puncture and intensive care unit admission. Broad spectrum antibiotic therapy is started when meningitis is clinically suspected and tailored toward the offending organism. A
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Figure 4 Intraoperative photo demonstrating round mass arising from and infiltrating the infundibulum with mass effect on the overlying optic apparatus. A full resection was performed, requiring transection of the stalk. Perforating vessels were preserved. Pathology revealed a granular cell tumor of the infundibulum. The patient, counseled preoperatively, developed panhypopituitarism as the only postsurgical complication. (Color version of figure is available online.)
workup should also be performed to evaluate for any concurrent CSF leak, which would also need to be addressed urgently, as well as an MRI to evaluate for an underlying abscess. The rate of intracranial abscess formation after endonasal skull base surgery is quite low, as most patients often come to medical attention before the frank development of cerebritis or a walled off abscess. A lumbar puncture may be contraindicated as this could represent a mass lesion with a risk of downward herniation with a spinal tap. In this instance, repeat operative intervention via an endonasal approach should be performed with the goal of obtaining a diagnostic culture and drainage of the intracranial abscess. Similar medical therapy is instituted and long-term clinical follow-up and imaging should be performed.
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sinonasal complications and timeline for return to normal function. Endoscopic surveillance and timely intervention are critical in promoting healing of the sinonasal cavity. Postoperative management of the sinonasal cavity after endoscopic skull base surgery follows the well-established principles for wound healing after endoscopic sinus surgery. The goals include maximizing wound healing, restoring mucociliary clearance, maintaining ostia patency, preventing synechiae, and avoiding rhinosinusitis. Prevention of postoperative sinonasal complications begins in the operating room by preserving native mucosa, avoiding raw surfaces in close proximity, and maintaining sinus ostia patency. Postoperatively, care of the sinonasal cavity includes medical management with saline irrigation, topical or oral antibiotics, nasal steroid sprays, decongestants, and mucolytics. In addition, postoperative nasal endoscopy with debridement is imperative for enhancing sinonasal healing and preventing sinonasal complications. Crusting occurs after all endoscopic sinonasal surgery secondary to mucosal damage and impaired mucociliary clearance. It is often more extensive after extended skull base procedures. Topical therapy with saline irrigation, antibiotic sprays, and mucolytics as well as postoperative debridements improve mucosal healing, encourage mucociliary function, and decrease synechia formation. The disadvantages of debridement include bleeding, mucosal avulsion, and minor discomfort. Several randomized, blinded clinical trials confirm that, although patients undergoing debridement have additional bleeding and discomfort, they experience fewer synechiae and less nasal obstruction over time.27 Postoperative synechia may occur after endoscopic skull base surgery despite meticulous surgical and postoperative care. They are typically found between the septum and lateral nasal wall or septum and inferior turbinates (Figure 5). Soft, immature synechia may be easily transected with topical anesthesia in the early postoperative period by the otolaryngologist. Mature synechia require a formal lysis of synechia, which involves topical and local anesthesia, fol-
Sinonasal complications Expanded endoscopic approaches to the anterior skull base increase the risk of sinonasal complications. These include excessive crusting, synechiae, septal perforations, vestibular sores/burns, and rhinosinusitis (acute and chronic). Although endoscopic skull base approaches are frequently coined, “minimally invasive,” extended approaches can often have a “maximally invasive” impact on the healing and postoperative function of the sinonasal cavity. The surgical approach, extent of surgery, complexity of skull base reconstruction, and patient comorbidities influence the extent of
Figure 5 Postoperative synechiae. (Color version of figure is available online.)
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lowed by resection of scar tissue, and often placement of splints to avoid scar reformation. Lysis of synechia is important to ensure good nasal airflow and prevent sinonasal obstruction and rhinosinusitis.20 Vestibular burns, sores, and abrasions are uncommon, but may occur during extended skull base surgery. This is largely secondary to the frequent movement of the endoscope, and other instruments (drills, aspirators, electrocautery) through the nose. Topical antibiotic treatment and local wound care are usually sufficient for treatment. Acute rhinosinusitis is rare after endoscopic pituitary or skull base surgery. More common is crusting, accompanied with mucoid secretions without significant mucosal inflammation. Medical management with antibiotics is well-supported in the literature to eradicate bacteria from the sinuses, hasten recovery, and improve quality of life.28 Adjunctive treatments, which include decongestants, corticosteroids, saline irrigation, and mucolytics, may provide symptomatic relief to patients. Topical therapy, including nasal sprays and irrigation, must be used cautiously in the immediate postoperative period to avoid disturbing the skull base reconstruction, specifically hastening the dissolution of dural and tissue sealants. Although amoxicillin is the first-line therapy for acute bacterial rhinosinusitis, this may not be the appropriate choice in patients after endoscopic skull base surgery. High-dose amoxicillin-clavulonate (4 g d⫺1 amoxicillin equivalent), a respiratory fluoroquinolone (levofloxacin, moxifloxacin), macrolides, or a third-generation cephalosporin (ceftriaxone) may be better choices for antibiotic therapy in these patients. Topical therapy, including nasal sprays and irrigation, as well as postoperative surgical debridements are performed cautiously in the postoperative period. Nasal sprays and irrigation encourage sinonasal healing but theoretically may displace the multilayer reconstruction and/or hasten the breakdown of dural and tissue sealants. Postoperative debridements must also proceed with significant caution given the risk of disturbing the skull base reconstruction. Crusting can often be adherent to the healing skull base reconstruction and aggressive attempts to remove it can result in a CSF leak or one-way valve, causing pneumocephalus. Meningitis is a rare but possible complication in the setting of acute bacterial rhinosinusitis. Recent literature points to a rate of less than 3% for intracranial complications such as meningitis, CSF leaks, and pneumocephalus in the perioperative period after endoscopic endonasal skull base surgery, including extended approaches.29
Conclusions Complications are inherent in surgical procedures, especially when addressing complex pathology of the skull base. Multidisciplinary surgical teams must strive to prevent postoperative complications by conducting a comprehensive
preoperative assessment (history, physical examination, laboratory studies, and imaging). Meticulous hemostasis, safeguarding of vessels, solid skull base reconstruction, and careful preservation of sinonasal structures are critical for minimizing postoperative complications after endoscopic skull base surgery.
