Introduction



I would even go further than Dr. Goodeve and maintain that there exists a natural, although by no means necessary connexion between the two states of the blood vessels above described. It is the task of the vaso-motor centres to regulate the calibre of the blood vessels all over the body, and it does so by means of the vaso-motor nervous system. And we know how it is done. Stimulation of a vaso-motor nerve causes contraction, while depression causes dilatation of the arterial blood vessels under its control. When, therefore, the flow of blood stagnates in one part of the body, we may be sure to find some other region of the same body where there is a corresponding increase of the flow of blood; and under certain climatic conditions or epidemic influences, this increase, or flux of blood, is likely to take place within the abdominal viscera. In fact a diarrhoea following a chill is an example-on a small scale, it is true, yet a fair example-of what is going on in spasmodic cholera at the stage of vomiting and purging. Cold, as is well known, has the effect of contracting the arterioles; there arises in consequence a local congestion; and we find often enough that such a congestion is followed by loose stools, as a sign of increased circulation and more or less serous exudation within the intestinal canal.

We have then only to suppose the morbific agent in the case of cholera to be a specific poison-that is to say a poison which, within certain limits invariably observes the same course of action in order to understand how it comes, that in this disease the venous congestion in the lungs is invariably connected with certain specific phenomena occurring within the alimentary canal.

In advocating the purely neurotic nature of this cholera variety I repeat, that I do not mean to say that the blood is, throughout the whole attack, free from any morbid changes, considering that it must necessarily become deficient in oxygen at the very onset of the disease and in the measure as the disease advances and profuse watery discharges from mouth and rectum take place in the shape of vomiting and purging, there is a new source of impoverishment of the blood; known as it is, that these discharges contain, besides the watery importance, various salts in solution.

But while there cannot be the slightest doubt that the cholera poison tends to de-vitalise the blood of its victims, it may still be doubted whether the haematic poisoning is brought about directly, or by means of the vaso-motor nerves. If we are entitled to judge from the march and nature of a phenomenon upon the way and mode in which it is brought about, then we cannot help coming to the conclusion, that in the spasmodic variety of cholera the spasms are primary, and all the further changes ensuing during the progress of the disease are secondary to those spasms. Of course, in speaking of the spasms peculiar to cholera as the source of all the ensuing disorders, I do not merely mean the spasms of the extremities, but those of the pulmonary arteries, as manifested at the onset of the disease by the intense dyspnoea.

This dyspnoea might be, and actually has been accounted for, by the supposition that the cholera patient labors patient labors all along under a state analogous to gaseous asphyxia. In fact some pathologists went actually so far as to call the spasmodic variety of cholera, Cholera Asphyctica. According to their view it was invariably and in all varieties, the blood which was primarily poisoned in cholera. The incipient dyspnoea, it was contended, is owing to the blood having been rendered unfit to absorb oxygen.

Since Dr. Parkes has, however, observed that the autopsy of cholera victims shows the pulmonary capillaries to be invariably empty; that the blood is moreover arrested within the arteries of the lungs, before reaching the capillaries, there cannot be any further doubt about the spasmodic nature of the disease, at least as far as the pulmonary circulation is concerned.

I quote here again from Dr. Goodeve:-`When death occurs in collapse, the disease has not lasted long enough to cause organic changes; such changes as there are, are chiefly in the distribution of the blood. The capillaries of the surface are empty and the blood is chiefly found in the large vessels of the lungs and right side of the heart and in the veins and various capillaries of the intestines.

And then Dr. Goodeve mentions that previous to Dr. Parkes’s observation, it was commonly thought that the lungs are gorged all over with venous blood; but Dr. Parkes has shown, and his observations have since then been repeatedly confirmed, that the gorged parts in the lungs are the vessels on the right side of the heart and the pulmonary artery in the roots of the lungs, from the right side of the heart to the smaller branches. While the smaller vessels, the pulmonary capillaries, the pulmonary veins and the left side of the heart were nearly empty. In fact the blood is not arrested in the capillaries of the lungs as in common asphyxia, but in the arteries short of them.

