Fevers and Blood poisoning

Another proof that death when it occurs is from failure of the circulation is, that in non-fatal cases with well-marked gastro- enteric symptoms, the temperature rises gradually during the first four hours, and as gradually subsides; whereas in fatal cases it rises rapidly to 104 degree F., and then declines rapidly to below the normal before death, thus indicating failure of the heart. In fatal cases from larger doses, the above symptoms increase to intestinal haemorrhage, purging, collapse, and death.

Post-mortem.-There is found extravasation of blood in patches underneath the endocardium of the left ventricle, sometimes on the papillary muscles, sometimes on or in the neighbourhood of the valvular curtains. Similar though less marked appearances are seen in the right ventricle. There are similar points of ecchymosis on the pleura and pericardium. The spleen is enlarged and full of blood. The mucous membrane of the stomach and small intestine is intensely injected with detachment of the epithelium and exudation of sanguinolent fluid distends the lumen of the gut.

These appearances indicate a general tendency to congestion and capillary haemorrhage as well as locally, congestion and capillary stasis of the gastro-intestinal mucous membrane with shedding of the epithelium, as the nature of the disorder. The state of the blood plays a great part in the morbid process; it is darker in hue, and the corpuscles arrange themselves in clumps instead of rolls; many of the blood- corpuscles are partially dissolved in the liquor sanguinis, communicating to it a red colour: a large quantity of the haemoglobin is lost by evacuation of the bowels, and conversion into bilirubin; the partial disintegration of the white corpuscles, by liberating the fibrino-plastic ferment, is supposed to be one cause of the capillary stasis.

“The symptomatic and pathological effects are substantially the same in man, and indeed, the analogy between the symptoms and morbid appearance and state of the blood in septicaemia after wounds and the experimental poisoning with Sepsin is very close.

“Now, granting that the powerful agent producing these remarkable effects may be expected to act therapeutically as an alternative in morbid states which present the pathological simile to them, what are these morbid states, and how are they to be recognised in the complex phenomena of fever in the human subject? To answer this we must inquire what is the cardinal point in the proximate cause of pyrexia with which we have to deal in employing a directly acting remedy? To this question-at least as regards the chief phenomenon which determines the name pyrexia, viz., the increased heat-the critical review of the experiments of Senator, Leyden, and others by B. Sanderson, {* See Blue Book, 1876, No 1 Appendix.*) gives a reply.

“The temperature of the body being dependent on the production and discharge of heat. of which the former is a function of living protoplasm, the later a function of the organs of circulation, respiration, and secretion, the question arises, whether pyrexial increase of temperature depends upon the former or the later.

To this Dr. B. Sanderson thus replies (p. 45):- “Two possibilities are open to us. One is, that fever originates in disorder of the nervous centres, that by means of the influence of the nervous system on the systemic functions, the liberation of heat at the surface of the body is controlled or restrained, so that “by retention” the temperature rises, and finally, that the increased temperature so produced acts on the living substance of the body, so as to disorder its nutrition. The other alternative is that fever originates in the living tissues, that it is from first to last a disorder of the protoplasm, and that all the systemic disturbances are secondary.

The facts and considerations we have had before us are, I think, sufficient to justify the definitive rejection of the first hypothesis in all its forms; for, on the one hand, we have seen that no disorder of the systemic functions, or of the nervous centres which preside over them, is capable of inducing a state which can be identified with febrile pyrexia; and, on the other, that it is possible for such a state to originate and persist in the organism after the influence of the central nervous system has been withdrawn from the tissues by the severance of the spinal cord. We are, therefore, at liberty to adopt the tissue- origin of fever as the basis on which we hope eventually to construct an explanation of the process.’ It is elsewhere concluded that it is in the protoplasm of the blood and the muscles that take place those changes of activity and disintegration on which depend the changes of temperature, and no doubt the other essential phenomena which characterize fever.

