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Premature and Congenitally Diseased Infants

by Julius H. Hess, M.D.

Chapter X
Diseases of the Respiratory Tract

Asphyxia Neonatorum

Asphyxia is a condition produced by any interference with oxygenation of the blood. It may be present at birth or it may occur subsequent to that event. Asphyxia in the new born is characterized by an absence or feebleness of respiration which is accompanied by cardiac action, showing that life is present. Asphyxia occurring after birth is most frequently due to prematurity or to congenital weakness.

During intra-uterine life the wants of the fetus are supplied from the maternal blood stream through the placenta, oxygen being present in sufficient quantities so that respiration is unnecessary. Normally this state of apnea terminates at birth and respiration is established, in all probability, as a result of the decreasing supply of oxygen derived from the placental circulation, and of the increasing amount of carbon dioxide which is accumulating in the fetal blood, and upon which the stimulation of the medullary center depends, the fetus passing from a condition of apnea to one of dyspnea. At the same time the heart action is slowed and the blood-pressure raised, both the result of the carbon-dioxide stimulation. Since the respiratory center is only with difficulty affected in the premature, it is sluggish in responding to the increase in carbon dioxide, and if this increase is slow in appearance respiration may not be attempted at all. Cutaneous stimulation from extraneous influences in the outer world also plays a part in the establishment of primary respiration.

Etiology. -- Asphyxia of the premature newborn may be due to any one of the many causes which interfere with the oxygen supply of the fetus either before or during labor. These causes may be listed as follows:

  1. Abnormally strong and prolonged labor pains. Such lengthy and oft-repeated uterine contractions may interferer with the exchange of gases in the placenta or with the oxygen-laden umbilical blood stream.
  2. Unequal pressure exerted by the uterus after the membranes have ruptured, if applied to the placenta or the cord, may prevent oxygen reaching the fetus.
  3. Compression or tearing of the placenta.
  4. Twisting or tearing of the cord or its compression while in the uterine cavity or prolapsed.
  5. Premature separation of the placenta, either complete or partial.
  6. Slow labor the result of weak pains or contracted pelvis.
  7. Premature respirations resulting from attempts at version or from the application of forceps. In this instance the aspiration of amniotic fluid of vaginal mucus usually forms the obstruction to respiration.
  8. Maternal anemia or asphyxia from renal, cardiac, or pulmonary affections, diseases of the blood, eclampsia or other forms of toxemia such as are produced by morphine, chloroform, etc.

In the extra-uterine variety of asphyxia the infant attempts respiration after birth but is unsuccessful. The reason for this failure may be due to the presence of mucus, blood, or liquor amnii in the respiratory passages; to the presence of anomalies of the heart or lungs; to injuries of the skull; to the pressure from cerebral hemorrhage; or to inherent constitutional weakness or weakness of the respiratory muscles. In the premature infant the respiratory center is but insufficiently developed, the respiratory muscles are weak and the lungs are in a state bordering more or less closely upon fetal atelectasis. All of these factors favor the development of asphyxia, and the younger the fetal age of the infant at the time of the birth, the more pronounced are these conditions, though it must be remembered that not all premature infants are debilitated (see Atelectasis).

Cerebral pressure from injuries of the skull or from intracranial hemorrhage causes anemia of the medulla and consequently prevents stimulation of the respiratory center with resulting lack of respiratory activity, or with stimulation of the vagus with excessive slowing of the pulse, which interferes with the exchange of gases through the placenta or the lungs.

Our present belief is that the asphyxia occurring immediately after birth is due to oxygen deficiency and to paralysis of the respiratory center by overloading the blood with carbon dioxide. The presence of atelectasis and pulmonary congestions and edema favors the development of this state, which is so common in prematures and leads to general acidosis. Ylppö demonstrated in living premature infants alkalinity of the blood lower than that ever found in the blood of adults. Conditions are thus favorable for excessive acidification of the organism, not only by carbon dioxide but also by the other acid products of metabolism. Because of the abnormal reaction of the blood the irritability of the respiratory center is early very reduced, leading to asphyxial attacks. In addition, it must be borne in mind that the frequency of cerebral and spinal hemorrhages in prematures will explain asphyxia attacks occurring in the first two or three months of life. Finally, traumatic lesions of the respiratory center may, in themselves, lead to disturbances in respiration and to interference with oxygen intake.

Morbid Anatomy. -- Examination of the body of a premature new-born infant, dead of asphyxia, shows besides the evidences of prematurity, marked congestion of the internal organs. The right heart, sinuses of the dura and the great vessels are filled with blood. The brain and the organs in the thoracic and abdominal cavities are congested and edematous. Small hemorrhages are found in the pleura, pericardium, peritoneum, liver, kidneys, adrenals, and retina. Occasionally effusions are seen in the serous cavities. In the lung areas of aerated tissue are seen along with areas of atelectasis, and the trachea and bronchi may be found filled with mucus or amniotic fluid. Edema of the extremities and scrotum may be present. Extravasations of blood are found in the skin and mucous membranes as well as in the internal organs.

Symptoms. -- The strong premature infant at birth behaves much as does the full-term healthy child; it breaths deeply, utters a more or less vigorous cry, and the skin which at first is of a purplish hue rapidly becomes pink. If asphyxia exists two sets of symptoms may present themselves, depending upon the variety of asphyxia, asphyxia livida or asphyxia pallida.

In aspyxia livida or asphyxia of the first degree the skin has a reddish-blue or bluish tinge, the face is swollen, the eyes protrude somewhat and the conjunctivae are injected. The extremities remain passive though the muscles retain their tonicity or are even hypertonic; the heart beats strongly and the apex-beat is often apparent to the eye; the vessels of the cord are filled with blood and pulsate; the respiratory efforts may be absent or shallow and infrequent. These infants can be roused and made to cry, respirations being established after suitable measures of resuscitation have been used.

In asphyxia pallida, or asphyxia of the second degree, the vasomotor center is overstimulated by the excess of carbon dioxide in the blood and this overstimulation causes contraction of the peripheral vessels with venous engorgement of the deeper vessels, thus further overloading the heart. The face is of a waxy pallor, the visible mucous surfaces are cyanosed, the muscle tone is lost and the extremities hang lax. The reflex irritability is lost; there is no attempt at respiration or at the most very feeble efforts; the pulsations of the heart are weak and either fast or slow, and the pulsations in the cord are absent or only weakly perceptible. The distinguishing feature that separates this condition from asphyxia livida is the lack of muscle tone in the pallid form, these infants having a corpse-like appearance and only the presence of the heart action and a few respiratory gasps show that the infant is not dead.

Further Course. -- If an asphyxiated infant is revived it frequently remains somewhat apathetic, cries very little and does not nurse well, requiring artificial aid in obtaining nourishment. In the stronger infants, however, this condition tends to clear up, so that in a few days the cry is vigorous, the movements active and the ability to nurse is good. In the weakling, whether premature or full-term, such improvement is much slower. The poorly developed respiratory mechanism results in superficial and irregular breathing and the existence of areas of atelectasis tends to delay development of the lung. These weak infants may have breathed spontaneously at birth though not enough to have dilated the alveoli of the lungs to a sufficient degree and as a result repeated attacks of cyanosis occur. These attacks of cyanosis are accompanied by a condition of apnea which lasts a moment or longer, during which the infant ceases to breath entirely. These attacks appear without warning and may be very frequent in the weaker infants during the first two weeks of life, and are evidently the result of lowered irritability of the respiratory center. The outlook for the infant in these spells is not good, despite the fact that treatment is undertaken, because they are an indication of inherent weakness in the individual. In those cases which are to recover, these attacks of cyanosis become less and less severe and less frequent.

