Abstract Introduction Pituitary apoplexy (PA) is an acute, potentially fatal clinical syndrome resulting from hemorrhage and/or infarction of the pituitary gland, which may require emergency surgery in some cases.The most common clinical complaint is severe headache, often accompanied by nausea, vomiting, visual disturbances, and altered consciousness. Life-threatening hypotension may also occur due to involvement of the anterior pituitary gland. Non-functioning pituitary adenomas (NFPA), specifically macroadenomas, appear to have the higher risk of apoplexy. We present a case of pituitary apoplexy presenting with nausea and vomiting following severe headache. Clinical Case A 77-year-old male patient presented to an external center with complaints of severe headache, nausea, vomiting, hypotension, and decreased vision for 15 days and was referred to us with a preliminary diagnosis of panhypopituitarism. In his medical history, it was learned that he had been followed up for 13 years due to non-functioning pituitary macroadenoma and that he was examined for a hypertensive attack one week ago and started on olmesartan + hydrochlorothiazide combination therapy. Laboratory tests were as in Table 1. Prednisolone 4*20 mg/day was started due to secondary adrenal insufficiency. Contrast-enhanced pituitary MRI revealed a 14x17x20 mm, hemorrhagic, non-enhancing macroadenoma mass that expanded the sella, extended into the bilateral cavernous sinuses and suprasellar cisterns (Knosp grade I), and compressed the optic chiasm. This was interpreted as apoplexy secondary to hemorrhage (Figure 1). Visual field evaluation revealed bitemporal hemianopsia and optic disc effacement on the left side. Since these changes were evaluated as signs of chronic compression and the patient benefited from steroid treatment, emergency surgical intervention was not considered by the neurosurgeon. Due to the development of central hypothyroidism during follow-up, levothyroxine sodium 1*25 mcg was added to the treatment and the patient was discharged with prednisolone 8 mg/day by decreasing the steroid treatment. Conclusion No large case series have been reported on the development of PA in the elderly. In this patient group, the frequent presence of comorbidities such as hypertension or diabetes, as in our case, increases the risk of PA. PA development is more common in non-functioning macroadenomas than in microadenomas. An ideal treatment approach for pituitary apoplexy has not been established. While urgent decompression may be necessary in patients with progressive visual field defects and deteriorating consciousness, conservative treatment is also an option in selected patients. It is important to note that the degree of symptoms at presentation and the clinical course of PA vary considerably among patients.Figure 1:Contrast-enhanced pituitary MRIA 14x17x20 mm, hemorrhagic, non-enhancing macroadenoma mass that expanded the sella, extended into the bilateral cavernous sinuses and suprasellar cisterns (Knosp grade I), and compressed the optic chiasm Table 1:Laboratory workup*ACTH:Adrenocorticotropic hormone, TSH: Thyroid Stimulating Hormone, FSH:Follicle stimulating hormone, LH: Luteinizing hormone, IGF-1: Insulin-like growth factor-1
Benli et al. (Thu,) studied this question.