Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 83

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

USA > Ohio > Hancock County > Findlay > Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens > Part 83

Note: The text from this book was generated using artificial intelligence so there may be some errors. The full pages can be found on Archive.org (link on the Part 1 page).

ince the predisposing cause for the spondylolisthesis he same as in Case I, and we likewise had to do ubtedly congenital spondylolysis interarticularis of the fifth lumbar vertebra. from which the olisthesis eloped. At the time of death the olisthesis was leveloped, but it would in all probability have in- ent had the individual lived; since, in the absence on of synostoses, no mechanism existed to check g.

[useum specimen 6651 (Figs. 5, 6 and 7). This ained from a 55-year-old peasant who committed ging, August 9, 1909. The history gave no inti- existence of any abnormality on the part of the in, and the skeleton was tolerably strongly built. he viscera at autopsy, it was noticed that the . the fourth and fifth lumbar vertebrae was more usual, and also that the left transverse process bar vertebra was very wide.

ful examination, it was found that a slight olis- ttent of 1 cm. had occurred, so that the body of ar vertebra projected over the anterior margin of

was made possible by a spondylolysis in both rtions of the fourth lumbar vertebra. The lower ertebra was drawn out in a lip-like manner, more

particularly in its anterior portion, which was united by lig- amentous structures with a similar lip-like hyperostosis, about 1 cm. thick, arising from the anterior and upper margin of the body of the fifth lumbar vertebra.

The separation in continuity in the interarticular portions of the fourth lumbar vertebra lay somewhat more posteriorily on the left than on the right side. On the right side it extended be- tween the lower and middle third of the joint surface of the upper articular process, while on the left side it extended only through the lower end of the upper articular process. An irregu- larly bowed bony process extended from the upper articular proc- ess on the right side and grasped like a claw the corresponding interarticular portion. The two fragments of the vertebral arch of the fourth vertebra lay about 1 cm. apart and the intervening space was filled with ligamentous structures.

As compared with the spinous processes of the third, second and first lumbar vertebrae, that of the fourth vertebra was very prominent. The fifth lumbar vertebra presented no lesion in continuity in the interarticular portions, but the inferior margin of its body, like the upper margin of the first sacral vertebra was somewhat hyperostosed. The right transverse process of the former appeared normal, but on the left side there was a bony plate about 3 cm. in diameter and concave below, which was firmly united by ligamentous structures with a correspondingly formed protuberance arising from the upper surface of the left wing of the first sacral vertebra.

The sacrum was made up of six vertebra of which the sixth was formed by the 30th vertebra, which was definitely assimilated to the sacrum, below which came three fused caudal vertebra. On the left side of the 29th and 30th vertebræ there was an irregularly formed, jagged exostosis, while the entire left half of the former appeared to be irregularly hyperostosed. Four sacral foramina were present on either side. The ilio-sacral joints were open and their anterior margins somewhat hyper- ostosed. The pelvic inclination appeared normal. The descend- ing ramus of the right pubic bone presented a fracture, which had healed with a perceptible hump, while the ascending ramus of the left ischium likewise presented a fracture, which had healed by hyperostosis.

Pelvic measurements: Distance between crests, 23.5 cm .; be- tween anterior superior spines, 20.5 cm .; between superior poste- rior spines, 7 cm. Superior strait: Conjugata vera, 9.3 cm .; transverse diameter, 15.5 cm .; right oblique, 11.2; left oblique, 11.2 cm .; right sacro-cotyloid, 9 cm .; left sacro-cotyloid, 9 cm. Plane of greatest dimensions: Antero-posterior diameter, 11.5 cm .; transverse, 10.5 cm. Plane of least pelvic dimensions: Antero-posterio diameter, 11.5 cm .; distance between ischial spines, 8 cm. Pelvic outlet: Distance between tubera ischii, 8 cm. On either side, the sacral portions of the innominate bone measured 7.5 cm .; iliac portions, 6 cm., and pubic portions, 6 cm. The sacrum was 12 cm. in height and 11 cm. in width.

In this specimen, the olisthesis of the fourth lumbar vertebra was likewise the result of a spondylolysis interarticularis. Leav- ing out of consideration the fact that the olisthesis involved the fourth lumbar vertebra, I consider that the interesting feature of the case is the probability that the spondylolysis interarticu- laris could be attributed to a fracture. This would seem to be borne out by the irregular outline of the separation of the interar- ticular portions, which on the right side extended through the superior articular process itself, and in addition by the presence of undoubted traces of fracture on the anterior wall of the pelvis and the lower end of the sacrum. The hyperostosis of the left transverse process of the fifth lumbar vertebra, as well as that of the left ala of the first sacral vertebra might also have resulted from a fracture, but I consider it more likely that they are sec- ondary processes resulting from the olisthesis.

