<unk>  is a life-threatening complication of severe postpartum hemorrhage (PPH) that results in mild to severe maternal hypopituitarism.<unk>  is less prevalent in developed countries, but it is still one of the most common causes of hypopituitarism in underdeveloped and developing countries. During pregnancy, enlarged size of the pituitary gland and decreased blood supply due to any cause can result in ischemic necrosis of pituitary gland. Severe PPH, glandular hypertrophy and hyperplasia, smaller sella size, autoimmunity, and disseminated vascular coagulation (DIC) are thought to play an important role in the pathogenesis of<unk> . The most common causes of<unk>  include massive hemorrhage during parturition, vascular compression, and vascular occlusion.<unk>  needs to be differentiated from diseases causing hypopituitarism and other diseases like lymphocytic hypophysitis, pituitary apoplexy, hypothyroidism, addison's disease, empty sella syndrome, hypogonadotropic hypogonadism, simmond's disease, hypoprolactinemia, and menopause. Risk factors for<unk>  include pregnancy, severe/massive PPH, pituitary mass, pre-existing vascular diseases, smaller and rigid sella, traumatic delivery, multiple gestations, placental abnormalities, and type 1 diabetes. If left untreated,<unk>  can lead to panhypopituitarism and empty sella syndrome. Common complications of<unk>  include adrenal crisis, hypotension, hypothyroidism, and hypopituitarism. Prognosis is generally excellent, providing early diagnosis and management may result in complete reversal of symptoms. Diagnosis of<unk>  is made on clinical basis with a recent/remote history of traumatic delivery or delivery complicated by hypotension. The most common presentations include postpartum lactation failure, amenorrhea, loss of sexual hair, fatigue, anorexia, and weight loss. Clinical features depend on the severity of hypopituitarism that results from<unk> . Almost all the patients have growth hormone (GH), prolactin, and gonadotropin deficiency; and the majority of the patients have ACTH and TSH deficiency. Laboratory evaluation in patients with<unk>  gives a picture of partial or panhypopituitarism. Other laboratory findings include hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, anemia, pancytopenia, eosinophilia, hypoalbuminemia, low fasting plasma glucose, and decreased levels of anterior pituitary hormones (free thyroxine, estradiol, and cortisol levels). The most sensitive test is inadequate prolactin and gonadotropin response to stimulation. ECG findings associated with<unk>  include QT interval prolongation, type-1 Brugada-like ECG pattern (due to adrenal crisis), findings suggestive of cardiac tamponade (sinus tachycardia, low voltage QRS, and electrical alternans), and dilated cardiomyopathy. CT scan findings in case of acute<unk>  may show non-hemorrhagic pituitary gland enlargement, while chronic presentation may show an empty sella or decreased sella volume. Findings on MRI suggestive of<unk>  include decreased sella volume, empty sella, pituitary remnant tissue or CSF in the sella. The treatment of<unk>  involves appropriate hormone replacement therapy, which must be taken for the rest of the patient's life, results in significant improvement and reversal of not only the physical symptoms, but also the psychological symptoms.
Sheehan's syndrome
Addison's disease
Addison-gull syndrome
Addison-Gull syndrome
Zieve's syndrome
Klinefelter's syndrome
Kallman syndrome
Angelman syndrome