Hypernatremia
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:
- Hypothalamic granulomatous meningo-encephalitis.
- Hydrocephalus Hydrocephalus.
- CNS lymphoma Lymphoma.
- 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):
- Gastrointestinal losses.
- Vomiting Vomiting.
- Diarrhea.
- Sequestration (ie small intestinal obstruction Intestine: obstruction ).
- Third space losses:
- Peritonitis Peritonitis.
- Pancreatitis Pancreatitis: chronic.
- Burns.
- Renal losses:
- Osmotic diuresis (diabetes mellitus Diabetes mellitus , mannitol administration Mannitol ).
- Chronic renal failure Heart: congestive heart failure.
- Non-oliguric acute renal failure Kidney: acute kidney injury (AKI).
- Post-obstructive diuresis.
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 9 (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.