by Julius H. Hess, M.D.
Sprue (Thrush, Soor or Mycotic Stomatitis). -- Etiology. -- Premature infants, weaklings, and more especially those suffering from nutritional disturbances are subject to this affection. It occurs only where a lesion of the mucous membrane is present. The abrasions of the epithelium may, however, be very slight and in the premature is usually caused by wiping out of the mouth or through other mechanical injury. The source of infection is very commonly from the nipple. However, it may be carried into the mouth through utensils or soiled pledgets.
Symptoms. -- The importance of thrush is probably always secondary and its significance above all symptomatic. It is improbable that thrush itself may cause a general serious infection. It may be an indicator of a serious general affection or an essentially lowered resistance; not infrequently it is seen in those apparently in good health. In the premature it sometimes invades the esophagus, and it has been described as invading the blood stream. In the more robust premature infants it is usually seen as small white punctiform and flat eruptions on the tongue, gums and inside of the cheeks. In infants with lowered vitality it may assume the form of extensive membrane covering the whole buccal cavity. The latter is especially true where it accompanies septic diseases. In the severe forms it is also frequently associated with Bednar's áphthae.
Usually the most serious symptom is the inclination on the part of the infant to refuse its food. However, it may be associated with vomiting and as has been stated, is frequently a complicating factor in the severe nutritional disturbances.
Prognosis. -- While thrush is usually curable within a week in the full-term infant, in the premature, unless the treatment is very carefully undertaken, the traumatism in the course of local applications may cause new local lesions which become readily infected, thus frequently prolonging the course of the disease.
Treatment. -- Prophylaxis. -- Thrush being due to lack of cleanliness and trauma, these two factors should by all means be avoided, and every effort made to avoid trauma of the mucous membrane in the first care of the mouth of the new born. It is not contagious and if the proper prophylactic means are observed in the daily routine, it should not be spread from one infant to the other. In the breast-fed the mother's nipples must be washed with a saturated solution of boric acid and moistened with one-half strength alcohol, which should be allowed to evaporate from the nipples before nursing. In the bottle-fed the nipples and bottles should be carefully boiled after each nursing, and only such nipples should be used as can be completely everted so that both the inside and the outside can be thoroughly cleansed, following which they should be preserved in a borax solution of one ounce to a pint of water. The nurse should use every precaution in the care of hands, dress and all objects which may be carried between the cribs.
Local Treatment. -- Every form of local treatment must be carefully and gently applied so as not to abrade the sensitive mucous membrane. Gently sponging the mouth with a solution of borax, 10 grains to 1 ounce of boiled water (this is preferable to boric acid), using a very soft pledget of cotton on the finger if the mouth is not too small, otherwise on a swabbing stick or toothpick after each feeding, will usually cure the disease. Traumatism of the tender mucous membranes must be avoided. The solution may also be used as an irrigation by allowing it to come gently in contact with the infected surfaces, including the tongue if involved, the infant being turned on its side so that the solution will flow out of the mouth. A small sucker containing equal parts of borax and sodium bicarbonate may be placed into the mouths of larger infants for a few minutes four or five times daily. In severe and persistent cases it may be necessary once or twice daily to gently paint the mucous membrane with a one-fourth of 1 per cent solution of silver nitrate. Following the application of the silver nitrate 2 drops of olive oil or castor oil can be used in the mouth to allay the irritation. Mixtures of honey and borax as well as all sugar preparations should be avoided.
Internal Treatment. -- Where the infant refuses to nurse it may be necessary to resort to feeding with spoon, medicine dropper, Breck feeder or even to gavage. Every effort should be made to improve the general health of the premature infant by proper feeding, cleanliness and good hygienic surroundings.
Various Types of Stomatitis. -- The term "stomatitis" is applied to inflammations of the mucous membrane of the mouth. In the full-term infant three types are usually described: the catarrhal, the aphthous and the ulcerative. The classification in the premature is far less distinct that in the full-term. The types as most commonly seen are the traumatic ulcerations, usually involving the palate. They may be very slight and superficial or by secondary infection become serious lesions. The simple traumatic patches are usually seen as yellowish, superficial lesions often covered by a slimy membranous film which can be easily removed, such removal being followed by small punctate hemorrhages. They are usually seen from the second to the fourth day after birth, decreasing in intensity and showing a tendency to rapid healing with proper care, usually disappearing within a week. Even in the premature this variety is usually harmless, except insofar as it interferes with nursing. However, the dangers of secondary infections must never be overlooked.
Etiology. -- Although the cause may vary it is usually trauma of the mucous membrane through cleansing of the mouth. This is especially true of the handling of asphyxiated and cyanotic premature infants and follows injury due to mechanical removal of mucous from the mouth. More serious lesions over the pterygoid processes which have been described as Bednar's aphthae and which are usually due to more intense trauma of the mucous membrane in the cleansing of the pharynx, may lead to more serious complications. Similar ulcerations may be found in other areas where a thin mucous membrane is in close contact with the hard bony structure.
Syphilitic stomatitis is not uncommon in infants suffering from congenital syphilis. The ulcerations are more commonly seen about the lips unless secondary to trauma.
Gonorrheal stomatitis is a rare condition. The tongue, palate and gingival folds are the seat of small whitish deposits, usually appearing on a non-inflammatory base. It is rarely manifest before the fifth or sixth day after birth. After one or two days the patches assume a yellowish color and become elevated above the surrounding tissue.
Prognosis. -- The tendency to secondary infections and deeper ulcerations should always lead to a guarded prognosis, because of the influence on the future health of the infant and the difficulties of feeding.
Gonorrheal stomatitis, while usually healing without unfavorable results in the full-term infant, when properly treated, is always a serious complication in the premature.
Treatment. -- Prophylactic. This should consist of the avoidance of all trauma at birth and the absolute prohibition of subsequent mechanical cleansing of the mouth, unless there are special indications. The latter is entirely superfluous when the proper care is taken in the preparation and administration of the infant's food. Infants suffering with ulcerative stomatitis should be isolated to impress the attendants with the dangers of spreading the infection by careless handling.
Curative. The curative treatment is the same as that described under thrush and even greater care should be taken in the application of local treatment. The deeper ulcerations in the mouth can be treated to advantage with small quantities of peroxide of hydrogen or 1 per cent potassium chlorate solution, or careful application of 1 or 2 per cent of nitrate of silver solution. In all cases, however, in the premature infant the attendant should not become overzealous in the administration of local treatment, because of the dangers of further traumatizing the sensitive mucous membrane. The feeding offers the same difficulties as in the severer cases of thrush necessitating hand feeding of expressed milk in most cases.
In syphilitic and gonorrheal stomatitis the local measures are the same as for the other varieties of stomatitis. The general measures for the former are such as are described under the treatment of congenital lues.
Cancrum Oris (Noma). -- Etiology. -- No single microorganism has been proved to be the cause of noma. Spirillae and fusiform bacilli have been found (Weaver and Tunnicliff ) not only in the necrotic tissue, but in the surrounding healthy parts. Whether these organisms represent the primary cause of the lesion or only secondary invaders is not known. In other instances the Bacillus diphtheriae alone has been found.
Symptoms. -- The site of the disease is usually the inner side of one or both cheeks. The gangrenous process usually begins as a small inflamed, infiltrated area in the mucous membrane. Localized destruction of tissue follows, and this process extends with great rapidity until the tissue sloughs away in masses.
Prognosis. -- The disease usually occurs in weakly, marantic infants, who die from exhaustion and sepsis within ten days or two weeks from the onset of the disease. Hemorrhage is rarely a complication. The disease is usually fatal even under the best management.
Treatment. -- Treatment at best is very unsatisfactory. The procedure followed in ulcerative stomatitis together with the use of surgical measures affords the best possibilities. Nicoll  reported a case which had resulted in recovery following the intravenous injection of salvarsan.
In a consideration of this very important section as relating to the premature infant, we must recognize: (1) The possibility of congenital malformations and other prenatal factors which might have an important bearing on the function of the digestive organs; (2) the lack of proper physiological development necessarily present in the prematurely born, the importance of which varies inversely with the fetal age; (3) postnatal pathological conditions, developing in the gastro-intestinal tract; (4) the importance of systemic infections in their influence on the processes of metabolism.
