SAT-476 - Adrenal Hemorrhage and Posterior Reversible Encephalopathy Syndrome: Vascular Companions?

Risk factors for Adrenal hemorrhage (AH) include conditions such as sepsis, coagulopathy, burns, pregnancy, anticoagulant therapy etc. Bilateral AH can cause primary adrenal insufficiency, and if undetected, can lead to adrenal crisis. Posterior reversible encephalopathy syndrome (PRES) is a neurological disorder which presents with acute or subacute neurologic symptoms such as encephalopathy, seizures, headache or visual disturbance. It is usually precipitated by acute hypertension. Prognosis is typically favorable in PRES, however in severe cases short-term functional disability can occur. Both entities carry significant morbidity, and a question of shared underly pathophysiology arises. We present an unusual case of AH precipitated by PRES in a healthy female.

A 59-year-old woman with no known medical history presented with acute onset headache and abdominal pain. MRI revealed multifocal T2 flair hyperintensities in occipital lobes with initial BP 201/76 mmHg, HR 64 bpm, concerning for PRES. CT abdomen with contrast revealed bilateral adrenal enlargement with fluid and masses along with a rim of hyper attenuation, suggesting bilateral adrenal hemorrhage. Labs showed AM cortisol 21.3 mcg/dL (6.27-22.6), ACTH 23 (6-50). ACTH stimulation test: baseline cortisol 6.6 mcg/dL, 60-minute cortisol 16 mcg/dL. Plasma metanephrines 0.15 nmol/L, normetanephrines 0.21 nmol/L, Aldosterone 3.3 ng/dL, renin 0.2 ng/mL/h, and normal hypercoagulable workup. CT abdomen four days later, noted a 3 x 1.6 cm left adrenal nodule of -14 HU, and nodular thickening of the right adrenal, suggestive of benign left adrenal adenoma, and adenomatoid changes in the right adrenal without hemorrhage. During her hospital stay she had early morning dips in BP. She eventually became normotensive with treatment of high BP. Given bilateral AH, she was discharged home on stress dose hydrocortisone. At follow-up in six weeks, she was asymptomatic with good BP control.

While risk factors for AH and PRES appear unrelated, both occur in the setting of vascular dysfunction. PRES is related to endothelial dysfunction due to hyperperfusion from hypertensive surges causing extravasation of protein and fluid into interstitium leading to vasogenic edema. AH occurs with sudden increase in adrenal vascularity leading to a cascade of venous stasis and rupture of thin-walled adrenal venules. AH can cause significant morbidity and mortality due to possible development of adrenal crisis if prompt diagnosis and treatment is not pursued.

This case highlights the importance of maintaining a high index of suspicion for AH, especially in patients with known adrenal adenoma, when they present with PRES, as undiagnosed bilateral AH can result in high mortality. Further studies are needed to explore potential shared pathophysiology in these entities.

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