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BASICS

Description

  • Serum sodium (Na) >145 mEq/L, indicating hypertonicity.
  • Reflects imbalance: total body water deficit relative to sodium.
  • Dehydration: water loss predominates.
  • Hypovolemia: loss of both salt and water.
  • Intact thirst and access to water usually prevent hypernatremia.

Epidemiology

  • More common in elderly and infants.
  • Incidence: 1% in hospitalized elderly; 9% in ICU patients.

ETIOLOGY AND PATHOPHYSIOLOGY

Causes of Hypernatremia

Water loss (most common)

  • Transdermal: burns, excessive sweating (fever, heat, exercise)
  • Urinary: nephrogenic DI (congenital, renal dysfunction, hypercalcemia, hypokalemia, lithium), central DI (trauma, stroke, meningitis), osmotic diuresis (glucose, urea, mannitol), post-ATN diuresis
  • Gastrointestinal: osmotic diarrhea, enterocutaneous fistula, vomiting, NG suction

Impaired water intake

  • Hypodipsia or impaired thirst (intracranial lesions, mineralocorticoid excess)

Sodium gain (rare)

  • IV hypertonic saline or sodium bicarbonate (brain injury, metabolic acidosis)
  • Seawater ingestion
  • Excessive sodium bicarbonate antacids
  • Improper infant formula or tube feeding
  • Excess sodium in dialysate

Genetic

  • Some forms of DI hereditary.

RISK FACTORS

  • Infants and children
  • Elderly (decreased thirst response)
  • Intubated or altered mental status
  • Acute GI illness
  • Poorly controlled diabetes mellitus
  • Brain injury
  • Surgery
  • Diuretic therapy (especially loop diuretics)
  • Lithium therapy

DIAGNOSIS

History

  • Symptoms/signs of water loss or impaired thirst: nausea, vomiting, diarrhea, polyuria, fever, heat exposure, brain injury
  • Neurologic symptoms: thirst, anorexia, myalgia, weakness, twitching, lethargy, irritability, seizures, coma
  • Severity linked to rapidity and degree of Na increase (>160 mEq/L severe).

Physical Exam

  • Volume depletion signs: tachycardia, hypotension, orthostasis, dry mucous membranes, poor skin turgor
  • Neurologic: lethargy, weakness, tremor, focal deficits, confusion, seizures, coma

Differential Diagnosis

  • Diabetes insipidus (DI)
  • Hyperosmotic coma
  • Salt ingestion
  • Hypertonic dehydration
  • Hypothyroidism
  • Cushing syndrome

Diagnostic Tests

  • Serum sodium, potassium, BUN, creatinine, glucose, calcium, osmolality
  • Hemoglobin/hematocrit (may be elevated due to hemoconcentration)
  • Urine sodium and osmolality:
  • Low urine osmolality (<300 mOsm/kg): DI
  • Intermediate (300-800): hypovolemia, osmotic diuresis, partial DI
  • High (>800): extrarenal water loss, salt ingestion
  • Urine sodium:
  • Low (<10 mEq/L): volume depletion
  • Intermediate: osmotic diuresis
  • High: salt ingestion

Follow-Up

  • ADH stimulation test to differentiate central vs nephrogenic DI
  • Imaging: head CT/MRI for central DI or hypodipsia to exclude lesions

TREATMENT

General Measures

  • Treat underlying cause.
  • Assess duration (acute vs chronic).
  • Acute hypernatremia: D5W infusion 3-6 mL/kg/hr to reduce serum Na by 1-2 mEq/L/hr; check Na every 1-2 h.
  • Chronic hypernatremia (>48 h): avoid rapid correction to prevent cerebral edema.
  • D5W at 1.35 mL/kg/hr; check Na every 4-6 h.
  • Correct at max 0.5 mEq/L/hr or 10-12 mEq/L/day.
  • Hypernatremia with hypovolemia: initial isotonic fluids, then hypotonic saline.
  • Hypernatremia with hypervolemia: diuretics + water correction.
  • Consider oral water for mild cases.
  • Dialysis if severe AKI or refractory.

Medications

Diabetes Insipidus

  • Central DI: Desmopressin acetate (DDAVP), parenteral for acute, intranasal/oral for chronic.
  • Nephrogenic DI: diuretics, NSAIDs; lithium-induced treated with thiazides, indomethacin, or amiloride.

Second Line

  • NSAIDs for nephrogenic DI.
  • Continuous renal replacement therapy (CRRT) for severe cases in critical illness.

ISSUES FOR REFERRAL

  • Nephrology for renal-related hypernatremia.
  • Neurosurgery/neurology for central DI.

INPATIENT CONSIDERATIONS

  • Symptomatic Na >155 mEq/L requires IV fluids.
  • Monitor frequently for neurological status and electrolytes.

ONGOING CARE

Monitoring

  • Neurological checks during correction.
  • Daily weight, electrolytes, glucose post-correction.
  • Urine osmolality and output in DI.

Diet

  • Maintain nutrition.
  • Sodium restriction in nephrogenic DI.

Patient Education

  • Avoid salt; maintain hydration in nephrogenic DI.

PROGNOSIS

  • Most patients recover.
  • Rapid hypernatremia increases risk of neurologic complications.
  • Serum Na >180 mEq/L associated with high mortality and CNS damage.

COMPLICATIONS

  • CNS thrombosis, hemorrhage.
  • Seizures.
  • Neurologic damage with chronic or severe hypernatremia.

REFERENCES

  1. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.
  2. Sterns RH. Disorders of plasma sodium—causes, consequences, and correction. N Engl J Med. 2015;372(1):55-65.
  3. Bagshaw SM, Townsend DR, McDermid RC. Disorders of sodium and water balance in hospitalized patients. Can J Anaesth. 2009;56(2):151-167.
  4. Hannon MJ, Finucane FM, Sherlock M, et al. Clinical review: disorders of water homeostasis in neurosurgical patients. J Clin Endocrinol Metab. 2012;97(5):1423-1433.
  5. Huang C, Zhang P, Du R, et al. Treatment of acute hypernatremia in severely burned patients using continuous veno-venous hemofiltration with gradient sodium replacement fluid: a report of nine cases. Intensive Care Med. 2013;39(8):1495-1496.

Clinical Pearls

  • Hypernatremia results from relative water deficit to total body sodium.
  • Most cases due to impaired access to water or excessive water loss.
  • Avoid rapid correction of chronic hypernatremia; goal max 10 mEq/L per 24 h to prevent cerebral edema.
  • Serum sodium monitoring and adjustment of water replacement are critical as formulas estimating water deficit have limited accuracy.