Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 81

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

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I found a specimen in the Prague Museum which probably belongs to this group of cases. The fœtus was a male, and had reached the fourth month of development. One could not actually demonstrate that the amniotic cavity had been con- tracted, but could prove that the cause of the deformity was abnormal pressure against the amnion in the locality of the affected parts (Fig. 8). The left upper extremity of the fœtus was rudimentarily developed, and supplied with only one digit. The limb was attached in a deep fossa upon the left wall of the thorax where the cartilages of the third, fourth and fifth ribs were absent, and the pectoralis major muscle, as well as the neighboring intercostal muscles, were very thin. In this instance, it seems fair to suppose that the amnion which enclosed the left upper extremity had been too small, and that perobrachia was produced in that way. Ritter, Ganghofner and Eppinger have described cases of the same character.

Viewed from the standpoint of pathological anatomy, it is not impossible that malformations and even death of the embryo may result from an abnormally spacious amnion, or to a premature collection of amniotic fluid. Yet, actual ob- servations, so far as I know, have not been made to substanti- ate this opinion ; nor have I observed cases which would seem to belong in that category.

What do we know concerning the cause and mode of forma- tion of either Simonart's bands or of an abnormally small amniotic cavity ?

Originally, Simonart's bands were thought due to an or- ganization of lymph (Montgomery), which was referred to some inflammatory process (Simpson, Gratzer, Simonart). Many authors, including Virchow, accepted the inflammatory hypothesis. In 1854, G. Braun expressed the view for the first time that Simonart's bands were in reality abnormally disposed portions of the amnion itself. He inferred that they originated in consequence of pathological folding of the amnion, and that this phenomenon, in turn, depended upon a scant quantity of amniotic fluid.

C. Braun explained the presence of these bands through the formation of plastic adhesions. Kustner elaborated the theory,

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and suggested that intimate contact was established between the amnion and the embryo during the early days of develop- ment. He considered that narrowing of the amnion, a defi- ciency of amniotic fluid and the formation of folds in the membrane might bring about adhesions between it and the young embryo. These adhesions gradually became firmer and occasioned the malformation. Possibly, other outgrowths might later develop from the amnion, but in that event the epithelium covering the surface of the fœtus would have to die before adhesions could occur. Finally, Kustner believed that a deficiency of amniotic fluid made it possible to have sec- ondary adhesions arise in connection with fissure formation when the epithelium of the medullary folds or of the intestinal wall was elevated. Later Kustner described a case of con- genital amputation of hands and feet by amniotic threads, which resulted from a rent in the amnion due to the mother lifting a heavy load during the second month of pregnancy. The amnion had entwined itself about the umbilical cord, and entangled the extremities of the embryo, thereby affect- ing their amputation. Olshausen discussed tearing of the amnion as a source of amniotic threads, and concluded that the amnion may rupture spontaneously if its cavity be too small. Stoeckel has quite recently collected a series of these cases in which extra-amniotic pregnancy was associated with amniotic bands.

My own view is that adhesions between the epithelium of the amnion and the ectoderm of the fœtus are of primary im- portance in the formation of Simonart's bands. Although we are not as yet sufficiently familiar with the development of the amnion (Graf v. Spee holds the interesting view that the amniotic cavity in the human arises as a closed cavity within the blastodermic vesicle and develops from the ectoblast) still we know that it is formed very rapidly, since the youngest human ova which have been described already possess a closed amnion. Embryos of 10 mm. are closely surrounded by amnion. Embryos of 11-15 mm. are separated from the amnion by a distance of only 1-3 mm., and it is only when a length of more than 20 mm. has been attained that the quan- tity of amniotic fluid becomes commensurate with the size of the embryo, thus insuring an appropriate separation between it and the amnion (Marchand, Kollman).

With these facts in mind, it is not difficult to understand how the human embryo may become adherent to the amnion during the early weeks of pregnancy. The ectodermal cells on the inner surface of the amnion, as well as those covering the surface of the embryo, are young and active, and can fuse together easily if they are not sufficiently separated from one another. The union will gradually grow firmer. Later, when the amniotic fluid begins to develop, the adhesions are drawn out and become Simonart's bands, stretching from amnion to fœtus, or from one part of the fœtus to another. Inasmuch as these adhesions occur during the earliest stages of develop- ment they cause the most extreme types of deformity, one can imagine. This conception, which includes a primary adhesion and a later fusion of the two epithelial surfaces belonging respectively to the amnion and to the embryo, agrees per- fectly with the histological findings in Simonart's bands.

