Reconstruction of Clival Resorption with Pontine Pneumatosis Secondary to Cocaine-Induced Skull Base Defect

Introduction: Intranasal cocaine use can result in various degrees of destructive craniofacial lesions. Direct irritation and local vasoconstriction commonly affect nasal mucosa without intracranial extension. Heavy cocaine usage resulting in destructive skull base lesions affecting the intracranial compartment has been reported. We describe the surgical management of complete clival resorption and associated pontine pneumatosis secondary to prolonged cocaine use.

Case Presentation: A 41-year-old man presented with mild dysarthria and ataxic gait; there was no clinical evidence of cerebrospinal fluid (CSF) leak. The patient reported cocaine use over the last 20 years. Computed tomography (CT) of the head along with CT angiography showed complete clival destruction, air in the pons and filling defects in the distal basilar artery (Fig. 1A, B). Magnetic resonance imaging (MRI) of the brain showed restriction on diffusion weighted imaging (DWI) sequences and partial enhancement with edema on T1-weighted with contrast and T2-weighted sequences (Fig. 1C, D). Nasal endoscopy revealed a large perforation of the nasal septum, a missing left inferior turbinate, and crusting with surrounding mucous overlying the clival defect in the nasopharynx (Fig. 2A). Surgical repair of the defect was planned via a combined open and endoscopic approach and reconstruction using a pericranial flap. Anatomical constraints precluded a nasoseptal flap as a viable option. Postoperatively the patient had transient right hemi-body weakness that resolved spontaneously. Tissue cultures were equivocal and only grew normal flora. He was nonetheless started on a six-week course of wide-spectrum antibiotic therapy. The patient consented to anonymous use of this clinical information for purposes of education and publication.

Surgical Technique: Surgery was performed in the supine position with the head fixed in a clamp. The length of the required pericranial flap was determined preoperatively using preoperative imaging (Fig. 3A, B). A bicoronal skin incision was done extending more posteriorly than usual to harvest a large enough graft. Next, we proceeded with a full house left functional endoscopic sinus surgery. This provided access to the left half of the anterior skull base. The clival defect (1 × 1 cm. was explored and prepared to receive the pericranial flap. Next, we harvested a unilateral pericranial flap and passed it into the left nasal cavity by drilling a bony window in the glabella. Under endoscopic guidance, the left pericranial flap was then laid along the left anterior skull base, lateral to the left middle turbinate, all the way to the clival defect at its distal tip. The clival defect was repaired in a multilayered fashion. Two layers of fascia lata were placed, one at a time, onto the clival defect as an onlay followed by the left pericranial flap. Valsalva maneuver revealed that the left pericranial flap provided a seal with no clinical evidence of CSF leak (Fig. 2B). At 1-year follow-up, an MRI showed reduced inflammation (Fig. 4A, B).

Conclusion: Combined endoscopic–open clival reconstruction is a feasible option in cases where there is complete clival destruction secondary to substance use.

Publication History

Article published online:
05 February 2024