References 1. Gardner PA, Kassam AB, Thomas A, et al: Endoscopic endonasal resection of anterior cranial base meningiomas. Neurosurgery 63:3652, 2008 [discussion 52-54] 2. Hadad G, Bassagasteguy L, Carrau RL, et al: A novel reconstructive technique after endoscopic expanded endonasal approaches: vascular pedicle nasoseptal flap. Laryngoscope 116:1882-1886, 2006 3. Leng LZ, Brown S, Anand VK, et al: “Gasket-seal” watertight closure in minimal-access endoscopic cranial base surgery. Neurosurgery 62(suppl 2):ONSE342-ONSE343, 2008 [discussion ONSE343] 4. Luginbuhl AJ, Campbell PG, Evans J, et al: Endoscopic repair of high-flow cranial base defects using a bilayer button. Laryngoscope 120:876-880, 2010 5. Harvey RJ, Sheahan PO, Schlosser RJ: Inferior turbinate pedicle flap for endoscopic skull base defect repair. Am J Rhinol Allergy 23(5): 522-526, 2009 6. Oliver CL, Hackman TG, Carrau RL, et al: Palatal flap modifications allow pedicled reconstruction of the skull base. Laryngoscope 118: 2102-2106, 2008 7. Zanation AM, Snyderman CH, Carrau RL, et al: Minimally invasive endoscopic pericranial flap: a new method for endonasal skull base reconstruction. Laryngoscope 119:13-18, 2009 8. Tabaee A, Anand VK, Brown SM, et al: Algorithm for reconstruction after endoscopic pituitary and skull base surgery. Laryngoscope 117: 1133-1137, 2007 9. Carrau RL, Snyderman CH, Kassam AB: The management of cerebrospinal fluid leaks in patients at risk for high-pressure hydrocephalus. Laryngoscope 115:205-212, 2005 10. Singh A, McCoul E, Roberti FR, et al: Successful Management of Recalcitrant Cerebrospinal Fluid Leaks: Technical Considerations. 21st Annual North American Skull Base Society Meeting. Scottsdale, AZ, 2011 11. Singh A, Anand VK, Schwartz TH: Successful Management of Endoscopic Skull Base Surgery Complications: Transnasal Endoscopic Skull Base and Brain Surgery. New York, Stuttgart, Thieme, 2011 12. Placantonakis DG, Tabaee A, Anand VK, et al: Safety of low-dose intrathecal fluorescein in endoscopic cranial base surgery. Neurosurgery 61(suppl 3):161-165, 2007 [discussion 165-166] 13. Tabaee A, Placantonakis DG, Schwartz TH, et al: Intrathecal fluorescein in endoscopic skull base surgery. Otolaryngol Head Neck Surg 137:316-320, 2007 14. Kassam A, Carrau RL, Snyderman CH, et al: Evolution of reconstructive techniques following endoscopic expanded endonasal approaches [review]. Neurosurg Focus 19:E8, 2005 15. van Aken MO, de Marie S, van der Lely AJ, et al: Risk factors for meningitis after transsphenoidal surgery. Clin Infect Dis 25:852-856, 1997 16. Casiano RR, Jassir D: Endoscopic cerebrospinal fluid rhinorrhea repair: is a lumbar drain necessary? Otolaryngol Head Neck Surg 121: 745-750, 1999 17. Kassam A, Snyderman CH, Carrau RL, et al: Endoneurosurgical hemostasis techniques: lessons learned from 400 cases. Neurosurg Focus 19:E7, 2005 18. Cappabianca P, Briganti F, Cavallo LM, et al: Pseudoaneurysm of the intracavernous carotid artery following endoscopic endonasal transsphenoidal surgery, treated by endovascular approach. Acta Neurochir (Wien) 143:95-96, 2001
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19. Reich O, Ringel K, Stoeter P, et al: [Injury of ICA during endonasal sinus surgery and management by endovascular stent application]. Laryngorhinootologie 88:322-326, 2009 [in German] 20. Singh A, Schaberg M, Nyquist GG, et al: Post-Operative Sinonasal Management. Endoscopic Pituitary Surgery. New York, Stuttgart, Thieme, 2011 21. Germanwala AV, Zanation AM: Endoscopic endonasal approach for clipping of ruptured and unruptured paraclinoid cerebral aneurysms: case report. Neurosurgery 68(Suppl Operative):234-239, 2011 [discussion 240] 22. Barges-Coll J, Fernandez-Miranda JC, Prevedello DM, et al: Avoiding injury to the abducens nerve during expanded endonasal endoscopic surgery: anatomic and clinical case studies. Neurosurgery 67:144-154, 2010 [discussion 154] 23. Bleier BS, Schlosser RJ: Prevention and management of medial rectus injury [review]. Otolaryngol Clin North Am 43:801-807, 2010
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24. Tabaee A, Anand VK, Barrón Y, et al: Endoscopic pituitary surgery: a systematic review and meta-analysis [review]. J Neurosurg 111:545554, 2009 25. Honegger J, Buchfelder M, Fahlbusch R, et al: Transsphenoidal microsurgery for craniopharyngioma. Surg Neurol 37:189-196, 1992 26. Brown SM, Anand VK, Tabaee A, et al: Role of perioperative antibiotics in endoscopic skull base surgery. Laryngoscope 117:15281532, 2007 27. Bugten V, Nordgård S, Steinsvåg S: The effects of debridement after endoscopic sinus surgery. Laryngoscope 116:2037-2043, 2006 28. Rosenfeld RM, Andes D, Bhattacharyya N, et al: Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg 137(suppl 3):S1-31, 2007 29. Harvey RJ, Smith JE, Wise SK, et al: Intracranial complications before and after endoscopic skull base reconstruction. Am J Rhinol 22:516521, 2008
Management of postoperative complications of skull base surgery Ameet Singh, MD,a Anand V. Germanwala, MDb From the aDivision of Otolaryngology, George Washington University School of Medicine Rhinology and Skull Base Surgery, George Washington University Medical Center, Washington, DC; and the b Department of Neurosurgery, The University of North Carolina School of Medicine, Cerebrovascular and Skull Base Neurosurgery, The University of North Carolina Hospital, Chapel Hill, North Carolina. KEYWORDS Cerebrospinal fluid leak; Endoscopic skull base surgery; Vascular injuries; Cerebrovascular accidents; Meningitis
