Book - Contributions to Embryology Carnegie Institution No.1-5

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Mall FP. On the fate of the human embryo in tubal pregnancy. (1915) Contrib. Embryol., Carnegie Inst. Wash. Publ. 221, 1: 1-104.

   Fate of the Human Embryo in Tubal Pregnancy: Introduction | Acknowledgments | Tubal pregnancy with normal embryos | Tubal pregnancy with pathological embryos | Tubal pregnancy with pathological ova | Fertility and sterility | Implantation in tubal pregnancy | Normal implantation in uterus | Normal embryos in the tube | The trophoblast | Normal embryos from 6 to 9 mm in length | Normal embryos over 9 mm long | Conclusions regarding normal implantation | Pathological embryos in tubal pregnancy | Pathological ova in tubal pregnancy | Degeneration of villi and chorion | Summary | Cause | Normal implantation | Tubal pregnancy containing pathological embryos | Pathological ova | Addendum | Description of the individual specimens | Bibliography of papers cited | Explanation Plates 1, 2, and 3
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Summary

Cause

A review of those specimens which are accompanied by data bearing upon the cause of tubal pregnancy shows quite definitely that this condition is associated with inflammatory changes, which must have preceded the lodgment of the ovum in the uterine tube. Under normal conditions the tube is lined with a layer of ciliated epithelium, which constantly works in the direction of the uterus and therefore creates in the tube a stream of fluid from the ovaries to the uterus. The fertilized ovum gets caught up by this stream and if the conditions are normal is carried into the uterus. Any change which delays the ovum in its progress will favor tubal pregnancy. It is well known that abnormal diverticula or duplicate tubes may be the cause of tubal pregnancy. Numerous isolated cases have been described in which a blind tube or large diverticulum contained the implanted ovum. In rare cases the blind inner end of the tube left after an operation is subsequently found to contain an ovum which has arisen from the ovary on the opposite side, which contained the corpus luteum, whereas only on the opposite side was there a passage free between the uterus and ovary. However, these anomalies are rare and cannot be viewed as the rule in cases of tubal pregnancy.


Much more commonly associated with tubal pregnancy is a chronic inflammation followed by adhesions and kinking of the tube. This has been repeatedly observed, but it is difficult to associate adhesions on the outside of the tube with the arrest of an ovum within its lumen. A glance at the protocols of our cases brings out this point. Whenever histories are given, it is frequently stated that there were numerous adhesions binding together the pelvic organs. It is also noticed that tubal pregnancy usually takes place in women who have given birth to a child and then have been sterile for a considerable period. This fact is well known to gynecologists, and they are inclined to believe that the occurrence of tubal pregnancy indicates that the inflammatory condition in the tube, which prevents pregnancy for a number of years, is gradually disappearing, so that if tubal pregnancy had not taken place, the chances are that the tube would probably have become healed in a few years, thus permitting the fertilized ovum to reach the uterus. This theory receives strong support from the study of numerous cases of tubal pregnancy. If the ovum within the tube contains a normal embryo there is but little adjacent inflammation. If it contains a pathological embryo, the changes in the tube wall are usually marked, and when the ovum is well disintegrated the changes are still more pronounced. Read in the otherway this would mean that if the inflammatory condition is nearly healed, the ovum implants itself in the tube and grows normally, but if the results of infection are still pronounced, the ovum rapidly disintegrates. Such an inflammatory process is signalized not only by an inflammatory reaction in the tube wall, but also by very pronounced changes within the tube lumen, the most common of these being a condition known as follicular salpingitis (Opitz). The tubal folds hypertrophy, their tips becoming adherent, and, when sections are made, small cavities are seen between the folds; hence the term "follicular." Often this process is so marked that a section of the tube shows the folds as an extensive and delicate reticulum permeating the entire tube lumen. In such cases the individual meshes of the folds have projecting into them numerous fingerlike processes, reminding one very much of a section of the intestine. While this process is at its height, it is clear that an ovum can not pass through the tube and much less can the spermatozoon pass outward to reach the ovum. It is only after this process has abated somewhat that it is possible to have conditions suitable for the production of a tubal pregnancy.


Another type of change differs markedly from follicular salpingitis, but in a way seems to go hand and hand with it. This condition I have constantly spoken of as outpocketing of the epithelial lining. No doubt this is the variety first described by Werth. Here the muscular wall is thick and fibrous and numerous small diverticula reach out into the muscular coat. Sometimes these are markedly distended at their blind ends. In other species they seem to run in parallel lines, indicating that, instead of a single tube, we have numerous small tubes side by side. Either of these conditions would account for the arrest of the ovum. The ovum is taken up by the mucous membrane of the outer end of the tube and, owing to the impairment of the ciliated cells, is delayed in its progress. On account of this delay it grows too large to be carried through the narrow portion of the tube into the uterus. This condition would be aggravated when the tube lumen is greatly reduced at the uterine end, so we can easily postulate two kinds of changes to account for the two kinds of implantation so frequent!}' encountered. When the ovum lodges at the outer end of the tube, we should expect the outer end of the tube to be lined with fairly normal mucous membrane, but if the ovum is delayed in its progress and becomes too large to pass later through the uterine end of the tube, we should expect to find the tube lumen reduced in size in this situation.


