Abstract

Introduction: Spontaneous Adrenal Hemorrhage (SAH) in pregnancy is a rare occurrence with estimated prevalence of 0.03% to 1.8%. SAH usually involves the right gland and can be easily mistaken with other conditions due to its nonspecific symptoms. We hereby report 2 cases of spontaneous bilateral SAH that occurred during the 3rd trimester of pregnancy. Case 1: 28-year-old female with history of IBS presented during 35th week of her first pregnancy with right-sided abdominal pain. Abdominal MRI revealed a 4.7 x 2.8 cm right adrenal hemorrhage. Due to stability of her vitals, steroids were not initiated and she was discharged. She returned 4 days later with similar pain but this time on the left side. MRI did not reveal adrenal bleeding. Due to Blood Pressure (BP) of 90/70 mmHg, hydrocortisone IV 50mg every 8 hours was started. 36 hour later she became tachycardic and tachypneic. CT angiogram (CTa) ruled out Pulmonary Emboli (PE), but was remarkable for interval development of a 5.3 x 3 cm left adrenal hemorrhage. There were no findings indicative of Primary Adrenal Insufficiency (PAI). Patient was discharged home on physiologic dose of hydrocortisone and delivered a healthy baby 2 weeks later at term. Case 2: 30-year-old female with history of hypertension and polycystic kidney disease presented at 31st week of her 2nd pregnancy with left-sided abdominal pain. Abdominal CT scan showed a 2.3 x 3.1 cm left adrenal hemorrhage. Due to BP of 85/50 mmHg at presentation, she was started on hydrocortisone IV 50 mg one dose followed by 25 mg every 8 hours, which improved her BP. 3 days later she developed new right flank pain. MRI was remarkable for features indicative of adrenal hyperplasia but did not confirm presence of hemorrhage. 1 day later she developed hypoxia and underwent CTa to rule out PE, which was remarkable for a new right adrenal hemorrhage. She did not have findings indicative of PAI and was discharged home on physiologic dose of hydrocortisone. Unfortunately, the pregnancy resulted in intrauterine fetal death at 36 weeks. Discussion: Adrenal cortex hyperplasia secondary to physiological elevation of ACTH plus adrenal venous constriction due to increased catecholamine release, have been suggested as possible mechanisms for increased risk of SAH in pregnancy. Common manifestations of SAH include abdominal pain, fever, fatigue, dizziness, anemia and hypotension. Features of PAI such as hyponatremia and hyperkalemia should be expected in cases of over 90% damage of adrenal cortices. Management in pregnancy involves fluid resuscitation, close monitoring for findings suggestive of adrenal crisis, fetal monitoring and glucocorticoid +/- mineralocorticoid replacement if indicated. Possibility for development of bilateral SAH should always be considered in patients who develop unilateral SAH. If left unrecognized, SAH is associated with poor outcomes and high fatality rate for both mother and fetus.

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