Microscopically, these bands consist of a wavy mass of amniotic, connective tissue, exhibiting very few nuclei and no blo: vessels. They are covered by amniotic epithelium whic shades into the fœtal epidermis. As they approach the ex- bryo, the covering of these bands often presents the typisa. structure of skin, from which we may infer that they uls- mately draw out the skin, making it a part of the band.

In addition to the mode of formation just described, other occur, though much less frequently : thus, Simonart's band may arise in consequence of rents in the amnion. This appears to me to support the interpretation of the previously met- tioned case with corset-formation, which was attributed to contracture of the amnion combined with laceration of the membrane and the production of Simonart's bands.

Valuable contributions from the field of experimental terat - logy shed light upon the causation of narrowing of the amnion, and the mechanism by which it is produced. In this connection, reference should be made to the unusually inter- esting experiments of Dareste. By raising and lowering the temperature of an incubator, and by warming different parts of a hen's egg unequally, this investigator frequently st- ceeded in producing disturbances in the development of the amnion. Moreover, embryonic malformations, apparently d amniotic origin, were noted : cyclopia was occasioned by na: rowing of the head-fold, and symelia by narrowing of the tail-fold. These experimental observations support the os- ception that narrowing of the amnion has a very direct bearing upon the origin of certain human malformations. To be str. these results are not strictly analogous with similar human deformities, since the formation of the amnion in the click and in man are essentially different. In the former, the amnion is formed by the union of the folds which arise at t .: anterior and posterior ends of the body as well as at either side. These folds meet and fuse over the back of the embryo. With this mechanism, it becomes very easy to have serious interfer- ence with development of the embryo, since either the head, the tail, or one of the side folds may not rise sufficiently, and tho- fail to reach its proper destination. As a result of such aminotic defects, malformation of the embryo occurs.

In the development of the human ovum, according to His. the amnion is formed exclusively by the head-fold; this el- tends over the embryo toward the tail, and ultimately sha: in the amniotic cavity. None the less, here again it become entirely possible for the amnion to attain incomplete dereley- ment through one harmful influence or another, and a paths- logical narrowing of the cavity may result. We can als imagine the amnion becoming abnormally firm and rigid & consequence of some disease; so that it is incapable of th: distension requisite for the subsequent growth of the embr .. Of course that is only an hypothesis at present. We met: occasionally with cases which demonstrate that the amnie may undergo pathological thickening, and attribute it to : inflammatory change. In this connection, the interesting cas of v. Franque should be cited. There a number of wart-like nodules were noted on the fœtal side of the amnion, and near them superficial plaques were found. These had arisen through the proliferation of amniotic stroma about certain

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the fœtal skin (vernix caseosa, desquamated epi- Il clumps of lanugo hair), which had been de- . the amnion. Further, the fact should be men- so-called " wind eggs"-a name given cases in nbryo has perished-often present circumscribed ickening of the amnion. Microscopically, the con- s to be a proliferation of amniotic stroma and

portion of human malformations can be fairly n amniotic origin may be difficult to decide, but n exist that the number is large. Among 178 formation studied by v. Winckel, 29 cases (16.3 ere referable to Simonart's bands. My own ex- s me to a similar conclusion. Beside this group, other in which deformity is due to narrowing of cavity ; and the latter, according to my view, is rge as the former. Combining the two, I would '-third of all human malformations to some in- ed by the amnion. Such an estimate, moreover, e into account the deformities met with in cases )S.

3, it becomes impossible to demonstrate the am- of malformations. On the one hand, it fre- ›ens that the membranes are studied too super- on the other, Simonart's bands, as well as evidence ving of the amniotic cavity, may disappear in the 3 of pregnancy. For these reasons, it is desirable larger amount of material and study it more han has been done.

ion, I should like to speak of congenital defects, in the skin, especially about the head, and have to the traction of amniotic bands. Keller has wed cases of this sort and included a new ex- was observed in the Pathological Institute at The defect was located upon the skull, and dif- respect, from similar cases thus far reported. examination in this instance showed that hair present at the site of the defect. That finding > with the hypothesis that very early amniotic ted. Therefore, Keller, concluded, if the tear- mnintic adhesions was to account for the de- case, the adhesions must have developed after ith and not during the early days of embryonic Moreover, he held that some inflammatory ndamentally responsible and his opinion had t the mother had suffered from endometritis. as firmly attached to the uterus and its separa- plished with difficulty. Such a case certainly iflammatory changes in the amnion be given ation in future study of the development of

REFERENCES.

itnis der Störungen im Oberflächenwachstum des Gehirns. Ztschr. f. Heilk., 1886.