The after-life of these infants may be affected to some extent as the persistence of a degree of atelectasis renders them less resistant to infection.

Sequelae. -- Cerebral symptoms that develop later are not at all infrequent in children asphyxiated at birth and probably depend upon cerebral sclerosis secondary to minute intracranial hemorrhages. Development cerebral anomalies or injuries may, however, be primary causes of asphyxia and may later be evidenced by motor and psychic disturbances.

Diagnosis. -- Asphyxia must be differentiated from hemorrhage of meningeal or cerebral origin occurring during prolonged or abnormal labor or after the application of forceps. The symptoms of a slight hemorrhage resemble those of asphyxia, the breathing being very superficial with frequent lapses into stupor. Convulsions occasionally occur and the pulse may be slow or fast. Continued slow pulse with the occurrence of coma and convulsions speak strongly for a cerebral hemorrhage, especially after a prolonged labor or the application of forceps. The differentiation is extremely difficult during the first days of life in premature and weak infants and death frequently results before the etiological factor is ascertained. Delmas [1] recommends lumbar puncture as a diagnostic and therapeutic measure.

Prognosis. -- The outlook for strong prematures suffering from asphyxia livida is good, the majority recovering under proper treatment. In the weaklings it is always grave. In asphyxia pallida the prognosis is bad, the infant invariably succumbing if left to itself. If the heart action improves while attempts at resuscitation are being made it is a favorable sign. Endeavors to revive the infant should be kept up until the heart ceases to beat. At all times undue violence should be avoided, all attempts at resuscitation being applied gently and at regular intervals to avoid visceral injury. If cerebral hemorrhage is combined with asphyxia the outlook is very poor.

The cause of death in asphyxia may be a recurrence of asphyxia attacks, lowered irritability of the respiratory center, atelectasis of the lung or blocking of the air passages by inspired foreign matter or cardiac failure.

Treatment. -- The treatment of asphyxia is concerned with clearing the respiratory passages and supplying oxygen to the tissues. In the milder cases the finger is gently introduced into the pharynx, or the throat stroked downward, while the child is held in an inverted position, sufficient to clear out the obstruction to respiration. In the cases of asphyxia livida there is usually mucus in the trachea or bronchi, and this can frequently be removed sufficiently to allow of respiratory activity by inverting the infant and introducing a catheter as far as the upper opening of the larynx. Only in the larger infants is it possible to pass the catheter into the larynx. Suction is made with the lips and the mucus is drawn into the catheter. Occasionally it is necessary to repeat this maneuver several times. The dangers of a syphilitic infection are to be remembered.

Once the passages are cleared of mucus the reflex stimulation of respiration by external irritation is attempted. In the milder cases the back and buttocks of the suspended child are gently slapped, cool (90° F.) water is sprinkled over the body, or the latter is rubbed with a warm cloth. In the severer cases the child is immersed in hot water at a temperature of 40.5° C. (105° F.) for a few minutes and then in a cool bath for an instant. The warm bath relieves the vasoconstrictor spasm and the overloaded heart, the blood being brought to the surface. Weak mustard baths, warm enemata and careful compression of the chest are all advocated.

In the severest cases cutaneous stimulation is not sufficient and it becomes necessary to resort to artificial respiration.

Insufflation has dangers, especially for the premature infant whose pulmonary tissue is very delicate. If the lung is torn emphysema follows and only a slight tear is necessary because of the very poorly developed state of the elastic tissue in the lung of the premature. On this account it is best to use some method by which the amount of air to be forced into the lung may be measured. The capacity of the lungs being about 30 cc, the use of a thin rubber bulb of capacity smaller than this would obviate the risk of tearing the lung tissue. The difficulty of entering the trachea of these small premature infants must be kept in mind.

The choice of the method to be used in inducing artificial respiration depends upon the severity of the asphyxia. There is no use wasting time in spanking the back or making traction on the tongue in the severer cases. In the lighter forms the simpler measures usually suffice, but in asphyxia pallida more energetic measures must be practised. First the air passages are cleared and then Prochownik's method is used for thirty seconds. If this is unsuccessful the tracheal catheter is introduced with great care and the lungs dilated with air.

The treatment of secondary asphyxial attacks consists in the use of warm baths, oxygen insufflations and artificial respiration. The oxygen tank should be kept at the side of the infant's bed and either continuous or intermittent showers of oxygen given in the attempt to ward off cyanotic attacks (see Cyanosis).

The intracutaneous injection of oxygen with an aspirator has been recommended in the treatment of asphyxia by Delmas. [2] He advises injecting from 30 to 60 cc beneath the skin, from which region it is readily absorbed with beneficial effect. In the opinion of the author such injections, because of the considerable trauma and shock, might result disastrously in the treatment of premature infants.

Reanimation of asphyxiated infants by the insufflation method of Meltzer and Auer is, according to Plauchu, quite practicable and efficient. In this method a current of air, directed as far as the tracheal bifurcation through a small catheter, ventilates the lungs sufficiently to oxygenate the blood even if no respiratory movements occur. The necessary apparatus consists of a rubber bulb, a small mercury manometer and a No. 12 (French scale) rubber catheter. A rod of soft copper is placed in the lumen of the catheter to give it the proper shape for introduction and the catheter itself is marked with transverse lines at 8, 10, and 12 cm. from the tip, indicating the distance from the mouth to the bifurcation of the trachea in the 2000-, 3000-, and 4000-gm. child, respectively.

The method of the procedure is as follows: With the little finger or a small gauze sponge in the hold of a forceps any mucus in the infant's throat is removed and the child is then wrapped in a blanket and placed with the neck slightly overextended. The index finger of the left hand is introduced as far as the upper border of the larynx, finding the soft opening of the glottis. The catheter is introduced by the right hand between the tongue and the palmar surface of the left index finger into the laryngeal opening. When it has reached the proper distance the copper rod is removed, the insufflation apparatus attached and air injected with the bulb, the pressure not exceeding 10 or 15 mm. of mercury.

The insufflation may be continued as long as needed. Soon the child appears less relaxed and the heart tones become stronger and more regular and respiratory efforts begin.

In infants weighing under 2000 gm. the larynx and trachea are passed only with great difficulty because of their small diameter, and the danger of secondary infection due to trauma of the tissue is great.

The use of the pulmotor or lung motor, several modifications of which are on the market, is not to be recommended in treating the asphyxia of premature infants, because of the danger of rupture of the delicate pulmonary tissue.


Of all functions of the premature infant, that of respiration is usually the least developed at birth, evidencing to a marked degree the general lack of development of the central nervous system. Failure on the part of the respiratory apparatus to respond in a sufficient manner to the needs of the infant is the most frequent cause of symptoms of the gravest nature in these weaklings and indeed not seldom of death itself.

