OBJECTIVE: To propose a new hypothesis regarding the possible role of glucocorticoid excess in patients with an extended acute illness, based on a patient's presentation and therapy in a critical care situation. METHODS: We present a detailed case report, review the related literature, and suggest the need for prospective studies to determine the appropriate intervention in critically ill patients with pseudo-Cushing's syndrome. RESULTS: A 50-year-old woman with diabetes and obesity who underwent vertical banded gastroplasty had postoperative complications, including refractory gastrostomy leakage, peritoneal and abdominal wall infections, and multiorganism sepsis despite intensive antibiotic therapy and surgical drainage procedures. Her physical appearance, elevated and relatively nonsuppressible plasma cortisol levels, and radiologic study supported a tentative diagnosis of Cushing's syndrome in a critically ill patient. Intravenously administered itraconazole and rectally administered aminoglutethimide were used to suppress endogenous glucocorticoid synthesis. Glucocorticoids were administered at dosages that provided 1/3 to 1/2 of her expected maximal daily cortisol secretion during her complicated hospital course. Insulin resistance declined with adrenal suppression and infection control, and wound healing improved dramatically. Adrenal suppression was discontinued, and she was reevaluated for hypercortisolism. Results of all studies for Cushing's syndrome were normal and remained so 1 year later. CONCLUSION: In our patient, substantially increased glucocorticoid levels were associated with severe insulin resistance, retarded wound healing, and persistent infections. Suppression of endogenous cortisol production and replacement with more physiologic concentrations of glucocorticoid were associated with clinical improvement and appeared to contribute to her recovery. Review of the literature leads us to propose the following hypotheses: (1) that considerably increased stress-induced cortisol concentrations in critically ill patients may contribute to adverse outcomes and (2) that therapeutic suppression of the persistent and substantially elevated glucocorticoid levels in selected cases may be a beneficial therapeutic option.
OBJECTIVE: To propose a new hypothesis regarding the possible role of glucocorticoid excess in patients with an extended acute illness, based on a patient's presentation and therapy in a critical care situation. METHODS: We present a detailed case report, review the related literature, and suggest the need for prospective studies to determine the appropriate intervention in critically ill patients with pseudo-Cushing's syndrome. RESULTS: A 50-year-old woman with diabetes and obesity who underwent vertical banded gastroplasty had postoperative complications, including refractory gastrostomy leakage, peritoneal and abdominal wall infections, and multiorganism sepsis despite intensive antibiotic therapy and surgical drainage procedures. Her physical appearance, elevated and relatively nonsuppressible plasma cortisol levels, and radiologic study supported a tentative diagnosis of Cushing's syndrome in a critically ill patient. Intravenously administered itraconazole and rectally administered aminoglutethimide were used to suppress endogenous glucocorticoid synthesis. Glucocorticoids were administered at dosages that provided 1/3 to 1/2 of her expected maximal daily cortisol secretion during her complicated hospital course. Insulin resistance declined with adrenal suppression and infection control, and wound healing improved dramatically. Adrenal suppression was discontinued, and she was reevaluated for hypercortisolism. Results of all studies for Cushing's syndrome were normal and remained so 1 year later. CONCLUSION: In our patient, substantially increased glucocorticoid levels were associated with severe insulin resistance, retarded wound healing, and persistent infections. Suppression of endogenous cortisol production and replacement with more physiologic concentrations of glucocorticoid were associated with clinical improvement and appeared to contribute to her recovery. Review of the literature leads us to propose the following hypotheses: (1) that considerably increased stress-induced cortisol concentrations in critically ill patients may contribute to adverse outcomes and (2) that therapeutic suppression of the persistent and substantially elevated glucocorticoid levels in selected cases may be a beneficial therapeutic option.