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Hyponatremia
Synonym(s): Hyponatraemia
Introduction
- Definition: serum sodium concentration <149 mEql/L.
Normal ranges and abnormal values are dependent on equipment used and reference ranges established for that equipment. - Sodium major cation of extracellular fluid (ECF).
- It does not freely move into the intracellular space (ICF) but is dependent on the action of the Na/K ATPase and is therefore the major determinant of plasma osmolality.
- Water moves freely between the ECF and ICF following an osmotic gradient.
- Measured sodium concentration does not reflect total body sodium content but indicates the amount of sodium relative to the amount of the ECF water.
- Hyponatremia usually implies hypo-osmolality.
Presenting signs
- Clinical signs vary considerably and usually do not occur until serum sodium concentration is < 120 mEq/L. Signs also occur if drop is rapid (>0.5 m Eq/L/hr (DiBartolaet al, 2008)
- Clinical signs are related to rate and sodium gradient between the plasma and brain.
- More commonly sodium concentration decreases over days and the cells in the brain are able to protect themselves by expelling intracellular solutes (idiogenic osmoles, sodium, potassium) to decrease intracellular osmolality.
- Rapid correction of hyponatremia can also cause neurological signs as a result of myelinolysis, these include blindness, ataxia, paresis, seizures, coma, death.
- None if hyponatremia is mild or chronic.
- In more severe cases the following signs may be seen:
- Lethargy.
- Apathy.
- Obtundation.
- Head tremors.
- Seizure.
- Coma.
- Death.
- Anorexia.
- Vomiting.
- Signs attributable to underlying disease.
Acute presentation
- Acute hyponatremia causes hypo-osmolality of the extracellular space in the CNS and cerebral edema as a result of movement of water from the hypo-osmolar ECF into the relatively hyperosmolar cells and interstitium of the CNS.
- Vomiting.
- Collapse.
- Obtundation.
- Head pressing.
- Seizures.
- Coma.
Special risks
- Animals could be susceptible to volume overload or myelinosis with rapid correction.
- Associated with the volume status of the patients.
- Associated with the neurological status of the patient.
- Associated with the underlying disease.
Pathogenesis
Predisposing factors
General
- None.
Specific
- None.
Pathophysiology
- Serum sodium concentration is a reflection of the amount of sodium relative to the volume of total body water.
- Hyponatremic patients may have decreased, increased or normal total body sodium content. Evaluation of sodium should be undertaken alongside their volume status.
- Pseudohyponatremia:
- Artifact when sodium measured by flame photometry in severely lipemic or hyperproteinemic samples.
- Hyponatremia may occur with increased plasma osmolarlty (unusual). This happens as a result of the addition of an effective osmole to the ECF and shift of water from the ICF to the ECF.
- Hyperglycemia (ie diabetes mellitus Diabetes mellitus).
- Mannitol infusion Mannitol.
- Hyponatremia with decreased plasma osmolality (more common). It may be accompanied by normal, decreased or increased plasma volume.
- Normal plasma volume.
- Psychogenic polydipsia.
- Syndrome of inappropriate ADH secretion (SIADH).
- Drugs with antidiuretic effects (ie barbiturates, narcotics and vincristine, tricyclic antidepressants, beta adrenergics, cholinergics, NSAIDs, oxytocin, phenothiazine, cyclophosphamide, serotonin reuptake inhibitors).
- Myxedema coma (hypothyroidism).
- Administration of hypotonic fluid Fluid therapy: for electrolyte abnormality.
- Low sodium diet.
- Hyponatremia with hypo-osmolarity and decreased plasma volume.
- Hypovolemia stimulates ADH release and thirst to promote retention of water.
- Gastrointestinal losses (severe vomiting and diarrhea).
- Third-space losses (peritonitis, pleural effusion, gastric).
- Cutaneus losses (burns).
- Hypoadrenocorticism Hypoadrenocorticism.
- Diuretics.
- Renal failure.
- Hyponatremia with hypo-osmolarity and increased plasma volume.
- Associated with impaired water excretion as a result of activation of homeostatic mechanisms secondary to perceived volume deficit resulting in water and sodium retention.
- Congestive heart failure Heart: congestive heart failure.
- Advanced hepatic disease (cirrhosis Liver: cirrhosis, fibrosis or PSS).
- Nephrotic syndrome Nephrotic syndrome.
- Oliguric/anuric renal failure Kidney: chronic kidney disease.
- Pregnancy.
Timecourse
- If severe hyponatremia and the onset is acute then clinical signs develop quickly.
- If hyponatremia chronic ( over at least 2-3 days) potentially none or only minor clinical signs.
- If correction of hyponatremia is too fast (more than 1mEq/kg/h) neurologic signs of myelinosysis develop up to 3-4 days later.
Epidemiology
- None.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- de Morais H A & DiBartola S P (2008) Hyponatremia : a quick reference. Vet Clin Small Animal Practice 38 (3), 485-9 PubMed.
- Schaer M (1999) Disorders of serum potassium, sodium, magnesium and chloride. JVEEC 9 (4), 209-217 VetMedResource.
Other sources of information
- The Veterinary ICU Book (2002) Eds W E Wingfield and M R Raffee. Teton New Media, Jackson Hole, WY.
- Small Animal Critical Care Medicine (2008) Eds D C Silverstein and K Hopper. Saunders Elsevier, St Louis, Missouri.
- Fluid, Electrolytes and Acid-base Disorders in Small Animal Practice (2006) Eds S P DiBartola, Saunders Elsevier, St Louis Missouri.