### Patient Information
A 45-year-old man with no significant past medical history presented with persistent headaches and visual field deficits. Magnetic resonance imaging revealed a large pituitary macroadenoma measuring approximately 40 mm in maximum diameter, causing mild suprasellar extension and compression of the optic chiasm. Endocrinological evaluation showed nonfunctioning tumor characteristics. The patient was scheduled for transsphenoidal pituitary adenoma resection.
### Diagnosis
The patient underwent an uneventful standard endoscopic transsphenoidal resection of the pituitary macroadenoma. Intraoperative cerebrospinal fluid (CSF) leakage was noted and repaired. On postoperative day 7, the patient developed sudden right-sided hemiparesis and decreased level of consciousness. Neurologic examination revealed left middle cerebral artery territory deficits. Urgent neuroimaging with CT scan identified postoperative sellar hematoma and associated subarachnoid hemorrhage (SAH). Digital subtraction angiography (DSA) demonstrated severe multifocal arterial vasospasm predominantly involving the anterior cerebral circulation.
The diagnosis of symptomatic arterial vasospasm following pituitary surgery was established based on clinical presentation, imaging evidence of vasospasm, and temporal relation to surgery and postoperative hemorrhage.
### Differential Diagnosis
Other possible causes for the patient’s neurological deterioration were considered and ruled out:
– **Ischemic stroke due to embolic or thrombotic event:** No evidence of emboli or arterial occlusion unrelated to vasospasm on angiography.
– **Postoperative hemorrhagic complications without vasospasm:** Although hemorrhage was present, vasospasm correlated temporally with neurological symptoms.
– **Pituitary apoplexy:** The surgery excluded this preoperatively; clinical deterioration occurred postoperatively.
– **Electrolyte disturbances or metabolic encephalopathy:** Laboratory tests were unremarkable.
### Treatment and Management
The patient was managed in the neurointensive care unit with close neurological monitoring. Treatment was guided by protocols for aneurysmal subarachnoid hemorrhage-induced vasospasm:
– **Triple-H therapy:** Induced hypertension, hypervolemia, and hemodilution were initiated to augment cerebral perfusion.
– **Pharmacological therapy:** Nimodipine, a calcium channel blocker with neuroprotective effects on cerebral vessels, was administered orally.
– **Endovascular intervention:** Given the severity and multifocal nature of vasospasm, balloon angioplasty was performed on accessible arterial segments to mechanically dilate vasospastic vessels.
– **Supportive care:** Ventilatory support and fluid management were optimized. Serial imaging and transcranial Doppler assessments monitored vasospasm progression.
### Outcome and Prognosis
Despite aggressive intervention, the patient suffered significant ischemic injury resulting in persistent left hemiparesis and cognitive impairment. After 4 weeks in hospital rehabilitation, some motor function improvement was noted. At 3-month follow-up, neurological deficits remained but the patient was oriented and able to perform basic activities of daily living with assistance.
Retrospectively, this case aligns with data from our systematic review of 41 patients (including our case) with symptomatic arterial vasospasm post-pituitary surgery. The mean onset was approximately day 7 postoperatively, and the anterior circulation was predominantly affected. Although treatment approaches varied, outcomes were generally poor, with 22.5% mortality and 32.5% having residual deficits. Only 45% were discharged without neurological sequelae.
### Discussion
Symptomatic arterial vasospasm after pituitary adenoma surgery is an uncommon but devastating complication. Our systematic review revealed that several risk factors increase the likelihood of vasospasm, including intraoperative CSF leakage (84% cases), postoperative sellar hematoma, or subarachnoid hemorrhage (94%). These factors presumably contribute to blood breakdown products irritating cerebral arteries, triggering vasospasm akin to aneurysmal SAH mechanisms.
Clinicians should maintain a high index of suspicion when neurological deterioration occurs in the late postoperative period (around seven days). Early diagnosis utilizing vascular imaging and close neurological monitoring is critical.
Management parallels treatment of vasospasm following aneurysmal SAH, including triple-H therapy, nimodipine, and endovascular angioplasty. However, the evidence base is limited due to rarity, and individualized care is warranted.
Our review underscores the need for prevention efforts — minimizing intraoperative CSF leakage, meticulous hemostasis to reduce postoperative hemorrhage, and prompt management of any bleeding.
This case also highlights gaps in knowledge regarding standardized guidelines for vasospasm in this context, emphasizing the importance of multidisciplinary care and further research.
### References
Doat-Sarfati V, Lefevre E, Chiaroni PM, Shotar E, Abdennour L, Degos V, Jacquens A. Severe symptomatic arterial vasospasm following pituitary surgery: a rare case and systematic review of the literature. Pituitary. 2025 Oct 18;28(6):115. doi: 10.1007/s11102-025-01590-5. PMID: 41109912.
Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Statement for Healthcare Professionals from a Special Writing Group of the American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711-1737. doi:10.1161/STR.0b013e3182587839
### Table 1: Summary of Literature Review Findings
| Parameter | Value/Percentage |
|———————————|——————————-|
| Number of patients | 41 |
| Mean tumor size (mm) | 39 |
| Tumor type | Mostly macroadenomas |
| Surgical approach | 80% transsphenoidal |
| Intraoperative CSF leak | 84% |
| Postoperative sellar hematoma/SAH | 94% |
| Mean onset of vasospasm (days) | 7.3 |
| Affected vessels | Anterior circulation predominance; often multiple vessels |
| Treatment modalities | Triple-H 68%, Nimodipine 46%, Angioplasty 44% |
| Mortality | 22.5% |
| Residual deficits | 32.5% |
| Discharged without sequelae | 45% |