A third type of implantation usually takes place in the middle of the tube, and is the most common variety. In this type we most frequently encounter tubal inflammation and follicular salpingitis. It seems as though the ciliated cells can carry the ovum to the middle of the tube, but no further. The ovum then implants itself within the folds of the tube, and, soon becoming too large for the space it started to occupy, through secondary rupture is cast into the tube lumen. This process is always accompanied by considerable hemorrhage with marked distention of the outer end of the tube. In case the ovum is not aborted into the peritoneal cavity, it becomes larger and larger; it is encircled by a dense fibrous clot and disintegrates. Often the entire tube wall, which is thin and inflamed, has practically disappeared.


I have intentionally not taken up the question of the nature of the inflammation which appears about a tubal pregnancy. It seems, however, that in certain instances this inflammation is due to the tightening up of an old infection that had occurred at the time of a previous labor, although the evidence points more towards venereal disease as a more usual etiological factor. The more frequent incidence of tubal pregnancy in cities than in country districts and the frequent histories of gonorrhea in these cases point stiongly towards the latter as the chief cause of tubal pregnancy. I do not believe that the evidence we have now warrants a more definite statement than this, as the subject can not be determined by the histological picture. For the present, therefore, the question must still remain open.

Normal Implantation

In case the ovum becomes well implanted within the middle of the tube and ruptures into the broad ligament, conditions are brought about which favor the development of a normal embryo. Rupture on the free side of the tube would throw the embryo into the peritoneal cavity and therefore would probably terminate its life. The same is true when the implantation takes place near the uterus. Here the tube distends with difficulty. The ovum burrows into its thick wall and usually passes right through into the peritoneal cavity. We have numerous beautiful specimens illustrating this point.


Table 1, given on page 5 of this article, is arranged in three columns, each column being divided into two, marked "Examined" and "Unexamined," respectively. The specimens have been arranged in this way to facilitate the study of them statistically. When embryological specimens were first sent me only normal ones from tubal pregnancies were included, and this accounts for the large number of specimens in the first 500 of this collection containing normal embryos. For statistical purposes, only the columns marked "Unexamined" should be compared. In these cases the specimens were not selected by the surgeons who performed the operations, so that during a period of 17 years, since No. 109 was sent me, I have obtained 13 normal embryos, 20 pathological embryos, and 47 pathological ova, among 80 unexamined tubal pregnancies. Thus it will be seen that of the pregnancies which were not examined before the specimens were sent to this collection, 16 per cent, or nearly one-sixth of the whole number, contained normal embryos. I am rather of the opinion that this is too large a proportion, inasmuch as the small tubes containing a small ovum were generally not sent to us.


It seems highly probable that, when the ovum is normally implanted and contains a normal embryo, it is attached to the tube wall much as the ovum is attached to the uterus normally. It burrows through the mucous membrane and makes for itself a space between it and the muscular wall. This process is accompanied by a marked hemorrhage probably much more pronounced than is usually the case for a uterine implantation. The trophoblast promptly attacks the venous sinuses of the tube, first growing around them and then into them, but there is no response in the tube similar to that which takes place in the uterus. In the tube practically no decidua is formed, and as it seems that the decidua is an important factor in preventing extensive hemorrhage, it follows that from the beginning the implanted ovum in the tube must be surrounded by an excess of blood. The blood which is in immediate apposition with the trophoblast does not coagulate and is taken up by the syncytium, which is usually very markedly vacuolated and serves as pabulum for the ovum. All stages of the destruction of the blood corpuscles can be seen in suitable specimens. Particles of red cells are found within the cells of the trophoblast, where they still take on their characteristic stain. Soon these particles become so small that they blend with the protoplasm of the syncytium, giving to it the tone of the staining property of the red cells, so we can find all gradations and colors from red cells to the well-stained syncytium without demarking sharply the blood pabulum in its digestion by the trophoblast. If the hemorrhage is excessive the blood forms a clot that is, the antibody produced by the trophoblast to prevent coagulation of blood acts only in its immediate vicinity and does not penetrate the larger mass of blood. This clot then becomes a foreign body and can not serve further as pabulum for the ovum. As rapidly as the trophoblast punctures the venous sinuses of the tube it throws up a wall, so to speak, which prevents excessive hemorrhage into the intervillous spaces. If the blood dribbles in slowly, it seems to serve best as pabulum for the ovum. Extensive hemorrhages are prevented by the cells of the trophoblast, which soon change into vacuolated syncytium and thus seem to protect the intervillous spaces. The larger meshes in the syncytium take up groups of red corpuscles, which are held until they fragment and are taken up by the protoplasm in the process of digestion.