Therefore, I believe that this man had sustained a fracture of

Digitized by Google

JOHNS HOPKINS HOSPITAL BULLETIN.

[No. 1;

the pelvis, involving the arch of the fourth lumbar vertebra, from which the spondylolisthesis had gradually developed, while fixation had not occurred up to the time of his death. It is greatly to be regretted that a history of the case is entirely lacking.

RECENT LITERATURE UPON SPONDYLOLISTHESIS.

Bohn: Ein neuer Fall von Spondylolisthesis. Diss. inaug. Ber- lin, 1892.

Brandenberg: Ein Fall von Spondylolisthesis mit Missbildung des Kreuzbeins. Ztschr. f. orthop. Chir., 1908.

Braun v. Fernwald: Ein Beitrag zur Kenntnis des spondylolis- thetischen Beckens. Arch. f. Gynäk., 1896.

-. Wiederholter Kaiserschnitt in einem Falle hochgradiger Spondylolisthesis. Centralbl. f. Gynak., 1898.

Weitere Erfahrungen über das spondylolisthetische Beck- en. Arch. f. Gynäk., 1899.

Breus & Kolisko: Die pathologischen Beckenformen, 1900.

Buchheister: Geschichte der Aetiologie der Spondylolisthesis. Diss. inaug. Strassburg, 1894.

Chiari: Die Aetiologie und Genese der sogenannten Spondylo- listhesis lumbosacralis. Ztschr. f. Heilk., 1892.

-. Ueber ein neues spondylolisthetisches Becken. Prag. med. Wchnschr., 1905.

Engström: 3 klinisch beobachtete Fälle von spondylolisthetis- chem Becken. Mitth. a. d. gynäk. Klin., Helsingsfors. Cen- tralbl. f. Gynäk., 1904.

Herzfeld: Ein Fall von spondylolisthetischem Becken. Ap Wien. med. Ztg., 1892.

Hübl: Fall von Spondylolisthesis. Centralbl. f. Gynak., 1898. Jellinghaus: Ein neuer klinisch beobachteter Fall von Spondy- listhesis. Arch. f. Gynäk., 1896.

Zur Casuistik des spondylolisthetischen Becken. Ibide 1898.

Lane, Arbuthnot: Case of spondylolisthesis associated with pr gressive paraplegia. Laminectomy, Lancet, 1893.

Lawrence: The re-description of the specimen of spondyist thesis in the Museum of University College. Trans. Obs. Soc. London, 1900.

Neugebauer. Spondyl-Olisthesis et Spondyl-Izème. Paris, 1892 -. Bericht über die neueste Casuistik und Literatur de Spondylolisthesis. Zentralbl. f. Geburtsh. u. Gynāk., 189% Olshausen & Veit: Schroeder's Lehrb. d. Geburtsh., 1902. Schütte: Demonstration eines Uterus mit frischer Kai schnittsnarbe; Operation wegen Spondylolisthesis bei * tischer Periotnitis. Centralbl. f. Gynäk., 1898, u. Monatssch f. Geburtsh. u. Gynak., 1898.

Schwarte: Aetiolige und Genese der Spondylolisthesis. D's inaug. Strassburg, 1901.

Sonntag: Die Pathologie der knöchernen Beckens. v. Winckel Handb. d. Geburtsh., 1905.

Wedekind: Ein neuer klinisch und anatomisch beobachteter Fi von Spondylolisthesis. Diss. inaug. Halle, 1897.

Williams: A case of spondylolisthesis, with description of => pelvis. Am. Gyn. Trans., 1899.

ON DIABETIC ACIDOSIS .* By PROF. A. MAGNUS-LEVY, Berlin.

What do we understand by the term acidosis, a name first employed by Naunyn? Acidosis means the accumulation of acids in the body, in sharp distinction to the formation of acids which are produced, indeed, in every moment of normal life. In the normal metabolism substances of acid or alkaline properties are continuously being formed, but the tendency of metabolism is towards their neutralization. Probably all acids, which we encounter in pathological states, are produced as intermediary products in the normal change of matter. We know this to be true of uric acid, of oxalic acid and of gly- curonic acid, etc .; we may assume it of homogentisic acid, of oxybutyric acid and of others. We, therefore, are not justified in defining acidosis, simply as a formation or as an appearance of acids which do not occur in normal health.

