![]() In a patient who presents to the hospital with hyponatremia, it will be assumed to be chronic in nature. Since patients with SIADH have a fixed urine osmolality, solute loads (such as urea and sodium tablets) are used to increase maximum urine output by increasing dietary solute. In patients who have chronic SIADH, sodium or urea tablets can be used. Fluid restriction is the mainstay of therapy. In SIADH, the underlying cause should be treated concomitantly with initial treatment to raise serum sodium. History and physical examination is important when it comes to this patient population to effectively start correct treatment plan. In patients who have reduced EABV, treating the primary pathology will improve the serum sodium. Therefore, in patients with primary polydipsia, they will overcome the maximum urine output while patients with reduced solute intake will have reduced maximum urine output. Maximum Urine Output = 900 60 = 15 litres per day ĪDH absent states are high risk for over-correction therefore should be monitored closely. These patients can be given isotonic fluid is clinical evidence of hyponatremia. In patients with reduced dietary solute intake (such as chronic alcoholics), instituting a proper diet will correct hyponatremia. Normally the kidneys require solute to create urine therefore in patients with poor nutritional status, a normal amount of water/alcohol will cause hyponatremia. In primary polydipsia, fluid restriction would be ideal. In patients with ADH absent states, hyponatremia is caused because patient is drinking more fluid than the kidney can handle. See Figure 2.ĭepending on the pathology, hyponatremia will be treated differently. Typical dose of two ampules of hypertonic bicarbonate is equivalent to ∼200 ml of 3% saline. Hypertonic bicarbonate has the same tonicity as 6% NaCl and is usually the fastest medication to obtain in an emergency. If patients symptoms persist and sodium has increased by 6 mM and symptoms have not resolved, then further workup should be performed to check for alternative pathologies. Lab work should be obtained after hypertonic therapy is administered and the goal is to increase sodium by 3-5 mM which should improve patient’s symptoms. 3% normal saline can be used, 150 ml over 20 min. In patients who present symptomatically with hyponatremia, they should be considered as an emergency and given hypertonic therapy. Treatment of hyponatremia is based on underlying pathogenesis. When plasma sodium is high, vasopressin levels are also increased. In the presence of vasopressin, water is allowed to flow out of the collecting tubule in the nephron attracted by a high solute concentration of the surrounding medullary interstitium. Vasopressin binds to V2 receptors on the principal cells lining the renal collecting duct. Osmoreceptors are hypothalamic neurons that are responsible for adjusting thirst and vasopressin secretion based on plasma sodium. Consequently, an abnormal plasma sodium causes water movement across the blood brain barrier leading to either brain swelling or shrinkage. Brain capillaries have tight endothelial junctions lined by astrocytic foot processes creating the blood–brain barrier which sodium cannot cross. Sodium crosses systemic capillary membranes through clefts between endothelial cells therefore sodium concentration is identical in plasma and interstitial fluid. The body normally prevents plasma sodium to stray outside normal range (135 to 145 mEq/L or mmol/L) by controlling water intake and excretion. Changes in sodium are generally due to changes in total body water, not serum sodium, which regulates plasma tonicity and effective arterial volume. Serum sodium reflects the plasma tonicity and is inversely related to total body water.
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