The underlying factors in the production of cyanosis may be divided into inherent and extraneous. The inherent causes of cyanosis are:

  1. Lack of development of the central nervous system, especially of the respiratory center.
  2. Weakness of the general musculature and softness of the ribs.
  3. Persistence of fetal atelectasis which tends to delay development of the lungs.
  4. Congenital malformations of the heart or great vessels or myocardial asthenia.
  5. Malformations of the respiratory tract or of the diaphragm.
  6. Diseases or compression of the air passages.
  7. Injuries of the skull or cerebral hemorrhage.
  8. Obstruction to nasal breathing.
  9. A birth weight below 1200 gm. These infants almost invariably suffer from attacks of cyanosis.
  10. Cooling of the body is given as a cause by Budin, but many infants have a temperature of 95° F. or even 93° F. without the occurrence of cyanosis.
  11. Elevation of the body temperature to more than 102° F. is given by Zahorsky as a cause.

In the premature infant the causes among the above which are chiefly operative in the production of the characteristic attacks of cyanosis are the weak respiratory muscles, the softness of the ribs, the underdevelopment of the centers of respiration and the presence of fetal atelectasis.

Involvement of the heart is ordinarily of secondary occurrence, the diminished amount of oxygen in the blood resulting in a slowing and weakening of the heart's action. The atelectasis which is so frequently present, tends to hinder the closure of the foramen ovale and the ductus Botalli and these defects in turn predispose to cyanosis.

The extraneous causes include:

  1. The aspiration of food or vomitus into the larynx or trachea. The lack of development of the pharyngeal and laryngeal reflexes is responsible for the food reaching the air passages and the lack of reflex cough prevents its being ejected. Pneumonia not infrequently follows the aspiration of such foreign particles.
  2. Distension of the stomach from overfeeding. This is one of the most common causes of cyanosis and death in premature infants. This leads to interference with the action of the diaphragm.
  3. Meteorism, due to gastric and intestinal stasis.
  4. Attempts at drinking are often followed by cyanosis, either the direct result of the mechanical prevention of respiration or secondarily through the lessened oxygen content of the blood, resulting in a lack of stimulation of the respiratory centers (von Reuss).
  5. Undernourishment is strongly advanced by Budin as a causative of cyanosis, and he has shown that with increased feeding these attacks stop.
  6. An insufficient supply of water.
  7. The occurrence of a local or general infection.

Symptoms. -- Oftentimes, without apparent cause, attacks of cyanosis appear with frequency during the first few weeks of the life of the premature or weakly infant. Usually without warning the respirations, which have previously been superficial and irregular, become still weaker and then cease entirely for a minute or longer, somewhat resembling the Cheyne-Stoke's type of breathing. Accompanying the apnea is a deep cyanosis which gradually disappears as breathing is resumed. Not infrequently, if immediate steps to restore the respiratory activity to something like the normal are not taken, the infant dies; in other cases breathing is spontaneously resumed and the attack passes off, leaving the infant more or less prostrated. Care must be taken in pronouncing it dead before examination for heart sounds. In a few hours or days cyanosis recurs, the attacks gradually increasing in length and severity despite treatment, until death occurs; or they become less frequent until they cease entirely.

Occasionally the attacks are preceded or accompanied by convulsions. Generalized edema sometimes develops.

Diagnosis. -- From congenital cyanosis due to other causes, or acute affections of the respiratory tract with cyanosis, these attacks are differentiated by the history or other evidence of premature birth, and the frequently accompanying cyanotic edema, the respiratory weakness, absence of the normal vesicular breathing, particularly over the bases and the tendency to a subnormal temperature.

Prognosis. -- The prognosis of cyanosis in the premature infant varies directly with the severity of the attacks which in turn are more or less directly dependent upon the fetal age and the physiological development, the ability of the infant to maintain its body temperature, the quality of the food and the ease with which the infant digests it.

In no other condition to which these infants are subject is the previous training and experience of the attending nurse in the care and handling of this class of cases, of such vast importance.

Treatment. -- A premature infant must be carefully watched for signs of cyanosis, otherwise it may be found dead in bed. Should an attack occur while the child is being fed, the proceeding must be stopped and efforts made to restore respiration. The first thing to do is to ascertain if there is any obstruction in the upper respiratory passages. Should inspired food or vomitus be present, an effort must be made to dislodge these particles. Inserting the little finger into the pharynx while the child is in an inverted position often serves to clear out the respiratory tube, and then slight cutaneous stimulation by pinching, friction, or gentle slapping is often enough to reinitiate breathing.

Again, exhaustion of the infant may be solely responsible for the cyanosis. In these cases artificial respiration should be tried, the chest being rhythmically pressed upon, or one of the other methods of artificial respiration may be tried. Simple compression of the chest may be tried without removal from the incubator or bed, though removal will be found more serviceable generally.

The use of oxygen is of value in quickly reducing the degree of asphyxia after breathing is once established, although it will not of itself restore that function. A tank should be kept by the infant's bed and any sign of approaching asphyxia should be the indication for the generous shower of oxygen. The continued use of the gas when properly applied is advocated as a valuable measure in the checking of attacks. About 80 to 100 bubbles of oxygen gas from a partially protected mask should escape in close proximity to the infant's mouth.

Aromatic spirits of ammonia in one-half to two drop doses, diluted, is of value, and nitroglycerin, one drop of a 1:1000 solution may be placed on the tongue. The use of camphor, caffein, atropin, or other respiratory stimulants hypodermically does not offer much practical help.

Sprinkling the baby with cool water will occasionally stimulate respiration and as this means is always at hand it should be kept in mind.

Infants suffering from repeated attacks of cyanosis should be immersed in a hot bath at a temperature of 102° to 105° F., and subjected to gentle friction, more especially along the spinal column. The infant may be kept in the bath for from a few seconds to several minutes, when it should again be placed in its warmed bed, avoiding all chilling. The efficiency of the bath may be increased by the addition of a teaspoonful of mustard to the gallon of water. Care should be taken to avoid aspiration of the bath water, or its entrance into the eyes, and the danger of infection of the umbilical cord, although not great must be kept in mind. The bath may be repeated as indicated.

In our own experience the warm mustard bath has proven one of the most satisfactory means of overcoming prolonged attacks. It is quite evident that the facilities for preparing the bath must be prearranged and great care taken to keep it at an even temperature throughout the immersion. To facilitate handling and to prevent undue manipulation during the cyanotic attacks the infant should be wrapped in a blanket.

It cannot be too strongly emphasized that the manipulations used to relieve the cyanosis should be the minimum necessary to accomplish the result as cyanotic infants react poorly to trauma. After an attack is over the infant should be placed in a warm bed or bath in order to overcome the tendency to a reduction of temperature by the previous manipulations. Afterward it is also necessary to supervise carefully the feeding in order that two things may be accomplished: (1) That the occurrence of further attacks of cyanosis due to mechanical obstruction of food may be prevented; and (2) that the nutrition of these weaklings may be immediately bettered and thus the cyanosis indirectly controlled.

