How do you manage cerebral salt wasting?

How do you manage cerebral salt wasting?

Management of cerebral salt-wasting syndrome centers on correction of intravascular volume depletion and hyponatremia, as well as on replacement of ongoing urinary sodium loss, usually with intravenous (IV) hypertonic saline solutions.

What is cerebral salt wasting?

Cerebral salt wasting (CSW) is another potential cause of hyponatremia in those with CNS disease, particularly patients with subarachnoid hemorrhage. CSW is characterized by hyponatremia and extracellular fluid depletion due to inappropriate sodium wasting in the urine [5].

How is cerebral salt wasting different from Siadh?

A retrospective study by Arieff et al indicated that in patients with cerebral lesions who exhibit hyponatremia, urinary sodium excretion and urinary volume can be used to differentiate cerebral salt-wasting syndrome from SIADH.

What causes salt losing nephropathy?

The cause of renal loss includes diuretic use, adrenal insufficiency, osmotic diuresis, cerebral salt wasting syndrome (CSWS), and SLN. Diuretic use, adrenal insufficiency, and osmotic diuresis were ruled out clinically and endocrinologically.

Why does sah cause hyponatremia?

Background: Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states.

Is urine sodium high or low in SIADH?

In SIADH, the urine sodium concentration is usually above 40 mEq/L, the serum potassium concentration is normal, there is no acid-base disturbance, and the serum uric acid concentration is frequently low [1]. (See “Diagnostic evaluation of adults with hyponatremia”.)

What is salt losing nephropathy?

On the other hand, salt-losing nephropathy (SLN) is defined as a renal loss of sodium that leads to hyponatremia and ECV loss [2]. Differentiation of SLN from SIADH is important because treatment of SLN is opposite from that of SIADH.

How do you approach hyponatremia?

For serious symptomatic hyponatremia, the first line of treatment is prompt intravenous infusion of hypertonic saline, with a target increase of 6 mmol/L over 24 hours (not exceeding 12 mmol/L) and an additional 8 mmol/L during every 24 hours thereafter until the patient’s serum sodium concentration reaches 130 mmol/L.

When should nimodipine be given?

It is usually taken every 4 hours for 21 days in a row. Treatment with nimodipine should be started as soon as possible, no later than 96 hours after a subarachnoid hemorrhage occurs.

What are the symptoms of salt wasting?

Hyponatremia and cerebral salt-wasting syndrome. Symptoms include lethargy, agitation, headache, altered consciousness, seizures, and coma. [13] The severity of symptoms typically reflects the magnitude and rapidity of the decrease in serum sodium concentration.

What are mechanisms of Cerebral salt wasting (CSW)?

Cerebral salt wasting (CSW) is a syndrome of hypovolemic hyponatremia caused by natriuresis and diuresis . The mechanisms underlying CSW have not been precisely delineated, although existing evidence strongly implicates abnormal elevations in circulating natriuretic peptides.

Cerebral salt wasting (CSW) is a hyponatremic condition originally thought to cause all sodium losses in patients with cerebral disease. Pseudohypoaldosteronism type 1 is a rare disorder characterized by renal resistance to aldosterone which may present with a salt wasting crisis in infancy.