1/21/2024 0 Comments Sodium normal range at 146There don't seem to be case studies of patients who developed herniation due to over-aggressive sodium correction (unlike overcorrection of hyponatremia, wherein scores of case studies document harm from osmotic demyelination).Retrospective studies actually correlate slower correction of sodium with worse outcomes.Among adults over ~40 years old there is no solid evidence that rapid correction of sodium causes harm.( 24559470) Both choices appear to be equally arbitrary. However, some authors recommend twice this rate (1 mEq/L/hr). Traditional teaching is to target a sodium decrease of 12 mEq/L per day (0.5 mEq/L/hr).Rapidly dropping the sodium concentration could theoretically cause cerebral edema and herniation. Brain tissue will adapt to hypernatremia over about two days.Treatment: optimal rate of sodium reduction Thiazide diuretics may be helpful by causing mild hypovolemia that stimulates increased water reabsorption in the proximal tubule.The most important component of management is simply providing enough free water to keep up with losses. Patients may have chronically elevated free water requirements (e.g., chronic nephrogenic diabetes insipidus from lithium).However, vasopressin requires a central line and the dosing can be tricky. This has the advantage that it is titratable, so that it can be stopped if hyponatremia occurs. Alternative treatment: vasopressin infusion 0.001-0.01 units/minute, titrated until the urine output decreases to a relatively normal rate.Note, however, that if excessive fluid is provided, the patient will develop hyponatremia. This is effective in causing the kidneys to retain free water. The simplest treatment might be desmopressin (DDAVP) 2 micrograms IV q8 hours.The following situations require more advanced management. The treatment of most causes of hypernatremia consists of general treatment of the underlying disorder and supportive care (e.g., replacement of lost water and electrolytes). Alternatively, exogenous DDAVP may have little impact among patients with nephrogenic diabetes insipidus. (2) Exogenous DDAVP will cause a reduction in urine output and an increase in urine osmolality among patients with central diabetes insipidus.Failure to concentrate urine indicates diabetes insipidus (e.g., urine osmolality Normal renal response to hypernatremia is to conserve water and produce concentrated urine (e.g., >300 mOsm).(1) Urine osmolality may occasionally help establish a diagnosis of diabetes insipidus:. If they are intubated, they will lose this compensation and become hypernatremic. Has the patient been chronically exposed to lithium in the past? Some patients have chronic partial diabetes insipidus, which they compensate for at home by drinking lots of water.Are there specific disease states that cause hypernatremia? (e.g.lactulose, mannitol, ampules of bicarbonate) Are there medications that cause hypernatremia? (e.g.
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