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3. Putrefactions which develop in the alimentary residues produce poison.

The injection of 2.5 grammes of putrefied meat is sufficient to kill.

4. Fecal matter is toxic; this toxicity is due chiefly to potass. and ammonia; this represents about one fifth of the total toxicity to the union of organic principles, in which are included alkaloidal substances.

We know, then, from the preceding statement of Bouchard, demonstrated quite conclusively, that in normal or physiological conditions there is material for intoxicating, and how with a kidney functionally free, if the production of toxic material is accidentally abundant, it may accumulate in the blood in the proportion capable of causing symptoms of intoxication to arise. When fermentation has become active in the whole length of the digestive tube, we see produced characteristic phenomena.

The unusual development of gas determines abdominal meteorism and tympanites, arising either from stomach or intestines, or may be carried to the latter from the former.

May have eructations, belching, preceded by burning sensations in the stomach, or may have pyrosis in the esophagus or pharynx.

May have acid vomiting, the acidity of which is due to acetic acid, rarely hydrochloric. Changes in the teeth may be due to mouth acidity.

Contents of intestines may have become abnormally acid, provoking diarrhea by irritation of mucus membrane, but also irritative to the skin outside of the rectum, as in the acid dyspepsia of infants.

The red tongue being another prominent evidence.

Here there is substituted an acid reaction of the intestinal contents for the normal.

There is change in color of the stools; bile is expelled of a green color; sulphureted hydrogen is diminished.

Bismuth given with the idea of diminishing the diarrhea, gives no longer to the dejecta a black color, for there is no longer formed sulphide of bismuth.

There are ocular demonstrations of the production of acid fermentation in the digestive canal.

When fermentation of putrid character predominates, an excessive disengagement of sulphureted hydrogen, ammonia and its sulphate, which manifest themselves to our olfactories.

Paralled to these objective phenomena, there exist those of a subjective character, viz: fatigue, headache, buzzing in the ears and deafness, disturbances of sight, vertigo, and depression.

With a healthy kidney acting well there may be no further trouble, but if the renal elimination is insufficient, may have evidences of uremic intoxication, through simple exaggeration of intestinal fermentation.

If, as illustrated by Bouchard, abundant vomiting has produced oliguria, we may have coldness established, paralysis of the vessels of the skin, cramps, convulsions, coma, paralysis, death even, while the kidney itself may not be really diseased.

For the development of such accidents, it is only necessary that the quantity of toxic material introduced into the blood should exceed the eliminating power of the kidney.

The variations of urinary toxicity may be in similar cases the measure of the degree of toxicity, depending on the amount of urine eliminated ; and we find under intestinal fermentation an increase in the toxicity of the urine.

If intestinal fermentation is controlled or suppressed, there is a lessening of urinary toxicity.

There is only a lessening, not a disappearance, because only one of the natural sources of the toxicity is controlled.

The toxicity of the urine can be lessened by neutralizing the products of putrefaction, by acid or charcoal, preventing their absorption, or by preventing putrefaction through intestinal antisepsis by means of beta-naphthol, salol, benzosol, or iodoform.

This fact has also been proven by chemistry, by Staedler (1848) finding phenol in the urine ; 1877, Bauman found phenol in fecal matter, this no doubt passing from the digestive tube into the urine.

1826, Tildeman and Greulin, in the duodenum, discovered a substance which gave a red color with chlorinated water, indol.

Senator has more recently confirmed the above in his analysis of meconium. He does not find indican in the urine or idol in meconium.

Martin established that in every disease of the intestinal tract there was increase in urinary indican.

Salgowsky made researches and found phenol and cresol.

We see them increase like indican in the urine in certain forms of diarrhea and in intestinal obstruction.

It has been observed by Senator, Riess, and Litten not only in diabetes mellitus, leucocythemia, but in grave dyspeptic states, carcinoma of stomach, all cases in which anomalous fermentation is produced in the digestive canal.

We know, therefore, that if these putrid substances are found in excess, there may result an intoxication without disease of the kidney.

It is natural, then, to ask if there is no other protection than the kidney-possibly the liver?

The experiments of G. H. Roger in his injections of extract of putrid meat into the portal vein, found less toxic influence than when injected into the general circulation.

We can but conclude that the liver is an organ of protection to the economy; that it arrests more or less the general toxic effect.

Other channels may be by rapid intestinal action, active diarrhea, or the forming of the intestinal contents into a hard fecal bolus, almost inoffensive because it no longer allows for absorption.

The breath and skin of the patient have a disagreeable odor. Where the toxemia is of chronic type, there is an ashen hue due to the toxic pigment contained in the blood.

Bouchard explains the fever following an aseptic laparotomy as due to toxemia, and points to the relief usually obtained by intestinal evacuation.

Special forms of intoxication have been observed following the formations of sulphureted hydrogen in excess; the ingestion of fish, preserved goose, and sausage.