The limits of endoscopic skull base surgery have significantly expanded over the past decade. More complex and challenging skull base pathology continues to be treated using endoscopic approaches. The expanding role of endonasal skull base surgery has been possible by a concerted effort to prevent and manage postoperative complications such as cerebrospinal fluid leaks, vascular injuries, neurological deficits, cerebrovascular accidents, and infectious sequelae. © 2011 Elsevier Inc. All rights reserved.
Although complications are inherent in any surgical procedure, they are best prevented rather than treated. This is especially true when addressing the complex pathology of the skull base. Preventing, minimizing, and successfully managing complications with minimal morbidity and mortality remain paramount in endoscopic skull base surgery. This goal presents multidisciplinary surgical teams with an ongoing challenge because larger and more complex intraand extraaxial lesions continue to be treated endoscopically. The combination of successful management and, more importantly, prevention of complications is necessary to achieve excellent outcomes while minimizing morbidity in endoscopic skull base surgery.
Cerebrospinal fluid leak Separation of the intracranial and sinonasal cavities after skull base surgery is necessary to prevent cerebrospinal Address reprint requests and correspondence: Ameet Singh, MD, George Washington University Medical Center, Endoscopic Pituitary and Skull-Base Surgery, George Washington University Hospital, 2021 K Street, Suite 206, Washington, DC 20006. E-mail address: [email protected]. 1043-1810/$ -see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.otot.2011.09.007
fluid (CSF) leaks and to avoid the risks of meningitis and pneumocephalus. Postoperative CSF leaks have been coined the “Achilles heel” for the skull base surgeon, illustrating the challenge of successful skull base reconstruction. Initial reports of postoperative CSF leaks after expanded endoscopic procedures were as high as 40%.1 The introduction of closure techniques for extended skull base defects such as the vascularized nasoseptal flap,2 the “gasket seal,”3 and “bilayer button”4 have reduced overall postoperative CSF leak rates to well below 5%. Additional techniques such as the temporoparietal, turbinate,5 palatal,6 and pericranial7 flaps offer additional reconstructive options available for primary and revision endoscopic skull base procedures. Although these reconstructive options have significantly reduced postoperative CSF leaks, multilayered reconstruction remains the mainstay of any successful skull base reconstruction. A plethora of factors may play a role in postoperative CSF leaks. These include characteristics of the leak (high flow vs low flow), defect (size, location, dural and bony margins), type of lesion, extent of intracranial dissection (dead space volume, volume of leak), repair technique, and patient-related factors (previous radiation therapy, diabetes, renal failure, obesity).8,9 In a prospective, multiinstitutional
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study of 412 patients, there were 18 postoperative CSF leaks, 12 of which were managed nonoperatively, and 6 were returned to the operating room. Five of the failures included technical problems with multilayered closure (inadequate dead space elimination, dural-graft approximation, graft-bone approximation, and graft stabilization) or the pedicled flap (inadequate size, rotation, and excessive tension). Only one failure was directly attributable to patient comorbidities.10 Most postoperative CSF leaks are diagnosed clinically without any imaging or laboratory testing. CSF leaks usually present as clear rhinnorhea, exacerbated by head movement (reservoir sign). However, they may present with subtle nonspecific signs such as positional headaches, a “salty” taste in the mouth, and/or clear postnasal discharge. Meningeal signs, or unresolving pneumocephalus on imaging, may also portend a CSF leak. Subtle leaks may be diagnosed by leaning the patient’s torso and head forward, while asking the patient to perform a gentle valsalva. In addition, clinical improvement of a headache in a reclined position may also suggest the presence of a small postoperative CSF leak. Suspicion of a CSF leak without obvious clinical signs may require biochemical testing of nasal secretions for markers like -2-transferrin, or imaging studies such as a computed tomography (CT) cisternogram and/or radionucleotide study. Intrathecal fluorescein may also be used to diagnose and localize subtle leaks.11 Fluorescein is a green fluorescent dye introduced into the intrathecal space to help endoscopically identify small leaks in the skull base. Although initial reports warned of a risk of seizures with its use, subsequent studies have established its safety and efficacy.12,13
A noncontrast CT scan of the head is necessary to evaluate for clinically significant pneumocephalus in any postoperative CSF leak. Small CSF leaks with minimal or stable pneumocephalus may be treated with a combination of nonoperative measures such as lumbar drainage, bed rest, and stool softeners for a limited period. If this strategy is employed, serial CT scans or skull x-rays and frequent neurological monitoring are essential to monitor for any sign of expanding pneumocephalus.8 Expanding pneumocephalus, essentially a mass lesion, requires repeat urgent operative intervention to diagnose and fix the site of the leak (Figure 1A, 1B). The presence of a neurological deficit, including lethargy under such circumstances, requires immediate exploration, irrigation of the pneumocephalus cavity, identification of the leak, and repair through the above described techniques. Many surgeons prefer to return immediately to the operating room to revise the skull base reconstruction regardless of the leak characteristics. Large CSF leaks with or without clinically significant pneumocephalus are unlikely to seal without operative intervention and are best treated expeditiously to reduce the risk of bacterial meningitis, and increasing pneumocephalus.14 The use of the lumbar drainage as an adjunct in skull base reconstruction is controversial given the conflicting literature and lack of randomized studies. The advantages of lumbar drainage include temporary CSF diversion to facilitate healing of the skull base and potentially reduce the risk of postoperative meningitis.15 Once the patient exits the operating room, a routine CT scan of the head is performed to ensure the presence of only minimal pneumocephaly in the immediate postoperative state, prior to opening the lum-