The trophoblast also has a marked tendency to produce a peculiar necrosis of the maternal tissues with which it comes in contact, producing the so-called fibrinoid substance. Apparently this is formed primarily in the mesodermal tissue of the mother, but the fibrin of the blood, the epithelial cells, and the free trophoblast do not seem to escape in this form of necrosis. With the aid of the fibrinoid substance a strong wall is formed between the tips of the villi and the tissue of the tube. This mass then forms a line of demarcation between the ovum and the tube wall, even if the latter be ruptured. The implantation cavity then is lined with much fibrinoid tissue upon which are scattered cells of the trophoblast. Later these individual cells penetrate the fibrinoid substance, giving it in older specimens the peculiar appearance of cartilage. Tips of the villi penetrate this wall and from them streams of active trophoblast reach out and puncture fresh sinuses. In every respect the condition found in normal implantation in the tube seems to be identical with that found in the uterus, except that there is no formation of decidua. As the decidua may be viewed mainly as an agent to prevent excessive hemorrhage, it can be spared in the tube in case the trophoblast and fibrinoid substance take its place. In fact, in the latter part of pregnancy in the uterus, the decidua does not seem to play any great role.


All together 43 normal embryos in this collection were obtained from tubal pregnancies. The youngest specimen contains an embryo 4 mm. long, and the oldest a fetus 96 mm. long. Table 5 is interesting mainly as regards the time of implantation of tubal pregnancy containing normal embryos. The larger number fall in the sixth week; that is, our surgeons usually make a diagnosis during the sixth week of tubal pregnancy. No doubt many of those represented in the first part of the table would not have continued as normal specimens; for instance, in the one containing the embryo 4 mm. long there already were pathological changes within the spinal cord. Others had ruptured and the embryo was found free within the abdominal cavity. Thus we could not expect many of these to survive through the full period of normal pregnancy. No doubt they would have succumbed in a variety of ways, but what percentage it is impossible to determine. But of all those that do survive only one-fifth remain normal; the rest become pathological or turn into monsters, as shown by Von Winckel's studies.

Table 5. List of normal embryos, giving size and age

Template:Mall1915 table5

Length.


No.


Weeks.


Length.


No.


Weeka.



338c


5


18 . .


496


8



808



18 5


432






19


431



6 5


706


6


19 ...


456



g


359



19


634



g


612



20


790



9


352



Ovum 40X30X30. .


667



9


422



25


657



9 . .


597






10


426



28


183


9


10 5


109



Ovum 60X40X30. .


640



11


197



35


294



11


535






11


487



36


449


10





37


867



12 5


670


7


43


497



13


175



52


448



13


503



52


851



13


899






15


350



54


458


11


15


728






15


898



57


481


12


15 5 ....


390






16


256



70


179


13


17


576









96


484


14



It is interesting to note the fate of 13 specimens containing normal embryos which were not examined before they were sent to me. No. 808 was unruptured and contained what appeared to be a normal embryo; nevertheless, upon careful examination, after it had been cut into serial sections, it was found that a small portion of the spinal cord showed marked histolytic changes. These were limited exactly to the part of the cord giving origin to the motor roots, the dorsal part of the cord appearing to be normal throughout. No doubt had we examined all of the embryos which appeared to be normal we should have found slight changes in different parts of the body of some of them.


It is seen by table 6 that only the larger specimens are unruptured, showing that most of those containing younger embryos came to an end through rupture of the tube. The larger specimens (e. g., Nos. 576, 431, 657, and 484) reached this stage of development because they did not rupture. In these the tube is evenly distended. In other words only 4 pregnancies among 117, or less than 4 per cent, have survived. Only these are suitable for development to full term. We must look to this group for the specimens which become markedly deformed towards the end of pregnancy. According to Von Winckel, four-fifths of the fetuses are markedly deformed. Therefore the probabilities are that of 117 specimens under discussion only one might reach maturity as a normal fetus.

Table 6. List of 13 normal embryos lliat came to the laboratory without examination or selection before the specimens were sent

Template:Mall1915 table6


No.


Dimensions of tubal mass in mm.


Length of embryos in mm.


Remarks.


808 706 389


70X25X25 55X15X15


4 6.5 8


Unruptured. Histolysia of spinal cord. Ruptured. Menstrual age, 3 weeks. Aborted.


612 597 535 670

728


30X30X30 20X10 60X55X50 35X30X25


8 9 11 12.5 15


Ruptured. Aborted. Unruptured. Tube wall nearly destroyed. Just ruptured. Ruptured. Menstrual age, 9 weeks.


576 431

057

183


30X30X25 60X45X35 35X20X15


17 19 25

28


Unruptured. Unruptured. Uuruptured. Menstrual age, 3 weeks. Tube evenly distended. Embryo possibly atrophic. Aborting. Tube evenly distended.


