Sheehan (1937) reported that pituitary ischemia and necrosis associated with obstetrical blood loss could result in hypopituitarism. With modern methods of hemorrhagic shock treatment, Sheehan syndrome is now seldom encountered (Feinberg, 2005; Pappachan, 2015; Robalo, 2012). Afected women may have persistent hypotension, tachycardia, hypoglycemia, and lactation failure. Because deficiencies of some or all pituitary-responsive hormones may develop after the initial insult, Sheehan syndrome can be heterogenous and may not be identified for years (Tessnow, 2010). In one cohort study of 60 women from Costa Rica with Sheehan syndrome, the average time to diagnosis was 13 years (Gei-Guardia, 2011). Because adrenal insuiciency is the most life-threatening complication, adrenal function should be immediately assessed in any woman suspected of having Sheehan syndrome. Mter glucocorticoid replacement, subsequent analyses and replacement of thyroid, gonadal, and growth hormones is considered.
This rare autoimmune pituitary disorder is characterized by massive iniltration by lymphocytes and plasma cells with parenchymal destruction of the gland. vIany cases are temporally linked to pregnancy (Foyouzi, 2011; Honegger, 2015; Melmed, 2015). here are varying degrees of hypopituitarism or symptoms of mass efect, including headaches and visual ield defects. A sellar mass is seen with CT or MR imaging. A mass accompanied by a modestly elevated serum prolactin level-usually < 100 pgl mL-suggests lymphocytic hypophysitis. In contrast, levels >200 pg/mL are encountered with a prolactinoma. he etiology is unknown, but nearly 30 percent have a history of coexisting autoimmune diseases including Hashimoto thyroiditis, Addison disease, type 1 diabetes, or pernicious anemia. Treatment is with glucocorticoids and pituitary hormone replacement. he disease may be self-limited, and a careful withdrawal of hormone replacement is attempted after inflammation subsides (Foyouzi, 2011; Melmed, 2015).
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