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Hypernatremia

ISSN 2398-2950


Synonym(s): Hypernatraemia

Introduction

  • Definition: serum sodium concentration >165 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 >175 mEq/L in cats.
  • 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 Feline primary 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 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

Client history

  • Depends on underlying cause.
  • Ingestion of salt (or salt dough or seawater) or administration of a salt-water emetic. 
  • Polyuria/polydipsia:
  • Hypodipsia or adipsia:
    • CNS disease.
  • Straining to urinate:
  • Weight loss, lethargy, anorexia:
    • Chronic renal failure.
  • Gastrointestinal disease:
    • Associated with gastropathy.
    • Associated with gastrointestinal obstruction.
    • Chronic renal failure, pancreatitis, peritonitis.
  • Diarrhea:
    • Associated with gastrointestinal disease. 
  • Abnormal behavior and CNS signs. 

Clinical signs

  • Depends on underlying cause.

Diagnostic investigation

  • Blood work:
  • Urinalysis:
  • Other laboratory tests:
  • Abdominal ultrasound.
  • CT scan or MRI in patients:
    • To diagnose pituitary tumors with central diabetes insipidus.
    • To rule out any other CNS diseases.

Confirmation of diagnosis

Discriminatory diagnostic features

  • Blood work.

Definitive diagnostic features

  • Depends on underlying cause.

Gross autopsy findings

  • Depending on the underlying cause:
    • Micro-macro adenoma of the pituitary gland in case of central diabetes insipidus.
    • Smaller, abnormal and irregular kidneys in case of chronic kidney failure.
    • Hydrocephalus.

Histopathology findings

  • Depending on the underlying cause.

Differential diagnosis

  • Other differentials for polyuria/polydipsia Polyuria/polydipsia (PU/PD).
  • Hypertonic dehydration.
  • Other CNS inflammatory or neoplastic diseases.
  • Diabetes insipidus.
  • Salt intoxication.

Treatment

Initial symptomatic treatment

  • Address and treat the underlying causes.
  • Determine whether hypernatremia is acute or chronc: 
    • If hypernatremia is acute and has developed very rapidly (over hours, as in acute salt poisoning) it is appropriate to correct the serum sodium over the same timeframe. Rapid onset hypernatremia can be corrected rapidly. The rate of decrease in sodium can be 2 mmol/L/hour. 
    • If the hypernatremia is chronic it is essential to reduce the sodium concentration and osmolality and correct the fluid deficit SLOWLY, ideally over a 48 to 72 period. Ideally the sodium should be corrected no faster than 0.5 mmol/L/hour (or 10-12 mmol/L/day). Rapid reduction of sodium can result in movement of water into the brain and result in cerebral edema and convulsions.  

Acute hypernatremia 

  • Gut decontamination Gastrointestinal decontamination follow salt ingestion:
    • Consider an emetic if ingestion was recent (within 30 mins). 
    • Activated charcoal is of no benefit in salt poisoning.  
    • Following a very large ingestion there may be crystallization of salt within the stomach resulting in continuing absorption of salt. This should be suspected if the sodium concentration continues to rise. Consider gastric lavage Gastric lavage
  • Access hydration status closely. 
  • Replacement of water lost restores normal serum sodium. 
  • If the animal is able to drink, small amounts of water at frequent intervals should be provided). Free water can also be given by nasogastric tube. [‘Free water’ is any water not associated with organic or inorganic ions. This can be water or dextrose 5% in water (as the dextrose is consumed immediately)]. 
  • Concentrate on intracellular replacement since intracellular losses are greater. 
  • Calculate fluid deficit = Weight in kg x {[PNa present ÷ PNa previous]-1 }. 
  • 5% dextrose in water (dextrose converted to water inside cells so equal to giving pure water) used to replace intracellular water. 
  • Adjusted treatment according to response to therapy. 
  • If there is renal impairment, underlying cardiac disease or risk of fluid overload, furosemide Furosemide should be used in addition to IV fluid therapy to aid sodium excretion.  
  • Antiemetics may be given if vomiting is excessive, as it may exacerbate any dehydration.  
  • Diazepam, a barbiturate or propofol can be used in the management of convulsions Seizure: management.  
  • If cerebral edema is suspected or confirmed, mannitol Mannitol should be given. 
  • Elevate the head in recumbent patients (to decrease intracerebral pressure). 
  • Cautions: 
    • Hypotonic fluids (0.2% or 0.45% saline) Fluid therapy: for electrolyte abnormality could worsen pulmonary edema so should only be used with care. The more hypotonic the fluid the lower the infusion rate. 
    • Isotonic saline (0.9%) is not suitable to correct hypernatremia because the sodium concentration is not low enough to significantly alter the plasma sodium concentration. 

Chronic hypernatremia 

  • Pure water losses (usually not volume depleted).
    • Replacement of water lost restores normal serum sodium.
    • Concentrate on intracellular replacement since intracellular losses are greater.
    • Calculate fluid deficit = Weight in kg x {[PNa present ÷ PNa previous]-1 }.
    • 5% dextrose in water (dextrose converted to water inside cells so equal to giving pure water) used to replace intracellular water.
    • Replace deficit over 48 hours.
    • Correct sodium ≤ 0.5-1.0 mEq/L/hr.
  • Hypotonic losses (usually associated with hypovolemia).
    • Need to replace extracellular losses.
    • Because hypotonic losses create less movement from intracellular to extracellular than pure water losses see more evidence of extracellular depletion.
    • Isotonic fluid (0.9% NaCl, Normosol R, Plasmalyte, LRS) to replace extracellular volume losses more quickly Fluid therapy: for electrolyte abnormality.
    • Hypotonic fluid (0.45% NaCl, 2.5% and 5% dextrose-containing solutions, half strength LRS) once extracellular deficits corrected.
    • Hypotonic fluids commonly used to correct sodium and extracellular deficits in acutely hypernatremic or symptomatic (neurologic).
    • Isotonic or hypotonic fluids used if no neurologic signs.
    • Correct at 0.5 mEq/L/hr in asymptomatic chronic.
    • Gain of impermeable solute (usually hypervolemic).
    • Want to eliminate excess sodium and water.
    • Excess sodium in extracellular compartment pulls water.
    • If volume overload, heart failure or renal failure administer furosemide at 0.5-2 mg/kg IV as needed to normalize sodium and volume status.
    • If no volume overload, heart failure or renal failure administer furosemide followed by 5% dextrose in water or 0.45% NaCl solution as needed to normalize sodium.
    • Correct sodium ≤ 0.5 mEq/L/hr.
    • Monitor volume status.

Standard treatment

  • Diagnose and manage underlying diseases.
  • Correct hypernatremia as necessary.

Monitoring

  • Serum electrolyte concentration:
    • Serum sodium concentration every 1-4 hours depending on underlying cause and rate of decrease and to access response to treatment.
  • Weight gain and volume status.
  • Neurologic signs.

Subsequent management

Treatment

  • Depending on the underlying causes.

Prevention

Outcomes

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.
  • Schaer M (1999) Disorders of serum potassium, sodium, magnesium and chloride. JVEEC (4), 209-217 VetMedResource.

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, S 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.