484


110X100X80


96


Unruptured. Tube evenly distended.

Tubal Pregnancy Containing Pathological Embryos

Whenever the degree of alteration in the tube wall is pronounced and accompanied with marked infection, the ovum does not implant itself well and consequently the embryo does not develop normally, but becomes atrophic and degenerates. The more severe this process the more pronounced is the reaction upon the ovum; or, in case it begins to develop normally, excessive hemorrhage around the ovum detaches the chorion from the tube and strangulates the embryo within. It dies suddenly and shows no tendency to grow in an irregular fashion. Later it disintegrates.


The pathological changes found in the tube are well described by Werth 1 and appear in most specimens I have studied. First, there are marked outpocketings of the epithelial lining of the tube, with a thickening of the muscular layer. This condition was first described by Werth, and according to the study of my specimens it appears to be chronic, as it is not accompanied with any leucocytic infiltration. Secondly, an acute condition, which is more frequently found, consists of a hypertrophy of the folds of the tube, which subsequently become adherent, thus forming numerous small pockets in the tube. This condition was first well described by Opitz and is known as follicular salpingitis. The mucous membrane is swollen and infiltrated with leucocytes and there is often an extensive exudate. According to Werth this condition is usually associated with gonorrhea, and there is nothing in the history of my specimens which speaks against this opinion. The inflammatory process is more marked in those cases containing pathological embryos than \\hrn they are normal. In practically all these cases the tube lumen is present, sometimes as a large semilunar slit encircling the hemorrhagic ovum and sometimes as a simple tube on one side of it. It generally remains open throughout its course, showing that in them, as well as in those containing normal embryos, the implantation is interstitial. In general the tube lumen is small at the site of the implantation and becomes large on either side as the mass extends within the tube lumen. It is naturally encircled by the folds of the wall, as is well seen, for instance, in the sketch of No. 808. Rough serial sections demonstrate this point satisfactorily.


  • Werth, Die Extrauterineschwangesehaft. Vou Winckel's Handbuch Geburtshulfe. B.I. 1>, Ti-il 2, Wiesbaden, 1904.


Table 7. List of tubed pregnancies containing pathological embryos

Template:Mall1915 table7

No.


Dimensions of tubal mass in mm.


Length of embryoa in mm.


Form of body.


Character of change in embryos.


825


90X40X25


1



Mesenchvme containing a few epithelial cells.


349


30X 9 OX20


1



Small remnant of a greatly deformed embryo at the end of a


554


50X20X20


1


Nodule


large umbilical cord.


874


80X30X5


1



Chorion very active.


196 396


50X30X30 40X28X20


2.5 2


Greatly deformed


Tissued in active growth.


304


45X45X45


3 5



Pathological change in chorion.


697


55X30X30


3



Completely dissociated; menstrual age 10 weeks.


881 SOS


110X35X33 70X25X 9 5


4

4



Histolysis of ventral side of spinal cord in thoracic region.


477



5



Markedly dissociated; menstrual age 2 weeks.


567


55X30X25


5



Dissociated.


784 838


75X35X35 27X23X29


5

6


Dead; tube ruptured.


Dissociated; organs can not be outlined; menstrual age 8 weeks. Thoroughly dissociated; central nervous system can still be


729 S46


20X10X10 85X40X30


8 8


Normal (?); tube ruptured.


be outlined; cord fibrous; menstrual age 4 weeks. Completely dissociated.


804


50X40X40


8



Free cells fill a cavity 8 mm. in diameter.


ss"


60X45X40





766


55X45X40


10



Complete dissociation; menstrual age 6 weeks.


685


70X60X50


12



Disintegrating; menstrual age 8 weeks.


VM


70X60X50


15



Embryonic mass seems to be composed of the cord.


307


40X40X40


20



Thoroughly dissociated, with secondary changes in cartilages


17x


S5X60X45


22 5



Dead for some time (?)"; menstrual age 20 weeks.


314



24


Head atrophic


Tissues macerated, dissociated, and infiltrated.


479


90X70X70


80


Very edematous; tube ruptured.


Tissues edematous, with secondary changes and adhesions; menstrual age 13 weeks.


All of the specimens containing pathological embryos, whether examined or not, before being sent to the laboratory, are arranged in table 7. I have also included specimens Nos. 825 and 874, which were assigned to the column containing pathological ova, as well as No. 808 from the column containing normal embryos.

The specimens are arranged according to their length, and it at once appears that among those containing small embryonic remnants we have nodular and vesicular forms. Then we have a group of larger embryos, which are regular in form but atrophic. The tissues of these are also more or less dissociated. The third group consists of dead embryos which are markedly dissociated, some of which have fallen entirely into pieces. The change in these specimens indicates that the process was probably of short duration, as it is marked by extremely severe destructive changes. A comparison of the different varieties of ova obtained from the tube with the pathological ova obtained from the uterus is given in table 8.

