Fortunately, bilateral adrenal hemorrhage is a rare event. In situations of physiologic stress (e.g., postoperative state or sepsis), blood flow to the adrenal glands and cortisol production are markedly increased—the adrenal glands become edematous and susceptible to hemorrhage, hypotension, and venous infarction. Thus the typical clinical settings for bilateral adrenal hemorrhage include the postoperative period, trauma, neoplastic infiltration of the adrenal glands, anticoagulation therapy, and coagulopathies such as antiphospholipid-antibody syndrome. Typically, primary adrenal insufficiency, if present, is a permanent deficit. The case presented herein highlights the evolution of adrenal hemorrhage on computed tomography (CT) and the potential to recover adrenocortical function.

Case Report

This 68-year-old woman presented to the emergency department with severe left flank pain. Eleven days previously she had undergone left total knee arthroplasty. Following the orthopedic procedure she was placed on a 7-day course of low-molecular-weight heparin for deep venous thrombosis (DVT) prophylaxis. She had no history of DVT or blood clotting disorder. An abdominal CT scan was obtained in the emergency department and showed bilateral adrenal masses with imaging characteristics consistent with bilateral adrenal hemorrhage ( Fig. 68.1 ).

Axial images from unenhanced (A) and contrast-enhanced (B) abdominal computed tomography (CT) scan showed bilateral heterogeneous adrenal masses (arrows) that did not have the imaging characteristics of benign adrenal adenomas. The left adrenal mass measured 3.3 × 2.6 cm and the right mass 3.0 × 2.7 cm. The unenhanced CT attenuations were 59.7 Hounsfield units (HU) on the right and 49.3 HU on the left. There was soft tissue thickening or edema of the adjacent mesenteric fat bilaterally. After contrast administration, there was minimal enhancement. Given the imaging characteristics, the clinical presentation, and the recent history of anticoagulation, this likely represented bilateral adrenal hemorrhage.

INVESTIGATIONS

Laboratory testing showed hyponatremia, high-normal serum potassium concentration, and low serum cortisol concentration ( Table 68.1 ). The next study obtained in the hospital was a 250-mcg cosyntropin stimulation test that showed serum cortisol concentrations of 5.3, 6.1, and 6.4 mcg/dL obtained at baseline and 30 and 60 minutes post-cosyntropin, respectively. Serum corticotropin, although indicated in this setting, was not measured.

TABLE 68.1

Laboratory Tests

Biochemical Test	Result	Reference Range
Sodium, mEq/L Potassium, mEq/L Creatinine, mg/dL eGFR, mL/min per BSA 7:50 am serum cortisol, mcg/dL Aldosterone, ng/dL Plasma metanephrine, nmol/L Plasma normetanephrine, nmol/L	121 4.9 0.9 >60 3.1 <1 0.31 1.09	135–145 3.6–5.2 0.6–1.1 >60 7–25 ≤21 ng/dL <0.5 <0.9

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