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Overview of Salt Toxicity


Excessive salt (sodium chloride, NaCl) intake can lead to the condition known as salt poisoning, salt toxicity, hypernatremia, or water deprivation–sodium ion intoxication. The last term is the most descriptive, giving the result (sodium ion intoxication) as well as the most common predisposing factor (water deprivation.) Salt poisoning is unlikely to occur as long as sodium-regulating mechanisms are intact and fresh drinking water is available.

Salt poisoning has been reported in virtually all species of animals all over the world. Although salt poisoning has historically been more common in swine (the most sensitive species), cattle, and poultry, there are increasing reports of adverse effects in dogs from acute excess salt consumption. The acute oral lethal dose of salt in swine, horses, and cattle is ~2.2 g/kg; in dogs, it is ~4 g/kg. Sheep appear to be the most resistant species, with an acute oral lethal dose of 6 g/kg.

In general, animals can tolerate high concentrations of salt or sodium in the diet if they have continuous access to fresh water. Salt poisoning is often directly related to water consumption and can be reduced significantly or abolished completely by appropriate management of factors such as mechanical failure of waterers, overcrowding, unpalatable medicated water, new surroundings, or frozen water sources. Both swine and poultry on normal diets can be severely affected when water intake is completely restricted or when consuming high-salt diets with moderate water restriction. Increased water requirements increase the susceptibility of lactating cows and sows to salt poisoning, especially in response to sudden restrictions in water.

High concentrations of salt in the diet (up to 13%) have been used to limit feed intake of cattle. Salt-deprived animals or those not acclimated to high-salt diets can overconsume these feeds, making the animals prone to salt poisoning. Improperly formulated or mixed feed can be sources of excess salt. The use of whey as a feed or as a component of wet mash can add to sodium intake. Additional sources of excess sodium can include high-saline ground water, brine, or seawater.

Chickens can tolerate up to 0.25% salt in drinking water but are susceptible to salt poisoning when water intake is restricted. Wet mash containing 2% salt has caused salt poisoning in ducklings. High salt content in wet mash is more likely to cause poisoning than in dry feed, probably because birds eat more wet mash.

Sheep can tolerate 1% salt in drinking water; however, 1.5% may be toxic. It is generally recommended that drinking water contain <0.5% total salt for all species of livestock.

Companion animal exposures to excess salt have included the use of salt as an emetic (no longer recommended) and the ingestion of various salt-containing materials including rock salt and dough-salt mixtures. Dogs have been reported to develop hypernatremia after swimming/playing in the ocean (which contains 3.5% sodium) without having access to fresh water. Horses appear to be rarely affected with classic salt poisoning but can develop it under conditions of increased salt intake and sudden water restriction.

In pigs, early signs (rarely seen) may be increased thirst, pruritus, and constipation. Affected pigs may be blind, deaf, and oblivious to their surroundings; they will not eat, drink, or respond to external stimuli. They may wander aimlessly, bump into objects, circle, or pivot around a single limb. After 1–5 days of limited water intake, intermittent seizures occur with the pig sitting on its haunches, jerking its head backward and upward, and finally falling on its side in clonic-tonic seizures and opisthotonos. Terminally, pigs may lie on their sides, paddling in a coma, and die within a few to 48 hr.

In cattle, signs of acute salt poisoning involve the GI tract and CNS. Salivation, increased thirst, vomiting (regurgitation), abdominal pain, and diarrhea are followed by ataxia, circling, blindness, seizures, and partial paralysis. Cattle sometimes manifest belligerent and aggressive behavior. A sequela of salt poisoning in cattle is dragging of hindfeet while walking or, in more severe cases, knuckling of the fetlock joint.

In poultry and other birds, clinical signs include increased thirst, dyspnea, fluid discharge from the beak, weakness, diarrhea, and leg paralysis.

Excess salt intake in dogs results in vomiting within several hours of ingestion. The clinical signs can progress to weakness, diarrhea, muscle tremors, and seizures.


Postmortem examination may reveal some degree of gastric irritation, including ulceration and hemorrhages. The content of the GI tract may be abnormally dry. Histopathologic lesions may be limited to the brain and include cerebral edema and inflammation of the meninges. During the first 48 hr, swine develop eosinopenia, eosinophilic cuffs around vessels in the cerebral cortex and adjacent meninges, and cerebral edema or necrosis. After 3–4 days, eosinophilic cuffs are usually no longer present. Cattle do not develop eosinophilic cuffs but can have edema of the skeletal muscles as well as hydropericardium. Chickens can also have hydropericardium.

In acute cases, no gross lesions may be present in any species.

Serum and CSF concentrations of sodium >160 mEq/L, especially when CSF has a greater sodium concentration than serum, indicate salt poisoning. Brain sodium concentrations >2,000 ppm (wet weight) are considered diagnostic in cattle and swine. There is a lack of data on normal brain sodium concentrations in other common domestic species, making interpretations of brain sodium concentrations difficult. Characteristic history and clinical signs, along with clinical pathology, postmortem findings, and analyses of feed or water for sodium content are essential for establishing a diagnosis.

In swine, differential diagnoses include insecticide poisoning (organochlorine, organophosphorus, and carbamate), phenylarsonic poisoning, and pseudorabies. In cattle, differential diagnoses include insecticide and lead poisoning, polioencephalomalacia, hypomagnesemic tetany, and the nervous form of ketosis.

There is no specific treatment for salt poisoning. Immediate removal of offending feed or water is imperative. Fresh water must be provided to all animals, initially in small amounts at frequent intervals to avoid exacerbation of clinical signs. On a herd basis with large animals, water intake should be limited to 0.5% of body weight at hourly intervals until normal hydration is accomplished, usually taking several days. Severely affected animals can be given water via stomach tube. The mortality rate may be >50% in affected animals regardless of treatment. In small animals before the onset of clinical signs, the acute ingestion of salt can best be treated by allowing the animal access to water and closely observing it for several hours. Emetics may be used in dogs if known ingestions occur and the dog is not yet showing clinical signs.

For all affected animals, the treatment should slowly return the animal to normal water and electrolyte balance over 2–3 days. Quickly lowering the serum sodium concentration will increase the osmotic gradient between the serum and the brain, with water following the gradient into the brain and increasing the likelihood of severe cerebral edema.

Monitoring serum sodium concentration is the first step in treating individual animals. Serum sodium levels should be lowered at a rate of 0.5–1 mEq/L/hr. The use of slightly hypertonic IV fluids has been recommended to reduce the likelihood of cerebral edema. IV fluids can be made to approximate the serum sodium concentration of the animal, or a solution containing 170 mEq/L sodium can be used initially, with the concentration decreased as clinical signs improve. In dogs, a series of warm water enemas given at intervals of several hours has helped reduce acutely increased sodium levels. If brain edema is suspected, mannitol, dexamethasone, or DMSO may be helpful.

Last full review/revision December 2014 by Larry J. Thompson, DVM, PhD, DABVT

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