: Beitrag zur Lehre von den amniotischen Band- h Einfluss auf die foetale Entwicklung. Ztschr. d. Aerzte in Wien, 1862.

G. Braun: Ueber spontane Amputationen des Foetus und ihre Beziehungen zu den amniotischen Bändern. Ibid., 1854.

Dareste: Recherches sur la production artificielle des monstruo- sités ou essais de tératogénie experimentale. Paris, 1877.

v. Franqué: Zur Kenntnis des Amnionanomalien. Monatschr. f. Geburtsh. u. Gynäk., 1897.

Grätzer: Die Krankheiten des Foetus. Breslau, 1837.

Keller: Zur Kenntnis der congenitalen Hautdefecte am Kopfe des Neugeborenen. Diss. inaug., Strassburg, 1908.

Kustner: Amniotische Bander und Strange. Muller's Handbuch d. Geburtsh., 1889.

Kustner: Ueber eine noch nicht bekannte Entstehungsursache amputirender amniotischer Fäden und Stränge. Ztschr. f. Geburtsh. u. Gynäk., 1890.

Montgomery: Dublin J. for M. & S., 1830.

Olshausen: Spontanamputation durch amniotische Bänder, Verh. d. Gesellsch. f. Geburtsh. u. Gynäk. in Berlin, 1896.

v. Ritter, Ganghofner und Eppingtr: Ein Fall von angeborener Lücke des Brustkorbes, Oest. Jahrb. f. Paed., 1876.

Simonart: Amputations spontanées. J. d. conn. med. prat. Bruxelles, 1846.

Simpson: Edinb. M. & S. J., 1836.

v. Spee: Neue Beobachtungen über sehr frühe Entwicklungs- stufen des menschlichen Eies. Arch. f. Anat. u. Phys., 1896.

Stoeckel: Anomalien der Eihaute. v. Winckel's Handb. d. Geburtsh., 1905.

Virchow: Die siamesischen Zwillinge. Berl. klin. Wchnschr., 1870.

v. Winckel: Ueber menschliche Missbildungen. Volkmann's Saml. Vort., 1904.

II. NECROSIS OF THE PANCREAS.

Necrosis of the pancreas may arise from many different causes. It may be due to a severe trauma, directly affecting the organ, as for example in gunshot wounds; or it may be caused by corrosive poisons, such as sulphuric acid, acting through the stomach wall. Again it may develop from the perforation of a petic ulcer of the stomach, or result from an inflammation of the pancreas, in so far as extensive necrosis and putrefaction may follow suppuration of the organ. It is my belief, however, that much the most common cause of necrosis of the pancreas is autodigestion due to the tryptic ferment of the pancreas.

The corrosive action of the pancreatic secretion has been known for a long time, and the tryptic autodigestion of the pancreas has been pointed out likewise. In 1879, Klebs at- tributed pancreatic hemorrhages to the corrosive action of pancreatic juice. Guscenbauer in 1883 described a cyst of the pancreas which had been formed by the destruction of a melanosarcoma by the pancreatic secretion. Arnozan and Vaillard referred in 1884 to the post mortem autodigestion of the pancreas in animals. Selzer (1886) and Wölfler (1888) thought that the erosion of the walls of pancreatic cysts by the pancreatic secretion might lead to hemorrhages. Pelliet (1889) and von Hansemann (1894) noted the frequency of post mortem autodigestion of the pancreas. Tilger (1894) attributed the origin of pancreatic cysts to autodigestion in pancreatitis. Nimier (1894) emphasized the importance of the pancreatic secretion as a source of pancreatic cysts, follow- ing injury to the duct of Wirsung. In 1895 I described the occurrence of intra-vitam, intra-agonal and post mortem auto-

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digestion of the pancreas, and drew a comparison between this and peptic autodigestion of the stomach wall. Blume (1897) and Pförringer (1899) supported my views, and Blume, as well as Beneke, sought the cause for intra-vitam autodigestion in temporary ischæmia, and Pförringer in fat necrosis. I described in 1900 a case of focal intra-vitam autodigestion in all probability caused by arteritis obliterans. Gaylord (1901) reported autodigestion of the pancreas following gunshot wounds. In 1901 and 1902 Lazarus attributed anew the origin of pancreas cysts to autodigestion.

