Appendicitis by John H. Tilden (life books to read txt) 📕

the intestinal putrefaction was kept alive by feeding.]

“The pulse from the onset was comparatively frequent, regular and somewhat tense.

“The vomitus was at first composed of the gastric contents, the bile of a peculiarly pure, grass-green, biliverdin color mixed with a yellowish chyme-like material, and in the later stages of the disease showed thin masses having a fecal odor_ (ileus paralyticus)._ In regard to the dejecta, the two passages at the onset of the disease pointed to increased peristalsis; this was of short duration, soon changing to the opposite condition, and until the rupture of the perityphlitic abscess absolute constipation existed.”

[The vomiting would have gone to stay within three days if no drugs nor food had been given; as it was, when real vomiting ceased the opium nausea began.

This patient was not allowed to come into that state of peristaltic elimination that is due in all cases in three days at the farthest, and which would have come to this man if food and drugs had been withheld.]

“Pain upon urination and strangury was due to inflammation of the peritoneal coat of the bladder, in which a noticeable irritation was produced by slight distention as well as by contraction of the bladder. The albuminuria was the well known infectio-toxic ‘febrile’ form; indicanuria was in proportion to tile fecal stasis.

“In the course of the next few days a new symptom was added to this group: Exudation, which was demonstrable both by palpation and percussion. It was the natural consequence of inflammation of the peritoneum, and was both of diagnostic value as indicating general peritonitis and of special value in that, more definitely than the pain, it pointed to the original seat of the affection, which, according to present indications, could only have been an internal incarceration following right-sided inguinal hernia, or femoral hernia, or appendicitis. As neither the history nor the general status (normal condition of the hernial rings) furnished any points of support for the first view, only the diagnosis of appendicitis, that is, of perforation of the appendix, could be made with that degree of certainty attainable in diseases of the abdominal cavity in general.

“After the appearance of these symptoms, a more or less firmly adherent but limited perityphlitic abscess, and a less intense although well developed peritonitis in this region, were assumed; the latter, notwithstanding the painful meteorism, was not necessarily diffuse in the strict sense of the term; the omentum often protects the upper abdominal cavity from infection, as was proven in this case at the autopsy. It is possible that this diffuse peritonitis, which did not in the early period of the affection extend beyond the limited local focus, was not due to the intestinal contents and to bacteria, but chiefly to bacterial toxins which arose from the circumscribed original focus. This fact is pointed out by the prompt retrogression of the diffuse peritoneal symptoms after rupture of the abscess; the diffuse peritonitis of this stage might then be designated a nonbacterial ‘chemical’ inflammation, according to the terminology now in vogue; finally, it was positively a bacterial infection, although the postmortem finding of bacteria in the distant folds of the peritoneum is not proof of this; we know that during the terminal agony or after death these may wander a long distance from the perityphlitic focus.”

[The author plays so fast and loose with the words, “diffuse peritonitis,” that I am reminded of a remark made to me several years ago by a society lady who posed as a pace-setter in all matters pertaining to the intricacies of what one should and should not do. The subject was one that I did not know much about at that time, and upon which I am not much better informed at present. It was on diamonds. I complimented her on a very beautiful sunburst. She took the compliment modestly, of course. The center diamond was large and, I thought, of uncommon brilliancy, and I remarked, “That center stone properly mounted would make a very fine solitaire.” She then informed me that she once owned a cluster of solitares.

The author tells us that at first the diffuse peritonitis probably did not extend beyond the local focus; this of course is exactly what I am contending for from first to last and I insist that there was not peritonitis proper until the occurrence of the fatal relapse.

It is somewhat surprising that this article should be selected to represent the last word on this subject, when the author builds his treatment upon diffuse peritonitis; then enters into a lengthy analysis and explanation of symptoms to fit the diagnosis and treatment and before he is through with the subject he declares that the diffusion is confined to the focus of infection.

If I did not know something of the worth of words I am not sure but such an excellent explanation might persuade me!! If I did not know from experience that all this is theory, beautiful theory, it might be very hard to resist!]

“After the symptoms of local and general inflammation with their secondary signs in the stomach and intestine had lasted for six days, suddenly a complete change took place: The nervous, anxious, extremely distressed patient became feeble and scarcely complained at all; his formerly congested face was pale and elongated, the nose pointed and cool; the skin lost its turgescence and warmth and was covered with a cold sweat; the bodily temperature also fell, the pulse became small and frequent but remained quite regular, the abdomen became softer and to a great extent lost its sensitiveness; the vomiting decreased to a few painless attacks,”

[Wholly due to the opium and morphine given]

“and singultus disappeared: A picture which, to a certain extent, is a combination of collapse and narcosis although not to the degree of profound loss of consciousness, being the picture of an intoxication in sharp contrast to the preceding febrile state.”

