§ 694. Fatal Dose.—The smallest dose of oxalic acid known to have destroyed life is, according to Dr. Taylor, 3·88 grms. (60 grains); but recovery has taken place, on prompt administration of remedies, after eight times this quantity has been swallowed.
With regard to oxalate of soda, or binoxalate of potash, 14·2 grms. (half an ounce) have been taken without fatal result, although the symptoms were very serious; and it may be held that about that quantity would usually cause death. Oxalic acid is not used in medicine, save as a salt, e.g., oxalate of cerium.
§ 695. Effects of Oxalic Acid and Oxalates on Animals.—The first cases of poisoning by oxalic acid occurred early in the nineteenth century, a little more than fifty years after its discovery. Thompson[683] was the first who attempted, by experiment on animal life, to elucidate the action of the poison; he noted the caustic action on the stomach, and the effects on the heart and nervous system, which he attributed simply to the local injury through the sympathetic nerves. Orfila[684] was the next who took the matter up, and he made several experiments; but it was Robert Christison[685] who distinctly recognised the important fact that oxalic acid was toxic, quite apart from any local effects, and that the soluble oxalates, such as sodic and potassic oxalates, were violent poisons.
[683] Lond. Med. Rep., vol. iii. p. 382.
[684] Traité de Toxicologie.
[685] Edin. Med. and Surg. Journ., 1823.
§ 696. Kobert and Küssner[686] have made some extended researches on the effects of sodic oxalate on rabbits, cats, dogs, guinea-pigs, hedgehogs, frogs, &c.—the chief results of which are as follows:—On injection of sodic oxalate solution in moderate doses into the circulation, the heart’s action, and, therefore, the pulse, become arhythmic; and a dicrotic or tricrotic condition of the pulse may last even half a day, while at the same time the frequency may be uninfluenced. The blood-pressure also with moderate doses is normal, and with small atoxic doses there is no slowing of the respiration. On the other hand, toxic doses paralyse the respiratory apparatus, and the animal dies asphyxiated. With chronic and subacute poisoning the respiration becomes slower and slower, and then ceases from paralysis of the respiratory muscles. The first sign of poisoning, whether acute or chronic, is a sleepy condition; dogs lie quiet, making now and then a noise as if dreaming, mechanical irritations are responded to with dulness. The hind extremities become weak, and then the fore. This paresis of the hind extremities, deepening into complete paralysis, was very constant and striking. Take, for example, from the paper (op. cit.) the experiment in which a large cat received in six days five subcutaneous injections of 5 c.c. of a solution of sodic oxalate (strength 1 : 30), equalling ·16 grm.; the cat died, as it were, gradually from behind forwards, so that on the sixth day the hinder extremities were fully motionless and without feeling. The heart beat strongly. The temperature of the poisoned animal always sinks below the normal condition. Convulsions in acute poisoning are common, in chronic quite absent; when present in acute poisoning, they are tetanic or strychnic-like. In all the experiments of Kobert and Küssner, lethal doses of soluble oxalates caused the appearance of sugar in the urine.