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Basics

Basics

Definition

Serum sodium concentration below the lower limit of the reference range.

Pathophysiology

Sodium is the most abundant cation in the extracellular fluid. Hyponatremia usually, but not always, reflects hypo-osmolality and is typically associated with a decreased total body sodium content. Either solute loss or water retention can theoretically cause hyponatremia. Most solute loss occurs in iso-osmotic solutions (e.g., vomit and diarrhea) and, as a result, water retention in relation to solute is the underlying cause in almost all patients with hyponatremia. In general, hyponatremia occurs only when a defect in renal water excretion is present.

Systems Affected

  • Nervous-severe neurologic dysfunction is not usually seen until serum sodium concentration falls below 110–115 mEq/L. Clinical signs may be more related to the rate of decline in serum sodium concentration than the actual nadir. Dogs with chronic hyponatremia often have mild, if any, clinical signs.
  • Overly rapid correction of hyponatremia can also cause neurologic damage.

Signalment

Species

Dog and cat

Signs

  • Lethargy
  • Weakness
  • Confusion
  • Nausea/vomiting
  • Seizures
  • Obtundation
  • Coma
  • Other findings depend on the underlying cause.

Causes

Normal Osmolar Hyponatremia

  • Hyperlipemia
  • Hyperproteinemia

Hyperosmolar Hyponatremia

Hypoosmolar Hyponatremia

Normovolemic

  • Primary polydipsia
  • Hypothyroid myxedema coma
  • Hypotonic fluid infusion
  • SIADH

Hypervolemic

  • Congestive heart failure
  • Hepatic cirrhosis
  • Nephrotic syndrome
  • Severe renal failure

Hypovolemic

  • Gastrointestinal losses
  • Renal failure
  • Third space losses
  • Cutaneous losses
  • Diuresis
  • Hypoadrenocorticism

Diagnosis

Diagnosis

Differential Diagnosis

  • Hypoadrenocorticism
  • Severe GI disease
  • Metabolic or respiratory acidosis (DKA)
  • Congestive heart failure
  • Primary polydipsia

Laboratory Findings

Drugs That May Alter Lab Results

  • Mannitol can cause pseudohyponatremia.
  • Diuretic administration can cause hyponatremia.

Disorders That May Alter Lab Results

Hyperlipidemia, hyperglycemia, and hyperproteinemia can cause pseudohyponatremia.

Valid if Run in a Human Laboratory?

Yes

CBC/Biochemistry/Urinalysis

  • Low serum sodium concentration.
  • Other abnormalities may point to the underlying cause.

Other Laboratory Tests

  • Plasma osmolality is usually low; if plasma osmolality is normal or high, exclude hyperlipidemia, hyperglycemia, hyperproteinemia, and mannitol administration.
  • Urine osmolality <100–150 mOsmol/kg indicates primary polydipsia or reset osmostat. Urine osmolality >150–200 mOsmol/kg indicates impaired renal water excretion.
  • Urine sodium concentration <15–20 mEq/L indicates low effective circulating volume, pure cortisol deficiency, primary polydipsia with high urine output. Urine sodium concentration >20–25 mEq/L indicates syndrome of inappropriate ADH secretion, adrenal insufficiency, renal failure, reset osmostat, diuretic administration, or vomiting with marked bicarbonate loss.

Treatment

Treatment

Inpatient versus outpatient treatment depends on severity of hyponatremia, associated neurologic dysfunction, and the underlying disorder.

Medications

Medications

Drug(s) Of Choice

  • Treatment consists of addressing the underlying cause and increasing the serum sodium concentration if necessary. Overly rapid normalization of the hyponatremia can have potentially severe neurologic sequela and may be more detrimental than the hyponatremia itself. Therefore, isotonic saline is the fluid of choice in the large majority of cases. More aggressive correction of the serum sodium concentration with hypertonic saline is rarely necessary.
  • Hypervolemic (edematous) patients are typically managed with diuretics and salt restriction. Isotonic saline and furosemide may be useful in more affected patients.
  • Hypovolemic patients are managed by replacing the volume deficit with isotonic saline.
  • The use of hypertonic saline may be considered in selected patients with severe symptomatic hyponatremia. The sodium deficit is estimated by 0.5 × lean BW (kg) × (120 – serum sodium concentration). The serum sodium concentration is corrected by 10–12 mEq/L/day (0.5 mEq/L/h) or less. Once the serum sodium concentration reaches 120–125 mEq/L discontinue hypertonic saline and continue to slowly normalize the serum sodium concentration using isotonic saline or water restriction as dictated by the underlying cause of the hyponatremia.
  • Other therapeutic interventions are dictated by the underlying cause of the hyponatremia.

Precautions

Overly rapid correction of hyponatremia can result in neurologic damage (demyelination); avoid increasing serum sodium concentration by more than 10–12 mEq/L/day (0.5 mEq/L/h).

Follow-Up

Follow-Up

Patient Monitoring

  • Serial serum sodium determinations to avoid overly rapid correction of the serum sodium concentration and to assure appropriate response to NaCl and other indicated therapies.
  • Monitor hydration status.
  • Monitor other serum electrolyte concentrations as indicated by the patient's clinical condition and underlying disorder.

Prevention/Avoidance

Depends on the underlying disorder

Possible Complications

Depends on the underlying disorder

Expected Course and Prognosis

Depends on the underlying disorder

Miscellaneous

Miscellaneous

Associated Conditions

Other electrolyte and acid-base abnormalities are often associated with the clinical disorders that cause hyponatremia.

Abbreviations

  • ADH = antidiuretic hormone
  • DKA = diabetic ketoacidosis
  • SIADH = syndrome of inappropriate ADH secretion

Author Melinda Fleming

Consulting Editor Deborah S. Greco

Acknowledgment The author and editors acknowledge the prior contribution of Peter P. Kintzer.