bubble_chart Overview

Hypopituitarism is also known as Sheehan's syndrome.

bubble_chart Pathogenesis

The condition may originate from intrinsic lesions (tumors, ischemia, necrosis, infarction, injury, and inflammation, degeneration), accounting for approximately 80%; or it may be secondary to CNS and hypothalamic disorders, accounting for 20%. The most common clinical manifestation is hypopituitarism caused by pituitary ischemia and necrosis due to postpartum metrorrhagia, shock, and DIC, known as Sheehan's syndrome.

Mechanism of postpartum metrorrhagia-induced hypopituitarism:

1. During pregnancy, the anterior pituitary is highly sensitive to ischemia and hypoxia. For instance, the physiological compensatory enlargement of the anterior pituitary increases from 500mg to 1000mg during pregnancy, particularly with pronounced hyperplasia and hypertrophy of PRL cells, which secrete more PRL (Rasmussen 1938, Goluboff 1969). This requires a substantial supply of blood and oxygen. Therefore, perinatal hemorrhage, hypovolemic shock, and DIC can easily trigger the condition (Kovacs 1969). For example, the incidence of grade I hemorrhage during childbirth is 8%, while severe hemorrhagic shock leads to the condition in 53% of cases. Postpartum metrorrhagia accounts for 65% of cases of hypopituitarism in women.

2. Approximately 80% of the blood supply comes from the superior hypophyseal artery and the portal plexus, while 10–20% originates from branches of the internal carotid artery. Thus, once cerebral blood perfusion is insufficient, ischemia and hypoxia begin at the level of the pituitary stalk and extend to the anterior pituitary. The longer the ischemia lasts, the more severe the pituitary necrosis and functional impairment become.

3. The anterior pituitary has a strong functional compensatory capacity. Based on the extent of tissue necrosis and functional impairment, it can be classified into: (1) Grade III: Pituitary tissue loss ≥95%, with severe clinical symptoms; (2) Grade II: Pituitary tissue loss ≥75%, with significant clinical symptoms; (3) Grade I: Pituitary tissue loss ≥60%, with mild clinical symptoms; (4) Pituitary tissue loss ≤50%, generally without obvious clinical symptoms.

4. The clinical manifestations of hypopituitarism vary widely, ranging from a single hormone deficiency (commonly gonadotropin and prolactin) to defects in two or multiple pituitary hormone systems. In Sheehan's syndrome, the order and frequency of pituitary hormone deficiencies are gonadotropin (FSH, LH) - GH - TSH - ACTH. PRL deficiency occurs simultaneously with gonadotropin deficiency and is unique to Sheehan's syndrome, rarely seen in tumors or other disease causes.

bubble_chart Clinical Manifestations

Postpartum hemorrhage is followed by extreme physical exhaustion, lactation failure, anemia, and infection within 2 to 5 weeks. Progressive sexual dysfunction and menopausal syndrome manifest as regression of sexual characteristics, hair loss, amenorrhea, atrophy of genitalia and breasts (Purnell 1964).

GH deficiency presents as hypoglycemia, TSH deficiency as myxedema, and ACTH deficiency as Addison's-like symptoms, including hypotension, hypothermia, bradycardia, susceptibility to infections, and shock, though sodium metabolism remains normal. β-MSH deficiency is particularly evident in the loss of pigmentation in the areola, axillary, and perineal regions.

bubble_chart Diagnosis

A history of postpartum bleeding and shock, along with symptoms of pituitary hormone deficiency, and measurements of HPO axis and adrenal axis hormones can assess the nature and progression of pituitary dysfunction.

bubble_chart Treatment Measures

Corresponding hormone replacement therapy and nutritional support therapy.