Complications of Endoscopic Endonasal Skull Base Surgery

Complications of Endoscopic Endonasal Skull Base Surgery

S E C TI ON 2 Cranial Complications Endoscopic Surgery 36  Complications of Endoscopic Endonasal Skull Base Surgery PAUL A. GARDNER, CARL H. SNYDER...

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S E C TI ON 2

Cranial Complications Endoscopic Surgery

36 

Complications of Endoscopic Endonasal Skull Base Surgery PAUL A. GARDNER, CARL H. SNYDERMAN, ERIC W. WANG, JUAN C. FERNANDEZ-MIRANDA

HIGHLIGHTS • Cerebrospinal fluid leak remains the most common complication of endoscopic endonasal skull base surgery, but this has decreased dramatically with the use of vascularized nasoseptal flaps. • Lumbar drains have been shown to decrease the risk of cerebrospinal fluid leak after endonasal skull base surgery, primarily for larger anterior and posterior fossa defects. • Major vascular injury can be controlled during endoscopic ESBS, but it often requires immediate endovascular evaluation and/or treatment. • Nasal instrumentation should be avoided in the postoperative period unless under direct endoscopic visualization. • There is a significant learning curve with endonasal skull base surgery that should be respected to keep complication rates low.

Background Endoscopic endonasal skull base surgery (ESBS) has seen a dramatic increase in adoption since its introduction and development over the last two decades. Initially used only for pituitary tumors,1,2 the approach has expanded significantly to include the entire ventral skull base.3–6 However, multiple articles have demonstrated that there is a significant learning curve with these approaches,7–9 with improved resection and decreased complication rates such as cerebrospinal fluid (CSF) leak over time. In addition, the introduction of vascularized flaps such as the nasoseptal flap10 has significantly improved the reconstruction of the skull base after these approaches. With all skull base approaches, nerve and vascular injury make up the remainder of the majority of complications.11 In general, endonasal approaches were developed to allow wide and wellvisualized anterior access for tumors that originate in the midline or paramedian skull base and displace involved neurovascular structures laterally. Respecting this concept in approach selection, as well as the learning curve, helps minimize neurovascular complications.

Anatomic Insights The anterior cranial base slopes inferiorly from anterior to posterior with varying degree. During exposure, care should be taken not to violate the skull base during anterior to posterior dissection, especially during maneuvers such as middle turbinate resection. Excessive head extension during positioning may alter the trajectory and predispose to anterior skull base injury during exposure. A thorough understanding of vascular and neural anatomy is critical for navigating the skull base. The internal carotid artery (ICA) is a key anatomic landmark for orientation and classification of endonasal approaches (Fig. 36.1). Endonasal landmarks include: • The Eustachian tube lies medial to the parapharyngeal ICA as it enters the skull base. • The vidian nerve is located just inferior and lateral to the foramen lacerum ICA, and it crosses over the horizontal petrous ICA to connect with the greater superficial petrosal nerve (GSPN). • The pterygoid process marks the medial plane of the foramen lacerum and the pterygo-sphenoidal fissure (between pterygoid process and sphenoid sinus floor) and attaches posteriorly to the foramen lacerum ICA. • The middle clinoid process, when present, is located between the cavernous ICA and the clinoidal ICA.12 • The “medial optic-carotid recess (OCR)” is a landmark for the clinoidal segment of the ICA and dural ring. • The lateral OCR is located laterally between the clinoidal ICA and optic canal. Sphenopalatine artery anatomy (Fig. 36.2) is critical to understand for a multitude of reasons. It can be a source of postoperative epistaxis after pituitary surgery, is the key supply for the nasoseptal (posterior nasal artery) and other posteriorly based flaps, and must be dissected and managed to access the pterygoid canal and base of the pterygoid for transpterygoid approaches.13 Limitations for the endoscopic endonasal approach (EEA) are largely laterally located or displaced nerves and/or arteries. Crossing the plane of nerves defeats the main advantage of an endoscopic endonasal corridor, which is avoidance of neurovascular manipulation. Understanding these limitations and the 207

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DR PS

PC VN Pet

FL

PPh

• Fig. 36.1  Endoscopic endonasal view of a cadaver dissection showing the segments of the internal carotid artery (ICA) that create the lateral limit of many endonasal approaches. DR, Dural ring confluence; FL, foramen lacerum; PC, paraclival ICA; Pet, horizontal petrous ICA; PPh, Parapharyngeal ICA; PS, parasellar ICA; VN, vidian nerve.