When the great importance of the interdependency of the second and third factors is recognized even in the absence of any congenital anomalies, we at once realize the marked tendency toward the development of disturbances involving the nutrition and well-being of the entire organism. The use of the term "nutritional disturbances" rather than that of "digestive disturbances" is beyond any question more generally applicable to the premature than to any other stage of life, as in these individuals the rapid development of general nutritional disorders is the rule following even moderate causes.
It must also be borne in mind that all factors which affect the general well-being of the premature infant, such as exposure and infection, have an almost direct effect upon gastric and intestinal functions. The very important relationship between the fetal age of the infant and the quality of the food and the method of its administration will be emphasized in the chapter on "Feeding."
The subject of gastro-intestinal disturbances in the premature infant offers a far more complex problem than do those of the new-born full-term infant. As previously stated, they require a consideration of possible developmental defects, constitutional anomalies, a low grade of immunity to infection, and a general lack of physical and functional development. The last two often lead to inability to take and assimilate the required food. Further complications are due to rejection of the food or the development of gastro-intestinal irritation upon the slightest indiscretion in feeding. All of these have an important bearing upon adequate digestion, resorption from the intestinal tract and the further intermediary functions.
It cannot be too strongly emphasized that the immediate institution of the proper hygiene, and the establishment of the proper prophylaxis toward the prevention of nutritional disturbance by the early administration of human milk whenever possible, are absolutely necessary to avoid disaster. It cannot be disputed that a great number of premature infants die, not because their organs lack that degree of maturity necessary to proper functions, but because of early neglect, either through lack of adequate facilities or ignorance of exact methods of feeding and care.
Our acquaintance with the tendency to the rapid development of marasmus in premature infants leads us to give great consideration to the development of even the slightest nutritional disturbances. It should become the rule to give even moderate disturbances the consideration that is given to athrepsia (marasmus) in the older infant, which is always regarded as making the feeding of human milk imperative. As this also entails the feeding of minimal amounts of food the body temperature must necessarily in part be conserved by artificial heat.
(a) Difficult Nursing. -- The causes of difficult nursing are to be found either on the part of the infant or mother or both.
The Infant. -- Various factors may enter which may make nursing difficult or even impossible. Some of these will be treated under the chapter on "Methods of Feeding." Of the malformations, those offering the most difficulty are cleft palate, hare-lip and nasal deformities due to lack of cartilaginous development. The tendency to sleep constantly is often very perplexing. General weakness and lack of muscular development in the poorly developed premature are not infrequently sufficient to make nursing impossible. Infections of the mouth resulting in thrush, stomatitis, and ulcerative processes are always of serious import. All conditions interfering with proper respiratory functions, whether due to lack of development, such as atelectasis or pulmonary infections interfere with the proper taking of food. These are but a few of the many complications which may be cited as impeding proper nursing.
The Mother. -- On the part of the mother the various pathological conditions of the nipples and breast must be given due consideration.
(b) Anorexia. -- Premature infants born in the seventh and eighth months rarely show a disposition to feed spontaneously during the first days of life, and in a large proportion of cases we are forced to administer the food without the infant's taking active part. Only a small portion of the infants weighing between 1000 and 1500 gm. are able to nurse without assistance, and very few of them, unassisted, are able to suck with sufficient strength to take food from either the breast or the bottle. A very interesting fact which we have noted in premature infants weighing under 1500 gm., and occasionally in even larger infants, is a tendency to at least attempt to nurse spontaneously during the first two or three days of life, during which they, however, receive very little food. This period is followed usually about the third day by a marked somnolence, during which they show little or no inclination to nurse. This is usually associated with a rather rapid loss in body weight due to underfeeding. At later periods not infrequently infants who a repugnance toward food, which may follow periods of overfeeding or be seen in the course of the gastro-intestinal or systemic infections. At whatever stage of the infant's development anorexia is seen it must be given the gravest consideration and every attempt made to administer food sufficient to meet the demands of the organism. Gavage must be resorted to if the less drastic methods of feeding are unavailing. It has been our experience that occasionally the omission of one or two feedings with the administration of a one-half strength physiological salt solution per mouth will result in the further stimulation of the appetite by producing thirst.
During this period the fluids should be given in sufficient quantities to meet the infant's needs, about one-sixth to one-fifth of the body weight daily. The addition of one to three drops of brandy is often a beneficial stimulant.
(c) Inanition Fever. -- Unquestionably hyperpyrexia as seen in the first days of life and during the days when these infants are receiving a minimum of food need not necessarily be due to inanition. Many are undoubtedly due to infection or toxic products which enter the circulation through the gastro-intestinal tract. The products of decomposition as seen during the period of change from the meconial flora to the milk flora can undoubtedly give rise to hyperpyrexia, as is also true of the toxic products formed by decomposition of milk. The effect of products absorbed from the intestinal tract on the parenteral cells, as well as the by-products due to the rapid changes seen in the body tissues, may, any and all of them, following their absorption, give rise to increase in body temperature. Occasionally one sees cases of hyperpyrexia in the premature and in the new born in whom the high temperature cannot be due to the surrounding artificial heat, and who make a rapid recovery without after-effect by simply increasing the fluid intake of milk or water. The most striking cases that are seen are those in which water insufficient to meet the body needs has been given.
Treatment. -- This consists in the administration of fluids equal to at least one-sixth of the body weight of the infant in twenty-four hours and the administration of food per the rules on "Feeding of Premature Infants during the First Ten Days of Life." Of equal importance is the prevention of overheating by application of excessive external heat. When doubt arises as to the causative factor in so-called "inanition fever" a small dose of castor oil (5 to 10 minims) together with a colonic flushing with a saline solution should be given in addition to the increase in the amount of water and human milk administered.
(d) Vomiting. -- In general the vomiting in the premature is of greater or lesser importance depending on its intensity, and the result upon the general state of nutrition. Vomiting must be considered only as a symptom and not primarily as a disease, and again as a symptom which in its development is influenced by many factors peculiar to the premature infant. The relatively vertical position of the stomach in the sixth, seventh and eighth months, as described under the "Physiology of the Premature Infant," is a factor of considerable importance, as is also the poorly developed sphincter at the cardia.
Of equal importance is the fact that most of these infants are fed mechanically in amounts theoretically correct for their weights and ages. But these same quantities may not agree with Nature's idea of sufficiency, thereby leading to a rapid overfilling of the stomach through catheter and other mechanical means of feeding. Again the tendency toward abdominal distension and the frequent handling and manipulation of the infant all tend to promote regurgitation.
Vomiting persisting beyond the first or second week, even when varying in frequency and intensity, is likely to result in a considerable degree of undernourishment. There is also the added danger in the case of premature infants with a minimal development of reflex irritability, that due to the lack of proper response on the part of the laryngeal reflexes, the regurgitated food may be aspirated with resulting sequelae, such as cyanotic spells, asphyxia or even pulmonary infection.
Because of the great danger of underfeeding in the presence of small food intake there is the gravest danger of weight losses, with the consequent development of inanition.
Etiology. -- Previous to the taking of food the infant may vomit the various fluids such as liquor amnii and blood, which may have been swallowed during labor. These may easily be recognized by their character. Following the intake of fluid many factors must be considered, such as atresias in the digestive tract, excessive feedings, which may be due to too free nursing from an easily secreting breast by the older premature infants, or too rapid feeding of large quantities mechanically given to the smaller infants.
The dangers of compression of the abdomen due to improper holding or excessive handling of the infant are usually overcome by feeding in the bed. The tendency to habitual vomiting is not uncommon in the first months of life in the premature. This is not infrequently due to a general state of nervousness or a neuropathic constitution. According to Alfred F. Hess, this can easily be demonstrated by passing a catheter and exciting the pharyngeal, cardiac and pyloric reflexes, which in the normal child are but slightly developed, while in the neuropathic individual the passage of the catheter is easily noted by the reflex manifestations following its passage. Undoubtedly many of these cases are true instances of pylorospasm. That true cases of pyloric stenosis may occur has been proven beyond doubt. The fact that these infants not infrequently vomit quantities larger than a single feeding should not lead to the diagnosis of a hypertrophic stenosis, as is proven by the fact that the stools usually contain a considerable amount of food residue.
