SUN-421 Double Trouble - A Case of Bilateral Adrenal Hemorrhage

Abstract Disclosure: G. Gupta: None. M. Dillon: None. S. Rabieihashemi: None. V. Kantorovich: None. Introduction: Bilateral adrenal hemorrhage (BAH) is rare and can cause adrenal insufficiency (AI) with increased risk of mortality. This case emphasizes the challenges in diagnosing BAH and identifying its cause. Case: A 60 year old male with a history of hypertension, hyperlipidemia, transient ischemic attack on aspirin, and acid reflux came to the emergency room for worsening epigastric pain for weeks, unrelieved by antacid medications. He denied nausea, vomiting, diarrhea, or fevers, but recently took ibuprofen for the Flu. He smoked 45 pack years, and denied trauma, recent surgeries or coagulopathies. On arrival, blood pressure was 192/95 but normalized on home medications. CT abdomen pelvis noted fat stranding and thickening of adrenals. MRI abdomen noted bilateral adrenal enlargement, surrounding T2 bright fluid in the retroperitoneal space, and T1 bright nonenhancing regions in both glands consistent with BAH. It was unclear if there was venous thrombosis, and no anticoagulation was given. Initial labs showed AM cortisol 11.1 µg/dL, ACTH 13 pg/mL, DHEA-S 98 µg/dL, normal aldosterone, renin, chromogranin A, 17-hydroxyprogesterone, and plasma metanephrines; normetanephrines mildly elevated (161 pg/mL). Four days later, cortisol was 21.5 µg/dL, and after 1 month, cortisol, ACTH, and DHEA-S remained normal. CT abdomen after 3 months showed resolution of adrenal thickening and fat stranding. Discussion: BAH is often an unanticipated diagnosis until identified on imaging. Unilateral AH can be clinically silent, whereas BAH can cause primary AI and lead to adrenal crisis. Causes include sepsis, surgery, abdominal trauma, or coagulopathies. The adrenal “vascular dam” coupled with high ACTH/catecholamine states can cause vein thrombosis and hemorrhage from high venous pressure. Our patient lacked severe stress/illness or trauma. AH symptoms include abdominal pain, however, most common symptoms are from AI. Imaging findings on CT include central hypodensity with peripheral contrast and fat stranding, progressing to gland swelling and higher attenuation, resolving with size/attenuation decrease, possibly with pseudocysts or calcifications. MRI, the most sensitive and specific modality for AH, shows high T1 and low T2 signal initially, hyperintensity on T1/T2 subacutely and then chronic hypointensity. It is unclear whether our patient had venous thrombosis as his imaging did not show overflowing thrombi from left or right adrenal veins into the left renal vein or inferior vena cava respectively. In our case, it was difficult to determine a cause and diagnose BAH due to non-specific symptoms, especially without the presence of AI. Early recognition is key as patients require monitoring for AI to reduce mortality. Presentation: Sunday, July 13, 2025