Figure 1 Noncontrast axial CT demonstrating large intraparenchymal and intraventricular (A) and subarachnoid (B) pneumocephaly in a patient with sinonasal undifferentiated carcinoma of the skull base who developed osteoradionecrosis of the skull base and a CSF leak. Despite several attempts to fix the leak endoscopically, this patient ultimately went underwent a coronal incision and craniotomy for placement of a pedicled pericranial flap.
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bar drain. The disadvantages of this adjunct include increasing pneumocephalus, infection, herniation, nausea, and headaches. Many authors rarely use lumbar drainage without any increase in postoperative CSF rhinnorhea.16 Most surgical teams use lumbar drainage selectively, namely with large skull base defects, high flow leaks, preoperative CSF leaks, specific tumor pathologies, and patients with increased intracranial pressures, and limit drainage to 5 to 10 mL/h. CSF analysis is performed periodically to evaluate for infection.
Vascular complications Meticulous intraoperative hemostasis is important to prevent postoperative vascular complications. Detailed study of neurovascular anatomy on preoperative imaging [CT, magnetic resonance imaging (MRI), and CT angiography] and using tools such as image guidance and Doppler are important to prevent catastrophic intraoperative vascular injuries. Bleeding may be classified by vessel type (capillary, venous, arterial), volume of bleed, and bleeding location (extra- or intracranial). The spectrum of bleeding includes minor nasal mucosal bleeding, troublesome venous oozing from a tumor bed, brisk venous bleeding from the cavernous sinus, pulsatile arterial bleeding from a moderate sized vessel (eg, sphenopalatine artery), or devastating bleeding from the internal carotid artery. Several surgical techniques have evolved to manage intraoperative bleeding and prevent postoperative hemorrhage.17 Nasal mucosal bleeding can be managed with topical thrombin with epinephrine, monopolar cautery, warm water irrigation (110°F), and/or a variety of hemostatic agents. Sinonasal arterial bleeding is usually controlled by monopolar cautery or clipping. Bony bleeding can be stopped with warm water irrigation, diamond drilling, or bone wax. Venous bleeding from the cavernous sinus or basilar plexus is best managed with direct application of hemostatic agents such as FloSeal fibular gelfoam with gentle pressure. Arterial bleeding from small intracranial vessels is challenging because sacrifice of the vessel may result in ischemia. Direct cautery to “weld” the vessel is ideal, although application of hemostatic agents or warm water irrigation may work in some circumstances. Sacrifice of an intracranial bleeding artery is considered a last resort. Although rare, injury to the internal carotid artery can lead to massive arterial bleeding and pseudoaneurysm or carotid-cavernous fistula formation (Figure 2A-2E). Good communication between the anesthesiology and surgical team, and immediate hemostasis, often achieved by multiple rounds of compressive packing, are paramount. Once hemodynamic stability has been maintained, emergent angiography is warranted to assess the vascular injury and intracranial circulation. Aneurysm clips with single shaft appliers, which can be applied endonasally, should be present in the operating room if hemostasis is unable to be achieved with compressive packing. Options for endovascular intervention include embolization with coils and/or
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balloon placement,18 carotid artery sacrifice, and stent placement, which requires strong antiplatelet therapy,19 and should be considered carefully in the setting of possible future surgery. Long-term follow-up imaging should also be performed to assess for pseudoaneurysm recurrence, delayed fistula formation, coil compaction, or in-stent stenosis. Minor immediate postoperative bleeding requires a nasal drip pad and humidification to prevent vestibular crusting. Endoscopic visualization of moderate or severe bleeding is recommended for expedient hemostatic control and preventing damage to the skull base reconstruction. If the patient is cooperative, local anesthesia and various hemostatic measures (hemostatic matrix, electrocautery, packing) can be applied under endoscopic guidance to control the bleeding. These measures, however, may be impractical if the bleeding occurs in the immediate postoperative period. Furthermore, if the bleeding is brisk, the source is not clearly visualized, or compressive packing cannot be used, controlling the hemorrhage in the operating room is recommended. This is particularly critical in the immediate postoperative period given the risk of displacing the skull base reconstruction.20 Finally, if an intracranial source of bleeding is suspected, emergent angiography is indicated.
