8144 Hypertension in Sheehan Syndrome: A Diagnostic Challenge

Abstract Disclosure: E. Ahsan: None. F.F. Foo: None. C. Lesniak: None. M. Akula: None. K. Hu: None. R. Ong: None. K. Chalasani: None. J. Cheng: None. S. Holland: None. Introduction: Postpartum pituitary necrosis, commonly known as Sheehan syndrome (SS), is the term used to describe the necrosis of anterior pituitary gland cells that occurs after significant postpartum bleeding, hypovolemia, and shock. This typically occurs after delivery, during which the mother suffers significant blood loss. The pituitary gland fails to produce hormones due to this blood loss. Depending on the degree of tissue damage, SS can have an acute or chronic course, and patients may present with a wide range of clinical symptoms at diagnosis. Acute SS is associated with postpartum pituitary infarction, which can result in hypotension, shock, hypoglycemia, hyponatremia, headache, vision disturbances, unconsciousness, and an inability to lactate. We present a rare case of SS where the patient experienced hypertension instead of classic hypotension due to postpartum preeclampsia. Clinical Case: A 40-year-old female with no significant medical history presented to the hospital for scheduled induction of labor for polyhydramnios and underwent vacuum-assisted vaginal delivery and postpartum hysterectomy due to severe postpartum hemorrhage secondary to DIC. The postpartum course was also complicated by preeclampsia with severe features. Patients developed features like excessive fatigue, hypoglycemia, hyponatremia, hypothyroidism, polyuria, and failure of lactation, which were consistent with panhypopituitarism secondary to Sheehan syndrome. However, the patient was hypertensive to 145/91 before steroids were given. Labs were significant for serum sodium 116 mmol/L (135-145 mmol/L), FSH <0.7 mIU/mL (Follicular Phase: 2.5-10.2, Mid-cycle Peak: 3.1-17.7, Luteal Phase: 1.5-9.1, Postmenopausal: 23.0-116.3), LH <0.2 mIU/m (Follicular Phase: 1.9-12.5, Mid-Cycle Peak: 8.7-76.3, Luteal Phase: 0.5-16.9, Postmenopausal: 10.0-54.7), Prolactin: 2.4 ng/mL (Non-pregnant: 3.0-30.0, Pregnant: 10.0-209.0, Postmenopausal: 2.0-20.0), PM Cortisol on admission: 1.10 ug/dL (3.44-16.76 ug/dL), plasma ACTH 7 pg/mL( 6 - 50 pg/mL), TSH 0.430 uIU/mL (0.550 - 4.780 uIU/mL), FT4 0.59 ng/dL - 1.76 ng/dL). MRI of the brain pituitary showed- A 1.5 cm region of hypoenhancement and an additional 2 mm focus of hypoenhancement in the sella, findings represent evolving pituitary necrosis. The patient received 24 units of blood transfusion and hormone replacement therapy, followed by outpatient endocrinology follow-up. Clinical lessons: Although considerable blood loss causes hypotension in patients with SS, additional postpartum medical issues can sometimes result in atypical presentations. In our patient, postpartum preeclampsia caused hypertension. Identifying the atypical symptoms of SS is just as vital as identifying its typical features to prevent potentially fatal consequences. Presentation: 6/2/2024