The accumulation of acids, the essential character of acidosis, presupposes in each case a disturbance of oxida- tion. Whether, besides the disturbed oxidation an increased formation of acids is present in acidosis is another question, and must be answered separately in each single case. (If homo- gentisic acid is a regular intermediary product in the katab- olism of phenylamine and tyrosine, as some authors believe, its quantity will depend merely on the amount of katabolized albumen. The alcaptonturic individual will not produce lar- ger quantities of this acid than a healthy person, but in the normal individual total combustion of the intermediary prod-

* Paper read before the Johns Hopkins Hospital Medical Society, May 9, 1910.

ucts takes place, while in the alcaptonuric patient the ace is neither split up nor oxidized.)

Similarly with oxybutyric acid, the principal subject of =! lecture, we must consider whether it is formed in a large amount in diabetes than in normal life.

Besides these that I have mentioned, other acids occur # results of metabolism, such as lactic acid, volatile fscy acids, higher fatty acids, amygdalic acid and carbonic ac! Some among these display specific effects, even when presa only in small quantity, as does uric acid, oxalic acid and pe :- haps the lower fatty acids. These specific effects do not over under the term of acidosis, which simply means the genera result of acidification. This, indeed, takes place only wh acids accumulate in very large quantities, such as are sufficient: to disturb by their acid character the processes taking pla in the organism. If we leave out of question the end produit of all oxidation, carbonic acid, which has scarcely the char- acter of an acid, only one acid remains, to which we mar appir the name of acidosis in the above sense. This acid is the oxybutyric acid and dependent upon it diacetic acid. Whether besides this group another kind of acidosis occurs in pathology. namely, an acidosis produced by lactic acid, as yet seems doubtful.

You are all aware of the fact that oxybutyric acid undergies oxidation into diacetic acid, and that from the latter acetone can be formed. It is hardly necessary to speak at length of the latter body, which has been the subject for intensive nt

Digitized by Google

-- -

los They years. Two authors, Folin and Embden, ad simultaneously that the acetone present in the urine is eliminated as such at all, or only to a small part. It is a luct of self-disintegration of the diacetic acid transferred the kidneys from the blood into the urine. The acetone, which is exhaled by the lungs, is not present in the blood uch, but occurs in the form of diacetic acid.

Thenever tests for acetone are positive, we should consider etic acid to be present. The name acetonuria, still in use, be used as synonymous with acidosis. The strong and 'acteristic smell of acetone in the expired air is an excellent le for its diagnosis. With a subtle sense of smell one is to observe the presence of acidosis and even to differentiate intensity. In my experience the smell of acetone is ob- ed in almost every tenth patient entering the hospital. I Id like to emphasize here that acidosis is a very common irrence. Acetone bodies, which is a comprehensive name oxybutyric acid, diacetic acid and acetone, are temporarily ned in almost all diseases. Several, even numerous, forms cidosis or, as one called it formerly, acetonuria, have been ribed. But all these forms are identical when considered an etiological standpoint and are all to be classified under same head. In general, acetone bodies are eliminated tys when carbohydrates are lacking in the organism, or, n they are not utilized in a normal way. Under these litions, indeed, the oxidation of protein and of fat will be zient and oxybutyric acid will appear in the urine. Acid- will occur every time, when from any reason, the taking 'ood and especially of starch and of sugar, sinks to a imum.

his applies to all kinds of acetonuria-to the acetonuria 1 starvation or from exclusive animal food, to the ace- ria in fever, in gastro-enteritis and to the acidosis appear- in the latter stages of cancer. Only upon one point do we remain in doubt, whether besides the absence of carbohy- ?, there exist other circumstances, which, although they ot induce acidosis, yet may increase and modify it. Practi- this question is rather irrelevant, and I think it an un- sary discussion of the subject. Another question is of far er importance, and that is the difference between diabetic ion-diabetic acidosis. Except in diabetes the elimination etone bodies rarely exceeds 10 or 15 grams, and when quantities appear in urine, they do so only for a short in diabetes, on the contrary, the elimination may reach ) and more grams, and acidosis of this height may last onths and even for years. We know this fact since the eighties, a period when we did not yet employ alkalies. e I would like to call your attention to the very im- It deduction. that a patient with severe diabetes, and I very marked acidosis, may. under favorable circum- 1, live for years without suffering immediate damage to ilth. He is, it is true, according to Frerich's words, id by the danger of a certain and unexpected death, is end may not be reached for many years. And nger is imminent only in the diabetic patient, whose y for utilizing carbohydrates is extremely weakened.