The toxic vomiting as seen in the infants of eclamptic mothers and in the presence of sepsis, as well as hematemesis, will receive further consideration in the discussions on these topics. Vomiting may at any time become of serious moment and should always be given proper consideration. The relative loss of food as foretold by the scale, by weighing before and after feeding, and after vomiting, the weight curve and careful observation of the stools will give the best indications for therapeutic interference.
Treatment. -- In the majority of cases there is no indication for active treatment. The occasional or even more or less regular "spilling" in the presence of a normal gain in weight and general well-being need receive little or no attention. However, when vomiting is persistent and is attended by stationary weight, which is equivalent to loss of weight in older individuals, or when it is associated with nausea or is expulsive in character or contains bile, blood and other matter foreign to the normal stomach content, it should receive prompt and careful attention. No set rules for treatment can be prescribed, as the etiological factors in each and every case must be considered individually. The following general principles of treatment will in a great number of cases prove sufficient:
1. The infant should be subjected to a minimum of handling. It should, whenever possible, be fed without being removed from its bed, or where handling is necessary, all violence should be avoided.
2. The recumbent position with the head and shoulders slightly elevated assist in overcoming the tendency to regurgitation in the presence of a weak sphincter at the cardia.
3. Regulation of feedings is primarily indicated. This should cover first the number of feedings and the interval between feedings, and the amount of the individual meal. Not infrequently an infant who is receiving quantities too great for the stomach capacity will cease vomiting upon simple reduction of the size of the individual meal. Again it may be necessary to decrease the number of feedings, thereby lengthening the intervals between the feedings. Furthermore large meals at long intervals may be replaced by small meals at short intervals with a very beneficial result. Where the infant is nursing at the breast, simply reducing the time allowed for nursing in many instances will accomplish the desired end. The same may be true as regards the slower administration of the individual feedings in the bottle-fed.
4. In infants nursing directly at the breast where the shortening of the period of nursing is insufficient to control the vomiting, drawing the milk by expression or by a breast pump and feeding a measured quantity which can be retained, either by hand or catheter, is often successful.
It is customary to start such feedings by giving 2 to 10 gm. at short intervals, 10 to 12 if bottle fed, or 6 to 8 if fed by catheter, in twenty-four hours, preferably, although not necessarily, of freshly drawn milk, following this by gradually increasing quantities, and as soon as the proper quantity for growth is retained, lengthening the intervals, returning to direct nursing when the infant's general condition allows of the same. In the more severe cases the human milk may be boiled or a skimmed human milk should be used.
Under these conditions the milk supply should be protected through the emptying of the breasts by expression to prevent their drying up.
The question of even temporary starvation in the premature infant is one of serious import and should only be practised after the most careful consideration, because of the rapidly developing apathy in this class of infants. The presence of so-called "hunger stools," consisting of a brownish, stringy mucous substance with little or no food residue, is as a danger signal of almost equal importance with loss in weight.
If the above suggestions fail to accomplish the desired end, rather than to institute a starvation diet we prefer to empty the stomach by careful lavage, using a weak sodium bicarbonate or saline solution, and before withdrawing the catheter placing a small feeding of human milk into the stomach. Lavage is practised not so much with the idea of removing any decomposed food content, but because of the sedative action on the mucosa. The dangers of gastric irritation from repeated introduction of the catheter in careless hands must, however, always be remembered, also the dangers of promoting cyanotic spells, through the careless deposit of fluids in the pharynx and larynx. In the infants artificially fed the problem is far more serious, and offers for its solution greater difficulties unless human milk can be obtained. In our own experience a well-boiled milk, in which the casein has been precipitated as a fine flocculent curd by the addition of rennet, has given the best results when human milk was not to be obtained (see Preparation of Chymogen Milk). Diluting the milk thus prepared before feeding, or skimming before boiling may also be of benefit. Lactic acid milk mixtures may be used.
(e) Gastric and Intestinal Indigestion and Distention. -- These may be of very serious consequence in the premature through interference with the respiratory and cardiac functions, and the precipitation of cyanotic attacks. Although frequently following relative overfeeding this need not necessarily be the case. Most of the factors which result in vomiting also predispose to indigestion and distention. Abdominal distention is exceedingly troublesome in the premature infant, but does not necessarily imply that indigestion is present. It may result in restlessness, vomiting, colic, borborygmus, increased respirations and cardiac action, hypothermia, cold extremities and not infrequently cyanosis.
While we have seen abdominal distention result in hypothermia it is equally true that when hypothermia is present it is almost invariably associated with impaired digestion, and a tendency to cyanosis and syncope. Owing to the tendency to abdominal distention there is the danger of underfeeding due to low-food tolerance. Excessive external heat whether from the use of simple heating devices or the more complex incubators often cause increased body temperature and result in impaired digestion. I have not infrequently seen death result from a relative overfeeding, due to attempts to feed infants food sufficient for their needs; but even more frequently do we see grave catastrophes from underfeeding in the same class, with rapidly developing syncope due to inanition.
Indigestion may be followed by an increase in the number of stools, and they become green and foamy and contain curds. The inability of the infant to handle food sufficient for its maintenance without the development of functional derangement is a very grave deficiency, directly dependent upon the fetal age and factors predisposing to prematurity in the individual case. Less dangerous are the cases due to absolute overfeeding following early correction in the errors of diet, as are also the cases following indiscretions on the part of the wet nurse or mother. In the first few weeks of life severe indigestion is often fatal. This is especially true in artificially fed infants. Improper hygienic surroundings such as poor ventilation, oppressive humidity, and lack of personal cleanliness may be factors in the development of indigestion.
The role of intestinal and systemic infections will be considered under their respective headings.
Treatment. -- In the treatment correction of dietetic errors is most essential, and this is especially true in the artificially fed premature infants. It should always be remembered that the correction of the mild forms of indigestion are the life-saving measures. Severe indigestion has a high mortality. Stimulation of peristalsis and thereby emptying of the intestinal tract is usually accomplished by a low-pressure saline enema of 1 or 2 ounces. In some instances the addition of 1 gm. of glycerin to an ounce of water is of great assistance. Warm baths with or without very gentle abdominal massage may aid in increasing the peristalsis. Where the symptoms are persistent 5 to 8 drops of castor oil, 1 to 5 grains of sodium phosphate, or 5 to 10 minims of milk of magnesia, together with 3 to 5 minims of pepsin of good quality, after each feeding, can occasionally be administered with great benefit. But unless the hygiene and feeding of the infant are properly regulated little permanent good can be expected. Correction of dietetic errors in the breast-fed is best accomplished by reducing the size and lengthening the intervals between individual meals when the stomach is very irritable. However, decreasing the size of the feedings is always associated with more or less danger and where the same results can be secured by simply lengthening the intervals this offers the best solution. Starvation diet should under all circumstances be avoided, although it may be necessary in extreme cases to dilute the meals. While larger infants -- those weighing in the neighborhood of 2000 gm. -- will stand the reduction of the feedings to as low as 60 calories per kilogram, in the smaller infants 70 to 80 calories must be considered the danger zone for even a short period of time. In the artificially-fed every attempt should be made to obtain human milk and where this is impossible our best results have been obtained by feeding boiled milk, in which the curd has been finely precipitated. (See Artificial Feeding.)
