On Snake-Poison: Its Action and Its Antidote

by A. Mueller

The sensory sphere remains comparatively unaffected in mild cases, and in the early stages of more serious ones, but when paresis has deepened into paralysis, sensation becomes ever more blunted, and with the advent of coma, of course, quite extinct. Reflexes, both superficial and deep ones, are also completely abolished at this period of the poisoning process, and the nerves of special sense do not react against any, even the strongest possible stimulation. The eye stares vacantly into a glaring light held close before it, and the widely dilated pupil shows no sign of reaction. The ear also appears deaf to any noise, and strong ammonia vapour is inhaled through the nose like the purest air, whilst pricking, beating, and even burning the skin elicit not a quiver of a muscle.

Feoktistow's experiments with regard to reflexes, more especially their restoration by strychnine, differ in their results entirely from Australian observations. Whilst we have no difficulty in restoring them with the drug on man as well as the domestic animals, his experiments on frogs were a failure, and merely showed a decided antagonism between the two poisons. He did not succeed in restoring the reflexes, and, instead of following up with experiments on the higher animals, he trusted implicitly to his results on frogs, and thus lost his opportunity.

G. Irregularities in the Action of Snake-poison.

There is in the whole range of toxicology not a single condition known to us in which the symptoms, both in chronological order and in their strength and relation to each other, show as much variety as those of snake-poison. Experienced observers will agree with the writer that it is but rarely we find two cases of snakebite exactly alike in the symptoms they present. Some of these puzzling variations have already been alluded to, but it is necessary to consider them a little more in detail. Apart from quantitative differences in the poison imparted, they arise principally from the strange capriciousness with which the poison concentrates its action on special nerve centres and leaves others comparatively intact.

The nearest approach to regularity and orderly sequence of the symptoms, as described in the foregoing pages, we find in Australia after the bite of the tiger snake (Hoplocephalus curtus) and the brown snake (Diemenia superciliosa), more especially that of Queensland. Here we can trace the action of the poison distinctly from centre to centre, from the lowest part of the anterior cornua up to the cortex cerebri, and even throughout the sympathetic ganglia as far as they are patent to observation. The poison of these snakes is extremely diffusible and quickly absorbed. It spreads with rapidity and nearly equal force over all the motor centres, the symptoms following each other so quickly as almost to appear simultaneous, though, in reality, successive. But even the poison of these snakes leaves the arms only slightly paretic, when paralysis in all the other voluntary muscles is well pronounced, and does not paralyse them until coma has set in. It also touches the respiratory centre but slightly. Sometimes coma is light and the patients can be roused for a little while, at other times it is deep and lasts till death. But even greater variations are observed occasionally. In one very extraordinary case of tiger snakebite, the patient, a child of 9 years, remained conscious to the last, and after vomiting blood freely died under symptoms of heart failure. In rare cases the symptoms resemble those of cobra poison.

If we turn from these to the black snake (Pseudechis porphyriacus) a different picture presents itself. Its poison does not produce so deep a coma and often none at all. The patients generally feel drowsy and fall asleep, but are easily roused and sometimes awake spontaneously. There is also not the same amount of muscular paralysis. They are frequently able to walk a few steps with assistance and can move in bed, the arms especially being almost free from paresis. But the insidious poison none the less does its work, though its effects are less patent. It concentrates its action on the vaso-motor centre. The victims from hour to hour become more anæmic in appearance through increasing engorgement of the abdominal veins. Anæmia of the nerve-centres hastens the collapse, and from the combined effects of this and heart failure death takes place suddenly and quickly as if in a fainting fit. Here then we have an approach to the effects of viper poison which is also shown in the greater amount of swelling and effusion around the bite and in the bitten limb.

This approach is still closer in the poison of the death adder (Acantophis antarctica). There is generally much extravasation of blood locally. Muscular paralysis is also less pronounced, but sudden collapse from vaso-motor paralysis not unfrequently takes place, when the patients fully conscious are still able to sit up. That leading feature of viper poison, diapedesis with hæmorrhage, does not occur with either.

If we turn from Australian to Indian snakes, the peculiar tendency of the poison to concentrate its action on special nerve-centres becomes still more marked. The predilection of the cobra poison for the respiratory centre has already been dwelt on. More remarkable and strange is the action of the Indian viper-poison on the minute ganglia in the vaso-motor nerve ends, which control the capillary circulation, and by their paralysis bring about extensive hæmorrhage through diapedesis.

It is quite impossible for us with our present scanty knowledge to account for these peculiarities and irregularities in the action of a poison, which we know now to accomplish its destruction of animal life by one uniform design and principle of action. That the protean forms under which the poison-symptoms present themselves are one and all the result of reduction and suspension of motor nerve currents may now be accepted as a well proven and fully established scientific fact. But why the effects of one and the same cause are so varying in their appearance, why the poison of different varieties of snakes, and even that of the same variety under different circumstances, make such a capricious selection among the various motor nerve-centres we can not explain and probably never will. Chemical analysis of the dead poison, no matter how minutely and elaborately it may be effected, will probably never throw much light on the "why" of this strange puzzle, for the subtle phenomena of life are apt to elude the grasp of the analyst. We have to do with a poison transferred from one living organism into another one and modified in its action by the condition of the giver and the constitution and peculiarities of the recipient quite as much probably as by slight variations in its chemical composition. Accepting the "why" of these phenomena like that of many other ones, simply as a fact not to be accounted for at present, we must be content to know "how" they are effected, and, what is of more immediate and paramount importance to know, that we now have an antidote that will deal successfully with them all, that the convulsions and hæmorrhages of the Indian viper-poison and the asphyxia of that of the cobra will yield as readily to strychnine, when properly and boldly applied, as the coma and general paralysis following the bite of the deadly tiger snake.