Cerebral salt wasting syndrome distinct from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

Abstract

Two cases with pituitary tumour developed postoperative hyponatraemia which was not caused by inappropriate secretion of antidiuretic hormone. The one case with non-functioning macro-adenoma showed severe hyponatraemia (116 mEq/l) on day 11 after trans-sphenoidal surgery in association with diabetes insipidus (DI). The patients was treated by aqueous pitressin and saline administration to control urinary output and keep positive salt balance at the same time. The other case with GH-producing macro-adenoma showed progressive negative sodium balance with the total loss of 644 mEq resulting in hyponatraemia of 133 mEq/l. This was corrected by additional salt intake. The plasma atrial natriuretic polypeptide (ANP), antidiuretic hormone (ADH) as well as aldosterone levels were normal in the latter case. These patients were considered to manifest primary salt wasting disorder, which should be clearly differentiated from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Syndromes related to sodium and arginine vasopressin alterations in post-operative neurosurgery

“…the coexistence of DI and csWs (mixed syndrome) observed in our patients has also been described by yamaki et al 17 , who studied two patients postoperatively following surgery for pituitary tumor and observed the presence of severe natriuresis and hyponatremia in a study patient who developed DI (fluid loss >2.36 ml/kg/h), which led the authors to conclude that hyponatremia resulting from csWs in intracranial diseases may develop in patients with DI. similar findings were described by laredo et al 29 , who reported hypernatremia resulting from DI, followed by hyponatremia due to sodium urinary loss compatible with csWs, in the immediate postoperative period of two neurosurgical patients.…”

“…Initially, hyponatremia in patients with intracranial disease was attributed to cerebral salt wasting syndrome (csWs), as proposed by Peters et al in 1950 13 . later, the syndrome of inappropriate antidiuretic hormone secretion (sIADH), described by schwartz et al in 1957 14 , became accepted as the principal cause of hypona-tremia in neurological patients with excessive urinary sodium loss, and the original concept of csWs was abandoned 1,8,[14][15][16][17] . Hypernatremia is the sodium disturbance least frequently found in these patients and its principal cause is neurogenic diabetes insipidus.…”

“…Hypernatremia is the sodium disturbance least frequently found in these patients and its principal cause is neurogenic diabetes insipidus. Improved knowledge with respect to the physiology of arginine vasopressin (AVP), the possibility of its measuring by radioimmunoassay 2,[16][17][18][19][20][21] and the report of hypovolemia in the majority of neurological patients presenting hyponatremia and natriuresis, led investigators to question sIADH in brain disease. Many questions remain unanswered with respect to sIADH since few studies in which AVP was measured have been reported and results have been contradictory 1,2,7 .…”

“…However, it can also be influenced by several factors involved in the postoperative phase of neurosurgical patients, that are able to stimulate the non-osmotic secretion of AVP, such as stress, an increase in intracranial pressure (IcP), pain, use of medication (antipsychotics, tricyclic antidepressives, carbamazepine, morphine, anesthetics, metoclopramide), hypovolemia, prolonged recumbency and positive-pressure mechanical ventilation 4,7,16,[22][23][24][25][26][27] . considering that patients submitted to neurosurgery may frequently suffer sodium and AVP alterations of various causes and since differential diagnosis of these alterations is essential to guarantee adequate treatment, their accurate diagnosis is of great importance 17,18 . the objective of the present study is therefore to identify the presence of syndromes related to sodium alterations occurring in neurological patients during the postoperative period.…”

Cerebral Salt-Wasting Syndrome: Does It Exist?

“…Reports of CSWS have appeared intermittently with 1 or several cases with predominantly intracranial diseases that presented with hyponatremia, concentrated urines, and high urinary sodium concentrations [34, 35, 36, 37, 38, 39, 40]. Some justify the designation of salt wasting by various means, including clinical evidence of dehydration, postural hypotension that is responsive to saline, inappropriately low plasma ADH levels, and measurements of CVP, red cell volume, plasma volume (by radiolabelled serum albumin), and chloride or bromide spaces.…”