Discussion:
Previously, only three cases of significant hyponatremia following CEA have been reported.2-4  Of these, only one report described severe hyponatremia with a sodium of 119 mmol/L. Unlike previous cases, our patient developed profound hyponatremia with a sodium level of 109 mmol/L.
Patients undergoing CEA may be at increased risk for developing hyponatremia postoperatively due to higher vasopressin levels.5 A relationship between carotid baroreceptor activity and increased plasma antidiuretic hormone (ADH) levels has been demonstrated in patients status-post CEA.6 It is suggested that the endarterectomy related arterial injury results in the activation of platelets and humoral factors that are transported to the hypothalamus via carotid circulation stimulating ADH secretion.5Additionally, it is postulated that the decreased wall distension of the carotid arterial walls or the aortic arch due to atherosclerosis lowers baroreflex-mediated afferent nerve traffic to the nucleus tractus solitarii which causes an increased efferent sympathetic nerve activity and ADH release.7 Interestingly, an increased incidence of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) after neck dissections has been described as well.8