PNA

SPA

• Fig. 36.2

  Endoscopic endonasal view of the right pterygopalatine fossa showing the sphenopalatine artery (SPA) and key posterior nasal artery (PNA) branch. The latter provides blood supply to the vascularized nasoseptal flap and can also be a source of postoperative epistaxis when sacrificed.

anatomy of the cranial nerves in these key locations is critical for avoiding injury. In the suprasellar space, the optic nerves enter the dural sheath of the optic canal at the medial aspect of the optic strut/lateral OCR. The canal can be widely decompressed by carefully drilling

all bone overlying the medial canal. A suprasellar dural opening can be extended laterally to the medial falciform ligament above the optic nerve, to avoid injury to the ophthalmic artery, which often originates on the medial supraclinoidal ICA or loops medially before travelling to its usual position, just inferior to the optic nerve, until it crosses superiorly more distally. The sella is limited laterally by the ICA, but tumors can be dissected from the various compartments of the cavernous sinus, named based on their relationship to the genu of the cavernous ICA.14 The superior compartment (where most medially originating tumors extend) is related to the third cranial nerve, whereas the posterior and inferior compartments only have segments of the abducens nerve (CN VI). The lateral compartment contains segments of all cavernous cranial nerves (III, IV, V1, and VI). Though III and IV are generally ensheathed in the lateral cavernous wall dura, entrance into this compartment is generally reserved for aggressive tumors or those with symptoms indicative of oculomotor nerve involvement. The midclivus is bounded laterally by the petrous apex, Dorello’s canal, and the abducens nerve. This nerve is most likely to be injured during any transclival approach, so understanding its anatomy is essential. CN VI exits the brainstem at the vertebrobasilar junction and runs obliquely up to Dorello’s canal, which runs behind the upper half of the paraclival ICA. There is a venous channel, the inferior petrosal sinus, immediately below the nerve, which can be a conduit for tumor growth. “Gardner’s triangle” is a medial anatomic triangle providing access to the petrous apex. It is bounded superiorly by the abducens nerve, anteriorly by the paraclival ICA, and inferiorly by the petroclival synchondrosis. The lateral limitation in the lower clivus, below the foramen lacerum, is the hypoglossal canal and nerve. Extending exposure to this landmark increases access by 50%.15,16 Immediately above the canal lies the medial jugular tubercle and below it, the medial occipital condyle. Inferior extension of dissection beyond the tip of the odontoid process may cause craniocervical instability, especially if the anterior ring of C1 is disrupted.

RED FLAGS • Prior endonasal surgery increases risk of nasoseptal flap necrosis. • Chondroid tumors (chordoma and chondrosarcoma) have the highest risk of ICA injury. • Growth hormone–secreting tumors are associated with ICA ectasia and increased risk of injury. • Recurrent tumors, especially after radiation therapy, have an increased risk of both neural and vascular injury. • Nonadenomas invading the cavernous sinus are at much higher risk than adenomas for nerve and artery injury during cavernous sinus dissection. • Coronal plane (paramedian) approaches have an increased risk of complications, especially ICA injury.

