Bilateral adrenal infarction in Crohn's disease
A 25-year-old female patient presented with gradual onset right shoulder pain for 1 week, which was constant and achy in nature and radiated to the left shoulder, down to her back and bilateral flanks. The pain was worse on the right side. She also complained of weakness, decreased oral intake and nausea but did not have any fever, vomiting or diarrhea. She was diagnosed with Crohn's disease since the year 1995 with extensive perianal disease complicated by abscess formation and rectovaginal fistula. She had also been put on filgrastim, a granulocyte colony-stimulating factor (G-CSF) analog for chronic leucopenia secondary to azathioprine treatment for Crohn's disease. Physical examination at the time of current admission revealed pallor, mild tachycardia with a heart rate of 115/minute and blood pressure of 96/56 mm Hg. There was epigastric and costovertebral tenderness with mild voluntary guarding. There was no rebound tenderness and her bowel sounds were faint. WBC count was 4.5 × 109/L. Although the patient did not have significant electrolyte abnormalities (sodium: 137 mEq/L, potassium: 4.6 mEq/L), there was postural tachycardia and hypotension.\nMRI of the spine and sacroiliac joints did not reveal any evidence of infection/inflammation/disc disease that could be attributed as a cause of the pain. CT scan of abdomen and pelvis with contrast showed some edema in the rectum in keeping with her Crohn's disease as well as some mild terminal ileitis. There was also increased thickening and hypodensities in both the adrenals []. Further evaluation with MRI [Figure -] revealed that the adrenals were bulky bilaterally. They showed hypointense signal on T1WI and hyperintense signal intensity on T2WI without any demonstrable hemorrhage. Following administration of gadolinium-based contrast, there was no enhancement of the parenchyma signifying a lack of viable parenchyma, based on which a diagnosis of adrenal infarction without hemorrhage was made.\nBiochemical confirmation of adrenal insufficiency was made by low plasma cortisol (21 nmol/l) and ACTH stimulation test that failed to raise the plasma cortisol levels to more than 25 nmol/l. She did not have any altered skin pigmentation or any history of hypotensive episodes in the past making the possibility of a long standing primary adrenal insufficiency unlikely. The PTT and INR were normal. Anticardiolipin antibodies and Lupus-like anticoagulant were negative. She was put on replacement steroids for which she showed a good response. Her appetite improved and she was discharged with complete resolution of pain.