Numerous cases of intra-vitam tryptic autodigestion of the pancreas were, in my opinion, incorrectly interpreted, being described as hemorrhage of the pancreas, as pancreatitis hemor- rhagica and gangrenosa (Fitz) and as necrosis of the pancreas from other causes. Here are to be found many pertinent ob- servations, which resulted from investigation of cases of fat tissue necrosis by Balser (1882) which have since been proved to be due to a lipolytic ferment of the pancreas. The necrosis of the pancreatic tissue so frequently found has been considered, by most of the writers, as secondary in relation to the necrosis of the fat tissue, and even those authors who regarded the pancreas necrosis as primary, and the fat tissue necrosis as secondary, did not ordinarily think of a tryptic autodigestion as the cause of the pancreas necrosis, but rather assumed a primary pan- creatitis. Only a few writers (Dettner, 1895; Hildebrand, 1898; Konheimer, 1898; Kaufmann, 1891) took the position that the spontaneous fat tissue necrosis was due to an intra- vital tryptic autodigestion, rather than to a traumatic rupture of the ducts of the pancreas. In 1902, I expressed myself firmly of the belief that both these conditions regularly be- longed together, in the sense that the primary factor was the tryptic autodigestion of the pancreatic tissue, which was fol- lowed by the necrosis of the fat tissue, due to a pouring out of the fat ferment and its diffusion. I was also able to show that in post mortem and especially in intra-agonal autodiges- tion of the pancreas, it was not seldom the case that the fat tissue in the pancreas showed the beginning of the changes as they occur in necrosis of the fat tissue, and I explained further that the pancreas hemorrhages and pancreatitis acuta hemorrhagica and gangrenosa were nothing more than changes in the pancreas due to autodigestion. Necrosis is primary and possible inflammation is secondary. Then Weil (1904), Reitter (1905) and Truhart (1906) expressed similar opin- ions. In 1906 I maintained the view that the intra-vitam tryptic autodigestion of the pancreas might, on the one hand, be a most important process, leading to extensive hemorrhages in the pancreas and its neighborhood, to hemorrhagic cyst formation of the pancreas, to focal or diffuse necrosis of the pancreas and to suppurative pancreatitis and sequestration of the pancreas if pathogenic bacteria invaded it; but that on the other hand from circumscribed slight tryptic auto- digestion of the pancreatic tissue, harmless, small areas of pan- creas necrosis and fat tissue necrosis (secondary autopsy find- ings) might develop, which areas of pancreas necrosis might disappear entirely by absorption. But in view of this, tryptic autodigestion of the pancreas deserved the title of a morbus sui

generis. Williams and Busch (1907), Truhart (1908) c: most recently, Opie and Meakins (1910), have express: similar views, so that the doctrine of the tryptic autodigest necrosis of the pancreas seems to be well founded.

There is not the least doubt that the causes for the ore rence of a " spontaneous " intra-vitam tryptic autodigestion : the pancreas may be manifold. Anything which may leai injury of the tissues of the pancreas or to activation of tryptic zymogen, may induce tryptic autodigestion of the pes creas. I would call especial attention to the following iz portant etiological factors : slight trauma of the pancreas, se causing rupture of a duct; disturbances of the pancreatic d' culation, which may be looked upon (Benecke and Blume) a spastic anæmias, which may be caused by the frequently nie arteritis obliterans; stagnation of the pancreatic secretit entrance of bile into the duct of Wirsung in cases of chin lithiasis, as was first shown by Halsted and Opie in 1901: . finally entrance of the secretions of the stomach, or the (: tents of the duodenum into the duct of Wirsung (Hess. 19 and 1905; Beitzke, 1905). In individual cases one Er always recall, and consider, as Eppinger showed in 1905, tar the kinases which are able to activate the pancreatic secreti. may be of many different kinds. I will not deny that trypa autodigestion of the pancreas may arise from a primary : flammation of the organ, but I think it happens rarely.

The consequences of tryptic autodigestion of the panco. may vary widely. As I have mentioned, a grave disease Et result. Death may result from severe hemorrhage-the - called apoplexy of the pancreas. Within a few days death ri follow after symptoms of ileus and peritonitis, when (? usually finds extensive necrosis of the fat tissue in associatic with the reactive inflammatory necrosis of the pancreas. Tx cause of death in such cases is to be attributed either t. resorption of a pancreas toxin (Dobenauer, 1906) a proča: of necrosis, or to poisoning by trypsin (Guleke, 1906). Sus ing from the pancreas a diffuse abdominal tryptic destruc: 2 of the cellular tissue may arise, as I, myself, had opportun? to report in a case (1909). Suppuration and gangrene of the pancreas, with eventual sequestration of the organ, march velop. Cysts of the pancreas may form in consequence of the tryptic autodigestion. On the other hand, however, the trypta autodigestion of the pancreas may be an insignificant process: which induces small circumscribed necrosis of the tissue of ta pancreas, and small circumscribed areas of fat tissue necnes In the course of time all these foci may disappear, through absorption of the necrotic tissue, or at least of the foi! (necrotic) pancreatic tissue in which case we may conchos from the presence of old fat necrosis in the pancreas and neighborhood that there has been an earlier autodigestion the gland.