Neurologic complications The limits of intracranial endoscopic surgery continue to be pushed, with resection of large intra- and extraaxial tumors being performed with increasing frequency at multiple institutions. Recent reports have noted the treatment of intracranial complex vascular lesions with these techniques.21 With increasingly complex surgeries, surrounding neurovascular structures are at risk. With sellar lesions such as Rathke’s cleft cysts and pituitary adenomas, attention must be paid to the neural structures within the cavernous sinuses. The medial wall can be readily identified; however, inadvertent cavernous sinus entry, particularly in cases with tumor infiltration or repeat endonasal surgery, can lead to injury of structures within the sinus. The abducens nerve, the most medial parasellar cranial nerve, can be temporarily or permanently injured, leading to a lateral gaze palsy. Intraoperative electrophysiological monitoring, including free running electromyography, can be a useful adjunct in these situations.22 Although visual disturbances are rare following endoscopic endonasal approaches, they can lead to significant morbidity for patients. With intracranial approaches and resections, the location of the optic nerves/chiasm and their blood supply must be respected. Thermal injury during high-speed drilling can lead to vision loss; therefore, periodic irrigation is recommended during bony work. Drilling immediately over the optic nerves is avoided for this reason. Ischemic injury can occur by stripping the visual apparatus of its blood supply; hence, perforating vessels of the nerves and chiasm are rarely cauterized. Also, manipulation of the nerves can lead to vision loss and so direct retraction is
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Figure 2 Sagittal (A) and axial (B) contrasted preoperative MRI demonstrating large planar meningioma. Note proximity to the anterior cerebral arteries. Intraoperatively, during the resection, arterial blood was visualized from the A2 branch of the right anterior cerebral artery. This was controlled with multiple rounds of packing. The remainder of the resection was aborted. The patient was taken to the interventional suite where an arteriogram revealed a small 2-mm pseudoaneurysm arising from this vessel (C). This was embolized. The patient did not develop any neurological deficits. Postoperative imaging reveals a small amount of residual tumor and a vascularized nasoseptal flap for dural reconstruction (D, E).
avoided. Avoidance of any significant pressure on the optic apparatus is a must to avoid postoperative vision loss, and care must be taken to preserve perforating vessels. Cerebral
arteries located in the subarachnoid space in this area include the ophthalmic and superior hypophyseal arteries as well as chiasmatic perforators. Good knowledge of the neu-
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rovascular anatomy is vital to help prevent inadvertent injury. Inadvertent breaches through the lamina papyracea can injure the medial rectus muscle,23 leading to weakness of ipsilateral medial gaze and diplopia. Intentional approaches through the lamina papyracea for orbital lesions can lead to the development of orbital/retroorbital hematoma, injury to the extraocular muscles, and blindness from injury to the optic nerve or ophthalmic/central retinal artery in the orbit. At the conclusion of surgery, care must be exercised to ensure that no compression of the visual apparatus from the orbit to the intracranial portion of the visual apparatus occurs from intranasal packing. Immediate postoperative visual disturbances should be emergently explored with removal of packing and endoscopic exploration for the etiology. Orbital hematomas can be evacuated endonasally, accompanied with a lateral and/or medial canthotomy. A negative exploration mandates emergent noninvasive imaging and an ophthalmology consultation. Extradural transcribriform approaches can lead to injuring olfactory filaments, while intradural exposures in this region pose risk to the olfactory bulb/nerve, which can lead to permanent anosmia. Patients need to be counseled about the potential for loss of smell and subsequent taste in the preoperative setting. Most patients with pathology in this region likely have a preexisting component of anosmia. Such testing should be part of the comprehensive physical examination. Intradural transclival approaches permit access to the ventral posterior fossa. The location of the vasculature must be noted to prevent the initial dural opening from being immediately over the basilar artery. Intraoperative Doppler can be used to identify underlying such vascular structures. The location of underlying cranial nerves must also be identified. The abducens nerve, often found exiting the brainstem at the vertebrobasilar junction and traveling superolaterally, can easily be injured with wide dural exposures, and free running electromyography should be available. The cisternal segment of the oculomotor nerve can be seen coursing between the posterior cerebral and superior cerebellar arteries before it enters the cavernous sinus and care must be taken to avoid excessive manipulation. Injuring either of these nerves will lead to postoperative extraocular movement difficulties and diplopia, which may or may not improve over the course of several months. The use of bipolar cautery must be kept at a minimum in these areas. The vestibulocochlear complex, exiting the caudal pons, can be visualized with angled scopes prior to entry in to the porous. Pending the location of the lesion, the potential need for facial nerve monitoring and brainstem auditory evoked responses must be kept in mind. A significant amount of time should also be spent on dural reconstruction in this region. A combination of free abdominal fat grafting with a superimposed vascularized nasoseptal flap and several days of lumbar drainage are useful tools to help minimize the risk of postoperative CSF leak. Transpterygoid approaches pose a risk to the nerves of the pterygopalatine fossa, the small inverted space located
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behind the posteriomedial wall of the maxillary sinus. The maxillary division of the trigeminal nerve exits the middle fossa via the foramen rotundum and enters the perygopalatine fossa. Injury to this nerve leads to numbness of the cheek and infraorbital anesthesia. Just inferior and medial to the foramen rotundum lies the vidian canal, which transmits the vidian nerve and a small branch of the internal maxillary artery. Injury to the vidian nerve can lead to decreased emotional tearing and a dry eye. Recognition of the location of these nerves and the surrounding bony anatomy is important to avoid injury; however, tumors in this area often present with these neurological deficits preoperatively and a detailed preoperative examination is important.
