Intra-sellar aneurysms are a rare, but important consideration when evaluating pituitary masses. Identification of aneurysms is critical to appropriate treatment and avoiding perilous consequences. These vascular aneurysms can result in severe endocrine dysfunction due to mass effect, stripping of the vascular supply to the pituitary, or hemorrhage. Here we describe a novel case of spontaneous myxedema coma and pituitary apoplexy secondary to a large internal carotid artery aneurysm.
IntroductionAneurysms with components extending into the sella turcica a rare, but important consideration when evaluating sellar and parasellar masses. Mistaking a calcified and/or partially thrombosed aneurysm for a tumor can have catastrophic intra-operative consequences. Severe endocrine dysfunction is uncommon, but may result from mass effect, vascular steal phenomenon, or hemorrhage. Here we describe a rare case of spontaneous myxedema coma and pituitary apoplexy secondary to a large internal carotid artery aneurysm.
Case reportA 78-year-old woman presented with symptoms of sudden polyuria, headache, and vomiting for 24 h. Bradycardia (52 bpm), hypothermia (33.9°C) and hyponatremia (sodium 117 mmol/L) were present on initial assessment. She reported a history of a sellar mass initially diagnosed 24 years earlier. She had refused surgery and opted to monitor the lesion with serial imaging. Per the family and patient, her hormonal blood work was normal and the mass had been stable, not requiring treatment. She had a stable left homonymous hemianopsia for many years. A large mixed density sellar mass was confirmed on initial CT imaging and she was referred for urgent neurosurgical evaluation. Prior to evaluation, she became disoriented and hypotensive requiring hemodynamic support and intubation for airway protection. Exam was notable for Glascow coma scale of 9/15 (E3, V1, M5), minimal reactive pupils bilaterally, and delayed tendon reflexes at the biceps; no significant cranial nerve, motor or sensory deficits were identified. Formal visual fields were not testable. Her skin and mucosa were normal with minimal peripheral edema. She was empirically treated for myxedema coma and adrenal crisis due to presumed pituitary apoplexy. Intravenous levothyroxine (T4), liothyronine (T3), and hydrocortisone were initiated. Central hypothyroidism and central adrenal insufficiency were later confirmed with a low free thyroxine (0.4 ng/dL), low total T3 (76 ng/dL), low cortisol (0.7 μg/dL), inappropriately normal TSH (3.57 mIU/L) and normal ACTH (16.5 pg/mL), respectively. Prolactin was mildly elevated (56.2 ng/mL). MRI (Fig. 1) revealed a 5 × 3.2 cm heterogeneous mass centered in the sella turcica extending into the left cavernous sinus with lack of flow void in the petrous and distal cavernous portions of the left internal carotid artery. The optic chiasm was poorly visualized due to significant displacement by the mass. The differential diagnosis included hemorrhage within a pituitary macroadenoma, other tumors including osteosarcoma, osteo...