Session: SUN 1-16-Adrenal Insufficiency
Poster Board SUN-12
Case: An 83 year old male with no significant past medical history was discharged home in stable condition after undergoing a cholecystectomy. Four days after discharge he began having nausea, vomiting, weakness and lethargy. He returned to the ER 7 days post-op with a blood pressure of 80/50 mmHg, pulse 127 beats per minute and temperature of 101 degrees F. Sodium was 131 mmol/L (137-145), K 3.3 mmol/L (3.5-5.1), Cr 1.0 mg/dL, and glucose 137 mg/dL. Fluid resuscitation was initiated with good response. The following morning a fingerstick (FS) of 56 mg/dL was noted and D50 was administered. Three hours later the FS was 68 mg/dL. BP at the time was 121/67 and T was 96.7 F. Serum cortisol was 0.38 ug/dL (4-22). A cortisol level from his ER stay was 0.46 ug/dL. For his GI symptoms, a CT abdomen/pelvis was done that revealed incidental bilateral AH. A CT scan done at the time of surgery showed normal adrenal glands. The patient was started on hydrocortisone IV, which was later switched to oral. After a long and complicated hospital stay the patient was discharged.
Discussion: Often the diagnosis of AH is made at autopsy (1-3), with the incidence ranging from 0.12 to 1.1 % (4-6). The differential diagnosis of bilateral AH includes surgery, sepsis, coagulopathy, clotting factor deficiency, adrenal tumor, and antiphospholipid antibody syndrome. Post-surgical AH is seen in the elderly (7), but the actual incidence in geriatric population is unknown. Conditions such as adrenal cortisol stimulation and alteration of adrenal blood flow due to severe stress, coagulopathy secondary to anticoagulant therapy or antibiotics, and heparin-induced thrombocytopenia, predispose post-surgical patients to develop AH (8). Bilateral AH is an uncommon condition that may lead to acute adrenal crisis, shock, and death with a mortality rate of 15% (9). The signs and symptoms of AH often mimic sepsis or severe hypothyroidism and can lead to a delay in diagnosis, as adrenal insufficiency is clinically evident when greater than 90% of adrenal cortex is destroyed (10).
Conclusion: Signs, symptoms, and even the laboratory findings of adrenal insufficiency due to hemorrhage may be very nonspecific at presentation. High suspicion for all indexes of postoperative patients with integration of information and early empirical treatment may help to diagnose this fatal, yet highly reversible, clinical syndrome.
Nothing to Disclose: YKL, ZC, ASP, AB
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