Salt Toxicity

Salt Toxicity

Introduction

            Salt toxicity (sodium chloride, NaCl), which is more appropriately called “water deprivation sodium ion toxicosis” can result when excessive quantities of salt are ingested and intake of potable water is limited. Salt toxicity is unlikely to occur as long as salt-regulating mechanisms are intact and fresh drinking water is available. It has been reported virtually in all species of animals all over the world. It is more common in swine (the most sensitive species), cattle, and poultry. Sheep are relatively resistant. The acute oral lethal dose of salt is 2.2 g/kg in swine and 6.0 g/kg in sheep.

Etiology

            Salt toxicity is directly related to water consumption. Water intake in animals can be reduced significantly or abolished completely due to factors such as mechanical failure of waterers, overcrowding, unpalatable medicated water, new surroundings, or frozen water.

            With water deprivation, sodium propionate, acetate, or carbonate can produce the same toxicosis as sodium chloride.

            Excessive intake of dietary salts, the effects exacerbated by limited availability of drinking water; poisoning may occur via the diet when too much salt is included in food rations.

            Poisoning from overingestion arises when the salt is made freely available after a period of salt deprivation.

                       

Feeder pigs on feed containing only 0.25% salt have had salt poisoning when water intake was limited, yet even 13% salt in feed may not produce poisoning when adequate fresh water is consumed. Swine feed should contain 0.5-1% salt, and fresh drinking water should always be available.

            Feeding whey or brine containing 3-4% salt can result in toxicosis in most livestock and poultry species.

            Similarly, ingestion of 1-3 kg of salt in deprived animals can result in salt toxicosis even when water is available, especially in cattle.

           

Chickens can tolerate up to 0.25% salt in drinking water but are susceptible to sodium ion toxicosis when water intake is restricted.

            Wet mash containing 2% salt caused 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.

            Cattle and sheep on range can develop salt poisoning when a high percentage of mineral supplement is provided, and the water supply is limited or saline.

            Sheep can tolerate 1% salt in drinking water; however, 1.5% may be toxic.

            It is generally recommended that drinking water should contain <0.5% total salt for any species of livestock. Chronic salt poisoning in cattle can cause gastroenteritis, depressed appetite, weight loss, and dehydration.

Mechanism of toxicosis

            Sodium causes extracellular hyper-osmolality which results in very significant intracellular dehydration. Toxicity varies in relation to the availability of drinking water. If water intake is restricted and sodium chloride intake is normal, a relative poisoning occurs. If combined with water deprivation, polioencephalomalacia develops when the water intake returns to normal.

Toxic doses

Toxic dose in g/kg by mouth:

            Cattle – 2; horses – 2; pigs – 2; sheep – 6; dogs – 4.

Toxic dose as a % of the diet:

            Where drinking water is restricted:

                        Cattle – 1.5-2; horses – 1.5-2; pigs – 0.25; poultry – 0.25-2.

            Where drinking water is freely available:

                        Pigs – 10; poultry – 5-10.

Clinical Findings

            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 affect the GI tract and CNS. Salivation, increased thirst, vomiting (regurgitation), nasal discharge, 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. Dehydration in lactating animals.

           

In poultry, increased thirst, dyspnea, fluid discharge from the beak, weakness, diarrhea, and leg paralysis are some of the common signs of salt poisoning; respiratory difficulties, respiratory distress; paralysis.

            In dogs, vomiting, profuse watery diarrhoea with colic; convulsions, pronounced hyperexcitation; intense thirst (variable).

Lesions

            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.

            The GI mucosa may be inflamed and congested and may have pinpoint, blood-filled ulcers. Cattle do not have eosinophilic cuffs; they have gastric inflammation or ulceration (or both), edema of skeletal muscles, and hydropericardium. Renal congestion.

            Chickens have hydropericardium.

           

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

Diagnosis

            Serum and CSF concentrations of sodium >160 mEq/L, especially when CSF has a greater sodium concentration than serum, are indicative of salt poisoning.

            In brain (cerebrum), >1800 ppm of sodium (wet wt) is compatible with toxicosis. Characteristic brain lesions and analyses of feed or water for sodium content are useful for establishing a diagnosis.

           

In swine, differential diagnoses include insecticide poisoning (organochlorine, organophosphorous, 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

            There is no specific treatment.

            Immediate removal of offending feed or water is imperative.

            Fresh water must be provided to all animals, initially in small amounts at frequent intervals.

Ingestion of large amounts of water may exacerbate neurologic signs due to brain edema. Severely affected animals should be given water via stomach tube.

            The mortality rate may be >50% in affected animals regardless of treatment.

            In small animals, slow administration of hypertonic dextrose or isotonic saline may be useful.

            Symptomatic and eliminatory: Cardiac stimulants; diuretics (in particular carbonic anhydrase inhibitors).