Extension of Acute Invasive Fungal Disease through Vidian Artery May Be Cause of Internal Carotid Artery Thrombosis
Background: Thrombosis of the internal carotid artery (ICA) is seen in rare cases of extensive acute invasive fungal sinusitis (AIFS) involving the skull base. We propose that direct propagation of disease and thrombus through the vidian artery may cause ICA thrombosis.
Objectives: To present endoscopic, radiographic and histopathological evidence of AIFS disease propagation through vidian artery causing ICA thrombosis
Study Design: Case series and systematic review of the literature.
Methods: A retrospective review of electronic charts of patients who underwent surgical debridement with the senior author for AIFS between 9/2010–9/2013 was performed. Patients with radiographic demonstration of ICA thrombosis were included. Endoscopic imaging, operative reports and histopathology reports were reviewed. A systematic review of the literature was also conducted.
Results: Of twelve cases of AIFS that were surgically treated, three were noted to have thrombus formation within the ICA. Cavernous sinus thrombosis (CST) was present in only one of these patients. At presentation, all three had fixed globes, two had sluggishly reactive pupils and one had fixed, dilated pupil. Direct orbital AIFS invasion was noted in two. CST with ipsilateral ophthalmoplegia and V1 and V2 numbness was noted in the patient who had fixed, dilated pupil; he had no direct orbital AIFS invasion. Two patients had complete ICA thrombus occlusion, and one partial.
Operative reports documented necrosis in the pterygopalatine fossa and thrombosis of terminal branches of the internal maxillary artery (IMA) in all three patients. Operative and photographic documentation of vidian artery thrombosis was also found in all three. The basisphenoid bone was necrosed along the vidian canal until the junction with the petrous ICA in all. In two patients, limited bony erosion of the carotid canal within the sphenoid sinus was found; ICA adventitia was not necrotic in either. In the patient with CST, the cavernous sinus was debrided. Relatively healthy bone was drilled off the ICA. The paraclival, parasellar and paraclinoid ICA segments were thrombosed, but the adventitia appeared viable. Vidian artery histopathology showed necrosis and hyphae.
Orbital exenteration was performed in only one patient. Two patients suffered from thromboembolic strokes. The patient with partial ICA occlusion had a transient middle cerebral artery stroke. One patient had a rapidly forming occlusive thrombus, resulting in multiple strokes, ultimately fatal.
The systematic review did not yield any previous reports of our hypothesis. The mechanism by which ICA thrombosis in AIFS occurs is not well described. Some reports ascribe it to result from CST.
Conclusions: We propose that direct extension of AIFS into the ICA may occur through the vidian artery. AIFS commonly involves the terminal branches of the IMA, and involvement of the vidian artery may occur early. Further direct extension of AIFS through the vidian artery and canal may propagate thrombosis into the ICA. The carotid canal bone and ICA adventitia was noted to be viable/non-necrotic in our series. Our series illustrates that ICA thrombosis occurs even in the absence of direct orbital invasion or CST, and may result from AIFS and thrombus extension through the vidian artery.