Hypernatraemia in a Dog


Dr Clare A’Beckett BVSc


Case Report

An 18kg, 2 year old female speyed kelpie cross presented to  the Frankston Animal Emergency Centre after a visitto the beach, where she had ingested a significant volume of   seawater over a number of hours. After emerging from the  water at the beach the dog vomited, collapsed and developed mild convulsions.

On presentation the dog was collapsed, agitated and tremoring, with some mild seizure activity. Physical examination revealed a rectal temperature of 41.4oC and a heart rate of 200 bpm; all other vital parameters were within normal limits. An intravenous (IV) catheter was placed and diazepam 1 mg/kg IV was administered and active cooling commenced. Within 1-2 hours of active cooling, and once convulsions were controlled, the heart rate decreased to 90 bpm and the rectal temperature was 37.5 degrees celsius. 
Initial diagnostic evaluation included venous blood gas and acid-base analysis, serum electrolytes, packed red cell volume and total solids.  The abnormal findings were marked hypernatraemia (>180 mmol/L; reference range 139-150 mmol/L), marked hyperchloraemia (failed to read), a marked metabolic acidosis with respiratory compensation (pH 7.197, HCO3- 12.4 mmol/L, base excess -15.7 mmol/L, PCO2 31.8 mmHg), hyperlactataemia (4.14 mmol/L; reference range 0.6-2.9 mmol/L) and an azotaemia (creatinine 135 umol/L; reference range 44-115umol/L).

Intravenous fluids were administered at a rate calculated to reduce the plasma sodium levels no faster than 0.5-1.0 mmol/L/h.  When the dog was able, she was offered measured amounts of water to drink orally and the intravenous fluid plan was modified accordingly. The dog improved gradually, neurological signs resolved and she became ambulatory. 

The EPOC (venous blood gases, acid base analysis and electrolytes), and the PCV/TS were repeated 2 hours after initial presentation and then every 4 hours. Despite careful monitoring and adjustment of the fluid therapy plan, the plasma sodium levels decreased from >180mmol/L to 155 mmol/L over the initial 12 hour hospital period, a decrease of Na>1 mmol/L/h. After a period of initial improvement, the patient became laterally recumbent, with an obtuned mentation. The cause for this was suspected to be cerebral oedema following the rapid decrease of plasma sodium levels. Intravenous mannitol was administered 0.5 g/kg over 30 minutes, resulting in an immediate improvement in neurological signs.

The dog remained in hospital for 37 hours.  In that time the electrolytes returned to normal levels and the acidosis, hyperlactataemia and azotaemia all resolved. She made a full recovery and was discharged home.



Hypernatraemia can be caused by a sodium gain or free water loss. Where a sodium gain is present, the cause is often easily identified such as salt ingestion or administration of hypertonic saline or sodium bicarbonate. Free water losses can be more elusive and include inadequate access to water, primary hypodipsia, diabetes insipidus, fever, renal losses, gastrointestinal losses, third spacing, etc.

A helpful way of approaching a patient that has hypernatremia is to assess their volume status (Figure 1). Animals with sodium gain are often hypervolaemic.  Animals with a pure free water loss (e.g., diabetes insipidus, inadequate access to water) are normovolaemic. Those with hypotonic losses (water loss in excess of electrolyte loss) are usually hypovolaemic and include gastrointestinal and renal losses, and third spacing.

In cases of mild to moderate hypernatraemia there may be no clinical signs, especially if the rise in sodium has occurred over many days. However, once plasma sodium levels increase >170 mmol/L, neurological signs such as obtundation, muscular weakness, behavioural changes, disorientation, ataxia, seizures and coma may occur.

Sodium is the main determinant of plasma osmolality.  When there is excessive sodium in the extracellular fluid compartment it becomes hyperosmolar, and water moves from the relatively hypo-osmolar intracellular fluid into the extracellular fluid causing cell shrinkage. The brain can protect against neuronal water loss initially with fluid and ionic shifts and accumulation of organic solutes to prevent large volume loss from the neurones. However, rapid or severe changes to cell volume cannot easily be compensated for. Neurones are the cell-type least tolerant to changes in volume, resulting in a predominance of neurological signs in disorders of sodium balance.

Regardless of the cause, all cases of hypernatraemia are considered to have a free water deficit. Treatment of hypernatraemia involves correcting the free water deficit by providing the animal with water replacement. In mild cases, oral intake of water can be encouraged. However, in more severe cases, intravenous fluid therapy provides less margin for error in controlling the sodium decent. The intravenous fluid of choice is 5% dextrose as free water is the carrier and water is produced through glucose metabolism.

An animal’s free water deficit is calculated using the following formula:Free water deficit (L) = {(current [Na+] ÷ normal [Na+]) – 1} x (0.6 x body weight in kg)

The number of hours over which to deliver this volume is calculated based on the recommended limitation of a drop in sodium no faster than 1.0 mmol/L/h. This prevents rapid redistribution of water across the cell membrane into the intracellular space, which results in cellular swelling.

In the case above the free water deficit was calculated as [(180/144.5)-1] x (0.6 x 18) = 0.246 x 10.8 = 2.66 L.

To return to a normal sodium of 144.5 mmol/L, the plasma sodium in this animal would need to reduce by at least 35.5 mmol/L. Therefore, to reduce the sodium by a rate no faster than 1 mmol/L/h, the free water volume (2.66 L) would need to be administered over at least 35.5 hours. Therefore, the fluid rate of 5% dextrose to be administered would be 2660 ml/35.5 h = 75 mL/h.

Plasma sodium concentration should be measured at least every 4 hours while sodium levels are being corrected. The rate of free water replacement may need to be adjusted if the sodium concentration is decreasing more rapidly than 1 mmol/L/h.

Free water replacement leads to movement of water into cells. If this replacement occurs too rapidly, cells will swell. Neurones are particularly sensitive to this water intake and cerebral oedema can rapidly develop. The clinical signs of cerebral oedema are similar to those of hypernatraemia including obtundation, head pressing, seizures, coma, and changes in behaviour or movement. Cerebral oedema should be suspected when a symptomatic hypernatraemic animal initially improves with free water replacement and then deteriorates neurologically, or an asymptomatic hypernatraemic animal receiving treatment develops neurological signs.

If any of these symptoms develop during treatment, intravenous fluids or oral water intake should be ceased. Plasma sodium concentration should be measured to demonstrate a rapid decrease and treatment for cerebral oedema should be initiated. Treatment of cerebral oedema includes either a single dose of mannitol at 0.5-1 g/kg intravenously over 20 to 30 minutes or judicious administration of hypertonic saline.



DiBartola, SP. Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice. Elsevier 2012.

Silverstein DC, Hopper K. Small Animal Critical Care Medicine, 2nd Ed. Elsevier 2014. 


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