Compression of the necrotic intrasellar mass superiorly towards the optic nerves and optic chiasma causes visual symptoms in most (75 %) patients (Table 7.1) (Bills et al. 1993; Randeva et al. 1999; Ayuk et al. 2004; Sibal et al. 2004; Elsässer Imboden et al. 2005; Lubina et al. 2005; Nawar et al. 2008; Rajasekaran et al. 2011), including decreased visual acuity, visual field defects, especially bitemporal hemianopsia and also complete blindness and monoocular blindness. The visual signs tend to improve spontaneously in many patients, probably due to decrease in intrasellar pressure, when necrotic tissue absorption occurs after several days. However, early pituitary decompression will improve visual functions in most cases, including visual recovery in blind eyes (Bills et al. 1993; Randeva et al. 1999; Ayuk et al. 2004; Sibal et al. 2004; Elsässer Imboden et al. 2005; Lubina et al. 2005; Nawar et al. 2008; Rajasekaran et al. 2011; Turgut et al. 2010).

Both computerized tomography (CT) scan and magnetic resonance imaging (MRI) are performed in patients suspected to have pituitary tumour apoplexy, to define pituitary anatomical changes (adenoma size, invasiveness, chiasmal compression) and to establish the diagnosis (pituitary haemorrhage). CT scans indicate the presence of a pituitary tumour in most affected patients but have usually low sensitivity in detecting pituitary apoplexy at the acute phase (less than 2 days) and are diagnostic then in only 21–28 % of studied cases (Onesti et al. 1990; Ayuk et al. 2004; Sibal et al. 2004; Rajasekaran et al. 2011). MRI is the preferred imaging technique and can detect haemorrhage in a pituitary mass, thus confirming the diagnosis of pituitary apoplexy in 80–90 % of affected patients (Onesti et al. 1990; Randeva et al. 1999; Ayuk et al. 2004; Sibal et al. 2004; Lubina et al. 2005; Rajasekaran et al. 2011). Typically, in the acute phase (less than 2 days) pituitary haemorrhage is seen as hyperintensity on T1-weighted images (Fig. 7.1) and as hypointensity on T2-weighted images. Later, after 3 days, hyperintense signals are depicted on both T1- and T2-weighted images. Several weeks later, during the chronic phase, the digestion of blood and necrotic tissue will appear classically as a fluid level in the pituitary mass (Fig. 7.2).

Hypopituitarism is very common at the time of apoplexy presentation. Clinical hypopituitarism will occur only when 70–75 % of the anterior pituitary is destroyed, and complete pituitary failure requires more than 90 % loss of pituitary tissue. The extent and severity of pituitary hormone deficiency are poorly investigated in published series of patients presented with apoplexy. Moreover, as most patients with pituitary tumour apoplexy harbour macroadenomas, many of them would have preexisting pituitary insufficiency even before the acute apoplexy episode. This is reflected by the high rate (~50 %) of patients with clinical endocrine symptoms before the apoplexy, including hypogonadism, altered menstruation, impotence, cold intolerance, chronic fatigue and anaemia (Randeva et al. 1999; Ayuk et al. 2004). At presentation, most patients with apoplexy (about 80 %) have deficiency of one or more pituitary hormones (Randeva et al. 1999; Ayuk et al. 2004; Sibal et al. 2004). Hypogonadotrophic hypogonadism was reported in 50–79 % of patients, central hypothyroidism in 35–57 % and cortisol deficiency due to adrenocorticotropic hormone (ACTH) deficiency in 50–76 % of subjects presented with pituitary apoplexy (Table 7.2) (Randeva et al. 1999; Ayuk et al. 2004; Sibal et al. 2004; Lubina et al. 2005; Rajasekaran et al. 2011). Growth hormone deficiency with low IGF-1 levels was also noticed in a subset of patients (Elsässer Imboden et al. 2005). Hyperprolactinemia is noted in 30–40 % of studied patients (Ayuk et al. 2004; Sibal et al. 2004) and hypoprolactinemia in 25–40 % (Ayuk et al. 2004; Sibal et al. 2004). Hyponatremia is reported in up to 44 % of the patients in some reports (Randeva et al. 1999; Elsässer Imboden et al. 2005; Rajasekaran et al. 2011), but in other series this electrolyte disturbance is less common (Sibal et al. 2004; Lubina et al. 2005). Hyponatremia in these patients results from either severe hypocortisolism or inappropriate antidiuretic hormone (ADH) secretion (Ebner et al. 2010). On the contrary, diabetes insipidus is very rare despite frequent and significant suprasellar extension in many cases.