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Matthew McGuire

, and Subramaniam Pennathur

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date: 14 June 2021

  1. A. Introduction

    1. a. Definition. Hypernatremia is defined as a serum sodium concentration greater than 145 mEq/L.

    2. b. Severe hypernatremia is rare if a patient has access to water and has an intact thirst mechanism. Those prone to hypernatremia therefore include the very old, the very young, and the very sick.

    3. c. Plasma osmolality. Unlike hyponatremia, hypernatremia is associated with only one state of serum osmolality: hyperosmolality.

    4. d. Hypernatremia is usually due to water loss out of proportion to electrolyte losses.

  2. B. Clinical Manifestations of Hypernatremia. The clinical manifestations of hypernatremia depend on the cause, level, and rapidity of changing serum sodium.

    1. a. Symptoms may include thirst, muscle weakness, altered mental status, hyperthermia, delirium, seizures, and coma. Like hyponatremia, symptoms are primarily neurologic in origin owing to a contracted intracellular fluid volume, which leads to contracted brain cells.

    2. b. Polyuria and polydipsia may also be prominent if the underlying etiology is diabetes insipidus.

  3. C. Approach to the Patient. The first step to evaluating a patient with hypernatremia is to check volume status and urine osmolality. A high urine osmolality (>400 mOsm/kg) ensures that renal water conservation is intact. Dilute urine (<250 mOsm/kg) is characteristic of diabetes insipidus (DI).

    1. a. Hyperosmolar urine

      1. i. Nonrenal losses that are hypotonic (e.g., excessive sweating, respiratory tract or gastrointestinal water loss). Hypernatremia can occur if water intake cannot keep up with hypotonic fluid loss. Urine sodium is typically <10 mEq/L because of appropriate attempts to conserve total body volume.

      2. ii. Renal losses (e.g., due to hyperglycemia). Progressive volume depletion is caused by osmotic diuresis. During these conditions, renal sodium and water conservation is not present, and the urine sodium is typically >20 mEq/L.

      3. iii. Rarely, hypernatremia reflects an increased amount of total body sodium. Causes include hypertonic fluid administration (e.g., during cardiopulmonary resuscitation with hypertonic fluids), sodium chloride ingestion (e.g., sea water or soy sauce) without adequate water, and mineralocorticoid excess (e.g., primary hyperaldosteronism or Cushing’s syndrome). Patients appear volume expanded on physical examination. In these cases, urine sodium is typically >20 mEq/L.

    2. b. Hypoosmolar urine in the setting of hypernatremia suggests the presence of DI. Patients with DI are typically either euvolemic or mildly hypovolemic.

      1. i. Nephrogenic DI stems from renal resistance to the action of ADH. Causes include drugs such as lithium and demeclocycline, chronic kidney disease affecting the collecting ducts (e.g., interstitial nephritis and ureteral obstruction), and electrolyte disorders (hypercalcemia and hypokalemia).

      2. ii. Central DI is most commonly caused by lack of ADH production in the posterior pituitary. The most common causes include brain surgery in the area of the pituitary or hypothalamus or head trauma. However, 50% of cases remain idiopathic.

  4. D. Treatment. Treatment depends on extracellular fluid (ECF) status and the speed with which hypernatremia developed. Before the following steps are taken, the initial underlying disorder must be corrected. Intranasal desmopressin is used for central DI. The underlying cause of nephrogenic DI should be corrected. If that is not possible, the concentrating defect can be treated with a low-sodium diet and a thiazide diuretic.

TBW = total body water = 0.5 (for women) or 0.6 (for men) × ideal body weight

Free water deficit = current TBW × ([Na+] – 140)/140

Change in serum Na (per liter of infusate) = (Infusate Na + infusate K) – serum Na/(TBW + 1)

TBW may be 10% lower than this calculated value in patients who are significantly volume depleted with hypernatremia. Large urine or stool output also needs to be accounted for, in addition to TBW calculations.

  1. a. ECF depletion should be corrected by the addition of sodium and/or potassium to the infusate.

  2. b. ECF expansion can be treated with diuretics, preferably thiazide type (because loop diuretics induce a hypoosmolar diuresis, which can exacerbate hypernatremia). If renal failure is present, dialysis may be necessary.

  3. c. Fluid choice determines the rate of infusion. The more hypotonic the infusate, the slower the rate of infusion for correction. Care must be taken with dextrose-containing infusates to avoid hyperglycemia, which can cause an osmotic diuresis and exacerbate hypernatremia. Volume depletion or hypokalemia often accompanies chronic hypernatremia, and the addition of sodium or potassium to the infusate can correct these deficits simultaneously.

  4. d. Rate of correction is critical. Acute hypernatremia can be corrected to near normal in 24 hours without risk for neurologic sequelae. Chronic hypernatremia, however, should be corrected at no faster than 0.5 mEq/L/hr or about 10 mEq/L/day total to prevent cerebral pontine myelinolysis.

Suggested Further Readings

Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med 2000;342:1581–9. (Classic Article.)Find this resource:

Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332:702.Find this resource:

Sterns RH. Disorders of plasma sodium: causes, consequences, and correction. N Engl J Med 2014;372:55–65.Find this resource: