Etiology

• Sodium Sodium and chloride are essential minerals involved in many physiological processes.
• Salt is provided to cattle by provision of salt licks or through addition of salt to their feed rations.
• Salt poisoning can occur in various circumstances including:
  • Mixing errors in commercial oral electrolyte or milk replacers in calves.
  • Overdose of salt-containing feed supplement.
  • Limited or no access to drinking water, eg due to:
    • Over-crowding.
    • Insufficient water provided, particularly during hot weather.
    • Drinking water frozen.
    • Failure of mechanical waterers.
  • Drinking water containing a high concentration of sodium (≥ 500 ppm) such as:
    • Salt water ponds which remains available when fresh water has frozen.
    • Brackish water.
    • Water that has accumulated in salt lick blocks.
    • Oil well sludge, as brine is used as a flush during drilling of oil wells and effluent may contain up to 100,000 ppm of salt.
    • Water that has passed through a water softener. This may contain high sodium concentrations and should not be mixed with milk replacer unless verified to contain low concentrations of sodium <100 ppm).
  • Dehydration due to hot weather and insufficient water intake.
• A high salt intake can be tolerated if there is sufficient access to water.

Predisposing factors

General

• Animals with concomitant risk of dehydration, eg diarrhea, are more at risk.

Pathophysiology

• Sodium is a major contributor to the osmolality of the extracellular fluid and an increase in sodium will increase the plasma osmolality.
• This increase results in the extracellular fluid becoming hypertonic and water moving from the intracellular to the extracellular space.
• The net result is cellular dehydration and vascular overload.
• In the central nervous system this causes vascular stasis, thrombosis, brain shrinkage and shearing of intracerebral vessels with subsequent haemorrhage.
• If this initial phase is survived, brain cells increase the osmolarity of their intracellular spaces to avoid dehydration during hypernatremia, main the normal volume of the brain and protect the brain from the severe effects of extracellular hypertonicity.
• The increase in osmolarity occurs over several days and involves cell uptake of Sodium Sodium, Chloride and Potassium Potassium from the cerebrospinal fluid but more importantly there is accumulation of organic osmoles such as taurine, glutamate, glutamine and phosphocreatine within the intracellular fluid of brain cells.
• If hypernatraemia is corrected rapidly the osmolarity of the extracellular fluids falls below that of brain cell intracellular fluid, water moves into cells, causing brain cells to swell. This occurs because brain cells cannot remove organic osmoles from the intracellular spaces quickly.
• Brain cells then become hyperosmotic compared to extracellular fluid. Pressure builds up within the brain causing necrosis of brain cells, convulsions and death.
• Hypernatremia of brain cells results in inhibition of glycolysis.
• Diarrhea may occur due to saline catharsis and osmotic effects.
• The acute toxic dose of salt in cattle is said to be 2.2 g/kg but this depends on water intake.

Timecourse

• Onset depends on the concentration and duration of the salt intake, but signs can occur within a few hours of ingestion.
• Duration depends on the concentration and duration of the salt intake. Recovery can occur within 24 hours in mild cases.
• Death can occur within 4-24 hours after onset of signs.

Epidemiology

• Salt poisoning (water deprivation) may occur in very hot or cold weather due to additional effects of dehydration or frozen drinking water.