A principle analogous to atropine, producing redness, mydriasis, and dryness of the skin, was developed from the sausages.

Various psychic disturbances, chlorosis, and inanition are among the sequelæ of auto-toxenia.

The prognosis necessarily depends upon the cause: Where the retained material can be eliminated and the absorption cut short, the system is given a chance to react from the primary trouble.

Thus lavage in gastric dilatation does not cure the non-retracting stomach, but it relieves the headache, restlessness, etc., and permits assimilation.

Constipation represents the mildest form and strangulation the severest form of intoxication.

Absorption necessarily ceases when the feces become hardened, as in constipation.

The treatment of auto-intoxication is almost specific.

Since we are treating a symptom and not a disease, we must expect relief and not a cure always.

Prophylaxis consists not only in the avoidance of high temperature and the ingestion of pure foods, but also in the eschewing of such foods as each individual has found to be indigestible. Thus potatoes may be perfectly digestible by one person, yet another, apparently normal person, may fill with gas after their ingestion.

Lavage and enemata are the speediest ways of removing the poisonous material from the alimentary canal.

Einetics are dangerous, since they may be followed by oliguria, permitting the poison already absorbed to remain in the system. Non-depressing salines are useful.

The antipyretic becomes a matter of individual choice.

Among the favorites may be mentioned beta-naphthol, charcoal, salol-arsenite of copper—thymol, guaiacol and its compounds, boric acid, and the mineral acids.

Lavage, enemata, and auto-zymotic, and stimulation seem to formulate the approved treatment.

LOUISVILLE.

PUERPERAL ECLAMPSIA: ITS CAUSE AND INDICATIONS FOR

TREATMENT.*

BY W. B. STONE, M. D.

Puerperal eclampsia, as defined by all our authors, is epileptiform convulsions peculiar to and occurring in pregnant females before labor, during confinement, or after delivery.

For the sake of brevity and needless recitation, I shall purposely omit its symptomatology, and take it for granted that you are all historically, if not clinically, acquainted with its symptoms in detail.

Our older authors recognized three varieties, the hysterical, the apoplectic, and the epileptic, from their fancied resemblance to this malady.

That a paroxysm of hysteria, a stroke of paralysis, or a fit of epilepsy can and often does occur during pregnancy or shortly after delivery, all will admit; but that the clinical history or prodromic symptoms of puerperal eclampsia are wanting in hysteria, apoplexy, or epilepsy, no one can deny.

Thus we see, so far as these diseases are concerned, puerperal eclampsia has no relation to nor dependence upon the causes of either hysteria, apoplexy, or epilepsy, but is a disease sui generis.

*Read before Southern Kentucky Medical Association, 1898.

I believe there have been about five theories advanced upon puerperal eclampsia from Hippocrates down to the present time, each one purporting to approximate at least the true etiology of the disease, all adinitting, however, the true pathogenesis to be as yet undiscovered. The first theory was, “that it is a cerebro-spinal congestion;" (2) “that it is a general cerebral anemia;” (3) “ that it is an anemia of the cerebro-spinal centers with meningeal congestion ; " (4) "that it is a neurosis;" (5) that it is a blood poisoning, nephritic in its origin, the toxic agent by some claimed to be urea, by others carbonate of ammonia, and still by some one thing, by others another.

And I believe we might with prudence add the sixth theory, which admits all the claims of the other five, but asserts the etiological factor to be stipulated in the sum total of the fifth theory; that it is not urea, carbonate of ammonia, extractives nor soluble ptomaines alone, but a retention in the blood of all these excrementitious substances, which it is the function of the excretory organs, especially the kidneys, to eliminate, and that this inability to eliminate on the part of the kidneys is due to nephritis brought about by mechanical pressure on the renal vessels by the fetus during gestation.

As it would require too much time, and, besides, be beyond the scope of this little paper, to enter into an explanation and discussion of the merits and demerits of all these theories, suffice it to say that all, no doubt, are correct in so far as the pathological lesion claimed in each theory is often found, and incorrect in a great many of them, inasmuch as, no doubt, effect has often been taken for cause. That is to say, no doubt in one case there has been found cerebro-spinal congestion, in another general cerebral anemia, and another anemia of cerebrospinal centers with meningeal congestion, and still another a neurotic element may seem to play an important role in the precipitation of an eclampsia; yet these lesions are in all probability the post hoc rather than the propter hoc.

It is to the merits of this last or sixth theory, that the primary cause is a toxemia resulting from renal inflammation induced by inechanical pressure on the renal vessels by the fetus in utero during gestation, aided by excrementitious material accruing from all other sources, such as constipation, arrest of perspiration, and doubtless fetal metabolism, that I desire to call your attention at present.

While all our leaders assert the cause to be about as above stated, yet they all leave us in the dark as to how the mechanical pres

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