Direct salt poisoning may occur following ingestion of excessive salt. Chronic salt poisoning may also occur when animals are ingesting normal levels of salt (or slightly increased levels) and are also experiencing decreased water intake. The pathogenesis generally involves a combination of water deprivation, variable levels of salt exposure, and then unlimited access to fresh water.
Excessive salt ingestion may lead to acute poisoning with gastroenteritis resulting from local irritation to the mucosa of the stomach and intestines.
Chronic salt poisoning can result in accumulation of sodium ions in tissues including the brain. If animals then gain unrestricted access to fresh water, fluid moves to tissues to restore normal salt-water balance. The presence of elevated levels of sodium can lead to excessive fluid retention and cerebral oedema with increased intracranial pressure and nervous signs. The disease is more serious if there is access to salt or salty water during the period of water deprivation. Intravascular haemolysis may occur during rehydration as water is drawn back into red blood cells.
Animals subjected to long transport in hot dry conditions and that are offered free access to water of low salt content at the end of the journey may be at risk of developing this condition. This may happen in the live export process.
Within a few hours of quenching thirst there is onset of acute nervous signs similar to those of polioencephalomalacia. Affected animals are dull, blind and head press or they may stand with the head pulled back. Urine may be dark from haemoglobinuria caused by intravascular haemolysis. Collapse, convulsions, coma and death follow development of nervous signs.
At necropsy there may be flattening of the gyri of the brain (from swelling associated with cerebral oedema), intense congestion of the abomasal mucosa, and hydropericardium.
Laboratory confirmation requires brain submitted in buffered formalin for histology.
The dark urine that sometimes accompanies salt poisoning may serve to differentiate it from the main differential diagnoses of polioencephalomalacia, lead poisoning, enterotoxaemia and insecticide poisoning.
There are no specific treatments and the condition is usually fatal. Treatment with thiamine (vitamin B1) is not effective. Remove access to water and salt immediately.
Prevent access to salt and salt water during periods of water deprivation. Consider providing restricted access to water at frequent intervals following long periods of water deprivation. Aim to rehydrate animals over 24 hours.