When the interest in acidosis became general among practi- tioners, when the Legal-Gerhardt test, so often positive, re- vealed the frequency of strong acetonuria in non-diabetic dis- eases, a feeling of apprehension arose. The bad prognosis which persistent and marked acidosis gives in diabetes was transferred without reason to acidosis existing in diseases other than diabetes. But acidosis never is a threatening dan- ger in such patients. Acidosis as such has nothing to do with the symptoms and with the dangers of such diseases. The idea of the specialists in children's diseases was wrong, who, in studying the acidosis which occurs in the alimentary dis- turbances of nursing babies, ascribed the cachexia and death of the children to oxybutyric acid.

Furthermore, in diabetes acidosis, even when it has lasted for years, induces no immediate harmful consequences. Thus acidosis, which exists other than in this disease, being far weaker and of short duration, is without clinical interest and without prognostic value.

You are aware that the human organism, as well as that of carnivorous animals, defends itself against the action of ac- cumulated acids by forming an alkaline body, ammonia. A diabetic patient at any time has at his disposal 6 or 8 grams of ammonia. The neutralization of acids by ammonia prevents deprivation of alkalies and a change in the alkalinity of the most important cells. With 6 or 8 grams of ammonia, 40 or 50 grams of oxybutyric acid can be eliminated month after month, without acidosis becoming deleterious. A fatal acid- poisoning will occur only then, when the accumulation of the acids reaches twice or three times these amounts. There is a difference between acidosis, spoken of in the common sense, and a fatal acid-poisoning, a difference which though only in the quantity of acids, yet cannot be emphasized strongly enough. Outside of diabetes, such an enormous rise of the accumulation of acid never takes place, so far as we know at present. The coma produced by it is limited to diabetes and merits the name of coma diabeticum.

Stadelmann, a pupil of Naunyn, was the first, as you well know, to consider diabetic coma to be a fatal acid poison- ing. He compared it to the experimental poisoning by muri- atic acid in experiments with animals. According to Wal- ther's fine discovery, rabbits, after having been given 0.9 gram of HCI per kilo of body weight within 24 hours, die in a comatose state. The striking analogy between this form of acid poisoning and that of diabetic coma, emphasized by Stadelmann, exists in the similarity of the clinical symptoms, especially the changed and deepened breathing, further in the strongly diminished quantity of carbonic acid of the venous blood, together with the diminution of the alkalies as deter- mined by titration. Aside from these symptoms the occur- rence of ammonia in the urine is common also to both states. One link alone was missing in the chain of proofs furnished by Stadelmann. It had not yet been demonstrated that such an amount of acid, as was necessary to bring about the death of the rabbit, was present in a case of human diabetes. The urine of comatose diabetic subjects not only contained no larger amount of organic acid, but rather less than in the time pre-

Digitized by

Google

JOHNS HOPKINS HOSPITAL BULLETIN.

[No. 9

ceding the coma. With one exception this quantity did not exceed 20 grams. That is the reason the theory of Stadelmann was doubted. The total quantity of acid found in any given case appeared insufficient.

A mistake had been made, however, in looking for their presence in the urine of deceased patients; it would have been just as much of an error to have looked for muriatic acid in the urine of dying rabbits. The lessened alkalinity of the kid- neys diminishes the secretory power, the stream of urine de- creases rapidly, sufficient elimination of the acid either in- gested in an experiment, or formed within the body of a diabetic patient does not take place. Both the poisoned ani- mal and the diabetic patient do not die from the acid which has been eliminated in a neutralized state, but from the acid. which remains in the body. The presence of the acids was not to be looked for in the urine, but in the organs of the corpse. By laying stress upon this point of view I really have been able to find in the body by analysis of blood, liver, muscles, etc., quantities of 100 to 200 grams of oxybutyric acid. Cal- culated per kilogram and allowing for differences in molecular weight, these amounts are just as large, and even larger, than those which induced the death of Walther's rabbits.

In the urine also enormous quantities may be found, but only if the patient survives the comatose state, so that the elimination of acids takes place in a sufficient way. I was lucky enough to establish this fact in a boy under the care of my teacher, Naunyn. This boy, only 30 kilograms in weight, underwent a most severe coma, but was saved by the use of almost 200 grams of sodium bicarbonate in 24 hours. On this day the urine contained 160 grams of acetone bodies; the fol- lowing days the elimination sank to a lower level.