(f) Diarrhea. -- Constipation is the exception; loose stools or a tendency toward diarrhea in both the breast-fed and the artificially-fed premature infants is the rule. Therefore, frequency of bowel movements, especially in the breast-fed may be entirely physiological and unassociated with fever, vomiting and other evidences of gastro-intestinal disturbances. However, they may be due to contaminated food or bacterial infection, and every case should, therefore be carefully studied so that evidences of deep lesions may be immediately observed. In the infant nursed by its mother the colostrum will almost invariably result in frequent bowel movements. This is one of the prime reasons in the selection of wet nurses, who have passed at least two or more weeks of their puerperium. The early milk also has a tendency to be high in its carbohydrate and fat content, either of which may be factors in the causation of frequent stools. A gastro-intestinal infection may be unassociated with fever and may, therefore, go unrecognized and be of serious consequence. Changes in the mother's environment, when she is nursing her own infant, as is seen at the end of the puerperium when she leaves her bed and changes her mode of living, seem to have a very beneficial influence on the quality of milk secreted, and the mother and baby seem to adapt themselves more readily to each other. This beneficial change is, of course, not seen where the baby is fed by a wet-nurse.
At this point I desire especially to emphasize my experience with both mothers and wet-nurses who are given a too liberal diet. While the average mother can be allowed to select her own diet during the nursing period of a full-term infant, eliminating such foods as may cause colic, abdominal distention and diarrhea in the infant, in the case of the premature such liberties must under no circumstances be allowed as they result in an early disaster, cyanosis and death due to abdominal disturbances. Therefore, every wet-nurse should be made to adhere strictly to the limitations of diet as prescribed under the section on "Diet of Wet-nurses." So long as the infant is passing yellow stools of normal odor, without symptoms of indigestion and gaining in weight, even though the stools may number five to eight daily, no alarm should be felt, and the diet should be sustained.
The change of the yellow stool to a green color shortly after passage is the normal process of oxidation. However, the green, frothy stool containing small white curds and considerable mucus should always be considered abnormal. Such stools usually use their normal acid odor, cause excoriation of the buttocks, and are frequently associated with fever. This is not infrequently a finding in the breast-fed premature. In the treatment of such cases, while the care of the infant is of paramount importance, no less important is the careful regulation of the mother's surroundings, mode of living and diet and also her mental activity. Again every precaution must be taken in reducing the infant's diet, and the same dietetic measures which were instituted for the treatment of indigestion apply to every case of diarrhea with abnormal stools, as they are almost invariably attendant on an intestinal indigestion or infection.
Dehydration of the body tissues through excessive water losses must be met with sufficient water administration, so that a good working rule should lead one to administer at least one-sixth of the body weight daily in fluids, in all cases of diarrhea. Therefore, when the quantity of meals is reduced, or the interval lengthened, water should be added to the feedings or administered between. The normal infant's stool will form a water margin about the semi-solid mass about one-half to three-quarter's of an inch in diameter. When more water than this is lost with the stool, the infant must be carefully weighed and its water losses noted so that they may be compensated.
Tarry stools are always due to the presence of blood, and abrasions of the intestinal mucous membrane are likely to lead to fatal infections and must therefore always be given serious consideration.
(g) Constipation. -- The mechanical causes such as atresias in various parts of the intestinal tract, or an imperforate anus, must always be considered as possible causes. As has been previously stated, diarrhea is far more common than constipation. This, however, does not mean that a sluggish lower bowel is uncommon in the premature. In fact the lack of power of the muscular wall and the minimal reaction of the mucous membrane to mechanical and chemical stimulation are both important etiological factors and are often associated with intestinal distention. The first evidence of this lack of response is often noted in the inability of the premature infant to evacuate the meconium which has accumulated in the lower bowel, and this may require mechanical removal by the aid of a small saline enema or further irrigation with a soap or glycerin suppository. If these means fail, a single dose of 5 to 8 drops of castor oil may be administered without too great delay, as it is our rule to start feeding only after the first intestinal evacuation, so that the presence of an atresia may have been noted, and the meconium removed before it has become infected through bacterial ingestion. The next stage of the infant's existence which is associated with constipation is in the first few days of life when food ingestion is insufficient and below the caloric requirements of the infant. In such instances in the absence of other causes it may be considered as a certain symptom of underfeeding, as is the case at all times when "hunger stools" are present. Increasing the food judiciously removes the trouble.
As the infant's digestive function improves and it utilizes its food to the fullest advantage, constipation may result from the minimal amount of food residue. The best evidence of such a causative factor in the presence of sufficient feeding is the improvement in general condition and gain in weight. In fact, utilizing their food perfectly, they have a tendency to constipation so long as their food intake is not in excess of their required caloric needs. Therefore, feeding this class of infant moderately in excess of normal caloric needs usually overcomes the constipation.
In the treatment where the ability to digest food is minimal, increasing the water intake frequently is beneficial. Even premature infants are creatures of habit, and where it is necessary to assist them in the evacuation of their bowels, this should be practised at a stated hour, once or twice daily, either through the use of a saline or oil enema, non-irritating suppositories, or what is better, the tip of a well-oiled catheter. Medication in the form of laxatives administered to the mother in the hope of influencing the character of the milk, as well as drugs administered directly to the infant are more or less dangerous agents and should be avoided whenever possible. Ten to 15 drops of paraffine oil, 5 to 10 minims of milk of magnesia or equal amounts of castor oil, may occasionally be administered, but only after attempts at correction by mechanical irritation.
(h) Underfeeding. -- In order to consider this subject properly we must first take into consideration the types of infants with which we are dealing, that is: (1) Healthy premature infants, and (2) congenitally debilitated infants, either premature or full-term. We must again divide them into the classes of breast-fed and artificially fed, and lastly, as to whether the underfeeding occurs during the first days of life during the period when we may expect normally stationary weight, or weight losses, or at later periods, during which we are more likely to see the development of the completed picture of marasmus.
Before entering upon the details of this subject several factors which tend toward the development of inanition and marasmus not directly dependent upon underfeeding must be considered: (1) The danger of an imperfectly developed digestive tract, which even in the presence of sufficient food may soon result in a metabolic bankruptcy. These infants rarely survive the first days of life. (2) Improper hygienic surroundings of the infant, of which one of the most important is the danger of overheating, thereby interfering with heat regulation and associated with excessive evaporation from the body surfaces. This is especially disastrous in its effects in the presence of decreased humidity. Both of these factors predispose to atrophy. Lessened immunity with the added dangers of local and general infections and the secondary nutritional disturbances are especially common in this class of infants, as are the tendencies toward repeated nutritional disturbances once they are established. All of these factors which may tend to impair the general nutrition of the infant will but serve to emphasize the need of careful observation. It will, therefore, be seen that underfeeding may be a primary affair, or may result secondarily following previous nutritional disturbances.
II. Underfeeding in the Healthy Breast-fed Premature Infant During the First Days of Life. -- This represents the dangerous period through which most premature infants pass whose feeding is delayed, awaiting the secretion of milk from the mother's breasts. While the full-term infant may pass through this period with slight disadvantages to its future development, the life of the premature infant may be jeopardized beyond all hope of recovery.
It has been our experience that when feeding is too long delayed the infants, unless very carefully fed in minimal quantities, are subject to repeated digestive disturbances and secondary infection, the latter due probably to lowered resistance. In the premature infant this is true even though the infant's food be human milk. How much more important is the avoidance of long starvation in those who are to be fed artificially, can easily be surmised. Whereas the birth weight in the average premature infant is regained by the second or third week, in those who have suffered great initial weight losses through starvation the return to normal birth weight is greatly delayed. It is surprising, however, to note what minimal quantities of human milk alternated with water, with a total administration of one-eighth to one-tenth of the body weight of fluid in twenty-four hours, will tend to prevent great initial weight loss during the first few days. (See Section on "Feeding during the First Ten Days of Life.")
The removal to an institution supplied with wet-nurses or a wet-nurse in the home are the ideal remedies. Small quantities of milk obtained from other mothers to tide over the period of early lactation when secretion is delayed, as is not infrequently the case where labor is considerably before term, will prevent a critical condition. Where the prospects for human milk are much delayed, the anxiety of the family, due to the decrease in weight, may often be relieved by judicious artificial feeding, as suggested in the chapter on Feeding. It is always the part of wisdom to impress the family with the fact that stationary weight and fluctuating weight are to be expected for a much longer period in the premature than in the full-term infant, and that this stationary weight curve does not indicate a bad prognosis. Artificial feeding, if instituted should always be discontinued at the first opportunity.
In the congenitally debilitated infant, especially the premature, human milk is a practical necessity for a low mortality.
