I have nothing to add to what is generally known as to the cessation of all natural secretions, especially urine and bile beyond the remark that over and above all the physiological disorders previously enumerated, to which a cholera patient is subject, he must be considered as being more or less uraemic, considering that the secretion of urine is completely wanting. In fact the spasm may partly be due to this precarious condition of the cholera patient. Niemeyer seems to think otherwise, for he tells us that urine and bile are not secreted because there is nothing more contained in the blood to be secreted. When reaction begins, matter changes and as we shall see hereafter, death by uraemia is often met with. His statement to the fact that the intestinal mucous membrane is deprived of its epithelium during the cholera process, calls however for some correction. There may be no epithelial cells. We know, however, that uraemic symptoms often gradually makes their appearance even when the patient steadily declines without signs of reaction, we are then compelled to suppose, that there is throughout the whole course of the disease a small secretion of urea (small in proportion to the whole process of metamorphosis which is necessarily small) retained in the system, owing to arrest of renal action. It is worth studying in connexion with the above whether the cholera ejections contain urea or not (see Physiological and Pathological chemistry by Charles page 432), found in the choleraic stools; they are, however, invariably found within the intestinal canal a few hours after death; so that, strictly speaking, the shedding of those cells is more a post mortem, than a pathological effect. Inasmuch however as post mortem changes may be taken as an indication of the direction in which disorganisation during life takes place, we may still say, with a fair amount of plausibility, that the epithelial cells of the intestinal mucous membrane during the life of a cholera patient are in a state of disorganisation, whereby they are rendered unfit for the physiological task assigned to them. The villi may not be actually denuded during the life time to the cholera patient of their epithelial covering, but as far as the capacity of absorbing food is concerned, they are no better off, than villi actually denuded of their epithelium. This is no gratuitous assumption, for the total absence of the assimilative and even of the absorbing faculty is conspicuous in cholera patients. For further details on the subject under discussion you may consult details on the subject under discussion you may consult Dr. Machnamarra’s Treatise on Asiatic Cholera.
Cholera has often been compared to malarial fever of the malignant type. During the time of the Burdwan Fever I has myself seen some few cases of this class. The cold stage, says Dr. Fayrer in his Climate and fevers of India, is not always free from danger; when the action of the poison has been very intense, the nervous force seems to be overwhelmed by it; an algid state supervenes, the heart fails, the skin becomes cold and clammy and the patient may die in a state of collapse; or, after remaining for hours-it may be forty-eight hours-in this condition, reaction takes place and the hot stage sets in; in other cases after partial reaction, the symptoms of collapse supervene. Happily this is rare. It so closely resembles the collapse of cholera that if the patient be seen for the first time when in that condition, there might be some doubt as to the diagnosis. Instances are recorded by Macculloch and others, of persons having died in a few hours in the Maremma of Tuscany, from the intensity of the poison.
Examples of epidemics, manifesting at a large scale a still closer resemblance between malarial fever and cholera we find recorded by the same writer. Fever in the city (of Amritsar) did not appear in an epidemic form until September; it was preceded by cholera about the beginning of August, of an extremely fatal type, and later on, when marked by fever, there was some difficulty in recognising it in time. The fever which prevailed with its utmost force in September and the early part of October appeared to be of the relapsing fever species but with some affinity to cholera. There were the rigors, fearfully severe headache, insomnia, disordered bowels (often constipated), fever, suppression of urine, with death from coma frequently within a few hours after seizure; but then the ricewater evacuations and vomit of cholera appeared in very many instances during the course of an attack of the fever.
The two diseases, cholera and fever, supposing them to be distinct, certainly masked one another so effectually that diagnosis was extremely difficult at times. The people, by the end of October, began to show the exhausting effects of the epidemic fever, enlarged spleen, anaemia, debility, jaundice, and the usual sequelae told fatally on their enfeebled constitutions. This specific fever was strictly confined to the city, and to those only who had to go inside on duty.
I observed in Kohat, in 1869, an outbreak of fever very similar to the Amritsar epidemic, followed by cholera. It was then observed also that it was and impossibility to tell when the cholera commenced, the symptoms of many cases of the fever being so similar.
