How is post operative SIADH treated

What is the management of post operative SIADH?

Hyponatremia resulting from isolated SIADH is the most common cause for 30-day rehospitalization after TSS. It occurs in upward of 25% of TSS cases, with severe, symptomatic hyponatremia (i.e., sodium [Na] < 125 mEq/L) occurring in ≈ 7% of cases. Nadir sodium levels occur most commonly between postoperative days 5 to 9 when patients are unmonitored at home. Fluid restriction has been the mainstay of treatment for mild SIADH for many years and recent studies now support this approach in post-operative TSS patients. Specifically, in TSS patients without evidence of DI at the time of hospital discharge, recent studies support the implementation of a 1-week 1 to 1.5 L/day fluid restriction, and a routine 1-week postoperative serum sodium level check (as has been recommended by other pituitary experts/guidelines). On the basis of the serum sodium levels at the 1 week postoperative blood test and the patient’s symptoms, additional fluid adjustments can be made, using various published protocols.

The diagnosis of SIADH is based on the following criteria: serum sodium < 135 mEq/L, low serum osmolality (< 275 mOsm/kg of water), inappropriately high urine osmolality (> 100 mOsm/kg of water), high urinary sodium (> 40 mEq with normal salt intake), euvolemic status, and normal renal function. In addition, other endocrinopathies associated with hyponatremia, specifically hypothyroidism and adrenal insufficiency, should be excluded. Once in the hospital, patients are routinely placed on fluid restriction and monitored closely neurologically and with serial sodium levels (every 4 hours). A spot urine sodium, urine potassium and urine osmolality tests are recommended at the time of admission to assess for possible superimposed hypovolemia (as best indicated by a spot urine sodium <40 mEq/L) and/or refractoriness to fluid restriction. Specifically, a high urinary osmolality (> 500 mOsm/Kg of water) and a low renal electrolyte-free water clearance (i.e., Urine sodium + Urine potassium/Serum sodium > 1) predict failure to fluid restriction. An important caveat, however, is that diuretic use, adrenal insufficiency, and renal insufficiency may also present with high urine sodium and osmolality levels.

For patients with hyponatremia with significant neurologic symptoms (from cerebral edema), such as seizures, altered mental status, or coma, hypertonic saline (3%) should be given for a targeted serum sodium correction of 4-6 mEq/L over the first few hours, or until life-threatening symptoms improve. This usually correlates with a serum sodium level in a ‘safe’ range, generally defined as > 120 to 125 mEq/L. In general, in cases of chronic hyponatremia (> 48 hours’ duration), the correction of hyponatremia should be limited to < 10 to 12 mEq/L in the first 24 hours, and even slower correction rates (< 8 mEq/L/first 24 hr) when other risk factors are present for osmotic demyelination syndrome (i.e., hypokalemia, liver disease, alcoholism, or poor nutritional status). Lastly, although generally not prescribed by endocrinologists, vasopressin receptor antagonists (tolvaptan or conivaptan) can be considered in cases of refractory euvolemic hyponatremia.


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