Atrophy and marasmus as seen after the first days or weeks of life are even more dangerous than the evidence of inanition during the first days of life, because they are almost invariably secondary to previous underfeeding, errors in diet, or gastro-intestinal and systemic infections, and improper hygienic conditions, which are unfortunately frequently neglected or overlooked, even when attempts to overcome the conditions are made. In all late cases of marasmus in the premature, while removal of the underlying factors is an absolute essential, the furnishing of the proper diet in the form of human milk is of equal importance.
III. Secondary Digestive and Nutritional Disturbances Accompanying Systemic Infections (Parenteral). -- Just as digestive disturbances result in lessened immunity to infection, so do we find digestive troubles following the infections in the premature, such as infections of the skin, lungs, genito-urinary tract, ears and the general septic infections, which are of common occurrence in these individuals. These secondary conditions are also likely to run a more severe course than the primary nutritional disturbances.
Where it is possible to keep up the baby's nutrition by the proper administration of foods during the course of an infection, such children may be subject to little or no weight loss in the milder types. In more serious cases the food must be reduced both qualitatively and quantitatively. However, even in these, to avoid catastrophes, long-continued underfeeding or starvation must of necessity be avoided, and only in exceptional cases with resulting food intoxication must all food be withdrawn. Such cases furnish us with every indication for early feeding with human milk whenever possible. True alimentary intoxication is usually early recognized by the toxic symptoms -- facial expression, rapid respiration, and marked drops in the weight curve. In these cases temporary complete withdrawal of food in the absence of severe infection results in disintoxication. In parenteral infections this is not the fact, and starvation only leads to a further reduction in fighting power and therefore should not be long continued. The further treatment of these cases is the same as that to be described under "Infections of the Gastro-intestinal Tract."
IV. Infections of the Gastro-intestinal Tract (Enteral). -- No subject with which we have to deal in the care of premature infants calls for such mature judgment as the care and treatment of gastro-intestinal infections. In fact the entire hospital unit is more or less planned and constructed with the idea of prevention and isolation of these cases. Our thought should all be centered on their prevention, since once they become established their course is associated with the gravest dangers.
Infections of the intestinal tract are secondary in importance only to infections of the respiratory tract. It is well known that infection of either of these systems is likely to run rampant throughout hospital wards unless the individual cases are properly segregated at the outset. The infection may be spread through carelessness in handling the infant's utensils or lack in the care of the nose and mouth, through the nipples if nursing on the bottle, or by lack of asepsis in the care of the maternal breasts. Again it may be spread by the thermometer, unclean napkins, or it may be transmitted by flies and insects. The food is in all probability the most common source of transmission, and the milk may be infected either in the breasts themselves or in the handling. In the past before our wards were properly equipped to care for premature infants, doubt as to the advisability of instituting hospital treatment in preference to the home, even though the facilities for general care were limited, existed in our minds with good reason.
All intestinal disturbances must be considered serious because at the outset it is impossible to decide whether we are dealing with a simple indigestion or the first symptoms of an infectious diarrhea. Again it is quite difficult to determine whether we are dealing with the abnormal activities of the intestinal flora or with pathogenic bacteria or their metabolic products. It is also a well-known fact that the normal bacterial inhabitants of the bowels may under suitable circumstances either form toxic products or pass through the frail intestinal wall of the premature infant into the general circulation.
That we may have serious intestinal problems without infection is not to be denied. On the other hand, however, we have the findings of Schabort  who was able to isolate diplococci and staphylococci from the stools of every infant which he examined between the thirty-second and ninety-sixth hour after birth. He found that the sooner the staphylococci appeared, the sooner the stools took on a dyspeptic character, and when the intestinal symptoms were at their height, these organisms dominated the bacterial flora. Be believes that every infant has a staphylococcal enteritis in the first days of life. The etiological significance of these cocci is, however, questionable.
Von Reuss  states that he has not infrequently seen, usually toward the end of the first week of life, even temporarily, muco-hemorrhagic stools, dysenteric in character, which did not, however, impair the general health. He also states that the entrance of staphylococci into the oral cavity of the infant and from there into the intestine cannot be avoided, even with the most extreme care on the part of the attendants, because the cocci may come from the milk ducts or the genital canal of the mother. While the milder types of enteritis are brought about by the irritation of the bacteria or their products of decomposition of the normal intestinal content, they are distinguished with difficulty clinically from the forms of enteritis which are caused by pathogenic microörganisms.
Although in most instances the important element of time and lack of laboratory facilities precludes the making of a diagnosis as to the specific causative organism, in the light of the more modern work of Passini  in his studies of the new born, and Kendall and Day  and others in older infants, the results of their studies are equally applicable to infections in the premature. Passini found that with the introduction of human milk into the lower part of the intestinal tract the meconial flora consisting largely of the sporulating forms of the gas bacillus were changed to the fermentative, aërogenous forms, which were capable of forming irritative products which frequently resulted in an increase of stools more or less foamy, containing increased quantities of mucus. These stools are frequently seen during the first days of nursing and are the so-called "transitional stools." However, these products of food decomposition may reach a considerable degree of intensity and be associated with morbid manifestations (Von Reuss).
Having thus described the mild types of irritation of the first group due to the ingestion of staphylococci and of the second group due to the transformation of the gas-forming flora of the meconium into the aërogenous organisms, as seen after the ingestion of milk, with the resultant irritation due to the fermentative action on the milk sugar, we come to the large class of cases which may be due to one of many types of organisms. Those due to streptococcus infections through the maternal circulation before birth (which in itself may be the cause of premature birth), or the secondary infections through the mother's milk, lochia, or other products entering the gastro-intestinal tract by way of the mouth, are among the most virulent.
The Streptococcus enteritis may, therefore, make its appearance very early in life depending upon the time of infection. In premature infants it has a very high mortality. The various bacillary infections of the intestinal tract due to the colon bacillus, dysentery bacillus, typhoid, paratyphoid bacillus, etc., with the exception of the colon bacillus, are rarely seen during the first days of life, unless the mother is suffering with an infection due to one or the other organism. The clinical symptoms are dependent upon the fetal age and stage of development of the individual infant and upon the type and virulence of the infecting organism. The general health of the infant suffers in all cases. Weight has a tendency to become stationary or show a loss. The temperature curve varies directly with the influencing factors and the reaction on the part of the infant, in the milder types being dependent to a great degree on the absorption of the toxic products. Vomiting is an almost constant factor, and the stools which are first frequent, containing food material when developing after the first few days of life, or meconium if the infection be very early, show mucus and often gas, depending upon the infecting organism, and in the severe cases sooner or later blood. Even the premature infant will give evidence of pain and tenesmus as seen by its facial distortion, its low whining cry, and drawing-up of the lower extremities. In the great majority of cases the abdomen is sunken rather than distended. The skin becomes dry. The body fat is burned up and collapse becomes imminent. The prognosis is in each case dependent upon the exciting factors, the degree of resistant, but in all cases, however mild, the outcome remains in doubt.
Treatment. -- The therapy of these cases offers one of the most difficult problems confronting the pediatrician, because of the danger of marasmus following even short periods of starvation, and because of the limitations of dietetic treatment. Human milk is indeed the only food which can be given with any degree of safety, and this at the same time because of its high sugar content offers a splendid culture medium for the gas-forming organism. The frequent, somewhat foamy, mucous stools which are seen during the transitional period, that is, in the change from meconial stools to the normal breast-fed stools as well as the frequent stools of similar formation as seen after this period, when unassociated with temperature, loss in weight, and other symptoms indicative of serious trouble, should not lead to dietetic changes, but breast feeding should be continued as long as there is an absence of all signs of beginning general disturbances. When the infant is feeding on the milk of its mother similar but physiological stools are very commonly seen during the period in which she is secreting colostrum and are not to be confused with intestinal infection. Evidence of more serious infection should lead to a short period of feeding on inert fluids of proper volume. This period of starvation should not be continued over six, or at the most, twelve hours, and should be followed by gradual feeding of smaller quantities of human milk than has been previously given. Where there is question as to the mother's milk being the source of infection, wherever possible, the milk should be obtained from another source, or the mother's milk should be sterilized before feeding. This latter is easily accomplished because in most cases premature infants are hand-fed during the first few days of life. These measures should be carried out until bacteriological examination is completed.
