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- W4387008099 abstract "To the Editor: Determining the cause of hyponatremia in a critically ill patient can be challenging1. The broad differential diagnosis of this electrolyte abnormality and the inherent difficulties in evaluating fluid status may confuse the clinical picture and result in an incorrect diagnosis1-3. A 73-year-old man presented to us with a gangrenous, non-healing ulcer after undergoing a right great toe amputation for osteomyelitis. Angiography revealed occlusions of the proximal superficial femoral artery and a previous femoropopliteal bypass. The patient was taken to the operating room, where the right common femoral artery was resected, an external iliac to common femoral artery interposition graft was placed, and a right femoral-to-peroneal bypass was performed. The patient developed hypotension during surgery that was treated with volume resuscitation and escalating doses of phenylephrine and norepinephrine. His urine output remained brisk (1.5-2.5 mL/kg/hr) despite the hypotension. Point-of-care ultrasound demonstrated normal biventricular function and an inferior vena cava collapsibility index greater than 50%. Cardiac output measured with transthoracic echocardiography was 9 L/min, suggesting that vasoplegia was present. An initial plasma sodium (Na+) concentration was 136 mEq/L. Vasopressin was added, which reduced norepinephrine requirements, but a plasma Na+ concentration obtained 12 hours later was 130 mEq/L. The patient did not have neurological symptoms; however, his urine output fell to less than 0.5 mL/kg/hr despite aggressive administration of crystalloid. Urine Na+ and osmolarity were elevated (124 mEq/L and 503 mOsm/kg, respectively), and serum osmolarity was decreased (272 mOsm/kg) consistent with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The serum cortisol concentration was 15 μg/dL. The Na+ concentration subsequently fell to 129 mEq/L. Discontinuation of vasopressin resulted in prompt return of Na+ to 136 mEq/L over the next 12 hours and marked diuresis without other interventions. SIADH is characterized by impaired water excretion from elevated levels of antidiuretic hormone that leads to a euvolemic, hyponatremic, and hypoosmotic state3. Vasopressin exerts its effects on the kidney through V2 receptors to cause antidiuretic effects and water reabsorption in the renal tubules3,4. Administration of exogenous vasopressin can occasionally be associated with SIADH, as illustrated here4. The reported incidence of hyponatremia produced by exogenous vasopressin is low5,6, as only 1 of 396 (< 0.3%) patients who received it developed hyponatremia (< 130 mEq/L) in the Vasopressin and Septic Shock trial5. As our case illustrates, a high index of suspicion for iatrogenic hyponatremia should be maintained in patients with unexpected hyponatremia when exogenous vasopressin is used for treatment of vasoplegia. 1Androgue HJ, Madias ME. The challenge of hyponatremia. J Am Soc Nephrol 2012;23:1140-11482McGreal K, Budhiraja P, Jain N, et al. Current Challenges in the Evaluation and Management of Hyponatremia. Kidney Dis 2016;2:56-633Ellison DH, Tomas B. The Syndrome of Inappropriate Antidiuesis. N Engl J Med 2007;356:2064-2072.4Salazar M, Hu BB, Vazquez J, et al. Exogenous Vasopressin-Induced Hyponatremia in Patients with Vasodilatory Shock: Two Case Reports and Literature Review. J Intensive Care Med 2015;30:253-2585Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl J Med 2008;358:877-8876Obritsch MD, Jung R, Fish DN, et al. Effects of continuous vasopressin infusion in patients with septic shock. Ann Pharmacother 2004;38:1117-1122 This work was supported entirely by departmental funds. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper." @default.
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- W4387008099 date "2023-09-01" @default.
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- W4387008099 title "Hyponatremia in vasoplegia treated with vasopressin: a reminder" @default.
- W4387008099 doi "https://doi.org/10.1053/j.jvca.2023.09.031" @default.
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