Hypernatremia

Hypernatremia is defined as a serum sodium concentration ([Na⁺]) >147 meq/L (some texts use >150 meq/L). In the normal state, the response to increased serum osmolarity is stimulation of thirst (promotes fluid intake) and an increase in ADH (increases water uptake in the renal collecting tubule). Severe hypernatremic dehydration can be associated with a high mortality, particularly in young infants.

Differential Diagnosis

• Dehydration
  –GI losses, especially watery diarrhea or profuse vomiting (very common)
  –Impaired oral intake and inability to respond to normal thirst mechanisms (e.g., young infants, altered mental status, or iatrogenic administration of IV fluids)
• Central diabetes insipidus (DI)
  –Decreased or absent production of ADH
  –Idiopathic
  –Head trauma
  –Suprasellar or infrasellar tumors
  –Langerhans cell histiocytosis
  –Granulomatous disease (including tuberculosis, Wegener granulomatosis and sarcoidosis)
  –Infection
  –Cerebral hemorrhage
  • Nephrogenic DI (NDI)
    –Inability to respond to ADH
    –Primary (congenital abnormality)
    –Secondary (acquired renal tubular dysfunction, e.g., progressive renal insufficiency; medications, e.g., lithium)
  • Severe skin or other insensible losses
    –Excessive sweating
    –Persistent rapid breathing
    –Burns
  • Increased total body sodium (rare in children)
    –Salt intoxication from
          –Sodium chloride tablets
          –IV NaCl or NaHCO₃
          –Breast milk after significant maternal sodium load
          –Concentrated formula
    –Primary hyperaldosteronism

  Workup and Diagnosis

  • History
    –Vomiting, diarrhea
    –Poor oral intake, recurrent dehydration
    –Medications or salt supplementation
    –Bicarbonate administration
    –Burns
    –Renal disease
  • Symptoms
    –Lethargy, seizures, coma
    –Polyuria, polydipsia
    –Headache, vision changes
  • Family history
    –Recurrent dehydration or early infant death (NDI)
  • Physical exam
    –Blood pressure
    –Assessment of hydration status (pulse, perfusion)
    –Midline defects (suggests presence of pituitary/hypothalamic defects/central DI)
    –Funduscopic exam
  • Labs
    –Chemistry panel
    –Serum osmolarity
    –Urinalysis
    –Urine osmolarity
  • Additional evaluation based on the clinical situation
    –Water deprivation test (to evaluate for central vs nephrogenic DI)
    –CT or MRI of the head

  Treatment

  • If dehydration is present
    –Fluid resuscitation with normal saline (20 cc/kg bolus)
    –Water deficit =0.6 ×weight ×(1 – 140/[Na⁺])
    –Administer hypotonic IV solutions to correct sodium and rehydrate over 48 hours
  • Too rapid correction can result in water shift into brain cells (due to the presence of “idiogenic” osmoles produced in response to the hypernatremia) resulting in cerebral edema
  • Central DI
    –Treat with exogenous vasopressin (DDAVP)
  • Nephrogenic DI
    –Treat with infusions of hypotonic saline or D5W (depending on the clinical situation and hydration status)
    –Allow free access to water

Book Source Details

• Book Title: In A Page: Pediatric Signs and Symptoms
• Author(s): Jonathan E. Teitelbaum, Kathleen O. Deantonis, Scott Kahan
• Year of Publication: 2007
• Copyright Details: In A Page: Pediatric Signs and Symptoms, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright Details: In A Page: Pediatric Signs and Symptoms, Copyright © 2008 Williams & Wilkins.

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More About This Book: Title: In A Page: Pediatric Signs and Symptoms Authors: Jonathan E. Teitelbaum, Kathleen O. Deantonis, Scott Kahan Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-4051-0427-9

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