The intestinal tract may be cleansed by the administration of a single dose of castor oil, varying from 10 to 30 minims, depending upon the age of the infant and the conditions at hand. The large bowel may be emptied by irrigations of normal saline solution, which later may also be given as small repeated nutritive enemata after the intestinal tract is once thoroughly cleansed. Vomiting may be allayed by very careful gastric lavage, small quantities of saline solution being left in the stomach after the washing. Lavage must be rapidly and dexterously performed to avoid attacks of cyanosis. Brandy (1 to 5 minims), or aromatic spirits of ammonia (1 to 2 minims), at regular intervals are the best forms of stimulation for oral administration. Minimum doses of paregoric (1/2 to 2 minims) will frequently allay the intestinal peristalsis and relieve tenesmus, both of which add to the dangers of the intestinal infection. Intestinal antiseptics are to be avoided. Hypodermic stimulation must be very carefully given because of the dangers of toxic effects and of local irritation. Small doses of camphor in oil (1 to 5 minims) are the best. In the artificially fed infant every effort should be made to obtain human milk.
Icterus Neonatorum. -- Two varieties must be distinguished -- icterus simplex and icterus gravis.
While the simple form of icterus is, as a rule, a very benign condition usually running its course without severe systemic manifestations, the grave type is especially fatal in premature infants in whom it is usually a clinical manifestation of liver insufficiency or bile-passage obstruction.
Frequency. -- The incidence of icterus neonatorum in premature infants varies with the observer from 15 to 100 per cent. This variation probably depends upon what the individual observer considers to be jaundice. If a yellowish tinge to the nose and cheeks is regarded as sufficient to make the diagnosis then the percentage will be high; should staining of the conjunctivae only be taken as evidence the number will be low. The term "true icterus" can be applied only to those cases in which the yellow discoloration of the skin is caused by a staining of the bile pigments.
Pathology. -- Autopsy in moderate cases shows that the intima of the arteries, the serous membranes and the various body fluids and the interstitial tissues are stained yellow, but the brain, the cord, liver, spleen and kidneys are usually only slightly discolored, if at all. In severe types, however, deposition of bilirubin crystals may be found in the cells of the skin, in the capillaries and lymphatics and also in the renal pyramids, blood, adipose tissues, brain and other organs.
Etiology. -- The recent work of A. Ylppö offers the most plausible solution for the occurrence of jaundice in the new born, and his experiments are well worth quoting in detail. His experiments were conducted through spectroscopic analysis of the blood for its bilirubin and biliverdin content. He found that biliary pigment secretion is small until the late fetal months are reached. Shortly before birth the secretion is rapidly increased, and this increase is intensified after birth.
This biliary pigment content of the blood increases up to the third to the tenth day and on the whole continues for a longer time in the premature than in the full term. He found that blood from the umbilical vessels averaged from 13,0-58,2 * 10**-5 [gm] per 100 cc of blood and that this increased from the third to the tenth. In those cases which passed 125,0 * 10**-5 gm. per 100 cc of blood, icterus developed, while it remained absent in those containing less than this amount. He also found that there was a direct parallel between the blood content of biliary pigment and the intensity of the icterus: Clinical manifestations of the icterus were absent in the mild cases, while in the severe ones the cholemia resulted in somnolence. He found little evidence that syphilis, sepsis and traumata influence the development of the icterus. From his studies he concluded that icterus neonatorum is hepatogenous in origin and is due to the fact that for some days after birth the liver continues to secrete bile into the blood stream by the same routes that this occurs in fetal life and that due to the fact that there is an intensified secretion of bile pigment shortly before and after birth, the blood content of bile is increased, and that these findings result in the development of the icterus when in excess. He therefore believes that it is a physiological process which, however, may become pathological when the blood content becomes excessive.
The earlier explanation of Knopfelmacher offers a closely related explanation. He describes two factors as concerned in production of jaundice in the new born, a hypersecretion of bile and a disturbance of excretion. The richness of the blood supply to the liver immediately after birth is responsible for a greatly increased production of bile at this time, while during the first few days of life there is only a rudimentary functioning secretory mechanism. Accordingly the tenacious and stagnated bile passes from the overfilled bile capillaries into the blood capillaries.
The increased viscosity of the bile during the first few days of life is explained by Pacchioni as being due to the loss of water sustained by the infant at this time, leading to a greatly slowed biliary current with absorption into the blood and lymph stream.
A hematogenous origin of the bile in icterus neonatorum may be excluded by the experiments of Minkowski and Nyuyn, who demonstrated that the liver is essential for the formation of bile and that without this organ jaundice cannot be induced. The connection of icterus with a stasis of bile, the result of the closure of the ductus choledochus by meconium (Franck), by desquamated epithelium (Cruse), or by a plug of mucus (Virchow), is not supported by the facts; neither is Birch-Hirschfeld's theory of edema of the capsule of Glisson, Bouchut's theory of a hepatitis, or Epstein's explanation that the cause is a catarrh of the small bile ducts.
Freirichs explained the jaundice by a marked anemia and decrease in pressure in the liver capillaries, which in turn lead to a lessened pressure in the bile capillaries and an overflow of bile into the blood stream. The great degree of congestion of the hepatic capillaries at birth precludes this belief, however, while the fact that the blood-pressure is raised in asphyxia neonatorum, in which condition icterus is especially intense also nullifies this theory.
Symptoms. -- In very mild cases the yellow color may appear only on the face, chest, and back, the conjunctivae being but faintly tinted and the urine and feces normal in appearance. In severer forms the urine may be high colored enough to stain the linen, and the jaundiced hue may extend to the arm and abdomen. Some infants present a yellowish discoloration of the whole body, with typical clay colored stools. In most cases the jaundice has disappeared by the eighth or tenth day. It may persist for several weeks. In rare cases, after having much diminished, it reappears with renewed intensity. The liver and spleen are usually unchanged, however; in the severer types liver changes are the rule and it is usually found enlarged.
An early type often seen from six to twelve hours after birth is not infrequent in small prematures. These are usually severe cases and although not of the septic type are slow in disappearing.
While most of the simple cases are unassociated with gastro-intestinal and febrile disturbances the severer types even of the simple form are associated with symptoms of indigestion which is always of grave import in the premature. They are also subject to febrile disturbances and are slow in overcoming their initial weight losses.
Diagnosis. -- Icterus neonatorum being a physiological condition, it must be differentiated from jaundice due to causes other than a mere disturbance of interrelation between formation and excretion. There must be excluded septic, syphilitic and familial jaundice, that due to deformities or obliteration of the biliary passages, and three or four rare conditions characterized by icterus.
Septic Jaundice. -- Gessner believes that many instances of so-called benign icterus neonatorum are dependent upon umbilical infection, and DeLee agrees with him. Other cases are thought to be due to intestinal infection.
In these cases the child is ill, the temperature is elevated and the skin shows a marked degree of icterus, which in the severer cases becomes a bronzing. Hemorrhages are often present, sometimes a foul-smelling pus exudes from the umbilicus, there is anorexia and the abdomen may be distended and tender. Blood cultures sometimes reveal the causative organisms or they can be demonstrated in the septic foci. The outlook for these children is poor, the younger and less mature the infant, the less is its chance of recovery.
Syphilitic Jaundice. -- This form of jaundice is usually present at birth or appears a few days later. It is generally rather intense and may persist, although sometimes it improves, only to recur again. Hemorrhages under the skin are not at all uncommon. It should be suspected if other signs of syphilis are present, especially a positive Wasserman test.
Family Acholuric Jaundice. -- This is a chronic condition characterized by jaundice of long duration, the presence of bile pigments in the stools and their absence in the urine. The spleen is usually but not always enlarged, there is, as a rule, more or less anemia present and some enlargement of the liver. The affection is compatible with life but occasionally there occur slight raises in temperature with malaise, diarrhea, abdominal pain and an increase in icterus. This jaundice has been explained on the basis of a simple cholemia, biliary cirrhosis, splenomegalic jaundice, or it may be that all the conditions are but different stages of the same affection.
