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For further information, see CMDT Part 21-03: Hypernatremia

Key Features

Essentials of Diagnosis

  • Serum sodium > 145 mEq/L (> 145 mmol/L)

  • Increased thirst and water intake are the main defense against hypernatremia

  • Urine osmolality helps differentiate renal from nonrenal water loss

General Considerations

  • An intact thirst mechanism usually prevents hypernatremia

  • The hypernatremic patient is typically hypovolemic due to hypotonic fluid losses or, less often, due to hypodipsia or adipsia

  • Hypotonic fluid losses can be

    • Renal, such as with diabetes insipidus or inappropriately dilute urine from diuretics

    • Nonrenal, such as from burns or gastrointestinal (GI) losses

  • Hypervolemic hypernatremia

    • Less common than hypovolemic hypernatremia

    • Can be an iatrogenic complication in hospitalized patients who receive substantial amounts of intravenous sodium salts

    • Can rarely occur in other settings, such as with sea water ingestion

  • Hypernatremia in primary aldosteronism is mild and usually does not cause symptoms

Etiology

  • Initial step is to determine whether the hypernatremic patient is oliguric, ie, urine flow < 0.5 mL/min, or nonoliguric

  • Oliguric patient (urine flow < 0.5 mL/min)

    • Reduced water intake from inability to communicate and/or limited access to water

    • Nonrenal causes, such as

      • Sweat

      • Gastrointestinal tract losses (diarrhea)

      • Respiratory tract losses (febrile patients on a ventilator)

    • Shift of water into cells; rarely, hypernatremia may develop from shift of water intracellularly due to intracellular gain of an effective osmole (eg, seizures or rhabdomyolysis)

  • Nonoliguric patient (urine flow > 0.5 mL/min)

    • Urine osmolality < 250 mOsm/kg

      • Hypernatremia with dilute urine

      • Central diabetes insipidus: Inadequate ADH

      • Nephrogenic diabetes insipidus: Normal or elevated ADH levels but kidneys less sensitive to ADH

    • Urine osmolality > 300 mOsm/kg

      • Hypernatremia with concentrated urine from osmotic diuresis (eg, glucose and urea can both promote polyuria with increased free water excretion)

Clinical Findings

  • With dehydration, orthostatic hypotension and oliguria are typical findings

  • Lethargy, irritability, and weakness are early signs

  • Somnolence and confusion can appear when the osmolality exceeds 320–330 mOsm/kg (320–330 mmol/kg)

  • Coma, respiratory arrest, and death can result when osmolality exceeds 340–350 mOsm/kg (340–350 mmol/kg)

  • Symptoms in the elderly may not be specific; recent change in consciousness is associated with poor prognosis

  • Osmotic cerebral demyelination is an uncommon but reported consequence of acute severe hypernatremia

Diagnosis

  • Urine osmolality > 300 mOsm/kg when renal water-conserving ability is functioning

  • Urine osmolality < 250 mOsm/kg when renal water-conserving ability is impaired

  • Serum osmolality invariably increased in the dehydrated state

  • Copeptin (C-terminal peptide synthesized with vasopressin, since difficult to measure vasopressin in plasma)

    • Elevated copeptin levels indicate elevated vasopressin and exclude central diabetes insipidus

Treatment

  • Correct both the cause of fluid loss and replace the water electrolyte deficit

  • Rate of correction

    • Chronic hypernatremia

      • Common clinical practice is to limit correction of chronic hypernatremia to < 12 mEq/L in 24 ...

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