Of the group of 13 normal specimens spoken of repeatedly, about 8 came to the laboratory ruptured and 1 was in the act of aborting; another was about to rupture (see table 5). Of 25 specimens containing pathological embryos only 6 were ruptured, showing again that ruptured specimens usually contain normal embryos. In other words, a live normal embryo is probably far more dangerous to the mother than a pathological one.

TABLE 8. Varieties of ova obtained from lubal pregnancy compared irith pathological ova obtained from the uterus.


Age.


Pathological

from uterus.


Pathological from tube.


Normal from tube.


Vesicular forms


19 1




Without embryo or amniou ....


29 15 (


52



Second week


4




Third week


18


3




21


7


o


Fifth week


13


6


2


Sixth week


27


2


11



10


3


10


Eighth week ... ,


o



g


Ninth week


1



3


Tenth week





5


Kleventh week .


1



1


Twelfth week





1


Thirteenth week


1


1


1


Fourteenth week . . .


1



1




Total


162


74


43




It is impossible to obtain any satisfactory data regarding the percentage of the different varieties of specimens obtained from tubal pregnancies. This fact has also been pointed out by Werth, who, however, expresses the opinion that only a small minority of tubal pregnancies live beyond the first month. Of those that become well embedded in the tube wall only a small percentage survive for any length of time, and probably much less than 1 per cent come to maturity. The chief difficulty in obtaining good statistics is that too few specimens fall into a single hand for study. Thus, our own specimens are only numerous enough to indicate the probable proportions. It is even impossible to obtain figures regarding the frequency of tubal pregnancy. The number of operations in a given hospital compared with the total number of patients does not give us any index at all of the true percentage. In fact, surgeons express very different opinions regarding the frequency of this affliction in different districts. Some state that it never occurs in colonial countries; others that it is uncommon in rural districts; and others that it is frequently encountered in cities. A parallel here with the probable prevalence of venereal disease is at once apparent. Beyond this we can not go at present.

In order to make comparison between the ova and embryos in tubal pregnancy and those obtained from the uterus, I shall first give a table modified somewhat from the one published in my article on monsters. That table rests upon all available statistics, most of which were obtained from Von Winckel. In it the pathological ova were put together, but according to my records of pathological specimens obtained from the uterus, there are 100 ova containing pathological embryos to every 63 without embryos. So, breaking up the probable number (7,048 pathological ova to every 100,000 pregnancies) according to this proportion, we have two numbers (4,330 and 2,718) given under this heading in table 9.

TABLE 9. Fate of 100,000 uterine pregnancies.



Pregnancies.


Births.


Abortion of normal embryos.


Pathological embryos.


Pathological ova.


Monsters at term.



100,000


80,752


11,765


4,330


2,718


615


Percentage. . . .


100


80


12


4.3


2.7


.6


For the sake of comparison it is best to reduce all these figures to a percentage. In each 100 uterine pregnancies 4.3 per cent contain pathological embryos and 2.7 per cent contain pathological ova or rather ova, without embryos.

Drawing upon the general table given in the beginning of this article that is, using only those specimens which came to the laboratory unexamined we can build up a similar table, but here instead of 100,000 cases to deal with we have only 80. All the tubal pregnancies in the collection could not possibly be used in drawing up this group of statistics, so I arranged the whole material into two groups with three subdivisions in each group. The first, called "examined," consists of specimens examined by physicians before the specimens were sent to the laboratory. The second group includes specimens not examined by the physician but sent to the laboratory for me to examine; this group is called "unexamined." It is seen at a glance that the specimens numbered less than 500 arrange themselves very differently from those numbered over 500. There are about 1,000 specimens in the collection and table 10 shows the distribution of tubal pregnancy among the first 500 and the second 500 specimens. It is seen that tubal pregnancies in the second 500 fall off markedly in normal embryos and increase greatly in pathological ova. The unexamined 80 specimens arrange themselves in a table in which the birth column is zero. 16 per cent of the specimens of tubal pregnancy contain normal embryos, 25 per cent pathological embryos, and 59 per cent pathological ova.

Table 10. Distribution of tubal pregnancies in first and second halves of about 1,000 embryologies I specimens collected

Template:Mall1915 table10

First 500 specimens.


Second 500 specimens.


1,000 specimens.


Examined.


Unexamined.


Examined.


Unexamined.


Examined.


Unexamined.



21 2

4


4

7 8


9

1


9 13 39


30 2 5


13 20

47



It is probable that the 59 per cent of the pathological ova would have disintegrated and disappeared in some way if they had not been removed by the surgeon. It is also probable that most of the specimens containing pathological embryos would also have disappeared. Then comes the question as to the fate of the 16 per cent of normal embryos. A glance at table 5 shows that most of them rupture or abort, but no doubt the few that remain within the tube may continue to the end of gestation, although some of them die and are aborted. In fact, Werth gives a case in which the skeleton of a very small fetus about the size of a bean was found encapsulated within the tube lumen at the end of thirteen years.


