Category: Adrenal Disorders

Type: e-Poster

Monitor: 8

8 - A CASE OF GESTATIONAL SECONDARY ADRENAL INSUFFICIENCY COMPLICATING SEVERE PRE-ECLAMPSIA

Thursday, Apr 25
11:00 AM – 11:30 AM

Objective : We describe a pregnant patient with severe pre-eclampsia and electrolyte derangements who was found to have adrenal insufficiency (AI) after betamethasone.


Methods : n/a


Results : A healthy 22-year old G1P0 woman at 25 weeks gestation presented with nausea, vomiting, and hypertension, found to have severe pre-eclampsia and intrauterine growth restriction. Anti-hypertensives and 12mg intramuscular betamethasone (IMB) were given. Baseline sodium and potassium were normal. She received a second IMB upon transfer to our facility on hospital day 1 (HD1). Her blood pressure stabilized with nifedipine. She had worsening peripheral edema, ascites, hyponatremia (nadir 116) and hyperkalemia (peak 5.4). There was no hypotension, orthostasis, or skin hyperpigmentation. On HD10, AM cortisol was 1.7mcg/dL (6.7-22.6) and ACTH 8.8 pg/dL (7.2-63.3). After cosyntropin stimulation, cortisol was 1.7 mcg/dL. Aldosterone was 16.4 ng/dL (0-30). Renin was 3.9 ng/ml/hr (0.2-5.4). Oral hydrocortisone (HC) 20mg in the morning and 10mg in the afternoon was initiated. Her electrolyte derangements persisted, and progressive anasarca developed. High dose IV furosemide led to improvement in electrolytes and volume status. On HD12, IV HC 25mg every 8 hours was started due to concern for malabsorption from anasarca, as well as the patient’s tenuous state.  She had a decline in renal function, nephrotic range proteinuria and HELLP. On HD22, fetal intraventricular hemorrhage prompted cesarean section. The patient received two additional IMB on HD21-22.  Post-partum, BP, creatinine, and volume status improved. She transitioned to oral HC 20mg qam morning and 10mg qpm.  At one month follow-up, cosyntropin stimulation testing showed cortisol of 4.6, 6.7 and 7.7 at 0, 30 and 60 minutes. HC was reduced to 10mg twice a day.


Discussion : We report a case of gestational secondary AI in an otherwise healthy young woman who suffered a complicated pre- and postnatal course. Betamethasone is a potent glucocorticoid with a long biologic half-life given to prevent neonatal respiratory distress syndrome, intraventricular hemorrhage and perinatal death. Betamethasone 12mg is equivalent to hydrocortisone 300mg. When given in successive doses, IMB has been shown to cause secondary AI which can persist for several weeks according to case reports. If untreated, secondary AI can increase maternal and fetal morbidity and mortality. Our patient’s postpartum stimulation testing demonstrates persistent adrenal suppression at 6 weeks after diagnosis and 4 weeks after last IMB exposure.


Conclusion : We conclude that intramuscular betamethasone contributed to our patient’s persistent adrenal suppression and continued hydrocortisone requirement.

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Emily Nosova

Endocrine Fellow
Mount Sinai Hospital
New York, New York

Emily is an Endocrine fellow at Icahn School of Medicine at Mount Sinai.

Grenye O'Malley

Assistant Professor
The Mount Sinai Hospital, Mount Sinai St. Luke's and Mount Sinai West

Dr. O'Malley practices endocrinology at Mount Sinai Hospital and its affiliates.

Maria Skamagas

Associate Professor
Mount Sinai Hospital, Mount Sinai Queens

Dr. Skamagas practices endocrinology at the Mount Sinai Hospital and Mount Sinai Queens.