Case Presentation: Addison’s disease, or primary adrenal insufficiency, is a rare disorder of glucocorticoid or mineralocorticoid deficiency caused by adrenal cortex dysfunction or destruction. Since the disease gradually progresses with nonspecific symptoms, patients are often misdiagnosed or diagnosed late. Consequently, patients receive delayed treatment and are at increased risk for Addisonian crisis, which continues to bring patients significant distress and life-threatening consequences.A 61-year-old African American male with a history of type 2 diabetes, end-stage renal disease, hypertension, and chronic obstructive pulmonary disease presented with hypoglycemia and altered mental status. Five days before admission, the patient completed arteriovenous graft placement for dialysis access and has since experienced left hand pain, increased confusion, decreased appetite, and hypoglycemia. The patient was admitted for vascular surgery evaluation for suspected subclavian steal syndrome causing delirium. His wife also mentioned that he often experienced severe delirium during previous hospitalizations. On examination, he was hypertensive (SBP 150-180s) and afebrile. Labs revealed a WBC 11.8, Hgb 12.3, RBS 60, recent HgbA1C of 4.4%, Na 133, K 5.6, and Cr 5.86. He was somnolent but did not have focal neurological deficits. The patient started IV D10W and glucose improved to 70-100s. CT head and MRI brain were unremarkable, and all CNS-acting medications were held. Blood cultures were also negative. The patient’s appetite improved, and the increased sugars were suspected to be reactionary postprandial. Studies of excess insulin from tumor secretion or exogenous insulin were also negative, and endocrinology recommended studies of insulin C-peptide, proinsulin, beta-hydroxybutyrate, AM cortisol, and hypoglycemic drug panel if another hypoglycemic episode occurred. The patient was weaned off IV D10W and underwent AV fistula ligation two days after admission. His left hand pain and mentation improved, but he had additional hypoglycemic episodes with persistent hypotension, hypoxia, hyponatremia, and hyperkalemia after dialysis sessions and eventually went into shock on the eighth day of admission. A cosyntropin test was performed and confirmed diagnosis of Addison’s disease. The patient started hydrocortisone and fludrocortisone and blood pressure and blood glucose recovered thereafter.
Discussion: This case illustrates the elusive nature of Addison’s disease progression and difficulty with diagnosis due to symptoms resembling other conditions like subclavian steal syndrome and ESRD. Early evaluation of Addison’s disease is important in preventing delayed diagnostic testing and Addisonian crisis development. Furthermore, atypical clinical features, such as lack of increased skin hyperpigmentation in a darker skin-toned patient, may have contributed to delay in diagnosis. Coordination between vascular surgery, endocrinology, and neurology services may have also contributed to delayed treatment during this admission.
Conclusions: Addison’s disease is a rare condition that has life-threatening consequences if not treated early. Diagnosis should be considered earlier in the evaluation of patients presenting with altered mental status and hypoglycemia. Recommendations for interventions include increasing disease awareness and improving communication between different services to avoid delayed patient care and consequences of prolonged hospital admissions.