Prognosis. -- It must be kept in mind that icterus neonatorum may be of prolonged duration and yet be only due to disturbance of bile secretion and excretion, and not dependent on malformation, sepsis or other disease. An increase in the intensity of the icterus during the second week should make one suspicious of some causative condition more serious than that responsible for a simple icterus neonatorum.
Treatment. -- There is no treatment for simple icterus of the new born, nor is any needed though small doses of calomel with sodium bicarbonate and sodium phosphate have been recommended.
Affections of the Excretory Bile Ducts. -- (a) Stenoses and Atresias. -- The common, hepatic or cystic ducts, one or all, may be affected in congenital stenoses. The more common etiological factors are as follows: (1) One or more of the ducts and even the gall-bladder may be totally absent; (2) fetal inflammatory processes of obscure origin may result in atresias; (3) pathological development at the distal end of the common duct with a valve-like formation may result in atresia (similar formations may be present in the mucous membrane at other locations in the bile passages); (4) hereditary syphilis may result in a perihepatitis, or cholangitis; and (5) occlusion may be due to inspissated bile or concretions.
Symptoms. -- Acholic stools are present where there is an involvement of the hepatic or common duct or both. This may or may not be evident in the meconium depending upon the causative factor. Progressive icterus is an almost constant finding. Urinary findings correspond to the degree of stenosis, and there is undigested fat in the stools when fat is contained in the infant's food.
Prognosis. -- Death soon follows in the cases where the stenosis is the cause of premature birth. However, in other cases where it is simply a part of the general picture of congenital lues, or occlusion is less complete, the infants may survive for a considerable time, depending upon the degree of system involvement. Death is usually due to intercurrent infection, which is not uncommonly through the gastro-intestinal tract, or inanition due to lack of fat digestion or to cholemia. All cases of complete occlusion are fatal in the premature.
Treatment. -- In all cases except those due to inspissated bile and lues the treatment would be surgical, but such interference is practically hopeless in this class of cases and is rarely to be advised in premature infants. The medical treatment of congenital syphilis is far from hopeless. A much poorer prognosis is offered in stenosis of the ducts than in those cases where jaundice is due to a hepatitis.
(b) Gall Stones. -- Cholelithiasis due to fetal inflammatory processes has been described by Bland-Sutton  and Cautley states that they are more frequent during the fetal age and early infancy than at any other period of childhood.
(c) Inflammations of the Bile Passages. -- Although they are rare they may be due to ascending infection, but are more commonly subacute conditions as seen in congenital syphilis.
Affections of the Hepatic Vessels. -- Phlebitis and thrombosis of the portal vein may result from an ascending infection through the umbilical vessels.
Congenital lues may be associated with a periphlebitis of the portal vein, or its intrahepatic branches, or gummatous infiltration about the hepatic vessels. When the portal vein is the seat of considerable obstruction, ascites, gastric and intestinal hemorrhages, enlargement of the liver and splenic tumor usually result.
Minkowski-Nyuyn: Arch. f. exper. Pathologie, 21, 1.
Frank, J. Peter: De curandis hominum morbis Epitome, 1805, 55, 183.
Cruse, P.: Arch f. Kinderheilk., 1, 353.
Virchow, R.: Gesammelte Abhandlungen, s. 847.
Birch-Hirschfeld, F. V.: Virchow's Arch., 1882, 87, 1.
Bouchut (quoted from Marcel Delestre): Étude sur les infections chez le prémature, Paris, 1901.
Epstein: Volkmann's Sammlung klin. Vorträge, 1880, Nr. 180.
Freirichs: Klin. d. Leberkrankh., 1858, p. 1.
Quinckie: Arch. f. exper. Pathol. u. Pharmakol., 1885, 19, 34; Virchow's Arch., 1884, p. 95.
Meckel, H.: Charité-Annalen, alte Folge 4, 1853.
DeLee: Principles and Practice of Obstetrics, Philadelphia, 1913.
Knopfelmacher, W.: Jahrb. f. Kinderheilk., 1898, p. 47; 1908, p. 67.
Hess, A. F.: Am. Jour. Dis. Child., 1912, p. 304.
Abramow, S.: Virchow's Arch., 181, 201.
Pacchioni: Rivista di clinics pediatr., 1911, 9, 333.
Ylppö, A.: Ztschr. f. Kinderheilk., 1913, 9, 208.
Affections of the Hepatic Parenchyma. -- Although the liver is readily influenced by toxic and infectious products, which easily pass through the permeable gastro-intestinal wall, nevertheless, it is exceedingly difficult to recognize the part which this great organ plays.
Among the most common affections of the liver is the predisposition to icterus, which appears especially early in prematures. Besides the physiological jaundice, icterus may accompany a variety of disorders. In the later life we see different types of icterus, aside from obstruction of the gall ducts, as: Septic icterus, Winckel's disease, catarrhal icterus, toxic jaundice and acute atrophy.
Parenchymatous and fatty degeneration of the liver is present in all septic diseases. Degenerative liver diseases are, however, seen where there is no focus of infection and these are probably due to toxins, which are absorbed from the placenta, as in the cases of infants born of eclamptic mothers, perishing shortly after birth. In some instances there may be no gross change but microscopically a high-grade degeneration exists. In addition, as previously mentioned, subcapsular liver hemorrhages occur quite frequently. Ylppö  was able to demonstrate such lesions in almost 80 per cent of the prematures under 1000 gm. birth weight, and only in 5 per cent of those weighing between 2000 and 2500 gm. At times the hemorrhages may be very extensive and with rupture of the liver capsule result fatally. Parenchymatous liver hemorrhages may also be found, but they are small and not of much significance.
In the literature one finds mention of cases of acute yellow atrophy of the liver with the finding of tyrosin and leucin in the urine, coagulation necrosis and hemorrhages into the parenchyma.
Septic icterus is characterized by a marked acute interstitial and parenchymatous hepatitis. In some cases there have been noted cyanosis, convulsions and digestive disturbances, which either disappeared in a few days or led to death. In these cases the liver symptoms are cloaked by those of general sepsis.
Icterus catarrhalis is often associated with duodenal catarrh and cholangitis, and is characterized by jaundice, acholic stools, bilirubinuria, and the prognosis is on the whole good.
Cirrhotic processes in the liver are usually associated with congenital syphilis or deformities of the gall tracts. One sees a diffuse interstitial luetic hepatitis under the picture of hypertrophic cirrhosis. With anomalies of the gall ducts there is a biliary cirrhosis.
Congenital Tumors of the Liver. -- These in themselves may be the cause of premature birth. However, most of the cases of malignant tumors described in the literature are those which have developed after birth in infants either born in seeming health at full-term, or those congenitally debilitated, but who did not give evidence of tumor formation until some time after birth; while the cases giving evidence of tumor formation at birth have been commonly agiomata or cystic degenerations.
Fetal Peritonitis. -- Intra-uterine peritonitis is usually chronic in character, and in premature infants usually results in death shortly after birth, if not already the cause of still birth.
Etiology and Pathogenesis. -- 1. Malformations in the digestive tract with emptying of the contents into the peritoneal cavity. It is also quite possible that some of the malformations described previously may result from secondary changes due to fetal peritonitis.
2. Malformations of the genito-urinary tract may likewise cause fetal peritonitis owing to the extravasation of urine into the abdominal cavity.
3. Spontaneous rupture of any of the hollow abdominal viscera with extravasation of their contents may result in peritonitis.
4. Congenital syphilis is frequently associated with fetal peritonitis (Simpson ). Maceration of the peritoneum, as frequently seen in still births in congenital lues, should not be mistaken for true peritonitis.
5. True congenital tuberculosis may be a causative factor and Mya  believes that the toxic bodies circulating in the blood of a tuberculous mother may in themselves cause peritonitis without the presence of the specific organisms.
6. Various septic infections may pass through the placental circulation into the fetal body and may among other lesions cause peritonitis.