There can hardly be any doubt concerning the reason, why in cholera unlike asphyxia, the blood is prevented from entering the pulmonary capillaries; it is the contracted state of the small arteries which does not allow the blood to pass through them into the capillaries. And this contracted state again is owing to the spasm of the muscular coat of the arteries, or, in first instance, to a morbid excitement of the vaso-motor nerves governing them.

Let us now compare spasms occurring during a state bordering on asphyxia-spasms known as asphyctic convulsions-with what is going on in the spasmodic variety of cholera as described by Hahnemann.

When an animal is placed in a chamber, in which the air is rarefied, the following occurs; With the impoverishment of oxygen which the blood undergoes under such circumstances, there is generally an increase in the carbonic acid of that fluid, and these changes in the gases of the blood as they make themselves felt in the medulla oblongata, the seat of the respiratory centres, at once cause the respiratory movement to become slower and deeper, under the influence of the accessory muscles of respiration; this change in the respiratory movements constitutes dyspnoea. Dyspnoea is a regulating act, for in the majority of cases it leads to an increase in the quantity of oxygen contained in the blood, and then itself ceases. If the impoverishment in oxygen proceeds further, general spasms of all the muscles of the body set in (clonic convulsions); the centre which presides over these convulsions is situated in the medulla oblongata, so that we must suppose that the stimulus which leads to normal respiration, if it be increased beyond a certain degree, exerts its action not only on the respiratory, but on neighbouring centres which were normally less irritable. Later on a contraction of the muscular coats of blood vessels occurs which exerts an action upon the heart. (Hermann.)

The succession of abnormal phenomena in the case of threatened asphyxia is then as follows:-1. Dyspnoea. 2. Clonic convulsions, following more or less the rhythm of inspiration and expiration; then 3. Contraction of the blood vessels.

In the spasmodic variety of cholera we find however, turning to Hahnemann`s description, the following succession of symptoms: 1. Dyspnoea, accompanied by tonic spasms and coldness all over, which means as much as contraction of the blood vessels. 2. Increased dyspnoea with clonic spasms. Now the tonic spasms preceding the clonic ones, cannot be owing to the respiratory struggle; they must then be idiopathic.

While there can then hardly be any reasonable ground for dispute, as to the mode of action of the cholera poison in the spasmodic variety, there seems to be room enough left for difference of opinion, with respect to the non-spasmodic variety of the disease. In this variety which represents by far the majority of cases, at least in India, there is always a premonitory stage, characterised by malaise, disordered digestion, diarrhoea. Cholera here is then ushered in by a state of mal-nutrition, which points to a vitiated state of blood. The temperature of the body is, besides, not disturbed during the premonitory diarrhoea, so that there is hardly ground to accuse the vaso-motor nervous system of the mischief going on in the visceral region. Here is what Professor Niemeyer has to say about this variety of cholera:

Out of the villi, which are denuded of their natural protection, takes place a constant, copious transudation of serum into the gut; therefore the rice-water discharges upward and downward, by which cholera is characterised. These villi, being deprived of their epithelium, lose their capability of absorbing the fluid which the patient takes as drink; consequently the patient constantly loses fluid, but gains none. The next natural consequences of this must be, that the blood becomes dark and thick in latter stages, even black, tarry, ropy, semi-coagulated. During the transudation into the intestinal canal, it appears that the diffusion currents from the blood into various structures are diminished, while on account of the density of the blood, the inverse currents from these structures to the blood are augmented in rapidity; in this way fluids are drawn from muscles, the viscera, and in fact from most of the tissues. Thus all the tissues become dry and reduced in volume; and nose becomes pointed, the cheeks fall in, the eyeballs sink back into their orbits, the skin wrinkles on the fingers like washerwomen’s and remains as a fold wherever pinched, and even pathological exudations, which had resisted all medication-for example serous exudations of the pleural cavities or within the synovial membranes of the joints-are completely absorbed, and moist eruptions and ulcers become dry like parchment. And further, it explains the cessation of all natural secretions, such as saliva, tears, sweat, urine and bile, simply because there is nothing more contained in the blood to be secreted.

Leopold Salzer
Leopold Salzer, MD, lived in Calcutta, India. Author of Lectures on Cholera and Its Homeopathic Treatment (1883)