Hyponatremia in patients with central nervous system disease: SIADH versus CSW

https://doi.org/10.1016/S1043-2760(03)00048-1Get rights and content

Abstract

The syndromes of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW) are two potential causes of hyponatremia is patients with disorders of the central nervous system. Distinguishing between these two causes can be challenging because there is considerable overlap in the clinical presentation. The primary distinction lies in the assessment of the effective arterial blood volume (EABV). SIADH is a volume-expanded state because of antidiuretic hormone-mediated renal water retention. CSW is characterized by a contracted EABV resulting from renal salt wasting. Making an accurate diagnosis is important because the treatment of each condition is quite different. Vigorous salt replacement is required in patients with CSW, whereas fluid restriction is the treatment of choice in patients with SIADH. Although most physicians are familiar with SIADH, they are much less familiar with CSW. This review emphasizes the need for CSW to be included in the differential diagnosis of hyponatremia in a patient with central nervous system disease. Distinguishing between these two disorders is of crucial importance because therapy indicated for one disorder but used in the other can result in negative clinical consequences.

Section snippets

SIADH is a volume-expanded state

The primary pathogenic mechanism underlying SIADH is excessive antidiuretic hormone (ADH) release causing renal water reabsorption and resulting in expansion of the ECF volume. Evidence for a volume-expanded state in SIADH initially came from studies of normal individuals given exogenous pitressin [7]. In these experiments, administration of pitressin resulted in an abrupt decrease in urine volume and increase in urine osmolality. The water retention produced by this antidiuretic effect

CSW is a volume-depleted state

The newly found appreciation for the diagnosis of CSW can be traced to reports in which blood and plasma volume were found to be decreased in patients who met the traditional laboratory criteria for SIADH. Nelson et al. [9] studied 12 unselected hyponatremic neurosurgical patients with subarachnoid hemorrhage, intracranial aneurysm and head injury. On an average, hyponatremia developed on the tenth day of illness and was associated with increased urine Na+ concentrations (>25 mEq l−1) and an

Pathophysiology of CSW

The mechanism by which cerebral disease leads to renal salt wasting is poorly understood. The most probable process involves disruption of neural input into the kidney and/or central elaboration of a circulating natriuretic factor (Fig. 2). By either or both mechanisms, increased urinary Na+ excretion would lead to a decrease in effective arterial blood volume (EABV), and thus provide a baroreceptor stimulus for the release of arginine vasopressin (AVP). In turn, increased AVP levels would

Differentiation of SIADH and CSW

Distinguishing between CSW and SIADH in clinical practice can be difficult, given the similarity in laboratory values and the overlap in associated intracranial diseases. Determination of ECF volume remains the primary means of distinguishing these disorders (Table 1). ECF volume is increased in SIADH, whereas it is low in CSW. Physical findings that support a diagnosis of CSW include orthostatic changes in blood pressure and pulse, dry mucous membranes and flat neck veins. Weight loss or

Treatment of CSW and SIADH

Making the distinction between CSW and SIADH is of particular importance with regard to treatment [31]. Fluid restriction is employed in SIADH because the primary abnormality is expansion of the ECF volume with water. Administration of NaCl is indicated in CSW because ECF volume is decreased as a result of renal salt wasting. Failure to distinguish properly between these disorders so that treatment indicated for one disorder is inappropriately used for the other can potentially result in an

References (34)

  • A. Leaf

    Evidence in man that urinary electrolyte loss induced by pitressin is a function of water retention

    J. Clin. Invest.

    (1953)
  • P.B. Nelson

    Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

    J. Neurosurg.

    (1981)
  • P.B. Nelson

    Hyponatremia and natriuresis following subarachnoid hemorrhage in a monkey model

    J. Neurosurg.

    (1984)
  • E. Wijdicks

    Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm

    Ann. Neurol.

    (1985)
  • J.P. Levine

    Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder

    Plast. Reconstr. Surg.

    (2001)
  • V. Sivakumar

    Management of neurosurgical patients with hyponatremia and natriuresis

    Neurosurgery

    (1994)
  • M. Filippella

    Very delayed hyponatremia after surgery and radiotherapy for a pituitary macroadenoma

    J. Endocrinol. Invest.

    (2002)
  • Cited by (0)

    View full text