Abstract Introduction Myxedema coma is a rare and life-threatening manifestation of severe hypothyroidism with an incidence of 0.22 to 1.08 cases per million per year. Shock, one of its most fatal sequelae, carries a reported mortality rate of 20-60%. Although several studies have described this complication, reports of distributive shock refractory to optimal resuscitative efforts remain exceedingly rare. We present one such case of myxedema coma complicated by profound, treatment-resistant distributive shock despite timely initiation of standard therapy. Case Report A 66-year-old female with a history of pancreatic cyst, polycystic kidney disease, hepatic cysts, alcohol dependence, tobacco use, peripheral vascular disease, and malnutrition presented to the emergency department for hematemesis and hypotension. On examination, she was confused, lethargic, hypothermic, hypoxic, with dry skin and bilateral lower-extremity edema.Initial resuscitation included intravenous fluids and norepinephrine infusion. Laboratory evaluation revealed severe hypothyroidism (Thyroid stimulating hormone 9.57 µIU/mL, free thyroxine 0.5 ng/dL, free triiodothyronine 1.0 pg/mL), hypoglycemia and anemia (Hemoglobin 6.8 g/dL). She was started on hydrocortisone 100 mg every 8 hours, intravenous levothyroxine 200 µg followed by 50 µg daily, and liothyronine 5 µg followed by 2.5 µg daily. Hemoglobin normalized after two units of transfused blood, and endoscopy was deferred until hospital stabilization.Although hemodynamics initially improved with continued above-mentioned resuscitative measures, she developed progressive shock subsequently requiring four vasopressors. Given her grave prognosis, her family opted for comfort-focused care. Discussion Shock in myxedema coma results from profound hypothyroidism, which reduces vascular tone and impairs cardiac function, leading to inadequate tissue perfusion despite normal intravascular volume. In severe hypothyroidism, vascular responsiveness to catecholamines is blunted due to downregulation of adrenergic receptors and impaired intracellular signaling, making vasopressors less effective. Thyroid hormones normally enhance cardiac contractility and maintain endothelial integrity; their deficiency causes low systemic vascular resistance and myocardial depression. Even with exogenous levothyroxine or liothyronine, tissue-level conversion and receptor uptake may be delayed in critical illness, explaining the slow or absent hemodynamic response.A prior case report described a patient with treatment-resistant shock in myxedema coma who required veno-arterial extracorporeal membrane oxygenation (VA-ECMO) as a bridge to orthotopic heart transplantation. Our patient deteriorated rapidly, before consideration of advanced circulatory support. VA-ECMO could have theoretically provided temporary hemodynamic support, potentially allowing time for the delayed biochemical recovery of hypothyroidism to take effect. This case underscores the importance of early recognition of refractory shock and timely discussion of advanced support options in myxedema coma. This abstract is funded by: None
Polavarapu et al. (Fri,) studied this question.