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General Critical Care

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Hyponatremia, characterized by low plasma sodium concentration (pNa), is the most prevalent electrolyte disorder in hospitalized patients, affecting about 15%. While the majority of cases are mild, with pNa levels at or above 130 mmol/L, about 4% of patients experience severe hyponatremia with pNa dropping below 130 mmol/L. The leading cause of this significant drop in pNa is the Syndrome of Inappropriate Antidiuresis (SIAD), which occurs due to an excessive release of arginine vasopressin (AVP) despite low serum tonicity. In cases of severe symptomatic hyponatremia, which may present with symptoms like vomiting, seizures, and a reduced conscious state, it is considered a medical emergency. Immediate treatment with a bolus of hypertonic saline, specifically 100 mL of 3% NaCl for up to three doses, is recommended to increase pNa by 4 to 6 mmol/L, aiming to reduce intracranial pressure (ICP).

For chronic or uncertain-duration hyponatremia, to prevent osmotic demyelination syndrome (ODS), the target pNa increase is set at 4 to 8 mmol/L over 24 hours, with a strict limit of 10 mmol/L/24 hours. In patients at higher risk for ODS, such as those with alcoholism or malnutrition, lower targets of 4-6 mmol/L/24 hours are advised. Fluid restriction of less than 1000 mL/day is the primary therapy for chronic SIAD, as per current guidelines, although it's only effective in about half of the cases. When first-line treatment is insufficient, second-line options include tolvaptan, urea, sodium-glucose cotransporter 2 inhibitors (SGLT2i), or high-dose salt tablets, with tolvaptan posing the highest risk for overcorrection. In instances where sodium correction exceeds the safe limit, reducing pNa with hypotonic fluid (oral water or intravenous 5% dextrose), with or without desmopressin to decrease urine output, becomes necessary.

Here is a nice review of SIADH from pathophysiology to management provided by Annabelle M Warren, Mathis Grossmann, Mirjam Christ-Crain, and Nicholas Russell:

Ibrahim Ameen
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