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Hypernatraemia occurs when plasma sodium concentration is above reference levels (usually 155 mEq/l or mmol/l in dogs, and 162 mEq/l or mmol/l in cats) (Benitah, 2010). Occurrence of clinical signs depends more on rapidity of onset of hypernatraemia than to magnitude of change. Neurological signs generally occur when serum sodium levels exceed 170 mEq/l or mmol/l in dogs and 175 mEq/l or mmol/l in cats (>350 mOsm/kg) (de Morais and DiBartola, 2008b). Hyper-natraemia can result from water or hypotonic fluid loss, or excessive sodium gain (Box 4.5).

Sodium and its attendant anions account for approximately 95% of the osmotically active substances in the extracellular water. Therefore hypernatraemia is associated with hyper-osmolality (de Morais and DiBartola, 2008b).

Box 4.5. Causes of hypernatraemia (modified from de Morais and DiBartola, 2008b).

Pure water deficit (normovolaemic hyper-natraemia):

• Inadequate water intake;

• Animal unable to drink or no access to water;

• Primary hypodipsia;

• Diabetes insipidus (central or nephrogenic).

Hypotonic fluid loss (hypovolaemic hypernatraemia):

• Gastrointestinal;

• Vomiting;

• Diarrhoea;

• Small intestinal obstruction;

• Renal:

• Osmotic diuresis (mannitol infusion, hyperglycaemia);

• Non-osmotic diuresis (furosemide administration);

• Chronic renal failure;

• Non-oliguric renal failure;

• Post-obstructive diuresis;

• Third-space loss;

• Pancreatitis;

• Peritonitis;

• Cutaneous;

• Burns.

Excessive sodium gain (hypervolaemic hypernatraemia):

• Hypertonic fluid administration (intravenous hypertonic saline, sodium bicarbonate, sodium phosphate enema);

• Hyperaldosteronism;

• Hyperadrenocorticism;

• Excessive sodium chloride intake (e.g. salt poisoning).