What is the difference between cerebral salt wasting and SIADH?

What is the difference between cerebral salt wasting and SIADH?

Both conditions are characterized by hyponatremia with elevated urine sodium, concentrated urine, and no edema. The key distinguishing factor is that in cerebral salt wasting the patient is hypovolemic versus in SIADH the patient is euvolemic to hypervolemic.

Does SIADH increase sodium excretion?

Generally, it is known to be helpful diagnosing SIADH when the patient exhibits urinary sodium and chloride excretion increased more than 30 mmol/L and fractional excretions of sodium and chloride more than 0.5% (33).

What is the difference between hyponatremia and SIADH?

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH) [1]. If water intake exceeds the reduced urine output, the ensuing water retention leads to the development of hyponatremia.

How can you tell the difference between CSW and SIADH?

The key difference is that SIADH is a euvolemic to mildly hypervolumic state, whereas CSW is a volume-depleted state. Unfortunately, the volume status is not always clinically apparent in every patient.

What is cerebral salt wasting syndrome?

Cerebral salt wasting syndrome (CSW) is defined as a renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. The pathogenesis of this disorder is still not completely understood.

What causes cerebral salt wasting?

Cerebral salt-wasting syndrome is a condition featuring hyponatremia and dehydration caused by head injury, operation on the brain, subarachnoid hemorrhage, brain tumor and so on.

How does SIADH affect sodium?

With SIADH, the urine is very concentrated. Not enough water is excreted and there is too much water in the blood. This dilutes many substances in the blood such as sodium. A low blood sodium level is the most common cause of symptoms of too much ADH.

Is sodium retained in SIADH?

It should be noted that aldosterone is unaffected in SIADH and the sodium balance will be usually normal. If isotonic saline is administered, the water will be retained and sodium will be excreted in urine, leading to possible worsening of hyponatremia.

What is the pathophysiology of SIADH?

Pathophysiology of SIADH The hormone increases water reabsorption in the distal nephron, producing a concentrated urine and diluted plasma. Vasopressin release is stimulated by any of the following: Increased plasma osmolality. Decreased blood volume.

What is salt-wasting?

First described by Peters et al in 1950, cerebral salt-wasting syndrome is defined by the development of extracellular volume depletion due to a renal sodium transport abnormality in patients with intracranial disease and normal adrenal and thyroid function.

What causes cerebral salt-wasting?

What is the urine specific gravity in SIADH?

Also, patients with hyponatremia (serum sodium ≤130 mEq/L), urine output < 3 ml/kg/hr, urine specific gravity ≥1020, and urinary sodium concentration >20 mEq/L were considered to have SIADH.