Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume .. Sivakumar V., Rajshekhar V., Chandy M.J. Management of  ‎Pathophysiology of RSW · ‎Differentiating SIADH · ‎Value of Determining. associated with the syndrome of inappropriate ADH secretion (SIADH), cerebral salt wasting . Identical acute cerebral insults may cause either SIADH or CSW. .. Rizzo V, Albanese A, Stanhope R. Morbidity and mortality associated with. This is usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) []. Cerebral salt wasting (CSW) is another potential cause of hyponatremia in those with CNS disease, particularly patients with subarachnoid hemorrhage.


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As water is retained and body weight Wt increases, there is a rise in urinary sodium excretion UNaV.

Cerebral salt wasting versus SIADH: what difference?

A fall in body weight induced by water restriction leads to a decrease in urinary sodium excretion despite the presence of a persistently concentrated urine. During exogenous administration of vasopressin when water intake is not limited and body weight is allowed to increase cerebral salt wasting vs siadh steady state is eventually reached in which urine sodium excretion stabilizes and is equal to dietary sodium intake.

At this time severe dietary sodium restriction will lead to excretion of urine that is essentially sodium free cerebral salt wasting vs siadh administration of a large isotonic sodium load is followed by rapid and almost quantitative urinary excretion of the infused solute [ 7 ].

The establishment of normal renal sodium handling despite a decreased serum sodium concentration is a characteristic feature of SIADH.

In SIADH expansion of ECF volume is not typically accompanied by overt signs of hypervolaemia such as oedema or distended neck veins since only one-third of retained water is distributed in the ECF space. Nevertheless modest expansion of the intravascular volume results in increased glomerular filtration rate and increased renal plasma flow.

In addition the volume expansion leads to decreased proximal sodium reabsorption and urinary sodium excretion is increased and equal to dietary sodium intake.

Cerebral salt wasting versus SIADH: what difference?

Substances such as uric acid and urea nitrogen, that are reabsorbed in concert with sodium proximally, also tend to be reduced because of diminished proximal reabsorption.

CSW is a volume-depleted state The concept of a CSW syndrome was first introduced by Peters and colleagues in in a report describing three cerebral salt wasting vs siadh with neurological disorders who presented with cerebral salt wasting vs siadh, clinical evidence of volume depletion, and renal sodium wasting without an obvious disturbance in the pituitary—adrenal axis [ 8 ].

This same constellation of findings was subsequently confirmed in additional patients with widely varying forms of cerebral disease [ 910 ]. In these initial reports, it was theorized that cerebral disease could lead to renal salt wastage and subsequent depletion of ECF volume by directly influencing nervous input into the kidneys.

Only in recent years has cerebral salt wasting again come into favour as a distinct entity.


Part of this new found appreciation for the diagnosis of CSW can be traced to reports in which measurement of blood and plasma volume were found to be decreased in patients who met the traditional laboratory criteria for SIADH. As compared to neurosurgical patients cerebral salt wasting vs siadh intracranial disease, 10 of the 12 patients had significant reductions in plasma volume and total blood volume.

These same investigators then examined sodium balance in a monkey model of subarachnoid haemorrhage [ 12 ]. Following the haemorrhage, seven of nine animals developed hyponatraemia in association with natriuresis and negative salt balance.

There was a slight decline in plasma volume, although it was not statistically significant. In contrast, sham-operated control animals did not become hyponatraemic or natriuretic and plasma volume did not change.

On cerebral salt wasting vs siadh average of 7 days following the event, nine patients developed hyponatraemia that met the criteria for a diagnosis of SIADH. Eight of nine patients were found to be in negative sodium balance, which preceded the development of hyponatraemia.

Interestingly, of the 12 patients without hyponatraemia negative sodium balance developed in four patients and plasma volume decreased in eight.

In one additional report of 21 neurosurgical patients with hyponatraemia associated with increased urine sodium concentration and an inappropriately concentrated urine, volume status was assessed by measurement of total blood volume and central venous pressure and determining the cerebral salt wasting vs siadh to volume cerebral salt wasting vs siadh [ 14 ].

In summary, a substantial number of neurosurgical patients who develop hyponatraemia and otherwise meet the clinical criteria for a diagnosis of SIADH have a volume status inconsistent with that diagnosis. Rather the evidence of negative salt balance and reductions in both plasma and total blood volume in these patients is more consistent with a diagnosis of cerebral salt wasting.

Pathophysiology of cerebral salt wasting The mechanism by which cerebral disease leads to renal salt wasting is not well understood. By either or both mechanisms, increased urinary sodium excretion would lead to a decrease in EABV and thus provide a baroreceptor stimulus for the release of AVP.

In turn, increased AVP levels would impair the ability of the kidney to elaborate a dilute urine.