“What, therefore, on these data are we to expect from an agent which shall act directly as curative of the pyrexial state? Not certainly any palpable disturbance of the nervous system which can in health lower temperature by promoting heat discharge, as is expected from large doses of Quinine, or from the merely physical action of cold baths; nor a general support of the vital powers till the specific disease runs its course, as is expected from alcohol, etc. But, on the contrary, a simple modification of the exalted and perverted protoplasmic action in which the proximate cause of pyrexia consists, which shall be of such a nature as to bring it back to health.

Let us assume (without any attempt to prove it, but merely to give an intelligible illustration in explanation) the hypothesis of Beale, that the essence of inflammation and fever consists in a degeneration in the scale of biological development of the bioplasts of the blood and tissues, which involves the production of a more rapidly growing and disintegrating kind of protoplasm; our most complete and perfect conception of a direct remedy would be that of an agent which would act as a specific stimulus to be affected protoplasm, and bring back its germinal development up to the normal plane. This has long been my view of the action of Aconite in inflammatory fever, or, at least, that it acted directly on the pyrexically affected protoplasm, and not on the vaso-motor nerves or centres of the heart, or of the spinal marrow; for reiterated experience has shown that its acts in far too small a dose to exert any directly effect on the heart or its nerves, or indeed, and perceptible effect on them at all.

Now, the living matter or protoplasm is capable of an almost infinite variety of kinds of morbid action according to the predisposing and exciting causes acting on it, and hence pyrexia may vary indefinitely in its character, even independently of the addition of the local lesion proper to the concrete specific fevers; so no directly curative remedy can be applicable to more than a few forms, or even to only one, e.g., Aconite suits inflammatory fevers, and Quinine malarious intermittents, while they would be powerless if interchanged. To what form, then, should we except pyrexin or pyrogen to be applicable?

The true clue to this is given, I think, by the state of the blood, for that is the most marked and important of the signs of septicaemia; the local congestions and extravasations not being so constant or so grave as respects the issue. If we contrast the characteristic hyperionotic state of the blood in inflammatory fever, displaying its bright colour, buffy coat, firm coagulum, and the adherence of the red corpuscles in rolls, with the septicaemic state of blood already described, showing its dark and dissolved state, loose coagulum, the red corpuscles adhering in clumps, and the increase of white corpuscles, we shall see well-marked grounds of distinction.

This latter state of the blood is very similar to, if not identical with, that which belongs to typhous or adynamic fevers, and, indeed, in describing fatal cases of septicaemia after wounds the analogy of the symptoms is so great with these fevers that the word `typhous’ is generally used in describing them. Hence the shortest discrimination of the indications for the use of Pyrexin or Pyrogen may be stated to be the typhous or typhoid character or quality of pyrexia, using these adjectives in their old fashioned sense.

For although the clinical discrimination of enteric fever from typhus is a great gain, it is unfortunate that the word `typhoid’ should have been appropriated to the former, as it either introduces confusion into our nomenclature or deprives us of a hitherto well- understood expression of the character of pyrexia from the name of a specific disease. We shall find it convenient to go back to the terms of Cullen, viz., synochal for inflammatory fever, the typhous or typhoid condition for the low adynamic or asthenic character or quality of fever, and synochus for the mixed kind, which is inflammatory at the beginning and typhous at the end.

I do not know that the more accurate discrimination of the typhous, enteric and relapsing fevers into distinct specific diseases gives any ground for denying the existence of the above distinctions of character in the pyrexial state in general, and therefore, we should still keep up the words inflammatory and typhous or typhoid, as expressive of different qualities or characters of fever, and not of distinct febrile diseases.

James Compton Burnett
James Compton Burnett was born on July 10, 1840 and died April 2, 1901. Dr. Burnett attended medical school in Vienna, Austria in 1865. Alfred Hawkes converted him to homeopathy in 1872 (in Glasgow). In 1876 he took his MD degree.
Burnett was one of the first to speak about vaccination triggering illness. This was discussed in his book, Vaccinosis, published in 1884. He introduced the remedy Bacillinum. He authored twenty books, including the much loved "Fifty Reason for Being a Homeopath." He was the editor of The Homoeopathic World.