Common salt poisoning

• Common salt is an essential nutrient & added to the

feed & ration of animals but it is the quantity
consumed which makes it toxic.

• Excessive ingestion of sodium chloride causes toxicity

& the condition is termed as water deprivation
syndrome.

• All species of animals including human beings &

poultry are poisoned but poultry & pigs are most
susceptible to salt poisoning.
• Feeds containing high quantities of common salt,
accidental over ingestion of common salt or
excessive licking of salt licks kept on the premises.

• One of the important determinants of salt poisoning

is the salt hunger & availability or restriction of water
supply as over consumption of salt can be tolerated
by the animals if sufficient quantity of water is
available to the animals immediately after ingestion
of salt.
• It is difficult to say sometimes about threshold toxic
dose of sodium chloride as consumption of sufficient
quantity of water facilitates excretion of sodium ions.
• 2.2g/kg of salt by mouth is the toxic dose for
ruminants, horse, pigs.
• 6g/kg for sheep, 4g/kg for dogs.
• Toxic dose of salt as a % of the diet is 1.5-2 for cattle
& sheep, 0.25 for pigs & 0.25-2 for poultry when
water supply is restricted.
• When drinking water is freely available, toxic dose for
pigs is 10% of diet while 5-10% for poultry.
 Mechanism of toxicity

• Exact mechanism is not known.

• But sodium ions & water balance are mainly disturbed.

• Excess sodium ions in GIT cause mild irritation & secretion of

water into the lumen of intestine & thus diarrhoea further
resulting into dehydration.

• Absorption of sodium results in hypertonicity of blood,

hypernatremia, shrinkage of kidney tubules, deposition of
sodium crystals in the tubules, anuria, uremia.
• Excess of Na+ in blood stream results in shrinkage of capillary
vascular endothelial cells in the brain & meninges which in
turn stimulate the capillary permeability & escape of water
from blood to extracellular fluid(intracellular dehydration) &
development of brain or cerebral oedema.

• As a result of cerebral oedema, there is increased

cerebrospinal fluid pressure & reduced blood flow to the
brain & thus hypoxia & the clinical signs & lesionsare
observed.
Clinical signs

• General signs of salt poisoning are anorexia,

excessive thirst, salivation, initially diarrhoea
followed by constipation, polyuria followed by
anuria, nasal discharge & weak pulse.

• Body temperature normal but ear & skin are cold.

• There is rigidity of muscles, hyper-irritability,

blindness, stumbling, walking backwards or in circle,
recurrent convulsive seizure, recumbency, coma &
death in a few houre to few days
• Vomiting in dogs, profuse watery diarrhoea with colic
in ruminants
• Diarrhoea with colic, mucus skin faeces, knuckling of
fetlocks, dehydration & prostration in lactating
animals.
• Pruritis, ataxia, dog sitting posture, blindness,
convulsions, comatose & paddling in pigs.
• Intense thirst, respiratory distress, fluid discharge
from beak, weakness, wet faeces & limb paralysis in
poultry.
 Post mortem lesions:
• Congestion & inflammation of gastrointestinal tract.
• Faeces are fluidy & dark or dry.
• Hydropericardium.
• Severe acute inflammation of gastric & intestinal lining.
• Oedema of tissues & body cavities.
• Renal congestion
• Oedema of the cerebral cortex, neuronal degeneration,
disruption of area between cortex & white matter.
• Congestion of liver in chicks, hyperaemia of the organs &
deposition of uric acid in kidneys, ureters & dropping in
mature birds.
Diagnosis:

• History of salt ingestion.

• Clinical signs of poisoning including excessive thirst.
• Post mortem lesion.
• Laboratory investigation indicating plasma sodium
levels of exceeding 150mEq/L in live animals & CSF
sodium level of > 145mEq/L and brain sodium level
>1800ppm in dead animals.
Treatment

• No specific antidote is available.

• Remove the toxic fee.
• Salt free fresh water be made available, however, initially
access of the animal to water should be restricted as large
intake of water will kill the animal by aggravating cerebral
oedema.
• Gastrointestinal tract sedatives.
• Sedatives to counter the CNS stimulation.