It is to be regretted that Dr. Fayrer does not mention anything about the temperature of the choleraic fever patients of the epidemic at Amritsar, which happened as late as 1881. Surely the thermometer should be able to tell us if we have to do with a case of malarial fever subservient to cholera, or vice versa. In malarial fever there is a rise of temperature at the very beginning of, and actually previous to the cold stage; while in cholera there is a fall, and often a very marked fall of temperature from the onset of the attack.
The choleraic fever type is by no means a new pathological evolution; it has been known to the ancient Hindoos, according to Dr. Annada Churn Kastogiri, by the name of Jawartishar, literally, fever with excessive diarrhoea (Indian Annals, January 1877). Dr. Kastogiri, a learned Bengali-physician and a graduate of Calcutta, further remarks:- It has been observed that both may break out simultaneously, or one follows in the track of the other. In practice mixed attacks of cholera and fever are frequently seen, an attack beginning with symptoms of fever may end with cholera, or vice versa.
Of the importance of the temperature as a diagnostic sign in cases of cholera mention has been made just before; the thermometer is, however, of no less value to us as an instrument of prognosis. It is not by the frequency of vomiting and purging, nor by the severity of the spasms that the degree of virulence of a cholera attack is to be judged, but by the depth of the fall of the temperature. Again when reaction has once set in, we shall best know how the patient goes on, by attending to the thermometer. Fluctuations of temperature augurate badly, however favourable the rest of the symptoms may be. A general brightening up of the patient, unaccompanied by any change of temperature often precedes final death. According to the observations of surgeons A. Leith Adams and F.H. Welch during the epidemic at Malta, the thermometer indicated that in the aged and delicate the vital powers gave in to the cholera poison step by step, commensurable with the severity of the attack. Collapse reached, a comparative quietness ensued, followed by the system asserting its superiority or succumbing rapidly. The course from the onset to the termination was gradual with no marked deviations. Not so with the young and healthy. Although the system was impelled to give way to the attack, it was not without a struggle; the collapse was marked by constant attempts at reaction, and this having once set in, the vital powers seemed to overreach themselves in their eagerness to resume their normal condition.
In speaking of the temperature in cholera we must guard ourselves against confounding the external temperature in the axilla, with the inner temperature of the rectum or vagina. In no disease is the difference so great as in cholera, where the cutaneous temperature may be far below, while the inner temperature may at the same time be far above the normal state. This difference of temperature is so much the more remarkable at the stage of collapse. In this stage there is almost a total absence of peripheral circulation, owing to a contraction of the cutaneous vessels, so that what remains of the blood-circulation is concentrated towards the inner parts.
There is another peculiarity connected with the variation of temperature in cholera; namely, the rapid rise of body heat soon after death, and often even a short time before death takes place. It might be suggested in explanation of this apparently strange phenomenon, that the vaso-motor centres, from having been for the most part during the cholera attack in a state of undue excitement, become paralyzed at the time of, and sometimes even soon before death. We have seen that it is the spasmodic occlusion of the cutaneous vessels which is the cause of the vast difference between the internal (high), and external (low) temperature. We further know from Claude Bernard`s experiments, that the spasmodic contraction of those arterial blood-vessels is owing to stimulation of the respective vaso-motor nerves, or of the vaso-motor centres governing them. This state of stimulation, kept up by the toxic action of the cholera poison, ceases with the approach of death, and the consequence would be, that the cutaneous vessels dilate to their natural calibre or even beyond their natural calibre and the difference between the blood contents of the internal and external blood vessels, and consequently between the internal and external temperature would cease to exist; thus the corpse would naturally become warmer than the living body was. But then the rise of temperature in cholera is not only external and relative; their is a real increase of heat production shortly before, or soon after death- an increase which might amount to about 3 or 4 degrees, and sometimes even to more than that. The question arises then: whence comes this increase of caloric production in a dead or a dying body? This is a question which interests the Pathologist, the Physiologist and the Medical Jurisprudent in a like manner, and I shall try to lay before you their respective opinions on the subject.