Cerebrovascular accidents Cerebrovascular accidents can occur in skull base surgery regardless of the approach. Vascular injuries with resultant ischemia, emboli, venous sacrifice, and hypotension are some of the most common causes for cerebrovascular accidents. A thorough knowledge of the vascular anatomy and meticulous tumor dissection is critical to avoid cerebrovascular complications. The treatment of suprasellar lesions or sellar lesions with suprasellar extension, such as large or giant pituitary adenomas, craniopharyngiomas, and epidermoid tumors, requires a thorough knowledge of the circle of Willis and perforating vessels. Clear visualization must be obtained at all times through the endoscope. Resection of these tumors requires sharp dissection and transection of arachnoid adhesions tethering the vasculature with traction/ countertraction, principles of microsurgery. Identifying the location of the anterior and posterior cerebral arteries, recurrent arteries of Heubner, and anterior/posterior communicating arteries are of prime importance (Figure 3A-3C). Electrophysiological monitoring, including somatosensory evoked potentials and electroencephalogram, are required if manipulation of the cerebral vasculature is a possibility during tumor resection. Arterial bleeding from the circle of Willis vessels can be disastrous and must be dealt with in a similar fashion as described above.
Endocrinological complications Diabetes insipidus (DI) is one of the more frequently encountered complications in transsphenoidal pituitary and craniopharyngioma surgery. Disturbance of the posterior pituitary, pituitary stalk, and neurons from the hypothalmus may lead to temporary or permanent imbalance of antidiuretic hormone-regulated water homeostasis. The overall incidence of transient and permanent postoperative DI in transsphenoidal pituitary surgery has been reported to range from 4% to 20% (transient) and 0% to 5% (permanent)24 but may be as high as 68% for transsphenoidal resections of craniopharyngioma.25 Recent literature has shown that patients with tumors, including macroadenomas, craniopharyngiomas, and rathke’s cleft cysts, with an associated intra-
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Figure 3 Sagittal (A) contrasted preoperative MRI demonstrating large cystic and solid mass. Intraoperative pathology revealed pituitary adenoma. Although the patient did not develop any symptoms, postoperative diffusion-weighted imaging revealed a small stroke involving the right caudate head (B), likely because of ischemic injury from the recurrent artery of Heubner. Sagittal contrasted MRI after resection demonstrated near total resection (C).
operative CSF leak may have an increased incidence of postoperative DI; such a finding may be explained by having a higher incidence of gland injury and concomitant CSF leak with more aggressive dissections. Also, reoperation can increase the risk of hypopituitarism because of increased scar, difficult dissection, and the challenge of identifying the normal gland. The fluid status and serum chemistries of patients need to be monitored postoperatively. Urine specific gravity and serum sodium should be measured when urinary output exceeds 300 mL/h. The combination of serum sodium ⬎145, urine specific gravity ⬍1.005, and such increased urinary output over consecutive hours should alert the treating physician to the administration of vasopressin. The immediate postoperative development of DI often remains permanent, while DI developing 1 to 2 days following surgery may be reversible. Following transphenoidal surgery, patients should be maintained on a small dose of steroids (often dexamethasone, 2 mg by mouth two times per day) in the setting of possible hypocortisolemia. The evening dose is typically held on postoperative day 1 and a morning serum cortisol is checked on postoperative day 2. A cortisol level less than 10 g/dL indicates adrenal insufficiency and the need for maintenance steroid therapy. This issue can be reevaluated weeks later to determine the potential need for long-term therapy.
Craniopharyngiomas and other lesions, including granular cell tumors that invade and infiltrate the infundibulum, often require transection of the infundibulum to achieve a cure (Figure 4). Depending on the goal of surgery, treating surgeons must decide on the aggressiveness of the resection. Patients need to be counseled preoperatively about the possibility of developing panhypopituitarism, which impacts fertility and requires lifelong medication.
Infection Despite the theoretic risk of infection by introducing sinonasal flora into the subarachnoid space with direct communication and passage of instruments, the overall infection rates are low and rival those of traditional craniotomy.26 Antibiotic prophylaxis is given preoperatively and is continued until removal of nasal packing. Frequent irrigation during surgery and good skull base reconstruction techniques help keep infection rates low. Patients presenting with symptoms of infection (fevers, elevated white blood cell count) and meningeal signs (headache, nuchal rigidity, mental status changes) warrant immediate evaluation with a CT scan followed by lumbar puncture and intensive care unit admission. Broad spectrum antibiotic therapy is started when meningitis is clinically suspected and tailored toward the offending organism. A
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Figure 4 Intraoperative photo demonstrating round mass arising from and infiltrating the infundibulum with mass effect on the overlying optic apparatus. A full resection was performed, requiring transection of the stalk. Perforating vessels were preserved. Pathology revealed a granular cell tumor of the infundibulum. The patient, counseled preoperatively, developed panhypopituitarism as the only postsurgical complication. (Color version of figure is available online.)
workup should also be performed to evaluate for any concurrent CSF leak, which would also need to be addressed urgently, as well as an MRI to evaluate for an underlying abscess. The rate of intracranial abscess formation after endonasal skull base surgery is quite low, as most patients often come to medical attention before the frank development of cerebritis or a walled off abscess. A lumbar puncture may be contraindicated as this could represent a mass lesion with a risk of downward herniation with a spinal tap. In this instance, repeat operative intervention via an endonasal approach should be performed with the goal of obtaining a diagnostic culture and drainage of the intracranial abscess. Similar medical therapy is instituted and long-term clinical follow-up and imaging should be performed.
