J Neurol Surg B Skull Base 2016; 77 - A076
DOI: 10.1055/s-0036-1579864

Nasoseptal Flap Necrosis: Incidence, Clinical Description, and Outcomes

Joseph D. Chabot 1, Chirag Patel 2, Nathan Zwagerman 1, Georgios Zenonos 1, Eric Wang 1, Carl Snyderman 1, Paul Gardner 1, Juan C. Fernandez-Miranda 1
  • 1UPMC, Pittsburgh, Pennsylvania, United States
  • 2Loyola University Medical Center, Maywood, Illinois, United States

Introduction: The vascularized nasoseptal flap (NSF) has become a mainstay for skull base reconstruction after endoscopic endonasal approaches (EEA) to the skull base. Spontaneous necrosis of the nasoseptal flap (NNSF), though rarely reported, has the potential for devastating infection requiring prompt intervention. We reviewed our institution’s experience with the NSF to describe the incidence, clinical presentation, risk factors, consequences and management of this complication.

Methods: The medical records of 1285 consecutive patients undergoing EEA at the University of Pittsburgh Medical Center between January 2010 and December 2014 were retrospectively reviewed. Patients were included for analysis if they underwent endoscopic re-exploration for post-operative meningitis or suspected cerebrospinal fluid (CSF) leak. Patients were excluded if they returned to the OR (RTOR) for staged surgery or hematoma. Two neurosurgeons and a neuroradiologist, blind to each other’s results, assessed the MRI characteristics of the included patients.

Results: Of 601 patients primarily repaired using a NSF, 51 returned to the operating room for repair of suspected CSF fistula within 30 days of EEA. Forty (6.7%) patients had confirmed CSF leaks and well vascularized flaps on re-exploration. Seven patients (1.2%) were found to have spontaneous necrosis of their NSF based on dark discoloration and lack of bleeding when incised. An eighth patient had iatrogenic flap death after embolization for epistaxis. Only three patients with NNSF had a CSF leak. The two groups were then compared with assess for risk factors and clinical/radiological characteristics.

MRI analysis revealed that 7 (87.5%) of the NNSF showed no contrast enhancement, while all but one of the vascularized NSF’s enhanced homogenously (p < .0001; kappa score = .85, p < .0001). All 8 patients with NNSF had clinical and laboratory evidence indicative of meningitis, compared with 9 (22.5%) of patients with CSF leak with intact NSF (p = .001). Four patients with necrotic flaps developed epidural empyema, compared with 2 in the non-necrotic group (p = .018). Patients who had a prior endoscopic endonasal approach were more likely to have a necrotic nasoseptal flap (p = .039) especially if this surgery was at an outside hospital (p = .008) or if they had 2 or more prior endonasal surgeries (p = .086). However, there was no association with re-use of NSF and necrosis. After debridement and removal of necrotic flaps, and repair with inferior turbinate flaps (5) and/or fascia lata (5), all patients were treated successfully with antibiotic therapy. Outcomes were similar with respect to length of stay and post-operative disability.

Conclusion: Patients presenting with signs/symptoms of meningitis after EEA even in the absence of CSF leak should be evaluated for NNSF. Lack of enhancement on MRI can confirm this diagnosis. Prior intranasal surgery increases the risk of this condition, although re-using a previously elevated flap does not. These patients (meningitis AND a non-enhancing flap) should undergo prompt exploration and aggressive debridement with salvage skull base reconstruction and long-term antibiotic therapy.