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Premature and Congenitally Diseased Infants

by Julius H. Hess, M.D.

Chapter II
Classification

For practical clinical purposes the group of infants comprising the premature and congenitally debilitated may be classified as follows:

  1. Premature infants, with no pathological changes.
  2. Premature infants, with pathological changes, due to:
    1. Constitutional disease and chronic infections in the parents.
    2. Maternal factors influencing the fetal nutrition, such as overwork, undernourishment, and acute illnesses during pregnancy.
    3. Local conditions in the mother.
    4. Multiple pregnancies.
    5. Constitutional defects and congenital malformations in the fetus.
    6. Infants born to parents late in life.
  3. Full-term infants with pathological changes due to the same causes as those enumerated under 2.

Etiology

The occurrence of premature birth depends upon many causes, which may be divided into those resulting in the expulsion of a healthy premature, and those which have a damaging effect upon the product of conception. In the first class may be included various injuries, falls, heavy lifting, overwork or other physical exhaustion, sudden emotional disturbances and premature rupture of the membranes, either accidental or intentional, occurring in those conditions whose existence does not affect the nutrition of the ovum, as in pelvic and spinal deformity in the mother, placenta previa, etc.

Conditions in the mother requiring operative procedure not involving the uterine cavity frequently result in premature labor either through shock or trauma, resulting from operations, as for ovarian conditions and uterine fibroids, or infection may be an added danger in cholecystitis, cholelithiasis, appendicitis, ileus, and renal operations.

The cases which fall within the second category all react to a greater or lesser degree upon the fetus, some producing only momentary weakness, as the milder acute infections, others causing a weakened physical condition as a result of their long-continued action upon the nutrition and development of the fetus.

The most frequent causes are the chronic infections. Syphilis plays the leading role, and is estimated as being a factor in from 50 to 80 per cent of all cases of repeated premature expulsion of the fetus, while Lesage and Kouriansky [1] state that syphilis is a factor in the causation of congenital debility of the full-term in 25 to 35 per cent. If the luetic infection is recent, abortion is the rule; but as the infection becomes older, the succeeding pregnancies terminate later and later until a living child with or without manifestations of the disease is born, usually prematurely.

Chronic nephritis is one of the most frequent causes of spontaneous premature labor, and the offspring of these mothers are often puny, due, either to the systemic affect on the mother, or resulting from impaired nutrition of the fetus due to placental hemorrhages and infarcts. Nephritis in the mother is also one of the most frequent indications for the induction of premature labor.

Pulmonary tuberculosis is less frequently the cause of premature labor, but the children, even at full-term, are often small and weak. Tuberculosis of other organs and tissues influences the fetus in proportion to the nutritional effect upon the mother or, again when involving the vertebral column or hip-joints may by their resulting deformities require premature induction of labor. Congenital tuberculosis is very rare, but does occur. In the majority of cases, not the disease per se, but the predisposition is inherited.

Premature birth occurs in 30 or 35 per cent of the cases of broken compensation in heart disease. The premature infants are, in these cases, often imperfectly nourished as a result of the poor aeration of the mother's blood. Exophthalmic goiter is occasionally the cause of premature emptying of the uterus. If chronic dyspnea exists, as a result of laryngeal or tracheal stenosis from pressure, the development of the fetus will necessarily be retarded.

Any of the acute infectious diseases may be responsible for the termination of pregnancy before the end of term. Pneumonia, influenza, typhoid fever, malaria, diphtheria, scarlet fever, measles, small-pox, Asiatic cholera and bubonic plague -- all have a deleterious effect on the continuance of pregnancy. Premature labor is very common in pneumonia and influenza, being more frequent in late pregnancy.

Of local conditions, diseases of the decidua or endometrium, gonorrheal infection and malpositions of the uterus frequently result in premature labor, but usually before the fetus is viable. Anomalous positions of the fetus in utero may be responsible for the premature expulsion of the uterine contents.

The occurrence of multiple pregnancy is a fruitful source of premature labor. About 70 per cent of twin pregnancies terminate prematurely and the length of practically all triplet and quadruplet gestations is considerably shortened in most cases due to lack of room in the uterine cavity. Miller's [2] figures are slightly smaller. He states that of 3380 plural births, 2040, or 60 per cent, were premature, and had a body weight of less than 2500 gm., and a length under 45 cm. Even when mature, twins are usually small and of low body weight. This, of course, is even more true of triple pregnancies, the reserve strength possessed by the mother not being sufficient to allow three fetuses to reach their normal development. Again in the presence of several fetuses the growth may proceed unequivocally so that one may be born with unimpaired vitality, and the others with greatly diminished strength (Fig. 9).

Faulty nutrition of the fetus, such as is found in maternal overwork or from lack of sufficient food, as well as that due to wasting diseases, the blood dyscrasias (pernicious anemia and leukemia), and intoxication from alcohol (acute and chronic), phosphorus, arsenic, mercury, or lead may -- any one of them -- cause either an early termination of pregnancy or so serious a lowering of nutrition of the fetus that the vitality at birth may be greatly impaired. In addition, congenital malformations in the fetus sometimes bring on premature birth. In diabetes prematurity is not infrequent, and the infants may show glycosuria.

Infants born to parents late in life are often born prematurely, perhaps because of the factor of undernourishment. This is also the case in prematures born of women who have had numerous pregnancies, at short intervals.

Finally, habitual miscarriage, without evident cause, resulting in the interruption of successive pregnancies, not infrequently at about the same stage, is not rare. The author has records of several such women without a history of syphilis or other constitutional disease, and in whom uterine deformity is not demonstrable.

The frequency of premature labors varies greatly in different clinics. Rommel [3] quotes the following figures from various clinics, noting the number of infants under 2500 gm. in weight and below 45 cm. in length.

Miller

5.0 per cent

Orphan Asylum

Moscow

Von Winckel

13.3 per cent

Maternity

Munich

Fehling

25.0 per cent

Maternity

Halle

Budin

10.7 per cent

Clinique Tarnier

Paris

Pinard

15.4 per cent

Clinique Baudelocque

Paris

It is stated that the percentage of premature births is greater during the colder months of the year.

Footnotes

[1] Congenital Debility and Atrophy, Nourrisson, Paris, July, 1919, No. 4, 7, 193.

[2] Peculiarities of the Disease of the Premature Infant, Jahrb. f. Khlk., 1886, 25, 129.

[3] Quoted from Pfaundler and Schlossman Handb. f. Kinderh., Leipzig, 1901.

 

Figure 1 Thumbnail

Fig. 1. Case of congenital goiter.

Figure 2 Thumbnail

Fig. 2. Case of congenital thymus (atrophy of gland following two exposures to roentgen ray).

Figure 3 Thumbnail

Fig. 3. Mongolian idiot.

Figure 4 Thumbnail

Fig. 4. Chondrodystrophia.

Figure 5 Thumbnail

Fig. 5. Chondrodystrophia.

Figure 6 Thumbnail

Fig. 6. Cretinism.

Figure 7 Thumbnail

Fig. 7. Dyspituitarism.

Figure 8 Thumbnail

Fig. 8. Case of Siamese twins. Thoracopagus tetrabrachius tetrapus. (From the service of Dr. Ludwig Simon, Michael Reese Hospital, Chicago.)

Figure 9 Thumbnail

Fig. 9. Triplets.


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