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sinonasal complications and timeline for return to normal function. Endoscopic surveillance and timely intervention are critical in promoting healing of the sinonasal cavity. Postoperative management of the sinonasal cavity after endoscopic skull base surgery follows the well-established principles for wound healing after endoscopic sinus surgery. The goals include maximizing wound healing, restoring mucociliary clearance, maintaining ostia patency, preventing synechiae, and avoiding rhinosinusitis. Prevention of postoperative sinonasal complications begins in the operating room by preserving native mucosa, avoiding raw surfaces in close proximity, and maintaining sinus ostia patency. Postoperatively, care of the sinonasal cavity includes medical management with saline irrigation, topical or oral antibiotics, nasal steroid sprays, decongestants, and mucolytics. In addition, postoperative nasal endoscopy with debridement is imperative for enhancing sinonasal healing and preventing sinonasal complications. Crusting occurs after all endoscopic sinonasal surgery secondary to mucosal damage and impaired mucociliary clearance. It is often more extensive after extended skull base procedures. Topical therapy with saline irrigation, antibiotic sprays, and mucolytics as well as postoperative debridements improve mucosal healing, encourage mucociliary function, and decrease synechia formation. The disadvantages of debridement include bleeding, mucosal avulsion, and minor discomfort. Several randomized, blinded clinical trials confirm that, although patients undergoing debridement have additional bleeding and discomfort, they experience fewer synechiae and less nasal obstruction over time.27 Postoperative synechia may occur after endoscopic skull base surgery despite meticulous surgical and postoperative care. They are typically found between the septum and lateral nasal wall or septum and inferior turbinates (Figure 5). Soft, immature synechia may be easily transected with topical anesthesia in the early postoperative period by the otolaryngologist. Mature synechia require a formal lysis of synechia, which involves topical and local anesthesia, fol-
Sinonasal complications Expanded endoscopic approaches to the anterior skull base increase the risk of sinonasal complications. These include excessive crusting, synechiae, septal perforations, vestibular sores/burns, and rhinosinusitis (acute and chronic). Although endoscopic skull base approaches are frequently coined, “minimally invasive,” extended approaches can often have a “maximally invasive” impact on the healing and postoperative function of the sinonasal cavity. The surgical approach, extent of surgery, complexity of skull base reconstruction, and patient comorbidities influence the extent of
Figure 5 Postoperative synechiae. (Color version of figure is available online.)
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lowed by resection of scar tissue, and often placement of splints to avoid scar reformation. Lysis of synechia is important to ensure good nasal airflow and prevent sinonasal obstruction and rhinosinusitis.20 Vestibular burns, sores, and abrasions are uncommon, but may occur during extended skull base surgery. This is largely secondary to the frequent movement of the endoscope, and other instruments (drills, aspirators, electrocautery) through the nose. Topical antibiotic treatment and local wound care are usually sufficient for treatment. Acute rhinosinusitis is rare after endoscopic pituitary or skull base surgery. More common is crusting, accompanied with mucoid secretions without significant mucosal inflammation. Medical management with antibiotics is well-supported in the literature to eradicate bacteria from the sinuses, hasten recovery, and improve quality of life.28 Adjunctive treatments, which include decongestants, corticosteroids, saline irrigation, and mucolytics, may provide symptomatic relief to patients. Topical therapy, including nasal sprays and irrigation, must be used cautiously in the immediate postoperative period to avoid disturbing the skull base reconstruction, specifically hastening the dissolution of dural and tissue sealants. Although amoxicillin is the first-line therapy for acute bacterial rhinosinusitis, this may not be the appropriate choice in patients after endoscopic skull base surgery. High-dose amoxicillin-clavulonate (4 g d⫺1 amoxicillin equivalent), a respiratory fluoroquinolone (levofloxacin, moxifloxacin), macrolides, or a third-generation cephalosporin (ceftriaxone) may be better choices for antibiotic therapy in these patients. Topical therapy, including nasal sprays and irrigation, as well as postoperative surgical debridements are performed cautiously in the postoperative period. Nasal sprays and irrigation encourage sinonasal healing but theoretically may displace the multilayer reconstruction and/or hasten the breakdown of dural and tissue sealants. Postoperative debridements must also proceed with significant caution given the risk of disturbing the skull base reconstruction. Crusting can often be adherent to the healing skull base reconstruction and aggressive attempts to remove it can result in a CSF leak or one-way valve, causing pneumocephalus. Meningitis is a rare but possible complication in the setting of acute bacterial rhinosinusitis. Recent literature points to a rate of less than 3% for intracranial complications such as meningitis, CSF leaks, and pneumocephalus in the perioperative period after endoscopic endonasal skull base surgery, including extended approaches.29
Conclusions Complications are inherent in surgical procedures, especially when addressing complex pathology of the skull base. Multidisciplinary surgical teams must strive to prevent postoperative complications by conducting a comprehensive
preoperative assessment (history, physical examination, laboratory studies, and imaging). Meticulous hemostasis, safeguarding of vessels, solid skull base reconstruction, and careful preservation of sinonasal structures are critical for minimizing postoperative complications after endoscopic skull base surgery.