Prevention Important aspects of prevention of complications during ESBS include preoperative preparation; a careful understanding of the normal anatomy from an endonasal perspective; proper imaging (computed tomography [CT] angiography) to assess the circle of Willis; evaluation of nasal structures if the patient has had prior



CHAPTER 36  Complications of Endoscopic Endonasal Skull Base Surgery

• Fig. 36.3

  Intraoperative endoscopic endonasal view showing a Kartush stimulator being used to dissect the abducens nerve from a petroclival meningioma. Identification and verification of cranial nerves with stimulating dissectors can decrease the risk of injury.

endonasal surgery; and full evaluation of hormonal and ophthalmologic function preoperatively. Intraoperatively, the use of image guidance and Doppler probes provides accurate localization of the ICA to avoid injury. Electromyography (EMG) (both free-running and stimulated) can help identify motor cranial nerves and is associated with lower risk of postoperative loss of function (Fig. 36.3). In addition, team surgery (two surgeons, 3–4 hands) has significant advantages with respect to visualization, dynamic endoscopy, and microsurgical dissection, as well as avoidance and management of complications. A second surgeon will often notice impending complications when the other does not. Two surgeons (especially from different specialties) will often focus on different aspects, thereby increasing the likelihood of complication avoidance. Postoperatively, close follow-up by both otolaryngological and neurosurgical teams will help avoid respective complications. Lumbar drainage has been shown to reduce postoperative CSF leak risk in patients with large anterior or posterior fossa dural defects.17 If CSF leak is suspected, early re-exploration is key to preventing subsequent complications such as meningitis. Frequent screening for deep venous thrombosis in the lower extremities with Doppler sonography is important in patients with prolonged procedures or hospital stays.

Management Nerve Injury In general, there is little that can be done for a nerve injury. Limited suturing ability combined with common sites of injury adjacent to or intimate with the ICA makes reapproximation difficult or impossible. If there is still a detectable EMG threshold across the nerve, no further measures are needed, although corticosteroids are often used intraoperatively and for a period of days postoperatively, depending on the severity of weakness and balanced with the

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impact of steroids on healing. There is some data on facial nerve injury suggesting that calcium channel blockers may aid recovery, but this has never been widely accepted or studied in other cranial nerves.18–20 If the two ends of the nerve can be placed into contact with each other, covering them with fibrin glue is a means of both re-approximation and protection against further injury. In general, vision loss after EEA is rare and seems to be less severe than with open approaches.8,21–23 Patients with greater severity of vision loss preoperatively may have a higher risk of worsening postoperatively. This may be a reflection of degree of compression or compromise of perfusion. If patients are worse on awakening, they should be closely monitored with a mean arterial blood pressure (MAP) floor of 80 or more, even if pressors are required, and high-dose steroids. Unless the source of injury is known, imaging with CT scan should be performed to look for early hematoma or overpacking with fat graft. Intradural fat graft in the suprasellar region due to the latter risk is generally avoided at our center. Delayed worsening should generally be treated in the same manner, though hematoma becomes a more likely scenario. If visual status is unclear, bedside ophthalmologic examination and urgent magnetic resonance imaging (MRI) can be used to determine need for reoperation. If there is any concern for mass effect associated with vision loss, reoperation to evacuate the source should be done as efficiently as possible. In the absence of compression, microvascular vasospasm of the superior hypophyseal branches and other optic apparatus perforators is the presumed cause. This is managed with hypertension, as described, and by considering the addition of calcium channel blockers such as nimodipine.