I have attempted to express in table 11 the redistribution of this 16 per cent in cases in which the fetus continues to grow to the end of pregnancy, using, as a guide, the proportion of anomalies in tubal pregnancy at term as given by Von Winckel. Of course this would not always be their fate, because most of this group die long before the end of gestation, but if this redistribution is made it is found that of 100 tubal pregnancies 3.3 per cent would have reached birth, the patholgical embryos would be raised from 25 per cent to 35.5, and there would be added about 2.2 per cent of monsters. This row of figures can now be compared with the percentage of specimens obtained from 100,000 uterine pregnancies. If this is done it is apparent that the pathological action in tubal pregnancy is far more severe than upon the pathological ova obtained from the uterus. In tubal pregnancy the embry< > is quickly destroyed, the ovum is easily detached and becomes necrotic, and is absorbed or aborted. A normal embryo eats through the tube wall, and many of them are also aborted. The appearance of a pathological embryo from the tube is much like that of one from the uterus, but the destruction of tissue is more severe. All this points more towards complete strangulation in the tube. The uterus appears to be a more favorable site for pathological embryos which continue to live. This variety is less frequently found in the tube. It is probable that all small monsters and pathological ova that remain in the tube disintegrate.

Table 11. 50 specimens of tubal pregnancy which had not been examined before being sent to the laboratory

Number.


Percentage.


Fate of the 10 por cent of normal embryos.


Percentage after redistribution of the 16 per cent of normal specimens.



SO


100



100


Births





3.3


3.3



13


Ifi





20


25


10.5


35.5



47


59



59



2.2


2.2



There is a marked difference between early and late monsters from the tube and those from the uterus. In the former there is a marked gap between these two varieties. In the uterus there is a finer gradation from one to the other. The conclusion of our study of tubal pregnancy regarding this point is that there is a break within the pathological group in the tube; thus we have the early stages in which the changes are very severe, and later stages which show special varieties but which seem occasionally to include specimens in which pathological changes must have begun very early. It may be that the change in the spinal cord in No. 808 might have continued to the end of gestation to produce a spina bifida. Otherwise the tubal monsters at term must have arisen from specimens which were normal up to the twelfth week. No doubt the normal specimens of the sixth, seventh, and eighth week, as given in table 4, are of the kind that produce the monsters at the end of pregnancy, as described by Von Winckel. In fact, there is every indication that No. 657 might have turned into a monster, as its head appears to be somewhat atrophic.


I have been unable to collect any good data regarding the frequency of monsters in tubal pregnancy, but, according to Joachimsthal, they are very rare, and according to Leopold they are relatively rare, while Martin and Orthmann, Huge, Olschausen, and Veit state that they are more common than in uterine pregnancies. It may be that the latter gynecologists confused early pathological embryos with older monsters, while the former did not. The line of demarcation between them is difficult to draw, hence the distinction is not frequently recognized.


Von Winckel has done us a service in collecting those fetuses from tubal pregnancies which continued to live and were removed alive from the abdominal cavity. His fetuses must have arisen from the 16 per cent of normal embryos found by me in unselected unruptured tubes. 84 per cent of the specimens were so markedly pathological and so far destroyed that they could not possibly have lived until the end of pregnancy. Von Winckel's cases are especially valuable for determining the fate of the embryos that must have been normal before the tube ruptured, that is, during the first months of pregnancy. He first gives the cases that have been published by others, as follows:

Table 12.

Date.


Author.


Number of specimens.


Number of monsters.


1876


Henniug


150 ...



1894


Orillard . .


6 (alive)


Q


1893


Schelling


257


25


1891


Kuchenmeistcr ....


43


7



Harris ....


45 (alive)


11


1901


Sittner


126 (alive)


36


1902


V. Winokel


13 (alive) .


13



Kehrer .



7



It will be seen that the percentage of monsters increases from year to year. However, Von Winckel thinks that it is safe to say that one-half of the fetuses in ectopic pregnancy are deformed, the most common deformity being defects of the hands and feet. He further collected 87 cases (14 of his own) and found that in 57 of them the fetuses were much deformed and in 12 were markedly monstrous. Among these there were 6 cases of hydrocephalus and 1 each of hydromeningocele, encephocele, anencephalus, omphalocele, spina bifida, and hyospadia. In addition, the head was found deformed in 57 specimens, the legs in 44, (he arms in 35; in 12 there were club-feet, and in 4 cases amniotic bands. The placenta was usually deformed, sometimes multiple, broad and thin, or short and thick, and often very hemorrhagic.