References 1. Gardner PA, Kassam AB, Thomas A, et al: Endoscopic endonasal resection of anterior cranial base meningiomas. Neurosurgery 63:3652, 2008 [discussion 52-54] 2. Hadad G, Bassagasteguy L, Carrau RL, et al: A novel reconstructive technique after endoscopic expanded endonasal approaches: vascular pedicle nasoseptal flap. Laryngoscope 116:1882-1886, 2006 3. Leng LZ, Brown S, Anand VK, et al: “Gasket-seal” watertight closure in minimal-access endoscopic cranial base surgery. Neurosurgery 62(suppl 2):ONSE342-ONSE343, 2008 [discussion ONSE343] 4. Luginbuhl AJ, Campbell PG, Evans J, et al: Endoscopic repair of high-flow cranial base defects using a bilayer button. Laryngoscope 120:876-880, 2010 5. Harvey RJ, Sheahan PO, Schlosser RJ: Inferior turbinate pedicle flap for endoscopic skull base defect repair. Am J Rhinol Allergy 23(5): 522-526, 2009 6. Oliver CL, Hackman TG, Carrau RL, et al: Palatal flap modifications allow pedicled reconstruction of the skull base. Laryngoscope 118: 2102-2106, 2008 7. Zanation AM, Snyderman CH, Carrau RL, et al: Minimally invasive endoscopic pericranial flap: a new method for endonasal skull base reconstruction. Laryngoscope 119:13-18, 2009 8. Tabaee A, Anand VK, Brown SM, et al: Algorithm for reconstruction after endoscopic pituitary and skull base surgery. Laryngoscope 117: 1133-1137, 2007 9. Carrau RL, Snyderman CH, Kassam AB: The management of cerebrospinal fluid leaks in patients at risk for high-pressure hydrocephalus. Laryngoscope 115:205-212, 2005 10. Singh A, McCoul E, Roberti FR, et al: Successful Management of Recalcitrant Cerebrospinal Fluid Leaks: Technical Considerations. 21st Annual North American Skull Base Society Meeting. Scottsdale, AZ, 2011 11. Singh A, Anand VK, Schwartz TH: Successful Management of Endoscopic Skull Base Surgery Complications: Transnasal Endoscopic Skull Base and Brain Surgery. New York, Stuttgart, Thieme, 2011 12. Placantonakis DG, Tabaee A, Anand VK, et al: Safety of low-dose intrathecal fluorescein in endoscopic cranial base surgery. Neurosurgery 61(suppl 3):161-165, 2007 [discussion 165-166] 13. Tabaee A, Placantonakis DG, Schwartz TH, et al: Intrathecal fluorescein in endoscopic skull base surgery. Otolaryngol Head Neck Surg 137:316-320, 2007 14. Kassam A, Carrau RL, Snyderman CH, et al: Evolution of reconstructive techniques following endoscopic expanded endonasal approaches [review]. Neurosurg Focus 19:E8, 2005 15. van Aken MO, de Marie S, van der Lely AJ, et al: Risk factors for meningitis after transsphenoidal surgery. Clin Infect Dis 25:852-856, 1997 16. Casiano RR, Jassir D: Endoscopic cerebrospinal fluid rhinorrhea repair: is a lumbar drain necessary? Otolaryngol Head Neck Surg 121: 745-750, 1999 17. Kassam A, Snyderman CH, Carrau RL, et al: Endoneurosurgical hemostasis techniques: lessons learned from 400 cases. Neurosurg Focus 19:E7, 2005 18. Cappabianca P, Briganti F, Cavallo LM, et al: Pseudoaneurysm of the intracavernous carotid artery following endoscopic endonasal transsphenoidal surgery, treated by endovascular approach. Acta Neurochir (Wien) 143:95-96, 2001
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19. Reich O, Ringel K, Stoeter P, et al: [Injury of ICA during endonasal sinus surgery and management by endovascular stent application]. Laryngorhinootologie 88:322-326, 2009 [in German] 20. Singh A, Schaberg M, Nyquist GG, et al: Post-Operative Sinonasal Management. Endoscopic Pituitary Surgery. New York, Stuttgart, Thieme, 2011 21. Germanwala AV, Zanation AM: Endoscopic endonasal approach for clipping of ruptured and unruptured paraclinoid cerebral aneurysms: case report. Neurosurgery 68(Suppl Operative):234-239, 2011 [discussion 240] 22. Barges-Coll J, Fernandez-Miranda JC, Prevedello DM, et al: Avoiding injury to the abducens nerve during expanded endonasal endoscopic surgery: anatomic and clinical case studies. Neurosurgery 67:144-154, 2010 [discussion 154] 23. Bleier BS, Schlosser RJ: Prevention and management of medial rectus injury [review]. Otolaryngol Clin North Am 43:801-807, 2010
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24. Tabaee A, Anand VK, Barrón Y, et al: Endoscopic pituitary surgery: a systematic review and meta-analysis [review]. J Neurosurg 111:545554, 2009 25. Honegger J, Buchfelder M, Fahlbusch R, et al: Transsphenoidal microsurgery for craniopharyngioma. Surg Neurol 37:189-196, 1992 26. Brown SM, Anand VK, Tabaee A, et al: Role of perioperative antibiotics in endoscopic skull base surgery. Laryngoscope 117:15281532, 2007 27. Bugten V, Nordgård S, Steinsvåg S: The effects of debridement after endoscopic sinus surgery. Laryngoscope 116:2037-2043, 2006 28. Rosenfeld RM, Andes D, Bhattacharyya N, et al: Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg 137(suppl 3):S1-31, 2007 29. Harvey RJ, Smith JE, Wise SK, et al: Intracranial complications before and after endoscopic skull base reconstruction. Am J Rhinol 22:516521, 2008