In the experimental poisoning by acid, there exists an experimentum crucis, which proves the death to be really due to the action of the acid itself and not to secondary factors. If the acid circulating in the body is neutralized by intra- venous injection of bicarbonate of soda, improvement follows immediately even when death seems to be imminent in the very next minutes. This experimentum crucis has suc- ceeded also in diabetic coma, though only seldom, just as it was postulated by Stadelmann. I myself have seen three cases survive pronounced coma by use of bicarbonate of soda, two of them being children, one a patient of sixty years.

Here in America the doctrine of Stadelmann-Naunyn was well received and also it has been developed farther. In Ger- many, too, it has been acknowledged more than formerly since the new proofs have been furnished. According to my per- sonal opinion, scarcely any other theory upon the entire field of metabolic science has better support and has been worked out more thoroughly both qualitatively and quantitatively. Yet it is proper that all objections which have arisen against it in the course of years should be considered carefully.

Four objections are to be named. The first one is the rela- tive inefficiency of the alkaline treatment. It must be con- ceded that only few cases are known, in which an advanced diabetic coma has disappeared under the use of bicarbonate of soda, in contrast to the absolute efficiency of alkalies in the

case of the rabbit. But it must not be forgotten that there s a marked difference between acid poisoning in experimenta to. in coma. In the first a certain limited and well-known amez of acid is introduced into the organism; when this quant" has been neutralized by the once-administered bicarbonate " soda, danger is over at once and will not reappear. Durch diabetic coma, on the other hand, the formation of acid de not stop a moment; new molecules enter continuously in: the metabolism, to such a degree that the ingestion of biz- bonate of soda does not keep step. In order to neutralize li- grams of oxybutyric acid, formed in the course of 24 hres a quantity of 120 grams of bicarbonate of soda is required Even when absorbed, the arrival of the alkali at the mensei. centers of the brain and its utilization there is by no means3 be taken for granted in every case. Only when the immit production of acids diminishes, or rather if oxidation take place again-which, however, is not the case, as long as (2) is at its height-will the alkalies ingested be sufficient neutralize the acids. The urine then becomes alkaline and t- diabetic patient will survive the coma. This quantitative d- culation reveals why bicarbonate of soda therapy fails so ofte in advanced coma, but at the same time it is obvious that the failure does not contradict the theory of Stadelmann.

The second objection to be mentioned seems to be of m: importance. It arose from the modern theories of acidity alkalinity. Since acidity and alkalinity have been definelt; the teachings of physical chemistry as the degree of concer tration in hydrogen and hydroxyl ions, it has been pointel that the fluids and the secretions of the body are fairly neutra if measured with this measure, with the single exception of the gastric and pancreatic secretions. The amount of hydrar. and hydrogen ions in the blood serum does not undergo marke: variations either in the various conditions of normal life er i: illness. Even in the acid-poisoning of rabbits only a slight derangement of the neutral point of the reaction occurs and slight decrease in the alkalinity takes place. In diabetic cara however, such a decrease has not been found. Silli and Bex dict, who carried out these experiments, therefore, deny 93! analogy between diabetic coma and the experimental aci :- poisoning. They deny that the former comes under the heat of acid-poisoning.

But their argument does not hold good. Besides other: objections, which could be made, the main difference lies in t' fact that Benedict, unlike Walther, did not inject the murittir acid into the stomach of the animals, but introduced it in the form of a continuous stream into the veins. The blood ws: mixed with the acid fluid directly, without the latter having been passed through the walls of the intestines, and the is- travenous injection was continued until death. Under the circumstances the actual concentration of ions at the moment of death, of course, is higher than that, which would have been reached if the acid had entered slowly and evenly from the stomach into the blood. I think, if the acid-poisoning had been produced in the same manner, as in Walther's exper- ments, the alkalinity of the ions would have been the same # in diabetic coma ; in other words, that here also the quantity

Digitized by Google

thị

t S

b 0

ions would not have been distinctly diminished. rt from these objections there is still another difference veen experimental poisoning and diabetic coma. In the mple of the rabbit the acid enters first the blood and only r that the cells; in the diabetic patient, on the contrary, acids are actually produced in the cells themselves, and a fraction of the total quantity enters the blood. Thus the same degree of- change of alkalinity in the nerve ers, upon which depends the death of the organism, the ease of alkalinity of the blood will be greater in the animal in the human patient. Death in both is not to be con- red simply as a consequence of the changed reaction of the d, but in reality as due to the poisoning of the vital center, which in particular are meant especially the respiratory ers.

Need help finding more records? Try our genealogical records directory which has more than 1 million sources to help you more easily locate the available records.

Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 83

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189