Vascular Injury Injury to the ICA or other intracranial vasculature is one of the most feared complications in any cranial base surgery, but especially during ESBS. The first step with any injury is control of the bleeding. This requires localization of the site of injury and maintenance of visualization. The former is obtained by using a large-bore suction to follow the bleeding while introducing a cottonoid to cover and contain it. If this cannot be achieved, other maneuvers should be used: adenosine (0.3 mg/kg) can give a 10- to 20-second cardiac pause; for ICA injury, firm percutaneous compression of the cervical ICA can provide a degree of proximal control. Hypotension can aid in initial control, but once compression is applied and/or the artery is occluded, it should be avoided in favor of perfusion. Small holes in an artery or avulsion of a perforator can be effectively controlled with careful, fine bipolar electrocautery on a lower setting with saline irrigation by the co-surgeon. Bipolar electrocautery can be an effective means of hemostasis while maintaining vessel patency, depending on the caliber. Other options such as aneurysm clips placed with a single shaft applier are possible, but the most reliable solution for a large vessel injury is packing with muscle, either from the abdominal rectus or temporalis muscle (if prepped), or from the nasopharyngeal capitis muscle, which can be harvested in-field once bleeding is controlled. Ideally, packing will be tight enough to control bleeding, but not so tight that it occludes the vessel. Doppler sonography can be critical to confirm maintenance of flow, and intraoperative neurophysiologic monitoring with somatosensory evoked potentials (SSEP) is an important adjunct to detect ischemia. The muscle graft (or cotton if used) ideally is covered with a tissue flap before placement of additional packing. This separates the site of injury from the sinus to prevent future contamination.

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An algorithm to this effect has been previously published.24 If control of the injury requires excessive or repeated manipulation of the artery, intraoperative anticoagulation should be considered, though this is often counterintuitive at a time of uncontrolled bleeding. However, once the vessel is controlled, the thrombus formation from endothelial injury can lead to complete occlusion or embolus. Immediate postoperative angiography (digital subtraction angiography [DSA] or CT angiography [CTA]) is critical in the setting of any vascular injury. Unless an injury is minor and easily controlled, minimal tumor resection should proceed, because vessel stenosis and/or manipulation can lead to unforeseen complications, such as thromboembolism, that can result in devastating but avoidable consequences. “Emergent” bypass is not pragmatic. The majority of patients will tolerate ICA sacrifice, and those who do not typically will infarct rapidly, much sooner than the 4+ hours it would take even the most skilled surgeons to complete a high-flow bypass. Therefore endovascular salvage remains the main reasonable option. The advantage of DSA is the ability to treat any active issue such as extravasation, stenosis, or pseudoaneurysm. Newer flowdiversion devices have improved coverage and can provide a good solution for all three of these. However, if this is not possible due to tortuosity of the carotid siphon, a large defect, or lack of technical expertise, coiling and even ICA sacrifice should be considered, assuming neurophysiologic parameters are stable. Delayed vascular imaging is also important, because vascular injuries will often result in pseudoaneurysm formation. Follow-up vascular imaging (CTA or DSA is preferred, but MR angiography is an option) typically is performed around 1 week, 1 month, and 3 to 6 months postoperatively in the setting of arterial injury without sacrifice.

Postoperative Cerebrospinal Fluid Leak CSF leak is the most common complication after ESBS.7–8,25 Early detection and treatment of leak are critical to prevent further sequelae. The introduction and widespread usage of the vascularized nasoseptal flap have led to a dramatic decrease in the risk of postoperative leak, and the flap is recommended in any high-flow leak setting.26,27 Proper healing requires removal of any intervening tissue (mucosa, blood clot) or foreign body (bone wax) between the flap and native bone or dura surrounding the defect. This maximizes contact between vascularized tissues. A multilayer reconstruction with an auto- or allograft onlay deep to the flap is sometimes necessary if the flap is not adequate to cover the defect with overlap. It is important to ensure that the flap is in contact with a demucosalized surface along its entire length, including the pedicle. Any part of the flap that is stretched across an air space will retract and cause shift of the flap in the postoperative period. Tissue glues play an unclear role but are used routinely. Nasal packing is important to hold the flap in place and counteract CSF pulsations exacerbated by the patient’s activities. There are also clear patient factors that contribute to CSF leak.28 Foremost among these is increased body mass index (BMI), a setting in which CSF leak rates were most significantly reduced with use of a nasoseptal flap. Posterior fossa tumor location has also been shown repeatedly to be associated with higher pressures and therefore higher leak rates. Also likely related to increased posterior fossa pressures is pontine encephalocele, a radiographic finding, typically without clinical sequelae, noted after wide bony and dural transclival resection.29 The pons can slowly herniate into the defect during the period of healing (Fig. 36.4). This complication can severely limit postoperative radiation fields and could create problems for repeat surgery.