From all this it is easily seen what an important rôle te tryptic autodigestion of the pancreas plays. It is surely (2 of the most important factors in the pathology of this onea: The practicing physician must be cognizant of this autodi; tion, since experience has shown that in the severe cases lite oftentimes may be saved by surgical measures.

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WYUMULIN.

III. SPONDYLOLISTHESIS.

Following the enunciation by Kilian in 1853 that spondy- ›listhesis is a pelvic deformity resulting from a gradual glid- ng forward, or an olisthesis, of the inferior surface of the last imbar vertebra over the anterior border of the first sacral ertebra, a large special literature has developed - upon the bject.

The spondylolisthetic pelvis is of the greatest practical in- rest to the obstetrician on account of the part which it may ay in the production of dystocia. On the other hand, the isthesis demands attention from the pathological anatomist an example of a peculiar acquired displacement of the rtebræ, whose mode of origin is not easy to understand. Practically every case coming within this category has been scribed and published, so that Neugebauer, who devoted rticular attention to its study was able to collect

11 clinical and 12 anatomical cases in 1882

1885

and 55 66 53

1892

" 1893,

xing a total of 115 cases. This, however, included 10 cases listhesis of the fourth lumbar vertebra, and one instance lving the first sacral vertebra. Furthermore, in 1899, liams described a new specimen, and collected 123 cases the literature, 62 of which were clinical and 61 ana- ical. He also stated that Dr. Authur Dean Bevan had rmed him that he had observed several cases in the dissect- room in Chicago.

cording to Olshausen and Veit about 130 cases had been rted up to 1902, 70 of which were described anatomically the remainder reported clinically.

llowing the publication of Williams, and including his nen, I have been able to collect 10 clinical and 7 anatomical so that the entire number thus far recorded amounts to At the same time, it must be admitted, particularly g the cases which were described clinically, that in not a he diagnosis was at least doubtful. Moreover, in several ens, which were described anatomically, only the pelvic n of the vertebral column or even isolated vertebræ were ble for study, so that Breus and Kolisko in 1900, in their mental work on Pathological Forms of the Pelvis, after ing the imperfect preparations, as well as those in which sthesis was only beginning, stated that only 18 examples Il-developed spondylolisthesis were on record, accom- by a satisfactory anatomical description of the pelvis, these they added two additional specimens which they scovered in Vienna.

cially from a clinical point of view, the means of diag- ting spondylolisthesis have been fully developed; and s of characteristic symptoms described, such as the rse furrow in the back above the lumbo-sacral juncture, nbar lordosis, the diminished pelvic inclination, and uliar "rope dancer gait " of the individuals affected At the same time, the importance of lumbo-sacral olisthesis has been accentuated on account of the im-

portant part it may play in reducing the size of the pelvis and thus interferring with the act of labor.

Anatomically the various changes in the shape of the bones and ligamentous structures have been described, and the effect of the olisthesis upon the form of the pelvis has been studied, more particularly by Breus and Kolisko. According to these authors, a fully developed spondylolisthetic pelvis is a " pelvis obtecta," which is composed of plump, massive bones. With the exception of the conjugata vera, the pelvic measurements are usually large. The former, however, as a result of the olis- thesis, is markedly shortened, in that the antero-posterior diam- eter of the pelvic inlet, which takes the place of the vera, will impinge posteriorly upon the ventral surface of one of the prolapsed lumbar vertebrae, instead of upon the promontory of the sacrum. The pelvic inclination is also diminished, the upper end of the sacrum appears to be inclined posteriorly, and the region of the symphysis pubis elevated. Frequently, the vertical concavity of the sacrum is markedly increased and the entire bone is retroposed, and the articulation between the first and second sacral vertebra gapes toward the sacral canal. The ilio-sacral joints are markedly developed, their ligaments strong and the acetabula deep. All of these changes are to be attributed to the forward displacement of the center of gravity of the body, and to the change in the manner in which the body weight is transmitted to the sacrum, and tend to become more and more pronounced until the olisthesis is checked by synostotic processes.

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 81

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

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