MON-347 Bilateral Adrenal Hemorrhage in a Patient with Myelodysplastic Syndrome and Clostridium Difficile Infection

Background: Acute primary adrenal insufficiency due to bilateral adrenal hemorrhage is an often-missed diagnosis, which can lead to shock and death if untreated. Risk factors include anticoagulation, hypercoagulable states, trauma, and sepsis. Clinical Case: A 67-year-old female with myelodysplastic syndrome (MDS), maintained on lenalinomide and periodic blood transfusions, presented with progressive nausea, vomiting, diarrhea, posterior chest pain, and dyspnea. Her medical history also included chronic hypothyroidism. She was afebrile with normal pulse and blood pressure, and no abnormalities on cardiac, pulmonary, or abdominal exams. The WBC count was 6.0 K/mm3 (baseline, < 4.0 K/mm3), hemoglobin was 7.5 g/dL, and platelets 497 K/mm3. Electrolytes were normal except for potassium of 3.0 mEq/L. PT was not prolonged. TSH was normal. There was no evidence for pulmonary embolism on chest CT scan. She was admitted for suspected gastroenteritis, and started on IV fluids, analgesics, antiemetics, and enoxaparin. On hospital day 3 the patient developed fever and disorientation, and was started on broad antibiotics. Several hours later, she became hypotensive, and received fluid boluses. The hemoglobin fell to 6.7 g/dL and sodium decreased to 132 mEq/L, with potassium remaining low at 3.1 mEq/L. The following day sepsis developed, with tachycardia, tachypnea, persistent fever, and recurrent hypotension. CT scan of the abdomen, ordered to rule out an occult abscess, revealed colitis and bilateral adrenal hemorrhages, and PCR for C. difficile in the stool returned positive. Immediately following a cosyntropin stimulation test, hydrocortisone 100 mg every 8 hours was started; the post-cosyntropin cortisol level returned at 3.8 mcg/dL. Oral vancomycin treatment was initiated. Over the following 24 hours the patient’s status improved, with normalization of blood pressure and mental status. Tests for other bacterial, viral, and fungal infections returned negative. The patient’s diarrhea improved, and she was discharged home on hospital day 10. The hydrocortisone had been tapered to 50 mg daily in divided doses, with plans to continue tapering as an outpatient, and eventually to re-test adrenal axis function. Conclusions: We present a patient with MDS who developed C. difficile colitis leading to sepsis, complicated by adrenal insufficiency due to bilateral hemorrhages. Individuals with MDS may have dysfunctional platelets and neutrophils, which may have increased the risks for bleeding and infection in this case; other risk factors for C. difficile infection were absent. The brief use of enoxaparin may also have been a predisposing factor. This report adds to the few cases in the literature of adrenal hemorrhages in the setting of MDS, and underscores the importance of maintaining a high index of suspicion for this rare complication with protean manifestations.