The prevention of cyanosis may be aided in several ways. The too rapid taking of food or distension of the stomach by overfeeding must be avoided (see Feedings). Underfeeding in cases where too frequent feeding is undesirable can be avoided by catheter feeding at longer intervals, although the maximum food quantities must be carefully ascertained by starting with minimum feedings, carefully increased according to the infant's tolerance. Catheter feeding is not well borne by all infants and may occasionally in itself induce cyanosis. The strength of the infant should be built up as rapidly as possible, and the temperature of the body should be maintained by the use of the heated bed inasmuch as a lowering of the body temperature not only favors the development of cyanotic attacks, but makes them more severe when they do occur. The use of oxygen may be of some value.

Insufficient supply of fluids should be avoided by the administration of water where the fluid intake is less than one-sixth of the body weight during the twenty-four hours.

Meteorism may be relieved by small quantities of low saline enemata, part of which may be left in the rectum to good advantage where the fluid intake per mouth is insufficient to meet the body requirements.

Gastric lavage must occasionally be resorted to as a means of last resort in overdistension of the stomach with paresis of its walls and should be performed with the infant's head at a lower level than the body to prevent aspiration of stomach contents, as passage of the tube very frequently results in vomiting. This procedure is always associated with great danger during a cyanotic attack. Occasionally the gas can be relieved by simple passage of the catheter into the stomach with slight pressure from without over the epigastric region.

Diseases of the Nasal Passages

The anatomy of the nasal passages of the new-born infant is such that comparatively small degrees of swelling or accumulations of mucus are sufficient to lead to obstruction of nasal respiration, thereby interfering with the act of nursing. When during sleep the tongue falls backward, thus occluding the passage between the pillars, attacks of cyanosis and dyspnea may result.

A nasal discharge present at birth or developing within the first two or three weeks of life should lead to a search for evidence of congenital lues. When the syphilitic infection is sufficiently virulent to cause premature labor the external manifestations usually appear early.

Other sources of infection of the nasal mucosa can be found in the passage of the child through the maternal birth canal, from the bath water or by direct transmission from an individual suffering from a similar infection. The organisms which may be concerned include the various pyogenic bacteria, the pneumococcus, colon bacillus, influenza bacillus and, less frequently, the gonococcus. The diphtheria bacillus is frequently seen as a cause in institutional infants.

Obstruction of the posterior nares is occasionally seen in the new-born premature, the opening being closed by either a membranous or a bony partition. When bilateral it favors respiratory obstruction and may be the direct cause of attacks of asphyxia and cyanosis. Nasal infections may threaten the infant by extension to the lower respiratory passages, while generalized septic processes may have their origin in a nasal infection.

Treatment. -- The prophylaxis of nasal infections requires that if the mother is suffering from any infection of the respiratory tract every effort should be made to prevent infection of the offspring. Coughing or direct breathing into the infant's face should be avoided and care taken that infectious material is not carried from one to the other in the hand, or by means of infected articles. The same precautions must be taken in case an attendant is the one infected. A vaginal discharge from the mother at the time of delivery requires that the infant's nose should be cleaned thoroughly but carefully with a cotton pledget after birth. Lowered resistance due to chilling of the infant is an important etiological factor and must be avoided.

It may become necessary to remove crust formation with instillations of normal salt or weak alkaline solutions. This must be carefully performed to avoid forcing the infection into the Eustachian tube and air passages, small quantities only being used. Pledgets of cotton saturated with 1:1000 solution of adrenalin chloride if placed within the nostril will temporarily relieve the nasal swelling. As curative agents some of the organic silver salts in weak solutions may be mentioned. The use of an ointment of the yellow oxide of mercury (ung. hydrarg. ox. flav.) of 0.5 or 1 per cent strength will be found of value. A portion the size of a small pea should be introduced into the anterior nares and the nostril then gently massaged in order to force the ointment as far into the nose as possible. In cases of syphilitic or diphtheritic infectios specific treatment must be instituted.

The breastfeeding of these infants with rhinitis offers some difficulty because of the interference with respiration which accompanies obstructions of the nose. Nursing at the breast is likely to be a difficult matter under the most ideal circumstances when the infant is as weak as many prematures are, and if added to this is an ability to breathe while sucking and swallowing. The difficulties are so great at times, even in infants approaching maturity, that it becomes necessary to fed expressed milk per catheter. This method of food administration must be instituted before the infant shows the results of inanition.

Congenital Stridors

Congenital Laryngeal Stridor. -- In the premature infant the presence of a stridor may go unnoticed for several days because of the weak inspiratory effort, in contradistinction to the full-term infant in which it is usually interpreted in the first days of life. It must, therefore, be expected that the croaking or crowing sound will be much more feeble than is usually heard in these cases. The stridor usually disappears when the infant is deeply asleep, which in the premature is the greater part of its day. Unless there is a considerable stenosis, the infant shows no distress and cyanosis is absent. During intense crying and in the presence of cyanotic attacks, signs of obstruction may become evident. It is often difficult to make an exact diagnosis in these cases because of the dangers of direct transillumination of the larynx in these small infants and the diagnosis is often dependent on the ability of the clinician to exclude other causes of inspiratory dyspnea. Two cases examined by the author at autopsy have in both instances shown similar findings, in that there was a marked narrowing of the lumen of the larynx with thickening of the aryepiglottic folds and deformity of the epiglottis. Nervous disturbances due to arrested development in the cortical centers with resulting disturbed coordination of the act of respiration may occasionally be a causative factor. Arrest of development affecting the center for the recurrent nerve may also be another factor.

Treatment. -- There is usually a spontaneous functional correction. The prophylactic care should consist in the prevention of respiratory infections.

Stridor Thymicus. -- The frequency of true thymic enlargement with direct tracheal pressure has undoubtedly been exaggerated by incomplete diagnosis. The most frequent sign proving stenosis of the upper air passages is the presence of suprasternal retraction. In the premature the tendency of the entire chest wall to collapse with each inspiration may be mistaken for this sign and easily lead to an error in diagnosis. The author has seen two such cases which were verified by palpation of a soft tumor mass in the fossa jugularis during expiration as well as by percussion with flatness to the right and left of the manubrium and substantiated by roentgen-ray findings. In both cases the stridor developed shortly after birth and disappeared spontaneously with diminution in size of the thymus gland, both infants making an uneventful recovery. The author has also seen a case of congenital thymus stridor in a luetic infant which died on the sixth day. At autopsy the thymus gland weighed 40 gm and was the seat of numerous miliary abscesses.

Prognosis. -- The prognosis varies with the cause of enlargment. The benign forms which disappear spontaneously undoubtedly belong to the vascular type. While the number of sudden deaths due to causes associated either directly or indirectly with the thymus gland are less frequent than one would be led to believe from a review of the literature, they do occur and must be given proper consideration. These deaths may be due to mechanical compression of the trachea by an enlarged gland either due to true hypertrophy or hemorrhage within the gland, or death may be caused by hypersecretion of the gland. Syphilitic changes in the thymus with miliary abscess formation has already been described as a cause of death under Thymic Stridor.

Treatment. -- An expectant attitude should be adopted in the absence of specific signs of stenosis. In the presence of congenital lues, specific treatment should be instituted. The only other form of treatment which offers any degree of encouragement is that of roentgen-ray exposure in the hope of creating rapid involution, with the development of moderate fibrosis. Friedlander [3] describes prompt results, stating that dyspnea is lessened even after the first treatment.

