What Causes Hypernatremia?

Patient Presentation
A 7-month-old male came to the emergency room with a 3 day history of watery diarrhea. The mother has tried some commercial electrolyte oral rehydration solution but the infant has refused the fluid for the last 1-2 days. She also tried his formula but he had refused that too. She said that she couldn’t tell when he last urinated because the diarrhea is so profuse. She denies any blood or mucous in his stool, and it currently is only brown water. He has been having increased sleepiness over the past 18 hours. She denies any fever but there was some emesis initially of the fluids she gave him. There is no one currently ill at home, but there is diarrhea in his daycare. There is no travel history nor exposures to pets other than the family dog. The past medical history shows a nasolacrimal duct obstruction as a neonate.

The pertinent physical exam showed that he was 8.640kg (75%) at his 6 month check and his current weight is 7.960 kg. Based on 75% for his age he should be ~9.00 kg. Therefore he is estimated to be 11.6% dehydrated. His blood pressure is 58/40, heart rate is 168 beats/minute, his respirations are 40/minute, and temperature is 37.8°C. He is lethargic but will awaken when stimulated and cry. His capillary refill is 4+ seconds on his trunk and longer in his extremities which are cold. He has poor skin turgor with mild tenting and his mucous membranes are dry. The rest of his HEENT, heart and lung exams are normal. His abdomen is relatively soft but he cries when examining him. His bowel sounds are hyperactive but there are no masses or organomegaly.

The diagnosis of severe dehydration with hemodynamic compromise due to enteritis was made and the patient was given 20 ml/kg of normal saline bolus. He continued to have low blood pressure and another bolus was given. The laboratory evaluation showed a serum sodium of 153 mEq/L, chloride of 116 mEq/L and potassium of 6.8 mEq/L.

The patient’s clinical course was that he was taken to the pediatric intensive care unit for fluid management. He was given additional fluid and then started on 0.2 normal saline to correct his hypernatremia over 48 hours. Ongoing diarrhea losses were also replaced by intravenous fluids. KCl was given after urination was established. He became more alert over this time and on day 3 began to take sips of fluid. The diarrhea also improved and he was sent to the floor on Day 4 of hospitalization. The cause of the diarrhea was Rotavirus.

Hypernatremia is a serum sodium of > 150 mEq/L. Basic causes are too much sodium or too little free water.

If body weight is normal or increased, there is an increase in total body sodium without an appropriate increase in total body water. Normally when the serum sodium is increased there is transient hypertonicity of the plasma which causes the thirst center to be stimulated and antidiuretic hormone (ADH) to be released. The thirst center tells the person to drink more water and ADH causes the kidney to retain free water. This normally will allow the plasma tonicity to go back to normal. Treatment is by treating the underlying cause and appropriate free water administration.

If the body weight is decreased, there is a lower amount of free water with a relative increase in total body salt. This occurs usually when there is hypovolemic dehydration such as diarrhea and inadequate free water intake. Normally ADH is produced to increase the free water but without adequate access to free water, the hypernatremia continues to be maintained. Treatment is by treating the underlying causes and appropriate free water administration.

Severe diarrhea is one of the most common reasons for hypernatremia. Patients with hypernatremic dehydration have both lower total body sodium and free water, but there is relatively more free water loss than sodium loss. Patients then develop hypernatremia. Because the hypernatremic plasma is hypertonic, intracellular free water passes into the extracellular environment which helps to maintain body’s hemodynamics. Therefore patients with hypernatremic dehydration usually are 3-5% more dehydrated than estimates based on clinical signs.

Patients who have had a prolonged period of hypernatremia should have their hypernatremia progressively decreased over a prolonged period of time to minimize the risk of cerebral edema. During hypernatremia, other osmolytes are produced intracellularly to help to balance the electrolytes extracellularly. These additional intracellular osmolytes are not created nor dissipated quickly. Therefore if additional free water is added too quickly to the extracellular environment to correct the hypernatremia, then as the serum sodium decreases, the extra free water can enter cells where the additional osmolytes are and this can lead to cellular edema.

While patients are given normal saline (sodium and fluid to expand the intravascular circulation immediately) if they are hemodynamically compromised, patients are often given Dextrose 5% (or 10%) + 0.2% normal saline (smaller amount of sodium and more free water) to correct the hypernatremia over 48 or more hours. Potassium and chloride are also replaced appropriately after the patient is voiding and it is obvious there is not a component of intrinsic renal disease. Patients should be monitored frequently (every 4-6 hours) and changes to the intravenous fluids made promptly. If the serum sodium decreases too quickly and cerebral edema and seizures occur, patients are usually given 3% saline to increase the serum sodium and the seizures usually stop after 4 ml/kg of 3% saline. Slower correction of the hypernatremia can then begin again.

Learning Point
Causes of hypernatremia include:

If body weight is normal or increased, there is an increase in total body sodium without an appropriate increase in total body water.

  • Urine sodium is high and urine osmolality is high
    • Salt poisoning
    • Excessive salt administration, such as salt tablets or medications such as sodium bicarbonate, hypertonic intravenous fluids, salt-water ingestion, excessive use of soy sauce, inappropriate mixing of infant formula, inappropriate use of salt instead of sugar
    • Cellular lysis such as tumors, rhabdomyolysis, crush injury
  • Urine sodium is variable and urine osmolality is low
    • Central hypodipsia
    • Reset osmostate – usually because of brain trauma
    • Hyperaldosteronism – infrequent
    • Cushing syndrome – infrequent
  • If the body weight is decreased, there is a lower amount of free water with a relative increase in total body salt
    • Urine sodium is low and urine osmolality is high
      • Diarrhea
      • Insensible water loss – fever, tachypnea, radiant warming of premature infants, burns
      • Excessive sweating
      • Lack of access to free water
    • Urine sodium is high and urine osmolality is isotonic to high
      • Diuretic
      • Glycosuria
      • Post urinary tract obstruction diuresis
      • Acute tubular necrosis, diuretic phase
      • Acute tubular necrosis, non-oliguric
    • Urine sodium is high and urine osmolality is isotonic to high
      • Diabetes insipidus
        • Central (non production of ADH)
        • Nephrogenic (non response to ADH)

    Questions for Further Discussion
    1. What causes hyponatremia?
    2. What causes hypokalemia? THE differential diagnosis is available here

    Related Cases

    To Learn More
    To view pediatric review articles on this topic from the past year check PubMed.

    Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

    Information prescriptions for patients can be found at MedlinePlus for these topics: Sodium and Dehydration.

    To view current news articles on this topic check Google News.

    To view images related to this topic check Google Images.

    To view videos related to this topic check YouTube Videos.

    Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1651-2.

    Moritz ML, Ayus JC. Intravenous fluid management for the acutely ill child. Curr Opin Pediatr. 2011 Apr;23(2):186-93.

    Powers KS. Dehydration: Isonatremic, Hyponatremic, and Hypernatremic Recognition and Management. Pediatr Rev. 2015 Jul;36(7):274-83.

    Donna M. D’Alessandro, MD
    Professor of Pediatrics, University of Iowa