In general, then, it is the poles of the body that suffer most, the head being deformed in 75, the legs in 50, the arms in 40, and the trunk in 4 per cent of the cases. But while it is clear that a good share of the difficulty is due to ordinary mechanical causes, in the 12 cases that were markedly monstrous these could not be the sole factor; for them we must hold the hemorrhagic placenta responsible, a growth that could be included under what I have termed faulty implantation. Therefore, 14 per cent of Von Winckel's 87 tubal cases which were normal in early pregnancy become monstrous, while in uterine pregnancies the percentage is below 1.


Pathological Ova

Pathological ova without embryos are very frequently encountered. In our selected cases 59 per cent fall under this heading, while in specimens obtained from the uterus there are only 2.7 per cent. Moreover, as Werth also admits, in both sets the figures are probably much too small, as no doubt many of the earlier specimens are lost or overlooked. We have no good data regarding the number of ova which disintegrate early, but the study of comparative embryology warrants the conclusion that many young ova degenerate and disintegrate. I am informed by Doctor Huber, who has studied with great care much material from rats, that some of the fertilized ova break down before implantation or what amounts to implantation. The same seems to be true regarding the pig. We usually find more corpora lutea in the ovaries than embryos in the uterus, indicating that all of the ova do not produce normal embryos.


Table 13, which includes all of the pathological ova studied, shows that most of them are less than 10 mm. in diameter. Many of them are small because they are collapsed. At one time they were larger, but as a result of excessive hemorrhage they became detached, and the collapsed ovum indicates that it is degenerating. Verj r few of them are in a process of abortion and none of them have ruptured through the tube wall. The ova are simply being disintegrated. This is indicated by the pathological condition of the magma, which is densely reticular and often very granular. The wall of the chorion is degenerating and the line of demarcation between it and the coelom is often obscure. Strands of cells extend from the chorionic wall into the coelom, and the main wall of the chorion is often ruptured. The villi usually show a variety of degenerative changes of which the most common is fibrous, but often mucoid. The trophoblast is usually scanty or necrotic, with disintegration of the nuclei, forming nuclear dust. When this is liberated, it is scattered through the specimen. The dead villi are soon invaded by the leucocytes and also by adjacent trophoblast which feeds not only upon them but also upon necrotic masses of trophoblast. As the ovum collapses it also begins to break up. The villi are detached and scattered in the blood clot. The isolated villi may continue to grow in case they are capped by active trophoblast, which continues to tap fresh vessels. As the blood clot becomes larger the single villi are separated more and more, ultimately undergoing complete degeneration. In a few instances the whole ovum breaks into pieces. It first becomes hourglass in shape, the two parts then separate, and in one case (No. 874), one part is aborting, whereas the other part is near the uterus, where it is still growing actively. Finally, the villi practically disappear and the clot becomes smaller and organized. These very small clots which are found in the tube are composed almost exclusively of fibrin con I Mining a few small degenerating villi. At any time during this process the whole tubal mass may be extruded and bring the pregnancy to an abrupt end. In case this does not take place the clot probably disappears entirely by absorption. My material does not warrant any statement regarding the ultimate fate of a small fibrous clot or of an excessive hemorrhage in the tube, which contains within it a few fibrous villi; nevertheless, the suggestion that the latter condition may have some relation to hematosalpinx, hydrosalpinx, and pyosalpinx is pertinent.


Table 13. Pathological ova

No.


Dimensions of tubal mass in mm.


Dimensions of ovum in mm. ; menstrual age.


Villi and coclom.


154



10X10X10



298



4X4X4 (3 weeks)


Fibrous.


361



10X10X10 (7 weeks)


Dense reticular and granular magma. Tubal abortion


367



10X7X5 (2 weeks)



369



(3 weeks)



378



12



415


40X20X20




418


50X25


7X4 (5 weeks)



430


60X35X35


25X20X15

472

Scattered fibrous villi.

488


495


30X25X25


12

507


50X35X35

513


70X30X30


15X10

514


15X SX 8

515


15X12

517


40X30X30

Granular mass in aninion.


519


Scattered villi.


520


60X35X30


5X3X3


539


40X 8X 8


10X6X6


Scattered villi .


540


50X16X16


2

553


50X23X23


5 (8 weeks)


Collapsed ovum. Manv Hofbaucr cells.


561


28X22X22


Collapsed (11 weeks)

570


25X14X 8


Collapsed (6 weeks)

575


40X23X18


5

602


50X25X25


13 (11 weeks)


Degenerate villi. Tubal abortion.


659


30X15X10


673


16X16X16


6X3 (11 weeks)



686


70X50X40

694


40X10


13X7X7.

720


90X30

726


60X40X30


(12 weeks)

734 741


50X25X25 70X50X40


Collapsed ovum (2 weeks) . 18X6 (20 weeks)


Mucoid and necrotic.


754


70X25X15


2X1 (1 week)

762


65X45X35

765a


75X30X30


5 (8 weeks)

772


30X30X15

773


55X20X15

775


70X40X35

Necrotic and fibrous.