It is self-evident that exposure of premature infants to the roentgen-ray, unless carefully guarded, may be disastrous not alone in the too rapid atrophy of the thymus gland which is so necessary to the growing organism, but also to the thyroid and other parenchymatous organs as well as the danger of skin irritation.

In our wards at Michael Reese Hospital, Dr. R. A. Arens makes use of the following equipment:

8 inch spark gap.
3 mm. aluminum filter.
10 inch S.T.D. (Skin-Target Distance)
5 M.A. (milliampères)
4 minutes exposure.

The treatment is guided entirely by the clinical course. Frequently one or two treatments are sufficient.

Stridor from Other Causes. -- These are most commonly due to congenital enlargement of the thyroid gland which is usually of the vascular type and disappears spontaneously without treatment. Congenital tracheal stenosis, deformities of the mouth, congenital tumors of the mouth and acute inflammatory conditions of the upper respiratory passages may be further causes.

Suffocation from External Causes

Death from suffocation due to external causes such as faulty position (infant on face), obstruction of breathing by clothing or overlying on the part of the parent have been responsible for the loss of many premature and weakly infants. These have often been described as instances of thymic death. Death from these causes is far less common in full-term, robust new-born infants, as the latter possess the ability to change the position of the head when threatened with suffocation.

Affections of the Bronchi and of the Lungs

1. Congenital Anomalies

Fetal Bronchiectasis. -- Fetal bronchiectasis is a rare condition of the new born which affects the whole or only part of one lung. Universal bronchiectasis is the result of hydremic degeneration of an entire bronchus, the lung structure being replaced by cystic formations which contain a serous fluid in which are found ciliated epithelium and nuclei.

The telangiectatic bronchiectasis is characterized by the formation either of individual cysts or less often of multilocular sacs, the walls of the cysts being lined with several layers of cuboidal epithelium.

A third variety known as atelactatic bronchiectasis is due usually to lack of development of certain portions of the lung which later become cirrhotic from pressure from a bronchus. (Birnbaum [4].)

Hypoplasia and Hyperplasia. -- These malformations are due either to lack of sufficient development or to excessive development. In hypoplasia a small airless structure is found in place of one lung. Since the healthy lung in such cases usually grows into the empty half of the thoracic cavity, deformity results, the thoracic wall not developing well over the healthy lung. The same is true of primary hypertrophy, which consists either in abnormal size or in formation of supernumerary lobes. (Birnbaum.)

Diagnosis. -- On account of the equalizing growth of the healthy lung the diagnosis is possible only in the presence of deadening of the sounds over one-half of the thorax. This is much more important in the new born than in older children, since in the latter the above mentioned physical finding is much more significant of an infiltration or exudation (von Reuss [5]). Roentgen-ray studies are of assistance in localizing the lesion although they may not determine the type of lesion.

Brochiectasis in the new born is not accompanied by any distinctive symptoms. In the premature their existence increases the respiratory handicap under which these infants labor, and if they are extensive, death with symptoms of asphyxia usually occurs soon after birth. The occurrence of inflammatory complications makes the outlook still graver.

Atelectasis. -- Atelectasis is also spoken of as acquired asphyxia though it may be congenital as it is a persistence of the fetal state in all or part of the lung. In the congenital variety the lung is not entirely expanded at birth, while in the acquired form collapse of the previously expanded lung occurs. The congenital variety is seen chiefly in the premature and debilitated, either due to a developmental anomaly or insufficient strength on the part of the respiratory muscles to inflate the lungs. The acquired form is most frequently due to obstruction f the bronchi or alveoli by intrathoracic exudates, diaphragmatic hernias and deformities of the spinal column.

Atelectasis is to a degree physiological during the first few days after birth, gradually disappearing with increasing strength. When associated with asphyxia at birth, it is often overcome entirely by the means used to revive the infant.

In the weak the methods used are not enough to cause complete expansion of the lung and collapsed areas persist, the soft and yielding thoracic wall and poorly developed respiratory muscles of the premature both favoring the non-expansion.

The cyanosis which is so frequently seen in those suffering from atelectasis may be directly due to the aspiration of food into the larynx, the absence of the pharyngeal and laryngeal reflexes favoring this. Mechanical interference with respiration during the act of drinking may also result in cyanotic attacks; interference with the action of the diaphragm through overdistension of the stomach (Birk [6]) and according to Budin [7] underfeeding, may both be responsible for cyanosis in the premature. (See Cyanosis.)

Pulmonary atelectasis also occurs after cerebral hemorrhage, due to injury to the respiratory center, and is characterized by small respiratory excursions and slight exchange of gases. In the premature the irritability of the respiratory center is low a priori, while in those suffering from natal asphyxia it is lowered by the asphyxia.

Pathology. -- The anterior portions of the lungs are most frequently the portions expanded, the paravertebral parts being atelectatic. Peiser [8] showed that in organs hardened in situ the portion near the hilus was also atelectatic, while the apices and borders were usually expanded, the expanded portions often being emphysematous (Holt [9]). When death occurred early a large portion of the lung was usually not inflated. The left lung is usually more atelectatic than the right. The involved parts are rich in blood and thus form sites of predilection for inflammatory processes.

Hemorrhages and edema frequently complicate this condition, which is made worse by the deficient heart action. These hemorrhages are chiefly in the region of the hilus. In vessel injuries of lesser degree there is no bleeding, only edematous extravasation.

The atelectatic lung is of brownish-red color, does not crepitate, is very vascular and shows the lobular outline on the surface. Usually both lungs are affected to the same degree. The heart frequently shows the presence of a patent foramen ovale or other congenital lesion, the liver and spleen are often congested and the latter may be enlarged. [Fig 152]

Symptoms. -- Very frequently the subjects of atelectasis give a history of asphyxia at birth; in others there may have been nothing to attract attention to the lungs. Some are noticeably quiet, cry weakly, sleep much, and their voices are feeble. The temperature is usually below the normal; occasionally there is some edema of the extremities or slight puffiness of the face, while the breathing is shallow and often irregular. The gain in weight is slight or absent, and the children remain small and delicate with poor circulation. At any time there may develop attacks of cyanosis, which occur without warning and which may be fatal in a few hours, often being preceded by convulsions. These attacks may occur as late as ten or twelve weeks after birth.

Physical Signs. -- Inspection. -- The breathing is shallow, often irregular and at times almost ceases.

Palpation. -- This is negative unless râles are plentiful, when fremitus may be felt. Vocal fremitus is absent.

Percussion. -- There is usually resonance over the entire chest and only posteriorly may diminished resonance be demonstrable. The collapsed areas are surrounded by areas which are overdistended with air and thus resonance is not much interfered with. Small areas of collapse give no dullness at all. If only one lung is involved a difference can usually be made out.

Auscultation. -- The breath sounds are very feeble and the expiratory sound in particular may be nearly inaudible. The sounds may be rather harsher than normal, but are rarely bronchial in character. The most marked physical sign is the presence of crepitant râles, the so-called atelectatic crepitation, which are best heard usually over the bases when the infant, by flagellation or otherwise, is induced to take a deep inspiration.

