Excessive sodium chloride intake can lead to salt toxicosis, also known as hypernatremia or as water deprivation–sodium ion intoxication. Salt toxicosis is unlikely to occur as long as sodium-regulating mechanisms are intact and fresh drinking water is available.
Salt toxicosis has been reported in virtually all species of animals worldwide. Although salt toxicosis has historically been more common in swine (the most susceptible species), cattle, and poultry, there are increasing reports of adverse effects in dogs from acute excess salt consumption.
Etiology of Salt Toxicosis in Animals
In general, animals can tolerate high concentrations of salt or sodium in the diet if they have continuous access to fresh water. Salt toxicosis is often directly related to water consumption and can be reduced notably or abolished completely in production animals by means of 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 toxicosis, 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 toxicosis. 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 toxicosis when water intake is restricted. Wet mash containing 2% salt has caused salt toxicosis 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 or playing in the ocean (which contains ~3.5% sodium) without having access to fresh water. Hypernatremia has also been reported in animals treated with improperly mixed oral electrolyte solutions, remedies for diarrhea, or secondary to treatment with activated charcoal. Horses appear to be rarely affected with classic salt toxicosis but can develop it under conditions of increased salt intake and sudden water restriction.
Mechanism of Action
As serum sodium concentration increases, water moves along the osmotic gradient out of the interstitium and intracellular fluid into the extracellular fluid. Rapid development of hypernatremia results in cerebral dehydration and neuronal cell shrinkage, with the brain then pulling away from the calvarium, which disrupts the blood supply to the brain and can cause tearing of vessels and hemorrhage. To prevent excess water loss to the extracellular fluid, cells of the brain increase their intracellular osmolarity through the generation of idiogenic osmoles. Sodium diffuses passively across the blood–brain barrier and eventually redistributes into neural tissues; however, high intracellular sodium concentrations inhibit energy-dependent pathways for transporting sodium out. With changes in cellular osmolarity in chronic water deprivation, once water access is restored, due to a rapid decrease in serum sodium concentration, intracellular water influx into neurons along the osmotic gradient can lead to cerebral edema.
The acute oral lethal dose of salt in swine, horses, and cattle is ~2.2 g/kg; in dogs, it is ~4 g/kg, but clinical signs of toxicosis can appear after ingestion of 2–3 g/kg. Sheep appear to be the most resistant species, with an acute oral lethal dose of 6 g/kg.
Clinical Findings for Salt Toxicosis in Animals
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 hours.
In cattle, signs of acute salt toxicosis involve the GI tract and CNS. Salivation, increased thirst, vomiting (regurgitation), signs of abdominal pain, and diarrhea are followed by ataxia, circling, blindness, seizures, and partial paralysis. Cattle sometimes display belligerent and aggressive behavior. A sequela of salt toxicosis in cattle is dragging of hind feet 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 after ingestion. Clinical signs can progress to weakness, diarrhea, muscle tremors, and seizures.
Postmortem examination after salt toxicity 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 hours, 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.
Diagnosis of Salt Toxicosis in Animals
History, clinical signs, and excess sodium concentrations in serum, CSF, or postmortem brain tissue samples
Analysis of food, water, or suspect material for sodium content
Serum and CSF concentrations of sodium >160 mEq/L, especially when CSF has a greater sodium concentration than serum, indicate salt toxicosis. Brain sodium concentrations >2,000 ppm (wet wt) 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 clinicopathologic findings, postmortem findings, and analyses of feed, water, or suspect material 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.
Treatment of Salt Toxicity in Animals
Controlling seizures if present, evaluating the animal's hydration and electrolyte status, and then, over several days, restoring the animal's normal balance of water and electrolytes
Other supportive care as needed
There is no specific treatment for salt toxicosis. Immediate removal of offending feed, water or other suspect material 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 treatment on an individual animal basis. This information can be used to correct the free water deficit in the animal, based on the following formula:
FWD = 0.6 × BW × (current [Na+]/desired [Na+] – 1)
where FWD is free water deficit (in L), BW is body weight (in kg), and [Na+] is serum sodium ion concentration (in mEq/L).
Not more than 50% of the FWD should be replaced in the first 24 hours, with the remaining deficit replaced in the following 24–48 hours. Serum sodium concentration should be lowered at a rate of 0.5–1.0 mEq/L per hour, with the slower rate recommended for cases of chronic hypernatremia. In dogs with acute hypernatremia, the use of warm-water enemas (6.6–11 mL/kg) repeated every 1–2 hours has been suggested. In acute hypernatremia without clinical dehydration, the use of 5% dextrose solution (at 3.7 mL/kg per hour) in combination with a loop diuretic has been suggested to decrease serum sodium at 1 mEq/L per hour. Diuretics such as furosemide can be used to prevent the development of pulmonary edema during fluid therapy.
The use of slightly hypertonic IV fluids has been recommended to reduce the likelihood of cerebral edema developing. Intravenous fluids should be made to approximate the serum sodium concentration of the animal, or the clinician may start with a solution containing 170 mEq of sodium/L and decrease this concentration as clinical signs improve. On an individual animal basis, seizures should be controlled (with diazepam or other seizure control agents); if brain edema is suspected, mannitol, dexamethasone, or dimethyl sulfoxide (DMSO) may be helpful.
Excess salt intake with lack of fresh water intake can cause hypernatremia on either an acute or a chronic basis.
Clinical signs differ depending on the species and chronicity (acute or chronic onset).
Treatment is directed at controlling clinical signs and slowly correcting hydration and electrolyte balance with monitoring of serum sodium concentration.
For More Information
Thompson LJ. Sodium chloride (salt). In: Gupta RC, ed. Veterinary Toxicology. 3rd ed. Academic Press, 2018;461–464.