ISSN 2398-2993      

Salt poisoning


Nicola Bates

James Breen

VPIS logoUniversity of Nottingham logo

Synonym(s): Sodium poisoning, Water deprivation


  • Cause: water deprivation or ingestion of fluid containing high sodium concentration.
  • Signs: gastrointestinal and neurological signs.
  • Diagnosis: high sodium concentration in biological and environmental samples.
  • Treatment: monitoring of sodium blood concentrations and fluid therapy.
  • Prognosis: generally poor even with treatment.



  • 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.
Water with a high salinity is a greater risk to livestock than feed containing a high concentration of salt because they have no access to fresh water to dilute it.

Predisposing factors


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


  • 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.


  • 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.


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


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login


This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login

Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Ollivett T L, McGuirk S M (2013) Salt poisoning as a cause of morbidity and mortality in neonatal dairy calves. J Vet Int Med 27 (3), 592-5 PubMed.
  • Senturk S, Cihan H (2004) Salt poisoning in beef cattle. Vet Human Toxicol 46 (1), 26-7.
  • Ross O (2000) The management of extreme hypernatraemia secondary to salt poisoning in an infant [letter]. Pediatric Anaesthesia 20, 110.
  • Van Leeuwen J A (1999) Salt poisoning in beef cattle on coastal pasture on Prince Edward Island. CN Vet J 40 (5), 347-348 PubMed.
  • Smith E J, Palevsky S (1990) Salt poisoning in a two year old child. Am J Emerg Med 8 (6), 571-572 PubMed.
  • Moder K G, Hurley D L (1990) Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature. Mayo Clinical Proceedings 65, 1587-1594 PubMed.
  • Hardy R M (1989) Hypernatremia. Vet Clin North Am Small Anim Pract 19 (2), 231-240 PubMed.
  • Pringle J K, Berthiaume L M M (1988) Hypernatremia in calves. J Vet Int Med 2, 66-70 PubMed.
  • Martin T, Morgan S, Edwards W C (1986) Evaluation of normal brain sodium levels in cattle. Vet Human Toxicol 28 (4), 308-9 PubMed.
  • Pearson E G, Kallfelz F A (1982) A case of presumptive salt poisoning (water deprivation) in veal calves. Cornell Vet 72 (2), 142-9 PubMed.
  • Sandals W C (1978) Acute salt poisoning in cattle. CN Vet J 19 (5), 136-7 PubMed.
  • Trueman K F, Clague D C (1978) Sodium chloride poisoning in cattle. Aust Vet J 54 (2), 89-91 PubMed.

Other sources of information

  • George L W, van Meter D C (2015) Salt poisoning (with or without concurrent water deprivation). In: Large Animal Internal Medicine. 5th edn. Ed: Smith B P. Elsevier Mosby, USA.
  • Sockett D, Behr M J (2014) Sodium toxicity in neonatal dairy calves. AAVLD Annual Conference Proceedings, Kansas City, MO. pp 85.
  • National Research Council (2005) Mineral tolerance of animals. 2nd revised edition. Washington DC, The National Academies Press, pp 361-371.
  • Osweiler G D (1996) Toxicology. Williams & Wilkins, USA. pp 351-358.
  • Osweiler G D, Carson T L, Buck W B & Van Gelder G A (1985) Clinical and diagnostic veterinary toxicology. 3rd edn. Kendall/Hunt Publishing Company. pp 167-170.

Can’t find what you’re looking for?

We have an ever growing content library on Vetlexicon so if you ever find we haven't covered something that you need please fill in the form below and let us know!


To show you are not a Bot please can you enter the number showing adjacent to this field

 Security code