A52-05 Use of Etomidate to Reduce Pressor Requirements in a Patient With Severe Ectopic Acth Syndrome Presenting With Shock

Abstract Background Patients with ectopic adrenocorticotropic hormone (ACTH) syndrome have excessive ACTH secretion, which promotes markedly elevated cortisol levels. High cortisol concentrations upregulate adrenergic receptor expression, causing vasoconstriction via α1-adrenergic receptors and increased vascular tone through inhibition of nitric oxide. Vasopressin raises blood pressure primarily by vasoconstriction, but its effect can be blunted by severe hypercortisolism.1 We hereby share our experience in managing a patient with ectopic ACTH syndrome who required high doses of pressors and was successfully treated with Etomidate to reduce pressor requirements. Case Description A 63-year-old female with a past medical history of small cell lung carcinoma metastatic to liver, thyroid cancer status post thyroidectomy and radioactive iodine therapy, type II diabetes mellitus, and paraneoplastic ectopic ACTH syndrome who was admitted for initiation of chemotherapy. The patient’s laboratory studies were significant for ACTH level of 1,191.9 pg/mL, cortisol level of 106.2 mcg/dL, and hypokalemia (∼3 mEq/dL). The patient was started on etoposide and carboplatin chemotherapy, and she received metyrapone for Cushing’s syndrome. Shortly after she developed severe hypoxia, septic shock, and new-onset atrial fibrillation with rapid ventricular response. She was transferred to the ICU, orally intubated, placed on mechanical ventilation, and started on broad-spectrum antibiotics. Initially, she required only norepinephrine to maintain a mean arterial pressure 65 mmHg, but 20 hours later due to escalation of norepinephrine dose to 30 mcg/min, the patient required addition of second vasopressor- vasopressin. Meanwhile, her cortisol level increased to 128 mcg/dL. A decision was made to initiate an etomidate infusion, which successfully reduced the cortisol level to ∼30 mcg/dL within five days, with continuation of vasopressin and reduction of norepinephrine to 5 mcg/min. The family ultimately elected for comfort care, and the patient passed away peacefully with family at the bedside. Conclusion Studies have shown that chronic excessive cortisol initially enhances norepinephrine’s effects by sensitizing the adrenergic system but eventually leads to receptor down-regulation. It also inhibits endogenous vasopressin release,2 causing dependence on exogenous vasopressin. In our case, the use of etomidate to suppress cortisol, although not sufficient to discontinue vasopressin, did allow for a lower overall pressor requirement. References: 1. Yang, S. and L. Zhang, Glucocorticoids and vascular reactivity. Curr Vasc Pharmacol, 2004. 2(1): p. 1-12. 2. Szczepanska-Sadowska, E., et al., The Interaction of Vasopressin with Hormones of the Hypothalamo-Pituitary-Adrenal Axis: The Significance for Therapeutic Strategies in Cardiovascular and Metabolic Diseases. Int J Mol Sci, 2024. 25(13). This abstract is funded by: None