Hypernatremia in Dogs (Canis) | Vetlexicon
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Hypernatremia

ISSN 2398-2942


Introduction

  • Definition: serum sodium concentration >158 mEq/L.

    Normal ranges and abnormal values are dependent on equipment used and reference ranges established for that equipment.
  • Sodium is the major cation of extracellular fluid (ECF).
  • It does not freely move into the intracellular space (ICF) of most cells but is dependent on the action of the Na/K ATPase pump and it is therefore the major determinant of plasma osmolality.
  • Water moves freely between the ECF and ICF following an osmotic gradient.
  • Measured serum sodium concentration does not reflect total body sodium content but indicates the amount of sodium relative to the amount of ECF water.
  • Hypernatremia always implies hyperosmolality.

Presenting signs

  • Clinical signs vary considerably and usually do not occur until serum sodium concentration is >170 mEq/L in dogs.
  • Clinical signs are associated with the rate and magnitude of change of sodium concentration. Signs are predominantly neurologic.
  • More commonly sodium concentration increases over days and the brain is able to protect itself by generating intracellular solutes (idiogenic osmoles) to increase intracellular osmolarity.
  • None if 'mild or chronic hypernatremia'.
  • Anorexia.
  • Lethargy.
  • Vomiting.
  • Diarrhea.
  • Polyuria/polydipsia.
  • Muscular weakness.
  • Behavioral changes.
  • Tachycardia.
  • Obtundation.
  • Disorientation.
  • Head pressing.
  • Ataxia.
  • Seizures.
  • Coma.
  • Volume depletion, eg weak pulses and poor CRT.
  • Dyspnea (volume overload).
  • Death.

Acute presentation

  • Acute hypernatremia causes hyperosmolarity of CSF and shrinkage of CNS cells due to rapid movement of water from within the cells of the brain to the ECF. As a result cerebral vessels may rupture and hemorrhage can occur. Signs that may be seen are predominantly neurological but may also include:
    • Vomiting.
    • Diarrhea.
    • Disorientation.
    • Ataxia.
    • Seizure.
    • Coma.
    • Death.

Special risks

  • None directly related to hypernatremia.
  • Associated with the volume status of the patients.
  • Associated with the neurological status of the patients.
  • Associated with the underlying disease.

Pathogenesis

Etiology

  • Free water loss.
  • Increased sodium intake.

Predisposing factors

General

  • None.

Pathophysiology

  • Serum sodium concentration is a reflection of the amount of sodium relative to the volume of total body water.
  • Hypernatremic patients may have decreased, increased or normal total body sodium content.
  • Hypernatremia must be assessed with volume status.
  • Hypernatremia may be acute of chronic:  
    • In acute hypernatremia the brain does not have time to adjust to the increased extracellular osmolality and an equally rapid decrease in sodium concentration should prevent brain intracellular dehydration and shrinkage. 
    • In chronic hypernatremia where the hypernatremia has developed slowly over days or weeks, the brain has had time to compensate and has responded to high sodium concentration with increased intracellular osmolarity. 
  • Hypernatremia associated with hypervolemia (impermeant solute gain):
    • Salt poisoning.
    • Iatrogenic:
      • Administration of hypertonic saline (3% or 7.5% NaCl).
      • Administration of sodium bicarbonate Sodium bicarbonate.
      • Administration of total parenteral nutrition.
      • Hyperaldosteronism.
      • Hypercortisolism (rarely severe hypernatremia).
  • Hypernatremia associated with normovolemia or mild hypovolemia (pure water loss).
    • Primary hypodipsia or adipsia.
    • Associated with:
    • Inadequate access to water.
    • Diabetes insipidus Diabetes insipidus :
      • Central (inadequate release of ADH).
      • Nephrogenic (inadequate response to ADH).
    • Fever (high insensible water loss).
    • High environmental temperature leading to high insensible water loss (often associated with panting).
  • Hypernatremia associated with hypovolemia (hypotonic fluid loss):
  • Third space losses:
  • Burns.
  • Renal losses:

Timecourse

  • Clinical signs more common with severe, acute hypernatremia.
  • If hypernatremia chronic (over at least 2-3 days) it is possible that there will be no or minor clinical signs.

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.
  • Ueda Y, Hopper K, Epstein S E (2015) Incidence, severity and prognosis associated with hypernatremia in dogs and cats. J Vet Intern Med 29 (3), 794-800 PubMed.  
  • De Morais H A & DiBartola S P (2008) Hypernatremia: a quick reference. Vet Clin Small Animal Practice 38 (3), 485-489 PubMed.
  • Pouzet C, Descone-Junot C, Loup J, Goy-Thollot I (2007) Successful treatment of severe salt intoxication in a dog. J Vet Emerg Crit Care 17 (3), 294-298.
  • Barr J M, Khan S A, McCullough S M, Volmer P A (2004) Hypernatremia secondary to homemade play dough ingestion in dogs: a review of 14 cases from 1998 to 2001. J Vet Emerg Crit Care 14 (3) 203-212. 
  • Adrogué H J, Madias N E (2000) Hypernatremia. N Engl J Med 342 (20), 1493-1499 PubMed
  • Schaer M (1999) Disorders of serum potassium, sodium, magnesium and chloride. Vet Emerg Crit Care (4), 209-217 VetMedResource.
  • Khanna C, Boermans H J, Wilcock B (1997) Fatal hypernatremia in a dog from salt ingestion. J Am Anim Hosp Assoc 33, 113-117 PubMed.

Other sources of information

  • Gray S L (2016) Salt. In: Hovda L, Brutlag A, Poppenga R, Peterson K (eds) Blackwell’s Five-Minute Veterinary Consult Clinical Companion. Small Animal Toxicology, 2nd edition. John Wiley and Son, Ames, Iowa, pp 521-528. 
  • 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.
  • The Veterinary ICU Book (2002) Eds W E Wingfield and M R Raffee. Teton New Media, Jackson Hole, WY.