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