FL FL FL

F NSF

FL

FL

B

A • Fig. 36.4  (A) Sagittal T1-weighted magnetic resonance imaging showing bulging of the ventral pons (arrow) into a large clival defect after endoscopic endonasal surgery (EES). (B) Intraoperative endoscopic endonasal view showing abdominal fat-graft as part of a multilayered reconstruction of a large clival defect, which lowers risk of pontine encephalocele. F, Fat-graft; FL, fascia lata autograft covering the entire bony and dural defect; NSF, nasoseptal flap.

CHAPTER 36  Complications of Endoscopic Endonasal Skull Base Surgery



NF

FP

• Fig. 36.5

  Intraoperative endoscopic endonasal view showing a necrotic flap in a patient who presented with meningitis but no cerebrospinal fluid leak. FP, Flap pedicle; NF, necrotic flap.

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Meningitis and young age increase this complication, whereas use of a fat graft as part of multilayer reconstruction (typically in between a deep allo- or autograft and the vascularized nasoseptal flap) lowered the risk by 91%. Another rare complication is nasoseptal flap necrosis (Fig. 36.5). Occurring in 1.2% of patients,30 it typically presents with signs of meningitis. Patients with prior nasal surgery are at higher risk, likely due to compromised vascularity of the flap pedicle or mucosa. Doppler sonography or ICG fluorescence endoscopy can be used to assess flap viability intraoperatively. Taking care to avoid narrowing the flap pedicle during harvest and protecting the pedicle during drilling and dissection are critical to avoid damage to the blood supply. A viable flap should enhance brightly on MRI. Failure to do so should lead to increased vigilance for necrosis and can be used to diagnose necrosis if the patient presents with meningismus or other signs of infection. Patients may also have a vaguely necrotic odor or halitosis. If symptomatic flap necrosis is suspected, MRI can confirm the diagnosis, and a lumbar puncture should be performed if there is any concern for superinfection. It is treated by endonasal exploration with debridement of the necrotic tissue and replacement with vascularized tissue whenever possible (inferior turbinate/lateral nasal wall flap is the first option). A lumbar drain can be placed, especially if there is evidence of increased intracranial pressure as a result of meningitis.

SURGICAL REWIND

My Worst Case (Video 36.1) A 39-year-old woman presented with florid acromegaly. Imaging showed an invasive adenoma with circumferential involvement of the right ICA (Knosp grade 4). Intraoperatively, the tumor was very fibrous and required sharp dissection and debridement. During the last portion of the surgery, an attempt at dissection of the ICA, which could not be visualized or accurately localized with Doppler sonography, resulted in torrential bleeding from the medial aspect of the cavernous ICA. Attempts at bipolar coagulation were unsuccessful. A cottonoid was placed over the bleeding site and compression held with a suction. Distal control with an aneurysm clip could be obtained at the paraclinoidal cavernous segment, but proximal control was unsuccessful due to tumor involvement, and neck compression did not slow the bleeding. A muscle patch was harvested from the rectus abdominal muscle while compression was once again held with a cottonoid. The muscle patch was placed at the site of bleeding and reinforced with multiple cottonoids. Mean arterial pressures were then increased as SSEPs began to decrease. The patient was taken immediately to the endovascular suite,

where the ICA was seen to be completely occluded with no evidence of contralateral cross-fill. Fortunately, deployment of a stent across the area of occlusion was adequate to reopen the artery. The patient was placed on aspirin and Plavix. Postoperative MRI showed a near-complete tumor removal and only minor, scattered watershed infarcts. The patient returned to the operating room more than a week later for removal of packing. Attempts at removal of the last cottonoid over the area of injury resulted in bleeding. This cottonoid was left in place but was covered with a vascularized nasoseptal flap to separate it from the nasal cavity. Repeat angiography showed that this resulted in a pseudoaneurysm that was treated with a flow diverter inside the previously deployed stent. Follow-up angiography showed resolution of the pseudoaneurysm. The patient was asymptomatic at this point and in biochemical remission. Later, she developed expected recurrence in the cavernous sinus, which was successfully treated with Gamma knife radiosurgery.