Symptoms. -- The symptoms depend upon the degree of peritoneal involvement and the nature of the cause. In living infants where the process is localized, there may be but few symptoms at birth, but such a process usually results in the formation of adhesions and the development of intestinal obstruction in surviving infants. More commonly the process is generalized, the abdomen distended, containing more or less effusion with resulting dyspnea and cyanosis and the early development of ileus.
Prognosis. -- Premature infants with fetal peritonitis rarely survive the first days of life and even the cases of localized peritonitis usually result in early death because of the inability of the individual to withstand surgical interference.
Acute Peritonitis. -- Etiology. -- It rarely occurs as a localized affection in the premature. The most common sources of infection are:
1. Hematogenous, either through general sepsis or local infection in some distant part.
2. Infections through the umbilical cord.
3. Infections through the intestinal canal either through rupture of the intestines due to trauma (this is usually located in the region of the sigmoid flexure), or the passage of bacteria into the peritoneal cavity, either through the uninjured intestinal wall, or through the inflamed, ulcerated or gangrenous bowel wall.
Symptoms. -- Violent vomiting, abdominal distension with either diarrhea or obstipation, usually temperature, although it may remain subnormal, rapid respirations and pulse, not infrequently marked icterus, and early collapse are the usual findings. The diagnosis is often impossible before death owing to the rapid development of similar findings in the premature from other causes, unless there is evidence of transmission from some localized source of infection, as about the umbilicus.
Prognosis. -- Entirely unfavorable.
Congenital Diaphragmatic Hernia. -- These hernias are described as true and false. The true diaphragmatic hernias are covered by the peritoneum and there is no direct communication between the pleural and the abdominal cavities. In the latter or false type there is really an extrusion of the abdominal organ, and therefore a direct communication between the abdominal and pleural cavities. The latter are by far the more frequent type and the left side is more commonly involved than the right. The diagnosis offers considerable difficulty in the premature and because of the commonly associated cyanosis they are usually diagnosed as congenital atelectasis, a diagnosis which is not greatly in error as the lung on the side involved is not infrequently entirely undeveloped. In contradistinction to full-term infants who may live to considerable age, premature infants usually succumb during the first hours or days of life with symptoms of asphyxia and cyanosis, usually due to gastric or intestinal distension within the chest cavity (Figs. 154 and 155).
Ventral (Lateral) and Lumbar Herniae. -- Etiology. -- They are usually due to defects or arrested development of the lateral abdominal or lumbar muscles. They may, however, result from increased intra-abdominal pressure.
Prognosis. -- This depends on the extent of the hernia and the general development of the infant. Three cases which I have seen in premature infants who survived resulted in spontaneous recovery.
Treatment. -- During the first months of life treatment must necessarily be limited to abdominal bandages or adhesive strips.
Umbilical and Inguinal Herniae. -- Navel and inguinal herniae are especially common in the premature. Ylppö  found herniae of one or both varieties in 84 per cent of the premature infants with a birth weight of less than 1550 gm. before the third month.
Weight in grams.
No. of cases.
1001 to 1500
1500 to 2000
2000 to 2500
Inguinal herniae are rarely observed at birth, usually developing when the infant is several days or weeks old, following intra-abdominal distension or severe crying in stronger infants. They are most frequently bilateral and are fairly common. The testicles are often undescended, leaving a direct communication with the abdominal cavity which is followed by rupture of the processus vaginalis communis through the canal. This is rather interesting when we note that the processus vaginalis is open at birth in the majority of infants prematurely born. The tendency to meteorism, which so commonly exists, enhances the development of hernias under these conditions. While incarceration is rare, and reduction is usually easy due to the elastic walls, strangulation does occasionally occur and is always dangerous if neglected.
Treatment. -- Operative interference is usually out of the question, and we of necessity have recourse to conservative treatment. Steel trusses almost invariably cause trauma and erosion, with the dangers of infection which are of graver importance than the dangers of strangulation due to the hernia. Conservative treatment by the use of yarn trusses as first devised by Fielder  or by the simple truss designed by Dr. Andrew A. Gour offers the simplest and best methods of treatment, and in the majority of cases results in spontaneous cure (Fig. 157).
The average mother or nurse can easily be taught to make the bandage from a good quality of poplin and of such size as will meet the infant's needs. It is usually necessary for the infant to wear the above improvised truss over a period of from one to three months.
Umbilical herniae are usually not extreme, most commonly developing during the first month increasing up to the third month. With proper care they often disappear completely by the end of the first year with the development of the recti and the other abdominal wall muscles.
This seems to be hastened when the child reaches the age of walking where the cases are not already healed. The chief factors in the causation of navel herniae are the weak abdominal walls, the tendency toward rectus diastasis and the delayed healing and falling off of the cord, which averages eight to ten days in the premature as compared with five to seven in the full term. The diaphragmatic respirations are also a factor. Although we may have hernia of the umbilical cord proper, that is, true congenital umbilical hernia, the condition more commonly described as navel hernia is the acquired hernia of the umbilical ring due to deficient closure, resulting in the protrusion of the omentum, or the intestines or both through the ring resulting from increased intra-abdominal pressure. With proper conservative treatment operative interference is rarely necessary.
The method as illustrated usually results in cure in from one to three months, and if a good grade of zinc oxide adhesive plaster is selected, there is usually little excoriation of the skin even in the premature, if the bandage is not applied until the umbilical would is entirely healed and all granulation tissue has disappeared. It is, therefore, necessary to treat the umbilical wound by the open method until thoroughly dried. A small "cigarette-like" roll is made of cotton about 1/2 inch in length and from 1/8 to 1/4 inch in diameter, depending upon the size of the hernia and the elasticity of the abdominal wall. This small cotton cigarette is then partially or entirely buried between the overlapping skin lateral to the hernia, and while it is being held by the operator (doctor, nurse or mother) a strip of adhesive plaster about 3 inches in length and 1 1/2 inches in width is applied directly over the umbilicus.
We have found the short strip of adhesive plaster preferable to the longer strips encircling the entire body, as it causes less irritation, allows greater motor activity on the part of the intestines, and is equally efficient in the treatment of these cases.
Fig. 156. Illustrating the application in inguinal hernia. A pure wool, white yarn 4-ply is wound into a skein of fifteen to twenty strands, from 15 to 20 inches in length, depending upon the size of the infant to which it is to be applied. To prevent tangling it is knotted by a single strand at six points. A single loop is made which is passed around the body at the level of the crests of the iliac bones, with loop coming directly over the hernia. Fixing the loop at this point with the finger, the free end is now passed from above downward between the strands, making a snug knot which is fixed over the hernia. The free end is then passed between the thighs where it is fastened to the main loop over the back by tying with tape or by the use of a narrow rubber elastic to which snap fasteners are sewed. They are made to meet the needs of each individual case. Such a truss should be worn for two or three months or longer. The strand passing between the legs can be protected from excreta by a cigarette made from oiled silk which can be slipped over the free end before fastening. Six skeins should be kept on hand. They can be washed in gasoline and soap and water. They should be stretched while drying.
Fig. 157. Inguinal hernia bandage with small oval metal pad inserted on left side. (Dr. A. Gour.)
Fig. 158. Pad designed by author for use with umbilical hernia bandage. An elliptical piece of fine pore rubber sponge is glued to a slightly larger piece of sole leather. The leather is perforated at four points so it can be stitched onto the bandage. The rubber pad insures close approximation and elasticity to the bandage.
Fig. 159. Umbilical hernia bandage: 1/2 inch cotton cigarette and strip of adhesive plaster.
Fig. 160. Umbilical hernia bandage. Cotton cigarette in place. The next step consists in burying the cotton by folding the skin over it.
Fig. 161. Umbilical hernia bandage. Adhesive strap in place.
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 Die Krankenheiten des Neugeborenen, Berlin, 1914.
 A Study of the Anaërobic Intestinal Bacteria, Jahrb. f. Kinderh., 1911, 73, 1911.
 Boston Med. and Surg. Jour., 1913, 169, 753.
 Gall Stones and Diseases of the Bile Ducts, 1911.
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