[That is exactly what I stated above—a case of narcotism. How is it possible that the author, recognizing the narcotism, feels it incumbent to give other explanations?]

“Just as the affection had suddenly developed to its full height at the onset of the disease, and much more swiftly than, for example, is the case in phlegmon of the external walls, so with extraordinary rapidity did the clinical picture assume a new type. In this respect we must consider the very great area of the peritoneal folds, their numerous lymphstomata, and their intimate relation to the circulation, and we are impressed with the fact that fluids and solubles, as well as formed products, are rapidly absorbed by the peritoneum.

“Somewhat less rapidly than this, but nevertheless in the course of a few hours, another change took place, a favorable turn following the rupture of pus into the intestine. Here we were dealing with a well known and familiar phenomenon; if this occurs in the peritoneum the effects are particularly well marked; similarly as in the case of a phlegmon which rapidly disappears with the discharge of pus even although the inflammation extend beyond the pus focus, the symptoms of diffuse peritonitis promptly disappeared after the rupture. Very likely, as has already been stated, the symptoms of diffuse peritonitis in the first stages of the disease are to be referred to a chemical inflammation of the serosa, i. e., one due to toxins and without the ingress of bacteria; and it must be remembered that the clinical picture of this chemical peritonitis cannot be differentiated from that of the severe bacterial form. With the rupture of the abscess, the entrance of poisons into the free peritoneal cavity, and their resorption by the extensive peritoneal surfaces, as well as the vomiting and the intestinal paralysis, ceased. The taking of nourishment again be came possible.

“The point of rupture formed adhesions, the natural drainage of the peritoneal ichorous focus ceased, perhaps a new influx of inflammatory material from the perforated appendix also took; place. There was a fresh relapse of the local peritonitis which extended beyond the boundaries of the limiting adhesions, and permitted the invasion by bacteria of the free abdominal cavity. This, time the severe toxic picture of collapse immediately followed, and with marked decrease in cardiac strength led to death.

“Doubtless the patient might have been saved in the first stages of the disease by the evacuation of the abscess; the incision would at first have acted similarly to spontaneous rupture into the intestine, but the relapse would have been prevented by permanent drainage, and a radical cure might have been brought about by the immediate or subsequent removal of the appendix.

“Opium, no doubt, had a favorable effect upon the affection. By relieving intestinal irritability, and by bringing about a mild degree of narcosis, the patient was kept quiet and this materially assisted in limiting the severe perityphlitic suppuration in the first stage of the disease.”

[All of which is positively not true, as I have witnessed for years.]

“If, as it unfortunately happened, the point of rupture had not immediately closed again, if it had remained open until suppuration ceased and contraction and healing of the perforated appendix had taken place, opium would have been regarded as instrumental in saving the patient, and unquestionably, at least to some extent, justly so. Among other factors in the treatment, the relief to the intestine by the suspension of nourishment was of paramount importance. The subcutaneous saline infusion had an obvious but, naturally, only a transitory effect.”

The subcutaneous saline infusion is another ridiculous habit. It would really be amusing if it were not so tragic, to see patients driven to the edge of the great divide and then see the innocent doctor throw out an impotent life line.

The absolute innocence displayed by this professional man, from first to last, his belief in himself and the mechanism of his theory and practice exculpate him from the charge of carelessness, neglect of duty or even that he didn’t know what he is doing. He does know what he is doing in a way. He works as exactly as a Waltham watch and he thinks about as much as the stem that winds the watch.

I cannot agree to the summing up of this case. There was not at any time, previous to the relapse and death of this patient, what we understand as peritonitis. A postmortem examination might have shown the intraperitoneal covering, of that portion of the cecum involved in the inflammation, slightly inflamed, but it is not reasonable to believe that the inflammation was of a toxic character unless adhesive inflammations can be so called.

Inflammation is always the same, it matters not what the exciting cause may be. It is an exaggerated physiological process. If there is inflammation of any part of the body it means that there is an exaggeration of function. Its intensity will be in keeping with the exciting cause. If the cause is intense heat or cold, or a corroding acid or alkali, the local action may be great enough to destroy the part; the inflammation following will be of the contiguous structure outside of the killing range of the cause, and it will be a simple—non-toxic—inflammation unless the secretions thrown out in excess of the reparative need are retained by dressings or prevented in some other way from draining away. If these secretions are kept bound on the raw surface by dressings until they decompose—yes, until the fermentation causes germs—the wound will become infected, and to what extent will depend upon the amount of malpractice—carelessness or ignorance—to which the case is subjected.

If the inflammation is caused by decomposition or a toxic agent, the extent of the process will depend upon the integrity of the part infected and the state of the general health, also upon the local environment—such as pressure interfering with the circulation of the blood.

In this fatal case there was the constitutional derangement and