NEUROSURGICAL SELFIE MOMENT

References

Complications of endoscopic ESBS generally fall into three categories: neural injury, vascular injury, and failure of reconstruction. Avoidance of all three requires a complete understanding of the relevant anatomy and respect for the learning curve associated with these approaches. Careful case selection, guided by the principle of minimizing neurovascular manipulation and the concept of team surgery, provides for the safe application of the EEA to the skull base.

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skull base surgery? A prospective, randomized controlled trial. J Neurosurg, submitted for publication. 2017;October. 18. Scheller C, Wienke A, Tatagiba M, et al. Prophylactic nimodipine treatment for cochlear and facial nerve preservation after vestibular schwannoma surgery: a randomized multicenter Phase III trial. J Neurosurg. 2016;124(3):657–664. 19. Scheller K, Scheller C. Nimodipine promotes regeneration of peripheral facial nerve function after traumatic injury following maxillofacial surgery: an off-label pilot study. J Craniomaxillofac Surg. 2012;40(5):427–434. 20. Lindsay RW, Heaton JT, Edwards C, Smitson C, Hadlock TA. Nimodipine and acceleration of functional recovery of the facial nerve after crush injury. Arch Facial Plast Surg. 2010;12(1):49–52. 21. Bander ED, Singh H, Ogilvie CB, et al. Endoscopic endonasal versus transcranial approach to tuberculum sellae and planum sphenoidale meningiomas in a similar cohort of patients. J Neurosurg. 2018;128(1):40–44. 22. Clark AJ, Jahangiri A, Garcia RM, et al. Endoscopic surgery for tuberculum sellae meningiomas: a systematic review and meta-analysis. Neurosurg Rev. 2013;36(3):349–359. 23. Stefko ST, Snyderman C, Fernandez-Miranda J, et al. Visual outcomes after endoscopic endonasal approach for craniopharyngioma: the Pittsburgh experience. J Neurol Surg B. 2016;77(4):326–332. 24. Gardner PA, Tormenti MJ, Pant H, Fernandez-Miranda JC, Snyderman CH, Horowitz MB. Carotid artery injury during endoscopic endonasal skull base surgery: incidence and outcomes. Neurosurgery. 2013;73 (2 Suppl Operative):ons261–ons270. 25. Koutourousiou M, Gardner PA, Fernandez-Miranda JC, Tyler-Kabara EC, Wang EW, Snyderman CH. Endoscopic endonasal surgery for craniopharyngiomas: surgical outcome in 64 patients. J Neurosurg. 2013;1119(5):1194–1207. 26. Zanation AM, Carrau RL, Snyderman CH, et al. Nasoseptal flap reconstruction of high flow intraoperative cerebral spinal fluid leaks during endoscopic skull base surgery. Am J Rhinol Allergy. 2009; 23(5):518–521. 27. Harvey RJ, Parmar P, Sacks R, Zanation AM. Endoscopic skull base reconstruction of large dural defects: a systematic review of published evidence. Laryngoscope. 2012;122(2):452–459. 28. Fraser S, Gardner PA, Koutourousiou M, et al. Risk factors associated with postoperative cerebrospinal fluid leak after endoscopic endonasal skull base surgery. J Neurosurg. 2018;128(4):1066–1071. 29. Koutourousiou M, Vaz Guimaraes Filho F, Costacou T, et al. Pontine encephalocele and abnormalities of the posterior fossa following transclival endoscopic endonasal surgery. J Neurosurg. 2014; 121(2):359–366. 30. Chabot JD, Patel C, Hughes M, et al. Nasoseptal flap necrosis: a rare complication of endoscopic endonasal surgery. J Neurosurg. 2018;128(5):1463–1472.