Diagnosis. -- The diagnosis of atelectasis is to be made more from the symptoms, the shallow breathing, the stupor, the asphyxia attacks and the debilitated condition of the infant than from the physical signs which are likely to be ambiguous and not well defined.

If the respiratory efforts of the infant are sufficient to supply the needed amount of oxygen the dangers from asphyxia disappear and only the inflammatory complications which may arise in the uninflated lung threaten its well-being. Any atelectatic area may become inflated (bronchopneumonic) and thus areas of collapse and bronchopneumonia may be present in the same lung. Pneumonia in an atelectatic lung is not easy of recognition. The presence of crepitant and subcrepitant râles, impaired resonance and the absence of respiratory sounds, accompanied by dyspnea and ineffectual cough, all speak of an inflammatory condition. The percussion note may be vesiculo-tympanitic and ausculatory signs of consolidation, such as bronchial breathing and bronchophony may be inaudible because of the diminished respiratory excursion.

Differential Diagnosis. -- A number of conditions must be considered in the differentiation of diagnosis, the most important of which are the following:

General debility with quantitative and qualitative lack of development attended with impaired respiratory cardiac and digestive functions. This is uniformly associated with lack of development of the thoracic wall and a tendency to collapse on the part of the costal cartilages, and a poorly developed respiratory musculature.

Cerebral injury associated with hemorrhage is one of the most difficult pathological conditions to differentiate, because of the tendency toward involvement of the respiratory centers, more especially in basilar hemorrhages. A careful inquiry should be made for a history of opisthotonos and clonic contractions of the extremities or facial muscles.

Hyperplasia of the thymus and occasionally the thyroid gland, with associated stridulous respiration, retraction of the diaphragm and local physical findings must be differentiated. When the chin is brought down upon the chest respiration becomes more difficult and, in turn, is made easier if the head is bent back.

Aspiration of foreign matter or food with lack of expulsitory effort resulting in cyanosis may lead to an error in diagnosis.

Underfeeding, with secondary asphyxia.

Congenital diaphragmatic hernia.

The differential diagnosis of this condition is based on the fact that the abdominal organs containing air enter the pleural cavity, thus giving rise to physical signs of pneumothorax. In addition, the following signs are presented: Respiratory movements on the affected side are absent or less marked than normal, and there is usually bulging of the thoracic wall on the same side; pectoral fremitus is slight or absent and the percussion note is deep and loud and in some cases tympanitic. Not infrequently succussion sounds can be elicited. The normal breath sounds are absent over the affected area and the heart is found displaced to the right. Moreover, these findings change with a change in the position of the patient. From the foregoing it will be seen that the findings of percussion and auscultation are important but variable, as they depend entirely on the amount of air or semisolid material contained in the abdominal organs present in the pleural cavity.

Radiographic examination is of special value in differentiating atelectasis pulmonum, hyperplasia of the thymus and diaphragmatic hernia.

Prognosis. -- This depends upon the degree of atelectasis which in turn usually depends upon the degree of debility of the child. When accompanied by attacks of asphyxia and cyanosis which appear with frequency during the first two weeks of life, the outcome is bad, despite the institution of proper treatment, as these attacks commonly result fatally. In favorable cases they become less frequent and finally cease. Pneumonia in atelectatic areas often leads to a fatal issue.

Infants who have suffered from congenital atelectasis may remain in delicate health for a long time, although many ultimately recover completely.

Treatment. -- The physical condition of these weaklings is oftentimes so precarious that undue roughness in the application of restorative measures can work infinitely more harm than they may do good, and so it must be remembered that the less the manipulation necessary to overcome the cyanotic attacks, the less is the danger of injuring the infant at this critical time either by overstimulation mechanically or by medication. The object of treatment is directed toward the expansion of the lungs through deep breathing. This is done by crying, and if the child does not cry strongly every day, it should be made to do so. In the mild cases cutaneous stimulation is sufficient, the child being very gently spanked thrice daily for fifteen or twenty times, thus tending to expand the collapsed portions of lung and to expel mucus from the bronchi. The mustard bath is made by adding one tablespoon of powdered mustard to one gallon of water at a temperature of 100° to 105° F. Alternate immersions in warm water with a temperature of 104° F. and cool water of 95° F. may be tried, always beginning and ending with the warm immersions. These may be repeated at intervals as indicated by the physical condition of the infant. The objects of the bath are the diversion of the blood from the lungs to the cutaneous vessels, and expansion of the collapsed areas. Expansion of the collapsed lungs is much easier during the first few days, the difficulty of doing this increasing proportionally with the length of time elapsing since birth.

The infant should not be allowed to lie quietly in one position, but its position must be changed frequently and the child picked up several times a day. Particularly where many infants are housed with but little individual attention atelectasis is seen most frequently. The further treatment should be similar to that advised for attacks of cyanosis.

As the temperature is so often subnormal, these children must be kept warm, either by being surrounded with hot-water bottles or else kept in some sort of heated bed. The feeding of these children is an important problem (see chapter on Feeding). It is essential to increase the general nutrition in order to increase the function of the respiratory center and muscles. Aside from this, it is improbable that increased feeding as recommended by Budin is of any direct value as a therapeutic measure.

During attacks of asphyxia, oxygen inhalations are recommended, and are valuable when the infant can be made to inspire, a tank being kept in close proximity to the infant's bed. Other measures of resuscitation mentioned under asphyxia (see Cyanosis) -- cutaneous stimulation and artificial respiration, or even the use of forcible means of inflating the lung with a catheter in the trachea -- may be necessary but their danger must not be underestimated. The use of drugs hypodermatically, such as camphor, caffeine, atropin, etc., is not of much value. Aromatic spirits of ammonia in one-half to three-drop doses, well-diluted, is worth trying.

Congestion and Inflammatory Changes of the Lungs.

Congestion of the Lungs. -- Congestion of the posterior lower portions of the lung most commonly results from long-continued rest without change of position, congenital or other anomalies of circulation. At first there may be extravasations of serum or blood in the alveoli and later, especially in the greater degree of congestion, tissue infiltration.

Clinically, the condition is manifested by disturbances of respiration, shallow breathing and asphyxial attacks. The impairment of resonance and auscultatory findings may be confounded with those of atelectasis or inflammations. The findings are usually bilateral and in dependent parts; these facts aid in the differential diagnosis. They develop post partum thereby differing from atelectactasis and are primarily associated with fever.

Congenital Pneumonia. -- That congenital pneumonia may exist seems to be well substantiated, although the number of cases reported in which the infection was hematogenous and transmitted by way of the placenta is small.

Infection of the fetus may also occur through infected amniotic fluid before labor. However, when it is the result of the aspiration of infectious material during the passage through the birth canal, these cases must be classed as extra-uterine pneumonia.

Post-natal Pneumonia. -- Etiology. -- Bronchitis during the first few days of life may be the result of aspiration of infectious material, or it may accompany a general septic infection. The fact that the vaginal secretion always contains microorganisms offers every opportunity for infection, should aspiration occur during the infant's passage through the birth canal. Infection of the bronchi may reach the child from an infected mother or attendant, or from a third person through the agency of feeding utensils, spoons, or other articles. Infections in the upper air passages may spread by direct extension to the deeper structure of the respiratory passages and there occasion a bronchitis or bronchopneumonia.

