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The Medical Woman.

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Contributed Articles

CARBOLIC ACID GANGRENE.

By W. E. LEIGHTON, M. D., Instructor in Surgery, St. Louis University.

My reason for presenting a paper on the subject of carbolic acid gangrene is: (1), to condemn the sale of such a powerful agent as carbolic acid to the public, who use it not only for all sorts of medicinal purposes; but often with suicidal intent; (2), to warn those members of the profession who use carbolic acid in the form of moist compresses that unpleasant results not infrequently follow its use when other less dangerous and more efficacious remedies could have been employed; and (3), to suggest a new factor, possibly two, in the production of carbolic acid gangrene of fingers and toes.

In regard to the first two reasons no further reference is required. The third reason, possible new factors in the causation of this form of gangrene, I have summarized at the conclusion of the article.

Following the discovery of Lister, the use of carbolic acid as an antiseptic became popular alike with physician and laity. The first reported case of gangrene following the use of carbolic acid seems to have been made by Kellock' in 1877, who reported two cases, one of which occurred in 1871. Many cases have since been reported, but up to 1900 Harrington' was able to collect only 132 published cases. Undoubtedly, however, this lesion is much more common than would appear from the literature, as the majority of cases probably go unreport ed. The author of the section on gangrene in Von Bergman's System of Surgery claims to have at least four or five new cases each year. Within two years I observed four cases of carbolic acid gangrene of fingers at the Jewish Dispensary of St. Louis, in the service of Dr.

*Read before the St. Louis Medical Society, November 21, 1908.

1 Kellock, (Canada Lancet, 1877).

2 Harrington, (American Journal of Medical Science, 1900).

Seelig, through whose courtesy I am reporting the cases.

Case 1. A young man of twnety-three came to the dispensary with the history of having cut his finger the previous night. He went to the drug store and was advised to use carbolic acid. He saturated a bandage and wrapped up the finger. The next morning on removing the bandage he found his finger had turned black and felt numb. Examination of the contents of the bottle showed it to be a 95 per cent solution of carbolic acid. The second and third

digits of the left third phalanx were discol

ored and cold. The skin was hard and was much contracted. An alcohol compress was applied but without relief. Several days later a line of demarcation having formed, the finger was amputated.

Case 2. A boy of ten years of age cut his thumb. The father applied a carbolic acid compress and brought the boy to the dispensary the following day. The thumb was discolored but showed some evidence of vitality. The strength of the carbolic acid was unknown. Alcohol compresses were applied and for several days the finger appeared to retain its vitality, but finally the terminal digit sloughed

away.

Case 3. A young man of nineteen applied a carbolic acid compress to a small abrasion on his finger. The next morning the finger appeared discolored but still showed circulation and was warm to the touch. Alcohol compresses were employed and although the skin sloughed away on the dorsum of the finger, we were able to save it.

Case 4. A little girl of eight appeared one noon at the dispensary with the following history: The night before while playing with her father's razor she cut her finger. The father procured from a drug store some carbolic acid, which proved on examination to be a 95 per cent solution. He washed the finger with it, but becoming alarmed at the skin becoming white, he washed the finger with water and bandaged it with a moistened cloth. On removing the bandage next morning, he found the finger blackened. He brought the child to the dispensary at noon within eighteen hours after

injury. (Fig. 1.) The index finger of the left

Fig. 1.

hand showed a superficial wound on the radial side of the first digit. The skin of the two terminal digits was blackened, hard and contracted. The finger was cold and there was no evidence of vitality. The condition was explained to the father and an alcohol compress was applied. Several days later the child came back to the dispensary. The finger at this time presented a condition of dry gangrene with a well marked line of demarcation. The patient was referred to St. Luke's Hospital, where the finger was amputated by Dr. Mudd, to whom I am indebted for the specimen.

Pathological Examination: The specimen was sectioned at different levels. A study of these sections proved most interesting. In the healthy tissue above the line of demarcationone of the main arteries presented marked arterio-sclerosis, a microscopical microscopical drawing of

Fig. 2.

which I have included. (Fig. 2.) This condition

of arterio-sclerosis was present throughout the entire finger. At the line of demarcation thrombosis of the vessels had taken place. Proliferation of connective tissue-cells and new formed blood vessels were seen throughout the section. Below the line of demarcation in the gangrenous area thrombosis was not marked and very little blood was to be seen in the vessels. All the tissues were necrotic. The features of special interest in this study were the presence of arterio-sclerosis in the healthy tissue and the absence of blood in the blood vessels throughout the gangrenous area.

In endeavoring to account for the cause of carbolic acid gangrene, several theories have been advanced, which have been best summarized by Freeman': (1) That all the carbolic acid fails to dissolve, the heavy molecules sinking to the bottom, thus forming a stronger application than was intended; (2) that the acid causes extreme contraction of the arterioles through the vaso-motor nerves; (3) that the difficulty arises from direct chemical action upon the blood vessels and tissues, accompanied by thrombosis; (4) that an acute edema is produced, the tension of which, in the resisting tissues of the toes and fingers, is destructive to vitality. It does not seem unlikely that any one of these factors might at times be at fault, or even all of them combined, and that tight bandaging also might be occasionally concerned, although this has been denied by some investigators.

One of the earliest contributions to the literature of the subject was made in 1886 by Neill of Edinburg, describing the action of carbolic acid on the peripheral nerves. "Kortum,' quoting the work of Neill, and referring to the well known local anaesthesia produced by this agent, concluded that trophic changes may be brought about in the nerves underlying the applied drug, and as a consequence the local death ensues."

