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Premature and Congenitally Diseased Infants

by Julius H. Hess, M.D.

Chapter IV.
Pathological Findings in Prematures.

Very little careful work has been done with reference to the pathological changes in the premature infant. The discussion which follows is a summary, largely taken from the recent excellent work of Arvo Ylppö. [1]

Premature infants must be classified into two groups: Those that are born "weaklings" owing to congenital deformities or malformations, congenital diseases, especially lues, and the congenital weaklings born of nephritic, eclamptic or tuberculous mothers, or those suffering from chronic toxemia. In the second group are those fully developed and normal for their fetal age.

One is often amazed at the life energy of these prematures, in view of the high grade pathological changes in the various organs, especially the hemorrhages into the brain and spinal cord.

Premature birth should be considered a traumatic process, in which the characteristic pathological processes are most frequently noted in three groups of organs, for which there appears to be a predilection:

  1. The skull with the brain and its membranes, inclusive of the spinal cord.
  2. The lungs.
  3. The gastro-intestinal canal.

Intracranial hemorrhages are especially important. Ylppö believes that they are responsible for 30 per cent of the deaths of prematures in the early days of life. In the skull there are subarachnoidal or intrapial hemorrhages, while in the spinal column they are extradural.

The so-termed subdural hemorrhages and those from tears of the tentorium, which are present in full-term infants, are only exceptionally seen in prematures.

Ventricular hemorrhages are frequently found in prematures, but hemorrhage into the brain substance proper is quite rare. High-grade edema of the pia is, as a rule, also present along with these intracranial hemorrhages. Bacteria easily settle in the injured brain membranes and meningitic processes are not uncommon.

In the later life of the premature the appearance of spastic states (Little) and of disturbances of intelligence are often seen and are explained as a rule, undoubtedly, as a consequence of old hemorrhages into the brain and spinal cord.

The condition spoken of in the literature as hydrocephalus of the premature, has, as a rule, nothing to do with hydrocephalus. The brain represents one-fourth of the body weight and appears normal macroscopically and developmentally. Ylppö suggests the term "megacephalus." This megacephalus is due to the fact that the brain develops at practically the normal rate, while the growth of the body is retarded.

Hemorrhages into the lungs appear not only under the pleura, but are scattered through the entire parenchyma. The alveolar septums are thickened because of the extravasations of blood. The normal circulation in the lung is hindered and in the extra-uterine life there appears a stasis, which hinders the taking up of air and predisposes secondarily to atelectasis. Following stasis and bacterial changes, there may appear in the lungs of prematures a high grade, almost total, inhibition of the circulation of the blood.

Inflammatory changes in the lungs or bronchi appear infrequently and atypically in the first days of life. Bronchopneumonia, after the second week of life, begins to play an important part in causing death.

Epicardial hemorrhages are of common occurrence. They appear just as do the subpleural hemorrhages and those in all the other organs.

Subcapsular liver hemorrhages are on a par with other subserous hemorrhages. They are important only insofar as they may be extensive, and with rupture of the capsule may result in hemorrhage into the peritoneal cavity with death.

Hemorrhages into the kidney are frequent. They have two predilections: In the interstices of the apices of the pyramids, or in the neighborhood of the venae et arteriae arciformes. Hemorrhages into the Malpighian bodies and cortex are rare. Infarcts appear in the same sites as the hemorrhages.

The hemorrhages of the digestive tract are next in importance to those of the brain. In small prematures, dying shortly after birth, one often finds hemorrhages scattered throughout the entire tract. The areas of predilection are: The lower portion of the esophagus, the cardia and fundus of the stomach, the mucous membrane folds in the corpus ventriculi, the duodenal margin of the pylorus, and the entire duodenal mucosa. In the deeper portions of the intestines, hemorrhages occur infrequently about the ileo-cecal valve and in the mucosa of the large bowel. These hemorrhages appear chiefly under the epithelial cells in the tunica propria. Blood often appears in the bowel lumen after rupture of the mucosa. These hemorrhages in extra-uterine life are important only insofar as they predispose to infection, which readily occurs. As a result, within one and a half days prematures may show a marked mucous membrane necrosis and peritonitis.

Inflammatory processes within the digestive tract, especially in the esophagus and duodenal mucosa are also common. From the inflamed intestinal mucosa, bacteria easily invade the blood, with a following general sepsis.

The mucosa of the stomach is frequently involved in the septic processes of the prematurely born, especially in their early days of life. Involvement of the stomach is often followed by peritonitis and by Bacillus coli septicemia.

The histopathological inflammatory processes, due to bacteria, appear atypically in prematures. This is associated with a very ineffective exudation of fibrin and scanty mobilization of leucocytes. Because of these factors general sepsis in all infections appears easily.

The hemorrhages are due to diapedesis, rhexis, or both, and vary with the intensity and duration of stasis and the grade of the infections -- toxic damage to the capillary walls.

The preceding summary of the pathological changes in the premature has been concerned chiefly with the question of hemorrhage. (Specific pathology will be discussed later under the "Diseases of the Prematurely Born.")

 

Footnotes

[1] Arvo Ylppö, Ztschr. f. Kinderh., xx, 212, 1919.


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Created 10/10/1998 / Last modified 10/12/1998
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