Atelectatic areas, so common in the lungs of the premature or weakling, and the frequency of aspiration of food or vomitus in the debilitated favors the occurrence of pneumonic inflammation. The richness of the atelectatic portions of the lung in blood and tissue fluids make them a most favorable medium for the multiplication of the invading bacteria.

The organisms found in the bronchopneumonia of early life are the pneumococcus and staphylococcus most commonly, less frequently the Bacillus coli, the streptococcus and the influenza bacillus.

Meyer [10] emphasizes the fact that the "grippe" with respiratory involvement may cause a surprisingly extensive infection.

Pathology. -- In the majority of cases both lungs are involved, the parts most frequently affected being the lower posterior portions. The principal lesion is an inflammation of the walls of the bronchi, and the walls of the alveoli surrounding the bronchi. Microscopically before section there is often no visible evidence of consolidation, and seemingly all of the lung can be inflated. The walls of the bronchi and alveoli are thickened and infiltrated with round cells. The involved alveoli are filled with an exudate which is at first composed of desquamated epithelial cells and later of leukocytes. On section there are seen grayish-red or yellowish-gray areas which correspond to the cut bronchi and the surrounding peribronchitis. From the cut bronchi the fluid contents exude, composed of epithelium, pus cells and mucus. Many of the smaller bronchi become occluded by the excessive exudate and collapse of the contributory alveoli follows. The collapsed portions are depressed beneath the surface of the surrounding lung and are of a beefy-red color.

In some cases, particularly in those instances where the streptococcus is the causative organism, the inflammation may be of a hemorrhagic nature. In these cases the blood vessels of the affected areas are deeply congested, the lung tissue is studded with small hemorrhagic patches whose size varies from that of the head of a pin to several centimeters in diameter, the latter being true infarcts. They are distinguished from the zone of congestion that surrounds them by their projecting above the surrounding tissues, their dark color and their durability. On section they are of triangular shape with the apex more or less deeply in the lung substance. They are seen particularly in the lower lobes. The mucous membrane of the large and small bronchi is the seat of a catarrhal inflammation with round-cell infiltration.

Death in the case of these prematures and weaklings is not always the result of the virulence of the invading organism but may be attributed rather to mechanical phenomena secondary to the involvement of the lung. Because of the excessive amount of exudate and intraparenchymatous hemorrhage the alveoli are filled with fluid, the bronchial ramifications are obstructed and the gaseous exchange limited or prevented almost entirely. Pneumonia, therefore, and particularly hemorrhagic bronchopneumonia kills the premature by asphyxia. In other instances death is the result of a true toxemia.

For contrast and comparison we have the recent investigations of Ylppö [11] who found that typical bronchopneumonic changes were very rarely observed in very young prematures.

The following table shows the frequency of lobar pneumonia in his series:

Frequency of Bronchopneumonia in Prematures


Death of the age of:

1 day.

2 days.

3 days.

4 to 15

1 mo.


Under 1000 gm.

Number of sections.







Bronchopneumonia in these.







1000 to 1500 gm.

Number of sections.







Bronchopneumonia in these.







1501 to 2000 gm.

Number of sections.







Bronchopneumonia in these.







2001 to 2500 gm.

Number of sections.







Bronchopneumonia in these.







Ylppö's histological investigations showed that the bronchopneumonic areas in prematures were not at all as frequent as the bronchopneumonic areas in the full terms in the first days of life. Hess Thaysen [12] stated that in newly born infants dying in the first three days of life there could be demonstrated small bronchopneumonic areas in 42 per cent of the cases. These changes are not due to aërogenous infection but to the aspiration of infected material from the mother during birth. Hochheim [13] showed that the vaginal secretion and amniotic fluid was aspirated and demonstrated the presence of foreign bodies, as squamous epithelium, fatty bodies, meconium and lanugo hairs in the lung alveoli.

Symptoms. -- The onset is most often insidious in the weakly new born. At first there is noticed possibly a slight nasal discharge and a cough of varying severity. Soon increased frequency of respiration makes its appearance accompanied by dilatation of the alae nasi. The cough in the more mature becomes worse and the respiration increases to 60 or 80 per minute. Now and again slight attacks of cyanosis occur, which in the severe cases are correspondingly more marked. There is great restlessness in older infants with inability to sleep, and the cyanosis becomes continuous. Convulsions occur with more or less frequency, while the temperature may be slightly elevated or may be subnormal even in the severest cases. There is a marked loss of weight, the stools become dyspeptic, and greenish with mucus and undigested particles. The prostration may be extreme.

There is often a singular lack of symptoms and the disease may go unrecognized. The respirations range from 40 to 60 or even 80 to 100 per minute, but are usually not labored, the pulse-rate is increased to 140, 160, or may be uncountable; the cough may be absent entirely, and there is often apathy and even deep stupor. The course in these infants is usually acute, either immediate improvement or death occurring.

The severity of these early symptoms is to be explained either on the basis of the sudden intense congestion of the small alveoli interfering with the bronchopulmonary apparatus almost as much as does consolidation, or their severity may be due to the intensity of the infection.

Physical Signs. -- The usual physical findings of a bronchitis or bronchopneumonia are often lacking or only suggested in the pulmonary inflammation of the premature and debilitated, especially when the involved areas are small in size. This is due to the fact the respiratory efforts are weak and their amplitude small. In addition it is often the atelectatic portion of the lung which is involved and if this is situated centrally the air may fail to gain access to it.

On inspection there is seen more or less marked dyspnea, with inspiratory retraction of the lower ribs; the face may be pale or cyanosed; cough if present is frequent, short and non-productive. Palpation may reveal nothing. Evidence of consolidation such as increased resistance may be entirely lacking.

Percussion may give indication of consolidation if impaired resonance or slight dullness is demonstrable, but this occurs only in the presence of massive involvement. Occasionally the note over the whole posterior chest may tend toward the tympanitic.

Auscultation usually offers the most reliable findings. The breath sounds are often entirely absent over collapsed areas or the respiratory sounds are weak and possibly higher pitched than normal. In other instances the breathing is exaggerated, and bronchial in character. Probably the most characteristic finding of pneumonia in these infants is the occurrence of fine sibilant or moist râles. These are often heard behind the lower lobes and are the most distinctive sign of the disease. The voice sounds are, as a rule, unchanged.

Diagnosis. -- Pneumonia may, in these infants, be easily confused with atelectasis. If the premature infant is strong and possesses a loud cry, congenital atelectasis may be excluded; in the weak the latter condition is most commonly present and the physical signs of pneumonia are absent. It must be remembered that the two conditions may exist side by side in the same infant. It may be necessary to make the infant cry or breath deeply by mechanical irritation in order to bring out the various abnormal sounds. A careful study of the history from birth may be of great assistance.

Prognosis. -- If the inflammation complicates infection in the upper air passages, such as rhinitis or bronchitis, the outlook is better than in primary pulmonary infections. Mixed infections with the influenza bacillus, staphylococci and streptococci, offer a more serious prognosis that primary pneumococcus. Involvement of a large portion of both lungs or an extremely weakened condition of the infant, both militate strongly against recovery. The younger the infant the shorter the intrauterine life the higher the mortality and when hypothermia exists death usually occurs soon. Cases which run their course with little or no temperature are usually fatal, probably because they occur in infants who are very feeble, of low vitality, with limited resistance to infection.