777 787


75X55X55 40X11X11


5, collapsed (11 weeks) . . .


Few necrotic villi.


794


60X20X20

None

Possibly a few trophoblast cells.


8096


60X40X30

809c


80X45X35

Scattered necrotic villi.


815


50X30X25


Collapsed (5 weeks)


Necrotic villi.


825


90X40X25

Double ovum with quite normal rhori'in.


835


40X30X30

Few scattered fibrous villi.

874 889


80X30X25 50X25X25


Ovum broken (7 weeks) . . .


Villi very active.


891


60X30X30


Ovum 10X5.

892


90X45X45


(11 weeks)


Fibrous villi.

Addendum

Since writing the above I have had an opportunity to examine 29 new specimens of tubal pregnancy; and this was done in such a way so as to test thoroughly the condition of the tube wall in each specimen. Most of the specimens came to me unopened and many of them were preserved in an approved manner in our laboratory.


As far as possible careful examination was made of the tube wall near its uterine end, in the neighborhood of the pregnancy, and at its fimbriated end. Examinations of the fimbriated end were not often possible, but in several instances they gave data of great value as regards the condition of the tube lumen (e. g., Nos. 928, 939, and 967a).


Twelve of the 29 specimens came from the Philippine Islands, and in these the inflammatory reaction in the tube lumen would appear to be more extensive than in those obtained from the United States. In two-thirds of these the accompanying clinical histories show that there had been an infection and that adhesions were found at the time of the operation. In only one of the 12 cases (No. 938) is it stated that the patient's condition was normal, and in this case no change was found within the mucous membrane of the tube. The same condition of the tube was found in 2 other specimens (Nos. 911 and 953). In all of the rest of the specimens follicular salpingitis, outpocketings of the epithelial lining into the muscular wall, or both, were found in some position of the tube lumen. This pathological condition was found 17 times in the uterine end of the tube, 14 times in the region of the pregnancy, and 6 times in the fimbriated end, and, as stated above, in some portion of the tube in 25 of the 28 specimens. The twenty-ninth specimen consisted only of a normal embryo, the tube not having been sent with it.


It is evident, then, that the changes within the tube lumen are frequently circumscribed; sometimes it was necessary to examine a second block from the uterine end before a pathological change was found in it. In one case this difference was most pronounced, the tube at its entrance into the uterus being normal, whereas one centimeter nearer the point of pregnancy a most pronounced follicular salpingitis was found.


In specimens Nos. 900/, 908, and 939, both tubes were examined. In the first and second there were outpocketings or follicular salpingitis in the uterine end of the pregnant tube, similar conditions being present in the same region of the nonpregnant tube. In No. 939 follicular salpingitis was found at the point of pregnancy and in the fimbriated end of the non-pregnant tube. A more detailed study, with the utilization of serial sections, would no doubt show pathological changes in the mucous membrane of the tube in every case, but at present such a study is entirely out of the question. For practical purposes the examination as recorded in table 14 is most satisfactory.


To make the causal study of tubal pregnancy complete, it will be necessary to determine with greater accuracy the norm of the mucous membrane of the Fallopian tube for various periods in its history up to the menopause, and numerous specimens for a study of this kind have already been collected. Furthermore, it will be necessary to make complete bacterial examinations from tubal pregnancies in order to determine their relation to venereal diseases.


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Pages where the terms "Historic" (textbooks, papers, people, recommendations) appear on this site, and sections within pages where this disclaimer appears, indicate that the content and scientific understanding are specific to the time of publication. This means that while some scientific descriptions are still accurate, the terminology and interpretation of the developmental mechanisms reflect the understanding at the time of original publication and those of the preceding periods, these terms, interpretations and recommendations may not reflect our current scientific understanding.     (More? Embryology History | Historic Embryology Papers)
   Fate of the Human Embryo in Tubal Pregnancy: Introduction | Acknowledgments | Tubal pregnancy with normal embryos | Tubal pregnancy with pathological embryos | Tubal pregnancy with pathological ova | Fertility and sterility | Implantation in tubal pregnancy | Normal implantation in uterus | Normal embryos in the tube | The trophoblast | Normal embryos from 6 to 9 mm in length | Normal embryos over 9 mm long | Conclusions regarding normal implantation | Pathological embryos in tubal pregnancy | Pathological ova in tubal pregnancy | Degeneration of villi and chorion | Summary | Cause | Normal implantation | Tubal pregnancy containing pathological embryos | Pathological ova | Addendum | Description of the individual specimens | Bibliography of papers cited | Explanation Plates 1, 2, and 3



Cite this page: Hill, M.A. (2021, May 9) Embryology Book - Contributions to Embryology Carnegie Institution No.1-5. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Book_-_Contributions_to_Embryology_Carnegie_Institution_No.1-5

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