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A 37-year-old woman with postpartum hemorrhage was transferred by ambulance to our hospital for emergency treatment. On arrival massive hemorrhage continued, and she developed tachycardia (130 beats/min), hypotension (60/30 mm Hg) and tachypnea (50 /min). She underwent blood transfusion and emergent hysterectomy, and her vital signs became stable. The estimated total bleeding volume was approximately 8 L, and pathological examination revealed placenta accreta. Five days later, she had disturbance of consciousness. Blood examination revealed hyponatremia. Despite attempting to correct hyponatremia, her serum sodium level decreased to be 112 mEq/L. The examination of serum hormone levels revealed reduced adrenocorticotropic hormone (2.1 pg/ml, normal range: 7.2 to 63.3 pg/ml), thyroid stimulating hormone (0.2 μIU/ml, normal range: 0.5-5 μIU/ml), prolactin (1.4 ng/ml, normal range: > 20 ng/ml in postpartum), luteinizing hormone (0.1 mIU/ml, normal range: 3–9 mIU/ml), and follicle stimulating hormone (0.1 mIU/ml, normal range: 4–9 mIU/ml). She underwent a brain magnetic resonance imaging (MRI) scan for evaluating the pituitary gland (Fig. 1). What is the patient's diagnosis?
Fig. 1Sagittal T2-weighted MRI (A) revealed an enlarged pituitary gland with heterogeneously hyperintense signal (arrow), and sagittal gadolinium-enhanced T1-weighted MRI (B) revealed the pituitary gland with rim enhancement and no internal enhancement (arrow).
The MRI findings suggested acute pituitary infarct. She was diagnosed with acute Sheehan's syndrome by considering the results of stimulation tests, and she has received hormone replacement treatment (L-thyroxine, hydrocortisone acetate, and estradiol). MRI performed 6 months postpartum revealed post-infarction shrinkage of the pituitary gland.
Sheehan's syndrome has decreased owing to recent advances in obstetrical care, but which is one of the most important causes of hypopituitarism. The mechanism of Sheehan's syndrome is considered postpartum pituitary infarction and necrosis result from severe hypotension and vasospasm of the hypophysial arteries [
The clinical differential diagnosis of acute Sheehan's syndrome is lymphocytic hypophysitis frequently seen in postpartum period. In acute Sheehan's syndrome gadolinium-enhanced MRI reveals a non-enhancing area in the pituitary gland [
]. On the other hand, in the most cases with lymphocytic hypophysitis enlarged pituitary glands and stalks with homogenous enhancement are shown on contrast-enhanced MRI. Thus, pituitary MRI with contrast enhancement can help in differentiation of these diseases.
Hyponatremia is the most common electrolyte imbalance in Sheehan's syndrome. Well-accepted mechanisms of hyponatremia are decreased free-water clearance by hypothyroidism and glucocorticoid deficiency and water retention from the increased secretion of antidiuretic hormone associated with glucocorticoid deficiency. Replacement therapy with corticosteroid and thyroid hormones should be performed for lifelong. But estrogen and growth hormone replacement therapy can be considered individually [
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