Treatment. -- Prophylaxis. -- The prevention of pneumonia in the premature requires that the little weaklings shall be protected against infection from every source. The lungs are most frequently the site of bacterial invasion, as there the organism finds a most favorable medium for its growth. In the adult there exist at the entrance to the respiratory tract defensive agents capable of stopping the invading bacteria but in the premature these defenses are absolutely rudimentary and consequently offer but slight impediment to the entrance of pathogenic germs (Delestre [14]).

The transmission of respiratory infections occurs by means of infected hands or other objects or through the medium of air. No one suffering from any infection of the nasal or respiratory passages should handle the infant. If the mother is affected with a coryza or bronchitis she should take care that her hands are not contaminated with nasal or bronchial secretions and that she does not breathe, or especially cough, in the face of the infant. A mask must be worn by the nurse or mother if she has a respiratory infection. In institutions where many babies are taken care of by one nurse, the hands of the attendant should be washed before the handling of each baby. Isolation of the premature should be practised if respiratory affections exist among other members of the family, or in the common wards if the infant is in an institution. Only if the attendants are thoroughly trained in the principles of aseptic nursing is it safe to leave the infant in close proximity to others suffering from respiratory affections. These of all infections are hardest to prevent. All utensils should be individual and should be sterilized before use; feeders, spoons, glasses, nipples, bottles, stomach tubes, etc., must all be boiled before they touch the child or its food. The French insist on the restricted use of the incubator in the management of premature and weak infants when the closed type is used, and believe that their success in the handling of prematures depends upon the fact that they remove them from the closed incubator as soon as the body temperature reaches 37° C. and their vitality permits. As soon as these babies can be removed from the incubators they are kept in large, well-ventilated rooms, which are not overheated. They should be given the benefit of open air and sunshine as their development warrants. In favor of the open-air treatment is the fact that most of the late deaths occur during bad weather. The mortality drops with improved atmospheric conditions.

General Treatment. -- The treatment of pneumonia is preëminently that of watchful expectancy, and overtreatment must be avoided, as these feeble infants are unable to withstand overmanipulation or stimulation. As a rule, pneumonia in robust infants is an acute self-limited disease, but in premature infants the course is apt to be somewhat sub-acute without the tendency to limitation. The indications in the treatment are to support the heart and conserve the strength. The feeding problem is difficult at any time in the premature and during an attack of pneumonia it becomes doubly difficult.

The hygeine of pneumonia requires that the child receive plenty of fresh air, and to insure this in an incubator of the closed type is difficult. The use of the open type in part overcomes this difficulty. The position of the child should be changed frequently in order to obviate any tendency to hypostasis. If the sick infant has been housed in a closed incubator with questionable ventilation it should be removed to an open, well-heated room, and placed in a properly warmed crib or incubator bed. The prime indication is for the promotion of elimination and sufficient administration of inert fluid. Stimulation of the respiratory tract is best accomplished by mild counterirritation to the chest and the use of hot applications to the extremities. The use of drugs such as cardiac and respiratory stimulants is not to be regarded with favor but strychnine sulphate in 1/500 grain (0.00012 gm.) doses, or atropine sulphate in 1/2000 to 1/3000 grain (0.00006 to 0.00002 gm.) doses given hypodermically may be of some help. The use of whisky or brandy is permissible in quantities varying from 3 to 10 drops every two or three hours depending upon the indications. Aromatic spirits of ammonia in 1 to 5-drop doses is one of the best stimulants at our command. Both the whisky and the ammonia should be given well-diluted in at least 8 parts of water. In cases of emergency, of sudden heart failure or of weakness accompanying a sudden fall in temperature, the use of camphor-in-oil 2 to 10 minims to the dose given hypodermically will be found to be a rapidly acting, reliable heart and respiratory stimulant.

If the infant shows a marked rise in temperature the use of hydrotherapy may be considered. Temperatures up to 103° F. are well borne, and do not require interference. As a general rule the temperature tends to remain subnormal in these weaklings and cool or even tepid baths must be avoided and instead warm or hot mustard baths resorted to. Even if there is an excessive amount of fever, should it be accompanied by a cold surface, feeble pulse and shallow respirations, cold is contraindicated. The best hydrotherapeutic measure used for the reduction of an unduly high temperature is the tepid pack. The use of cold baths or packs is probably never justified in the premature or weak infant. The temperature of the tepid bath may range from 100° to 105° F., depending upon the condition of the child.

The treatment of attacks of collapse with cyanosis, which are so frequent in the atelectatic prematures, should be prompt. The infant should be immediately placed in a mustard bath (one teaspoonful of powdered mustard mixed with one gallon of tepid water being of sufficient strength), of about 102° to 106° F. together with gentle massage. Respiratory and cardiac stimulants may be needed. Oxygen should be administered continuously.

Disturbance of the nervous system, occasionally so prominent in older and stronger children, is not marked in the premature during a pneumonic process. When present mild hydrotherapy offers the best results.

The use of the coal-tar products is contraindicated.

The diet is an extremely important part of the treatment of pneumonia and will be considered under "The Feeding of the Premature."

Frequent changes at regular intervals of the infant's position in its bed are imperative to successful care of the pneumonias in the premature.


Fig. 151 thumbnail

Fig. 151. Specimen of thymus gland weighing 40 gm., and resulting in thymic death.

Fig. 152 thumbnail

Fig 152. Congenital atelectasis. Magnification of 6 diameters.

Fig. 153 thumbnail

Fig. 153. Diffuse congenital atelectasis.

Fig. 154 thumbnail

Fig. 154. Incomplete diaphragmatic hernia (case of Dr. Irving Stein). Roentgenogram taken three and six hours after ingestion of bismuth. Stomach and bowel in chest.

Fig. 155 thumbnail

Fig. 155. Incomplete diaphragmatic hernia (case of Dr. Irving Stein). Roentgenogram taken soon after death with postmortem injection of bismuth in the bronchi. Only lower lobe of right lung admitted the bismuth emulsion. The gas distension of the stomach and bowels here beautifully portrays the extent of eventration.


[1] Le Progrès médical, 1912, 40, 88-89.

[2] La médicine infantile, 1912,16, 210.

[3] Am. Jour. Dis. Child., 6, 38.

[4] Congenital Disese of the Fetus, Springer, Berlin, 1909.

[5] Diseases of the New Born, Springer, Berlin, 1914.

[6] Leitfaden der Säuglingskrankheiten, Marcus and Webers, Bahn, 1914.

[7] The Nursling, Caxton Pub. Co., London, 1907.

[8] Jahrb. f. Kinderh., 1908, 67, 589.

[9] Diseases of Infancy and Childhood, D. Appleton & Co., New York, 1913.

[10] Über den Hospitalismus der Säuglinge, Berlin, 1913.

[11] Ztschr. f. Kinderheilk., 1919, 20, 212.

[12] Jahrb. f. Kinderheilk., 1914, 79, 140.

[13] Path. Anat. Arbeiten, Berlin, 1903 (Hirschwald).

[14] Étude sur les infect. des prématures, Thèse de Paris, 1901.

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