"In 1890, Frankenburg, writing on the subject, stated as a conclusion of his experiments, that weak solutions of carbolic acid 1 to 3 per cent are far more dangerous than strong ones. He observed disintegration of red and white blood corpuscle, stasis of the circulation, thrombosis first in the capillaries, then in the veins and arteries, resulting in gangrene."

"Joseph Levai" of Budapest, doubting the theories of Frankenburger and Kortum, that the gangrene was produced by the peculiar action of carbolic acid upon the nerves and blood vessels, began a series of investigations, which were published in 1896, showing that the death of the part is due to the direct chemical action on all parts of the tissue. He showed that car

3 Freeman, (Keens Surg.. Vol. 1).

4 Kortum, (Brougham, N. Y., Medical Record).

5 Frankenburger, (Broughan, N. Y.. Medical Record). 6 Levai, (Harrington American Medical Science, 1900).

bolic acid has no specific quality for the production of gangrene; but that other dilute chemical might produce the same effect. Five per cent solutions of muriatic acid, nitric acid, sulphuric acid, acetic acid, and caustic potash produced gangrene when applied for 24 hours in the form of a moist compress. The histological examination showed that in the beginning each of the dilute chemicals when so applied produced the same effect; the epithelial layers became edematous and loosened. As soon as a way has been prepared to the deep layers each agent produced in a different way the same result, namely necrosis of the tissues. The death of the part takes place in layers downward, and effects not only the nerves and vessels, but all the tissues at the same time. Maceration of the skin having taken place as the result of the prolonged action of a watery solution, the penetration of the chemical becomes easy.

In addition to the chemicals mentioned by Levai, weak solutions of creolin, lysol, and campho-phenique have caused gangrene when applied in the form of moist compresses.

In 1897, Honsell' concluded that following upon the destruction of the superficial layers of the skin, the carbolic acid penetrated to the blood vessels, causing at first contraction but later dilation. With this dilatation, the blood current slowed, and a transudate was poured out into the cellular tissue, which blocked the circulation, and the thrombosis resulted. The thrombosis of the vessel was not as Frankenburger believed, the cause, but the result of the necrosis.

10

Another point which was noted by Warfield and Brougham," of this country, and by Muller of Strasburg, was the fact that on plain surfaces gangrene was not apt to occur, but that complete envelopment of the part with a car bolic acid compress seemed essential for the production of the gangrene. It is this statement which brings us to the consideration of a new factor in the production of carbolic acid gangrene of fingers, which so far as I have been able to learn has never been mentioned before, i. e., the mechanical obstruction to the circulation of the part due to the peculiar action of the carbolic acid in causing a contraction and hardening of the skin.

The effect of carbolic acid on the skin is to produce numbness and tingling, followed by loss of sensation. The skin turns white, but depending on the length of the application, the color changes to yellowish brown, grayish black, or black. The skin becomes hard and shriveled. This contracted and leathery-like condition of the skin is very pronounced. It is

7 Honsel. (Lexer and Bevan, General Surgery).

8 Warfield. (Phil. Medical News, 1890).

9 Brougham. (N. Y. Medical Record, 1899).

10 Muller, (Gazette de Medical de Strasbourg, 1899).

this latter condition pictured so beautifully in Harrington's article and so noticeable in all our cases to which we would call attention. The skin of the finger was hard, and the cir cumference of the finger was less than on the corresponding side, in our cases. This hardened and contracted skin combined with the transudate poured out from the vessels underneath, as described by Honsell, appears to us to be a decided factor in the production of the gangrene.

A case described by Levai would seem to bear out this theory. He observed a patient who. had applied a carbolic acid compress to the middle of a finger resulting in a bandlike burn; the distal portion of the finger being uninjured. For several days pricking this part of the finger caused bleeding, almost proving that the circulation was unimpaired until the secondary inflammatory reaction occurred, blocking the circulation and causing gangrene.

In conclusion: The two factors which I have tried to present are the following: (1) The mechanical construction to the circulation due to the contracted and hardened skin, which acts like a tight bandage applied to the part. (2) The possibility of a sclerotic artery, which is not uncommon in the young, playing a part in some of these cases as it undoubtedly did in the case which I have just described.

GONORRHOEAL PARAURETHRITIS CAUSING FREQUENT AUTOINFECTION.*

By JOSEPH L. BOEHM, M. D., Professor Genito-Urinary Diseases, St. Louis College of Physicians and Surgeons.

In 1902, a case of diffuse septic peritonitis due to the formation of periurethral abscesses, rupturing into the pelvic cavity and burrowing into the peritoneum, was reported by me to the City Hospital Alumni Society. (Medical Fortnightly, Jan. 11, 1904.) I have the urogenital organs, removed at autopsy, in my possession and have often examined them with much interest. For the past six years I have closely observed cases of urethral fistulae and periurethral abscesses and have concluded that many cases of so-called urinary infiltration are primarily conditions of urethral follicular ab scesses. The leakage of urine into the sinuses, resulting from rupture of these chronic abscesses, is a secondary consideration, often attributed to urethral stricture or other complicating conditions.

This idea actuated me to closely and carefully observe the urethra and its numerous follicles and the following data of cases have

*Read at Urological Section meeting of St. Louis Medical Society, January 29, 1909.