Complications of venous sinus stenting in idiopathic intracranial hypertension

Venous sinus stenting (VSS) has emerged as an effective treatment for selected patients with idiopathic intracranial hypertension (IIH) who fail maximal medical therapy. With its expanding adoption, recognition of rare but catastrophic complications is essential. We present the case of a 21‐year‐old female with IIH who failed medical treatment and was found to have bilateral stenosis at transverse‐sigmoid sinus junction with manometry showing 12 mmHg and 13 mmHg pressure gradients on the left and right side respectively. A stent was deployed in the right transverse‐sigmoid sinus with successful reduction of pressure gradient to 4 mmHg. Intraoperative EEG and somatosensory evoked potentials (SSEPs) remained normal throughout the procedure. Following a technically successful procedure, upon awakening from general anesthesia, the patient was unresponsive, with non reactive pinpoint pupils, absent vestibulo‐ocular reflexes, and extensor posturing in all four extremities. Emergent flat panel CT didn’t reveal acute intracranial hemorrhage, and neither did a helical head CT, but acute cerebellar tonsillar herniation and basal cistern effacement with mild supratentorial hydrocephalus was noted. CTA confirmed stent patency, but showed hypoenhancement of vertebrobasilar system relative to anterior circulation, suggesting regional impairment in cerebral perfusion pressure (CPP). Repeat neurophysiological monitoring following minimal brain activity on clinical exam, 15‐30 min after the previous recording, revealed profoundly suppressed EEG and SSEP's. IV Mannitol was administered and repeat digital subtraction angiography (DSA) confirmed stent patency without in‐stent stenosis and no increased ICP or pressure gradient across the stent. After the second DSA, the patient started following simple commands, and was extubated. Her exam was remarkable for bilateral CN VI palsy with direction beating horizontal and vertical nystagmus, subtle right facial droop, as well as right sided drift, bilateral Hoffman's and sustained ankle clonus. Subsequent CT revealed improved patency of basal cisterns and re‐expansion of temporal horns, but showed new hyperattenuations in the interpeduncular cistern, tentorial leaflets, and falx concerning for subdural hemorrhage (SDH), as well as sulcal hyperdensities concerning for subarachnoid hemorrhage (SAH). MRI showed no acute ischemia. Within the next day, despite the new hemorrhagic findings, symptoms had largely resolved, except for persistent midline ataxia. This case highlights a rare but serious constellation of complications following VSS for IIH, including acute spontaneous cerebellar tonsillar herniation, transient brainstem dysfunction, and subsequent SDH and SAH. Rapid hemodynamic shifts and altered intracranial venous compliance in patients with longstanding venous hypertension may precipitate hydrocephalus and tonsillar herniation. Elevated posterior fossa pressure can in turn compromise vertebrobasilar CPP, providing a plausible explanation for the transient neurological decline. Potential mechanisms include acute intracranial hypotension, or transient venous outflow obstruction of the vein of Labbé at the stented site, either from the stent construct itself or acute thrombosis. Intracranial hypotension after pressure reduction might ultimately have caused tonsillar herniation with consequent tearing of fragile bridging veins resulting in SAH and SDH that appeared on subsequent imaging. This case underscores the importance of vigilant multidisciplinary post‐stenting monitoring. Timely identification and intervention is the difference between irreversible brain injury and full recovery as in this case.