Many patients with pituitary apoplexy will have pre-existing pituitary insufficiency due to the presence of pituitary macroadenoma and resultant pressure effect (Arafah et al. 2000). Approximately half of patients with pituitary macroadenoma have partial hypopituitarism (Dekkers et al. 2007; Karavitaki et al. 2007). While this is often undiagnosed, patients presenting with apoplexy commonly report long-standing symptoms of pituitary insufficiency on questioning (Bills et al. 1993).

Pituitary apoplexy results in extreme elevation of intrasellar pressure due to the rapid increase in pituitary contents when haemorrhagic necrosis occurs (Zayour et al. 2004). High intrasellar pressure reduces blood flow to the anterior pituitary (Kruse et al. 1992; Arafah et al. 2000). While this may reversibly reduce anterior pituitary hormone secretion, ischaemia and cell necrosis occur leading to irreversible pituitary damage. The potential reversibility of pituitary dysfunction likely depends on the degree of pituitary necrosis (Arafah 1986). Zayour and colleagues (2004) measured intrasellar pressure and prolactin in 13 patients undergoing pituitary surgery within a week of pituitary apoplexy. Pituitary pressure was inversely related to prolactin, high or normal prolactin (in non-prolactin-secreting adenomas) predicted recovery of anterior pituitary function. The six patients with prolactin level <2.5 mcg/L did not recover endocrine function after urgent surgery, whereas the seven patients with levels >3.5 mcg/L had at least partial preservation of pituitary function.

Clinical features of anterior pituitary hormone excess are detailed in Table 12.3. Biochemical investigation for acromegaly and Cushing’s disease will be guided by clinical suspicion and may be missed by routinely performed investigations. Therefore it is essential that features of these conditions are specifically sought in the clinical assessment. In some cases a patient with clinical features of hormone excess will have deficiency on endocrine testing due to resolution associated with tumour infarction; this is particularly relevant to Cushing’s syndrome where the presence of clinical features of cortisol excess does not exclude adrenal insufficiency following apoplexy (Alarifi et al. 2005; Fraser et al. 2009).

Clinical features of anterior pituitary hormone deficiency are detailed in Table 12.3. As clinical features of pituitary hormone deficiency are often vague and non-specific biochemical testing is required in all cases of apoplexy. The acutely life-threatening manifestation of pituitary hormone deficiency is hypoadrenal crisis secondary to ACTH deficiency. The key clinical feature of an adrenal crisis is shock; additional features include nausea, vomiting, abdominal pain, lethargy dehydration, confusion and coma. While severe thyroid deficiency (myxoedema coma) can be life threatening, this is rare, particularly unlikely acutely in the context of apoplexy (in part due to the long half-life of endogenous T4), and has not been reported.